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' ■Uiliiilll:-'- 'ijlliliililIinK iilliiiijiiiiiiiii " iiillllimiiuiii nifiiiiiniilDit ; iiiilliitii: ; ,!:rtrii:i" ".iiimiii-' .ttttllttf.'.: HUlin:; : .'.iniiiii . iiiiinii- ma liSBSBSBWP" iijJafiamiSsr»' -■\ J .it:!^^f™ .# 5!K* THE LIBRARY OF THE UNIVERSITY OF CALIFORNIA PRESENTED BY PROF. CHARLES A. KOFOID AND MRS. PRUDENCE W. KOFOID ESSENTIALS OF TROPICAL MEDICINE. BALE'S MiiDlCAL BOOKS AND JOURNALS. ESSENTIALS OF TROPICAL MEDICINE BY WALTER E. MASTERS, M.D.Brux.. m.r.c.s., L.R.c.p.Lond. Graduale of the Loiidoi School of Tiopical Medicine, Felloiv of the Society of Tropical Medicine and Hygiene, Fellow of the Koyal Geographical Society, Graduate and Felloiv of the Royal Institute of Public Health, Graduate and Member of the Royal Sanitary Institute, Late Medical Officer, Colombia, South America, Late Medical Officer, Belgian Congo, Late Surgeon, Whifps Cross War Hosfital, Present Rledical Officer, Gold Coast, Il'est Africa Xon^ou JOHN BALE, SONS & DANIELSSON, Ltd. OXFORD HOUSE 83-91, GREAT TITCHFIELD STREET, OXFORD STREET, W. i 1920 % vl(Ai LONDON : JOHN BALE, SONS, AND DANIELSSON, LTD. 83-gi, GREAT TJTCMFIEI D STREET, W.I. PREFACE. The subject of Tropical Medicine, considered in its broadest sense, has become vaster tlian any other specialized branch of the Medical Sciences. The comprehensiveness of the subject is only irealized when one undertakes a course of study at one of the Tropical Schools, a course particularly essential, but all too short in order to become acquainted with the various branches of the subject. The student finds that he must gather together his knowledge from as many imposing text-books in the three or six months of his study as he required for the whole of his cjualifying examinations, a task almost impossible in the lime. Also the busy tropical practitioner, who requires adequate essential information, cannot consult libraries or include large volumes in his limited equipment, and if he had them he would find it a somewhat laborious task to peruse them for the few essential facts he needed to know. This work contains nothing new. It is not intended to sub- stitute any other work. It is a digest of our knowledge of Tropical Medicine, including Skin Diseases, Eye Diseases, Venoms, Hygiene and Laboratory Hints in a form handy for ready reference : the vade-mecum of the student and busy tropical practitioner. It was commenced for the sole use of the writer, but it has been suggested that its utility would be appreciated in a wider field. In tlie event of another edition being- required the writer would welcome any suggestions for its improvement from medical men. For the illustrations the writer is much indebted to the authors of the following works and to the publishers through whose courtesy their loan was made possible : — " A Handbook of the Gnats or Mosquitoes, including a Revision of the Anophelin^e." By Lieut. -Col. George M. Giles, M.B.Lond., F.R.C.S.* Album of Photographs issued by the South Indian Branch of the B.M.A. Compiled by Major P. C. Gabbett, I. M.S.* " Amoebic or Tropical Dysentery : its Complications and Treat- ment." By W. Carnegie Brown, M.D., M.R.C.P.* "Beriberi." By Edward B. X'edder, A.M., M.D. New York: William Wood and Co. " Laboratory Studies in Tropical Medicine." By C. W. Daniels and H. B. Newham.* VI PREFACE " Reports of the Sleeping vSickness Commission of the Royal Society." By F. W. Mott, M.D., F.R.S.* " Researches on Egyptian Bilharziosis." Bv R. T. Leiper, M.D., D.Sc* " Sprue and its Treatment." By W. Carnegie Brown, M.D.* "The Animal Parasites of Man." By H. B. Fantham, M.A. Cantab.; J. W. W. Stephens, M.D.Cantab.; and F. V. Theobald, iAL A. Cantab.* " The Diseases of Warm Countries." \\\ Dr. B. Scheube.* "Webster's Diagnostic Methods." Philadelphia: P. Blakiston's Son and Co. "Tropical Medicine and Hygiene." Bv C. W. Daniels, ALB., F.R.C.P.Lond.* " Venoms : \^enomous Animals and Antivenomous Serum- Therapeutics." By A. Calmette, M.D.* W. F. M. London, 1920. * London : Bale, bons and Danielsson, Ltd. CONTENTS. SECTION I. Diseases Dle to Protozoa ... ... ... ... ... ... 1 SECTION II. Diseases Due to Bacteria ... ... ... ... ... ... 161 SECTION III. Diseases Due to Helminths 226 SECTION IV. Diseases of Uncertain Etiology ... ... ... 327 SECTION V. Diseases Due to Venoms and Poisons ... . . 419 SECTION VI. Diseases of the Skin ... ... ... ... ... ... ... 458 SECTION VII. Diseases of the Eyes ... 508 SECTION VIII. Troimcal Hygiene, Sanitation, &c. ... ... ... ... ... 530 SECTION IX. Laboratory Hints ... ... ... ... 603 APPENDIX 667 ESSENTIALS OF TROPICAL MEDICINE. SECTION I. DISEASES DUE TO PROTOZOA. INTRODUCTION TO PROTOZOOLOGY. MODES OF TRANSMISSION OF PROTOZOAL DISEASES. RELAPSING FEVER. SPIROCH.ETOSIS ICTEROH/EMORRHAGICA (WEILS DISEASE). NOTES ON TICKS. FRAMBCESIA TROPICA. THE DYSENTERIES. Amcebic. CiLIAR, Leishmanic. (See Kala-azar.) Laveranic. (See Subtertian Malaria.) PSEUDO-DYSKXTERIES. (See PSEUDO-DYSENTERIES. ) LIVER ABSCESS. AMCEBIC ABSCESS. TROPICAL LIVER. THE LEISHMANIASES. Kala-azar. Infantile Kala-azar. Dermal Leishmaniasis. Differentiation between Kala-azar and Oriental Sore. Naso-oral and Oro-phalangeal Leishmaniasis. Canine Leishmaniasis. Pseudo Kala-azar. M.ALARIA. The Malarial Mosquito. TRYPANOSOMIASIS. African Trypanosomiasis. South American Trypanosomiasis. The Tsetse Fly. Notes on Mammalian Trypanosomiasis. T 2 DISEASES DUE TO PROTOZOA DISEASES DUE TO PROTOZOA. INTRODUCTION TO PROTOZOOLOGY. The Protozoa are now definitely proved to be factors of the greatest importance in the causation of Tropical Diseases. It is essential that all tropical practitioners should be acquainted with the outlines at least of their life-history and comparative pathology. One only has to mention such diseases as malaria, kala-azar, trypano- somiasis, framboesia tropica, and relapsing fever to indicate the large amount of tropical pathology coming under this head. DEFINITION. Protozoa are unicellular organisms, occurring singly or in clusters, either non-parasitic, parasitic on the lower animals only, parasitic during part of their existence, or parasitic in different animals during different stages of their development, and reproducing themselves — Asexually by binary fission (schizogony) ; Sexually by budding (sporogony); Sexually by rejuvenescence by conjugation. ORIGIN OF INFECTION. Very probably the primitive form of protozoon had some of the characteristics of the simple amoeba. This could be taken into the alimentary tract, from thence into the blood-stream, consequently facilitating blood-sucking insecta in carrying out their part in the transmission of the protozoa in question. The blood of man may have been infected from human intestinal excreta or from infective material coming from the intestinal tract of some invertebrate. The first form was undoubtedly non-pathogenic, pathogenicity probably beginning in bats and birds, followed some time later by pathogenicity in man, the intermediate links being lost. Some protozoa cannot pass through the placenta, e.g., the malarial parasite, while others can pass through and infect the foetus, e.g., the spirochcetes and treponemata. Many of the insect "carriers" infect their eggs, and thus hand down the infection to a new generation of blood-suckers. The hasmatozoan types may live — In the blood-stream free, e.g., trypanosomes ; In the red blood cells, e.g., malarial parasite; In the white blood cells, e.g., Leishman-Donovan body ; In the endothelial cells, e.g., Leishman-Donovan body. INTRODUCTION TO PROTOZOOLOGY 3 MORPHOLOGY. It may be that all protozoa have not yet been recognized, but some of those known are large, e.g., the Sarcocystid^e in muscle; and some are small, e.g., the Ikemoprotozoa. The protoplasm consists of — A clear hyaline ectoplasm ; A dark granular endoplasm. The protoplasm contains — One or more nuclei, a complex body of chromatin and achromatic substance. It may be single or divided into two — One controlling the function of nutrition — trophonucleus ; One controlling the function of motion — kinetonucleus, or A macronucleus which is trophic and kinetic ; and A micronucleus Avhich is purely reproductive. Chromidiosomes are smaller particles of chromatin which give rise to the chromidia, intra- or extra-nuclear. Metachromniic granules consist of chromatic grains in process of ana- or kata-bolism. Volutine granules contain nucleic acid and food material for the nucleus. Metaplasmic granules are products of cytoplastic ana- or kata- bolism. Centrosomes, one or two granules outside the nucleus essentially concerned in binary fission. Archoplasm, the clear protoplasm around the centrosome. Rhizoplast, that portion of the flagellum which penetrates into the cytoplasm. Vacuoli, their function may be — Respiratory and excretory ; Digestive and excretory. Protozoa move by pseudopodia, cilia, or flagella, or they may become quiescent and encysted. LIFE-HISTORY. Under favourable conditions of food, moisture, temperature, &c., reproduction is asexual and may follow the methods of — (i) Binary fission. This is single division of the nucleus into two portions, followed by the cytoplasm. (2) Gemmation. The nucleus divides into two or more portions, Avhich separate at the periphery, each being surrounded by a differentiated portion of the cytoplasm. 4 DISEASES DUE TO PROTOZOA is) Spore Formation. A quiescent body, the schizont, is formed. The nucleus and cytoplasm divide into a number of asexual spores known as merozoites, leaving, as a rule, a " nucleus de reliqual," or rest-bodv. These merozoites enter new cells in the host, where they grow into tropho- zoites, and complete ?.n asexual life-cycle or the cycle of simple schizogony. Under adverse conditions, such as scarcity of food in the host, &c., the merozoites develop into more resisting forms or gametocytes. In these latter female and male elements are separated. Such elements, nuclear, may remain in the same cell or separate cells. Usuallv the male element of one fuses — zygosis — with the female element of another and forms a new individual, with a single new nucleus known as a sporont. This reproduces itself rapidly by binary fission or spore formation, the resulting spores being known as sporozoites. (4) Parthenogenesis.. This is a form of reproduction from the female type of parasite as may take place in malaria. The female gametocvte can resist drugs in the body and lie dormant until taken up by a blood-sucking insect, when the nucleus and protoplasm will divide, one portion disappearing, while the other forms merozoites, and starts the cycle of schizogony agam. PATHOGENICITY. The pathogenicit}^ of protozoa is considered under the diseases caused by them. CLASSIFICATION. There are live groups : — (i) The Sarcodina (Rhisopoda). These move by a protrusion of protoplasmic processes, broad and blunt or thin and sharp. They may or may not be covered in part with shells. They multiply by budding or fission. Occasionally spores are formed. (2) The Mastigophora (FJagellata). These have specialized motile protoplasmic processes known as flagellum or flagella. The shape of the parasite is defined and covered with a membrane. They multiply by longitudinal fission. (3) Sporozoa. (A) Telosporidia. In these the spore formation is distinct from and later than the trophic phase of the life-cycle. INTRODUCTION TO PROTOZOOLOGY (B) Neosporidia. The spore formation and trophic growth proceed simultaneously. (4) Ciliata {Infusoria). These possess cilia throughout their whole existence or only during the early stages of their life-cycle. The cilia are formed from the ectosarc only. Reproduction is by transverse fission and budding. Protozoologists may decide upon a rearrangement of this classi- fication later. Protozoa of pathogenic significance in man may be grouped as follows : — (i) Sarcodina. Pathogenic amoeb^u are dealt with under Amoebic Dysentery. The Chlamvdophrys stercorea, a rhizopod, is believed to be an ama:ba parasitic in man during one stage of its existence. It has been found in cows, rabbits, mice and lizards, (2) Mastigophora. The Cercomonas hominis is a rounded or pear- shaped single flagellated parasite found in normal faeces, also in the excretions of diarrhoea and cholera patients. The Cercomonas vaginalis is a similar parasite not uncommonly found in the vagina of Cingalese native women . The Tetramitus mesnili has a pear-shaped body with three flagella and a large cytostome. It may cause diarrhoea and dysentery. It has been seen in people from the Crimea, Bahama, Hawaii and West Africa. Trichomonas hominis may be found in some diarrhoea patients. Trichomonas vaginalis has been found in Central Africa, Ceylon and Kurope. Its name is descriptive. Its presence does not necessarily give rise to symptoms. Lamblia intestinalis with its pear-shaped body carries three flagella from its broad end and one from the narrow end. It has been found in the rabbit, cat, dog, sheep and large bowel of man. Its cysts can be found m the faeces. Pathological changes are not severe. Treatment is difficult. The Peucocytozoidae.are not found in man. The Trypanosomidae are dealt with under special headings. The Herpetomonas (Leptomonas, Crithidia) are not found in man. Trichomonas iu' testinalis from man, showing an- terior flagella, cyto- stomic depression anteriorly, undula- ting membrane, nuclei, and axo- style. X 2,500. Original. 6 DISEASES DUE TO PROTOZOA The Leishmania are dealt with under the Leishmaniases. The Histoplasma capsulatum is a round or oval parasite enclosed in a refractile capsule with an acentral nucleus and chromatic particles causing an acute specific disease known as Histoplasmosis. The parasite is found in the endothelial cells of capillaries and smrill blood- vessels in the liver, spleen, lungs, intestine and lymphatic glands as well as in the leucocytes. It causes an irregular fever characterized by disseminated hyaline pseudogranulomata in the lungs, splenomegaly, necrotic areas in the liver, ulceration of the large nnd small intestine, severe ana?mia, and with it a marked leucopcenia. Dr. Darling discovered it at Panama in igo6. Nothing is known as to treatment. Babesia has not been found in man with the doubtful exception of Babesia hominis in Spotted Fever of the Rocky Mountains (Manson, 1903)- Sambon believes that Blackwater Fever is caused by a minute babesia. See " Blackwater Fever." The Plasmodidai pathogenic to man are dealt with under Malaria. Pathogenic Spiroch^etes are dealt with under Relapsing Fever. The Treponema pertenue under Frambocsia tropica. (3) Sporozoa. (A) Telosporidia. Coccidium oviforme (Eimeria stieda?) occurring in the liver and bile ducts of rabbits has been found five times in man. In these cases there were : fever, enlarged liver and spleen, both of which contained coccidia, the infection of the spleen being probably via the blood- stream. H^mogregarines, in all probability, never occur in man. (B) Neosporidia. Sarcocystis tenell?e bubali is common in bufifalo meat in Ceylon, the parasites being known as "milk nerves," which appear as white patches lying amongst the muscle fibres of tlie tongue, larynx, diaphragm and skeletal muscles. The ingestion of the spores may cause : Irregular fever in man. S. lindemanni and S. muris have been described in man upon several occasions. There are — Regular fever, myositis, sometimes necrosis of muscle fibres. Spores may be found in the blood, and the parasites should be searched for amongst the muscle fibres. They are found normally in warm-blooded animals. In them the spore formation commences early and continues until a large size has been attained. The spore has two coats, a number of fibrous sectors dividing the spore, and remaining continuous with the inner coat. No human has died from the disease. MODES OF TRANSMISSION 7 Sarcosporidiosis was proved in a Barbadian negro; the sporozoa were found in a portion of the biceps muscle (Darling), but the disease aborted in three weeks, leaving the patient free. Rhinosporidium seeberi is similar to tlie above, but has a well- defined sporoblast. The parasite has been obtained from nasal polypi and penile papilloma (Ingram). The growth has a raspberry appear- ance, with white spots on a general red background. The dots are the cysts. The irritation of the parasite causes proliferation of the mucosa and sub-mucosa of the affected part. The source of the infection is unknown. The condition is known as Rhinosporidiosis. It has been seen in South America, India and Ceylon. The treatment is to remove the growth and cauterize the base. Balantidium coli and minutum cause diarrhoea and abdominal pain in man (enterocolitis). See the Dysenteries. (4) Ciliata. Numerous forms of ciliated protozoa existing in man but not pro- ducing any symptoms are not dealt with here. MODES OF TRANSMISSION. Insects become infected witii animal parasites in various ways : — (i) Insects suck up parasites with the blood when they are feeding upon that medium. Such parasites develop and multiply in the insects and are later injected into man during the act of drawing more blood. (2) The development of the parasite taken up with the blood may continue in the eggs of the host, which process of development is not completed until the eggs are hatched. Young ticks, having developed from an infected egg, may bite a warm-blooded host and infect him, although it has not previously fed on infected matter. This process takes place in the case of the piroplasma and spirochete. (3) Parasites drawn up with the blood may develop in the alimentary tract of the insect and infective sporozoites may be passed with the feces . (4) Larve of the invertebrate host living in water may become infected directly by means of their food. These larve and their ingested parasites develop simultaneously, so that by the time maturity of the insect is reached the parasites are very numerous. Such parasites may then be passed with the feces and live independently, to enter into other larve later. Flagella may thus be transmitted. This method applies not only to protozoa, but also to metazoa and bacteria. The following facts show briefly how the most important protozoal diseases are transmitted : — 8 DISEASES DUE TO PROTOZOA (i) The malarial parasites, P. vivax, P. malariie and P. falciparum have their reservoir in convalescents from primary attacks and for weeks after such attacks; the parasites leave the host, man, by blood drawn up by blood-sucking insects; the sexual stages or external development of the parasite takes place in some species or anophelines ; it re-enters man with the saliva of the biting mosquito. (2) In Yellow fever the parasite is not known, but the reservoir is the blood in the early stages of the disease; it leaves the host like the above; passes its external phase in a mosquito, Stegomyia calopus; and re-enters man by mosquito bites about ten days after feeding on infected persons, after which period the mosquitoes have become infective. (3) In Dengue fever the parasite is not known ; its reservoir is human blood, and is carried away with the blood by the Stegomyia calopus or Culex fatigans ; re-infecting man by the mosquito. (4) In Trypanosomiasis the parasite, Trypanosome gambiense or T. rhodesiense, has its reservoir usually in man in the former instance and usually in wild game in the latter case; it leaves the host with the blood; passes its external life in the Glossina palpalis or G. morsitans ; and re-enters man eighteen days or more after the fly has fed on an infected person by biting and sucking blood in the ordinary way. (5) In Kala-azar the parasites, Leishman-Donovan bodies, prob- ably have their reservoir in man ; leave the host in the leucocytes with the blood ; pass their extra-corporal life in bed bugs, Cimex rotundatus, and re-infect man by the bites of these bugs. (6) In Relapsing fever the parasite, Spiroch^ete recurrentis, has its reservoir usually in man ; leaves the host by the blood plasma ; passes its external life probably in the Pediculus, and re-infects man by its bites. (7) In African Tick fever the parasite, S. duttoni, has its reservoir in man or a progeny of infected ticks ; leaves man in the blood and saliva; passes its external life in the Ornithodorus moubata and re- enters man by its bites. (8) In SpirochcBtal diseases, Yaws, S^philis and some ulcers, the parasites, S. pertenuis and S. pallida, have their reservoir in man; leave the host by the discharges; have no external development, and re-infect man by contact usually with an abraded surface. (9) In Amoebic dysentery the parasite. Entamoeba tetragena, has its reservoir in convalescents from the disease, leaving the host in the fasces in an encysted form ; further developing while encysted, in earth, water or dust; re-infecting man by the mouth in water, milk, food, &c., contaminated by the parasite. RELAPSING FEVER 9 RELAPSING FEVER. DEFINITION. An acute infectious disease or group of diseases: — Caused by the SpirochcTtes, S. recurrentis, S. novyi, S. duttoni, S. carteri. Transmitted by bed bugs, body lice and ticks. Characterized by sudden onset, definite course (r to 7 days), rapid subsidence and indefinite relapses. HISTORICAL. A relapsing fever was known to Hippocrates in Thasos, which he described. The next notice of it was by Rutty of the Dublin epidemic in 1770. In 1873 Obermeier published his discovery of the causative spiro- ch^ete during a Berlin epidemic. In 1897 Tictin proved the bed bug as a carrier. In 1904 Philip, Ross and Milne in Uganda discovered that the tick Ornithodorus moubata was the carrier of the African Tick Fever. Dutton and Todd in the Congo confirmed this, and proved that the parasite could pass into the egg and larva, thus infecting succeed- ing generations. Napoleon's Grand Army was attacked by it in the great retreat from Moscow. The allied Armies were affected by it during the Crimean War, and both armies suffered from it in the Russo-Turkish War. DISTRIBUTION. Relapsing Fever is found in Europe, Asia, Africa, North, Central and South America, and probably in Australia. The Relapsing fever of Europe is caused by S. recurrentis or obermeieri ; The Relapsing fever of America is caused by S. novyi ; The Relapsing fever of Asia is caused by S. duttoni ; The Relapsing fever of Africa is caused by S. carteri. The number of the spirochaetes present in the peripheral blood during infection is variable according to the type of parasite; thus in the African type the infection is light, in the European type it is heavy, and in the Indian type it is variable. The different types will now be considered seriatim. EUROPEAN RELAPSING FEVER. ETIOLOGY. The causative organism is S. recurrentis (obermeieri), which is found in the peripheral blood during attacks, but is usually absent between them. Its absence from the peripheral blood during apyrexial 10 DISEASES DUE TO PROTOZOA periods is due to the formation of antibodies such as agghitinins and parasiticidal substances, but some spiroch^etes resist this attempt at cure and cause a relapse when they are in sufficient numbers. Resistant types of spirochastes develop during and after an attack. Spiroch^etes are usually present in the peripheral blood from the onset of the fever until the crisis, then suddenly and totally disappear, possiblv collect- ing in the spleen. They have never been found in the excretions or secretions. Some immunity is caused after an attack, but onlv for that specific spirillum. Gozony concludes that infection is possible through the damaged skin, healthy mucous membrane of the alimentary or genital tract, or possibly by the conjunctiva}. It is proved that the parasite is carried by the bed bug, Cimex lectularius, and lice by direct inoculation. The spiroch^etes multiplv by longi- tudinal and transverse fission. They are hereditarily transmitted from adult to young lice, and are thus maintained in nature. The infection can be transmitted from mother to foetus. On this point Nattan-Larrier, Breinl and Kinghorn conclude that — Both S. recurrentis and S. duttoni have been proved to transmit infection to the foetus in 80 per cent, of cases, but the number of spirochastes penetrating the placenta is not great ; this fact would explain the long incubation, small blood infection and short persistence of the parasite in the blood in these foetal infections, but their virulence is not attenuated. When pregnancy is nearing the end there may be a serious illness with death of the foetus in utero. No lesions of the uterus are necessary to facilitate the passage of the spirochaetes. Very little immunitv is given to young born of an infected mother. INCUBATION. Two to ten days, never after the fourteenth day, sometimes on the same day. SYMPTOMATOLOGY. Onset. — This is usually sudden with rheumatic-like pains, head- ache and constipation, which sometimes precede the rigors. There is severe frontal headache, pains in the back, limbs and epigastrium; weakness, giddiness, convulsions in the young, flushed face, injected conjunctivae, fever to io3°-io4° F., pulse-rate to 1 10-120, respirations increased, sometimes nausea and vomiting. Course. — The skin becomes yellowish, hot and moist. There is often a rose-coloured macular eruption on the thorax^ abdomen and legs for one or two days. The temperature keeps up until the eighth day, third to fourth day in Serbian cases. EUROPEAN RELAPSING FEVER ix There is thirst, nausea and vomiting of yellow-green matter. Constipation is common, but diarrhoea is rare. The liver and spleen are enlarged and tender. The pulse is 120 to 140, but not dicrotic. Respirations are 48-50. Red cells and Hb. are diminished. There is leucocytosis of the polymorphs. Spirocha?tes are found in the peripheral blood and engulfed in the leucocytes. A troublesome cough is common with rales and a scanty expec- toration. Muscle and joint pains continue and cause sleeplessness. Delirium is not uncommon, stupor is rare. The urine is febrile and often contains a little albumin. Sometimes herpes labialis is seen. There may be rose-coloured spots on the trunk and limbs. Crisis. — This takes place on the sixth or seventh day, usually by rigor. There is a violent perspiration and sometimes diarrhoea. Epistaxis is not uncommon. There is a sudden fall of temperature, pulse-rate and respirations, then a deep sleep, followed by rapid improvement. Sometimes there is a dangerous collapse at the crisis with old people. Intermission. — All appears to be normal, but it is the exception for the disease to end here. The patient usually desires to leave the hospital. About the fourteenth day from the onset there is a Relapse, with rigor and severe symptoms as before, lasting three or four days. The urine is increased, the pulse-rate goes up, and the prostration is often marked. The termination is by crisis which may end the illness. If there are more relapses, which is common, they become gradually milder in severity. The second relapse occurs about the twenty-first day from the onset, is milder, and lasts about three days as a rule. Convalescence is sometimes slow. COMPLICATIONS. Bronchitis, pneumonia, dysentery, diarrhoea, ha^matemesis. Cerebral haemorrhage, conjunctival haemorrhage, iritis, irido- cyclitis, corneal ulcers. Abortion during the tirst relapse is common. Nephritis, otorrhoea, neuritis, parotitis and adenitis are not un- common. Meningism, paresis with spasticity of lower limbs. Recurrent myocarditis, followed always by death (van Hoof). 12 DISEASES DUE TO PROTOZOA DIAGNOSIS. In the early stages one must differentiate it from Malaria, Typhoid, Typhus, Yellow fever. Seven-day fever and Influenza. The following are the main points to watch : — (i) For spirochaetes in the blood. (2) Malarial parasites in the blood. (3) Agglutination ; add a drop of suspected serum to a drop con- taining spirochastes, mix, cover with cover-glass, seal, incubate at 37° C. for half an hour. Clumping of spirocha?tes into non-motile masses is positive. (4) Typhoid by absence of leucocytosis. (5) Typhus by absence of spirochaetes, agglutination test and presence of rash. (6) Yellow fever by black vomit (7) Seven-day fever by slow pulse and absence of spirocha?tes. (8) Influenza, from a mild attack of Relapsing fever, not easy to differentiate apart from absence of spirochaetes. Relapsing fever may co-exist with Malaria, Small-pox, Measles, Plague. Diphtheria and Scurvy after famines. PROGNOSIS. This is good. Mortality 4 per cent, in Europe, 14 per cent, in Egypt (Sandwith). Marked jaundice is bad. Pregnant women usually abort. Death may be caused by : Toxaemia during the first attack ; collapse during the intermission ; complications intervening. TREATMENT. Rest in bed is essential. Salvarsan, neosalvarsan, galyl or kindred preparations are specific, and should be given intravenously or intramuscularly; the former is better. These drugs have revolutionized the treatment of these fevers. One should begin with small doses as some patients stand them badly, say with 0*30 grm. Relieve pains with salicylates, aspirin, antipvrin and quinine. Opium or morphia may be necessary. Vomiting with ice, champagne, bismuth mixture, morphia and codeine. Epigastric pains with fomentations sprinkled with opium tincture. Cough by codeine and heroin or expectorant mixture. AMERICAN RELAPSING FEVER 13 Constipation by laxatives and enemata. High temperature by cool sponging. Give appropriate feeding during the intermission. A serum has been promised. PROPHYLAXIS- Keep bugs, lice and biting insects away from the patient. Wooden bedsteads should be abolished and iron ones substituted. Practice the strictest cleanliness, disinfect clothing, houses, &c. Doctors, nurses, hospital attendants and laundry hands are very liable to attack. ~ - _ . MORBID ANATOMY. There is an enlargement of the spleen, five or six times its normal size, and may weigh five or six pounds. On section it is dark coloured^ soft with enlarged follicles, showing congestion and a cellular increase. There may be minute abscesses and wedge-shaped infarcts. The liver is enlarged up to five pounds in weight, the lobules are poorly defined with cloudy swelling, fatty infiltration and leucocytic infiltration into the portal system. The kidneys are enlarged, congested, cloudy swelling, and fatty degeneration. The stomach is congested. The heart is soft and flabby. The bronchi are congested, frothy mucus, lungs hypostatic con- gestion. The brain is congested. All the viscera may be stained vellow with bile. The bone marrow is hyper^emic. Sometimes there is a submucous petechias. AMERICAN RELAPSING FEVER. It is present in North, Central and South America. In the two latter instances the fever is similar, but the spiroch^ete has not yet been definitely classified. ASIATIC RELAPSING FEVER. The causative parasite is the S. carteri. The carrier is unknown. The disease has long been endemic in India, commonest in the Bombay Presidency. Infected bugs can convey the disease to monkeys, but Rogers suspects mosquitoes as human carriers, while Mackie favours Pediculus capitis. The spirochcetes are found in the blood during the acute attack, 14 DISEASES DUE TO PROTOZOA becoming more numerous towards the crisis, after which they com- pletely disappear. They are not always seen during the relapse, and may not be found at all during a typical attack. On the other hand, they have been known to be so numerous that the circulation of the blood has been hindered and a dusky lividity caused (Carter). Rigors are usually absent in this form. After the crisis, instead of feeling better, there is more often collapse, sometimes resembling that in a cholera patient. There is much debility. TIME MCMCMEMCMCMCMCMEMCM^MCMtMCMCMCHCMCMtMtMCMC r* ,I'_L,jA X^A 1 f\ IlZ^A ' : t "^-i I- J v4LV ^^ ~ " '" ,'- \ ^ '" + > _.-_U 1 J._A_Ac-^ 4- :! t==~= :::::ij^? +!: :!:!_:::::""s^'- M - ± ^t _ __ Relapsing fever. Indian. In 16 per cent, of cases there is a sudden rise of temperature during the first intermission period when spirochaetes are not found in the blood. Haemorrhage from the stomach and intestines is more common than in the other forms. Parotitis is present in 10 per cent, of cases. Bile in the urine is scanty. Epistaxis occurs in from 10 per cent, to 15 per cent, of cases. Vomiting of bile occurs frequently, 70 per cent, to 80 per cent. Diarrhoea is present in 10 per cent. Maniacal symptoms are known. The first relapse occurs about the fourteenth day from the onset, seventh day from the intermission. The second intermission may last longer than the first ten days. Second relapses are common, but the liver does not so markedly enlarge, and the crisis is not so well marked. A third relapse may occur after a secondary intermission of ten to seventeen days. The percentage of relapses to be expected can be seen from the following table : — With one relapse, 49*2 per cent. With two relapses, 20 per cent. With three relapses, 5 per cent. With four relapses, 2 per cent. ' In some cases the attacks may be more prolonged, irregular, AFRICAN RELAPSING FEVER 15 ending by lysis and ^vilh marked jaundice, 70 per cent, to 80 per cent, of cases. The mortality is higher than in the others, 18 per cent. In Bombay, 30 per cent, to 40 per cent., according to Daniels. Sudden death from heart failure is common. Heart stimulants should be given and collapse avoided by camphor, ether, strychnine, hot bottles, blankets, &c. AFRICAN RELAPSING FEVER (African Tick Fever). The causative organisms are S. duttoni and S. recurrentis (obermeieri) in West, East and Central Africa. The carriers are Ornithodorus moubata and Pediculus humanus. The disease is present in Angola, Congo State, Uganda, German East Africa, Portuguese East Africa and the Zambesi Valley. C Spirochoeia duttoni, a, blood form showing slight membrane ; &, granules or coccoid bodies clearly formed within the organism ; c, beginning of extrusion of coccoid bodies in the tick. (After Fantham.) The infection is by small spiroch^etal chromatin segments, which come from the lumen of the gut of the tick and contaminate the wound made by it. The chromatin segments pass into the wound as a result of the regurgitation of the gut contents or the Malpighian secretion, and also as a result of its faeces contaminating the abraised surface. Scratching after a tick bite is said to cause sufficient abrasion for the parasites to pass through the skin and cause the infection. i6 DISEASES DUE TO PROTOZOA There is often some local inllammatory reaction at the site of the bite. In this variety there is more vomiting and diarrhoea with blood- streaked stools. The spiroch^etes are very sparse in the blood, as compared with the other varieties, but heavy infections have been met with in Arabia. On the second day of the illness there is restlessness, thirst, splenic pain, cough, the temperature has a morning fall without any relief of the symptoms, and an evening rise. There may be delirium. The Hver does not enlarge, but the spleen does. There is polychromatophile degeneration of the red cells and a marked increase in the number of blood platelets. After the third or fourth day there is a crisis preceded by a pseudo- crisis. Relapses are very common, five to eleven, lasting three days each, and spreading over a month or more. All crises are preceded by pseudo-crises. In the relapses, oedema of the eyelids is a common feature. Iritis is a common complication. There is often an abrupt violent delirium (Porot). Some consider that there is a mild and a severe form of the disease. The mortality is not known, but it is generallv low. A rapid fall of temperature without improvement of the svmptoms usually indicates the approach of death. All Europeans should encamp 20 to 30 metres away from native huts, rest houses or caravans. The bed should be well above the ground, and a good mosquito net used with its lower ends well tucked under the mattress. In North Africa. In North Africa the causative organism is S. berbera, as a rule. It is probably spread by lice. It is common in Algeria, Egypt, Tripoli and Tunis. The surgeons of Napoleon's Army noticed the disease. The incubation is believed to be about twelve days. The fever reaches its height during the first twenty-four hours. The spleen and liver enlarge, but jaundice is generally absent. Vomiting is common, but not diarrhoea. Urethral Spirochcvtosis. ^lacfie found a case of acute urethritis on the Gold Coast due to spirochcete infection. The temperature was slightly raised and joint pains were troublesome. The name S. urethras was proposed for the parasite. SFIROCH.WrOSIS ICTERO HEMORRHAGIC A 17 SPIROCH.^TOSIS ICTEROH.EMORRHAGICA (WEIL'S DISEASE). DEFINITION. An infective febrile jaundice caused by S. icleroha^morrhagica and characterized by pyrexia, marked prostration, jaundice, albuminuria and haemorrhages. HISTORY. 1849, Larrey first described it. After him were several other French workers prior to Weil in 1886. 1914, Inada and Ito in Japan found the causative parasite. 1916, Martin and Pettit found the disease to be present amongst the French troops in Flanders. DISTRIBUTION. There are widespread epidemics in the United States. The disease is epidemic and endemic in Japan. It is also found in India, Africa, the Near East, and amongst the French troops in Flanders and on the Italian front. AETIOLOGY. The causative organism is the S. icteroh^emorrhagicae. They have been recovered from the blood and urine; from the former during the first days of the disease, and the latter from the ninth to the fifteenth day. They disappear at the end of the fifth week. They have also been found in the kidneys of the field rat, which animal is now held to be a reservoir host for the spiroch^etes. An immune body has been found during the disease in the blood which is said to destroy and dissolve the spiroch^etes. It is very difiticult to find them at all in some severe cases of the disease. Sera have been suggested for prophylaxis and treatment. Infection is probably by infected rats, passing infected urine and fouling the water and food such as could so easily happen in the trenches in Flanders. SYMPTOMATOLOGY. The incubation is doubtful, probably six to eight days. The onset is sudden. There are : conjunctival congestion, headache, general body pains, bilious vomiting, slight swelling of lymphatic glands, gastric disturb- ance, epistaxis (17 per cent.), fever, ioo°-i04° F., lasting ten to four- teen days, jaundice (60 per cent.) — this comes on the fourth or fifth day when present — albuminuria, constipation, liver and spleen slightly enlarged. Marked general weakness and prostration. 2 i8 DISEASES DUE TO PROTOZOA Herpes labial is (42 per cent.), which becomes hccmorrhagic. In severe cases liiere may be marked lic-umorrliages under ihe skin and from the mucous membranes. There is sometimes a secondary fever. Some workers describe a meningitis and claim lo have found tlie organism in the C.S.F. (Costa and Troisier). The attack lasts from ten days to three weeks. The attack may be so slight that few of the above svmploms may be present, while in severe infections all may be present and sudden death caused by rectal haemorrhages. In some cases the spiroch^etes seem to concentrate in the duodenum. There is inflammation of the mucous membranes and of the ])aj)il]a of Vater. The swelling causes obstruction of the bile flow along the common duct and jaundice results. In some cases the swelling of the affected mucous membranes causes mechanical obstruction of the bile in the liver itself, follow^ed by jaundice, or the swelling may be so slight that obstruction does not exist and jaundice is not seen. In any case the jaundice is not due to an increased formation of bile. PROGNOSIS. On the whole this is good, but marked haemorrhages are always bad. The mortality is under 6 per cent. On the Trentino and Isonzo fronts it was only 0*55 per cent. (361 cases). Some cases are so slight that only an inoculation of guinea-pigs will enable one to make a diagnosis at all. DIAGNOSIS. The spirochcCte can be recovered from the urine after the lenih day, but it is always difficult to find it even in centrifuged blood. An inoculation of a guinea-pig is preferable. Localized symptoms will exclude Gallstones and Cholecystitis. Blood cultures and Widal's reaction will exclude Typhoid and Paratyphoid. The spirochaetes can now be grown with comparative ease, hence as the sera of convalescent patients cause clumping — agglutination — 'of the spirochastes, we have an important diagnostic test. Severe forms of trench fever cannot be diagnosed from this disease in the slighter attacks when no jaundice is present. Acute yellow atrophy is not easy to exclude in some cases because we do not know the cause of it. It is suggested that one form of it may be caused by this spirochaete. NOTES ON TICKS 19 TREATMENT. As for Relapsing fever. Immune horse serum, three doses of 10 cc. each in the first twenty- four hours (Inada). Destroy all rats, especially those that are apt to foul water or food. Much of our knowledge may have to be revised and the above modified as we learn more about the disease. NOTES ON TICKS. Ticks belong to the Order of the Acarina, of which they are the largest specimens, always visible to the naked eye, and the females invariably larger than the males, some of the latter when engorged with blood being nearly half an inch long. They differ from insects by having four pairs of legs and in having the three parts of the body, thorax and head fused into one un- articulated mass. After impregnation the female attaches herself to the host, becomes enormously distended with blood, drops off, hides herself, deposits her eggs by thousands within two to ten days after leaving the host. After two to three weeks the eggs are hatched, the forthcoming larvae resembling minute moving grains of sand, with three pairs of legs, but no sexual orifice. The larva attaches itself to its vertebrate host, grows, moults, becomes a nympha with four pairs of legs, and a pair of stigmata behind the hindermost pair of legs. It moults thrice more and becomes adult. Then the sexes unite. After fertilization the male dies, but the female seeks blood. If blood cannot be found the female can fast for weeks, months or years, until blood can be found. The two families of ticks are : (i) The Ixodid^e, e.g., Ornithodorus moubata. (2) Agarsidse, e.g., Argas persicus. The former example transmits the spiroch^etes of African Tick Fever, and the latter of Miana disease, &c. Ticks are transmitters of important animal diseases due to Spiro- chastas and Babesise. Ornithodorus mouhata. It is found throughout Tropical Africa. The body is flattened, oval in outline, and greenish-brown in colour. The integument is hard, leathery, covered with closely set tubercles lined by grooves. It lives in native huts, hides during the day in cracks of walls, floors, thatched roofs, and is very active during the night. 20 DISEASES DUE TO PROTOZOA It attacks man and beast, feeds slowly; the victim must be asleep for it to receive a good feed which requires two to lliree hours. It deposits its eggs in batches of 50, 70, 100; these hatch in about Oniithodonis vioitbata. a. Ventral aspect ; />, dorsal aspect ; c, lateral aspect between second and third pair of legs. twenty days. The larval stage is practically omitted in this variety. After about thirteen days the eggshell splits, also the larval skin, and an eight-legged nymph throws off both covers simultaneously. FRAMBCESIA TROPICA 21 This tick is commonly found along the lines of travel, e.g., rest houses, caravanserai, &c. It may be carried long distances in bedding, mats, porters' cloths, &c. The natives protect themselves by applving cow dung to the floors and walls of their houses and by smoking the thatch. Pyrethrum powder is good when placed between the sheets. A little sprinkled down the backs of porters is a good measure. A night light is a protection. Argas pcrsicHS. This tick is in shape a flattened oval, yellowish green or red in colour, spotted on the back with many white granulations; its legs are a pale yellow, and the whole insect is much smaller than the one described above. Mouth-parts of Ixodes. Mouih-parts of Rhipicephalits It is found in Persia, Syria, Turkestan, Russia, China, Algeria and Cape Colony. It attacks poultry and humans. Its habits are those of O. moubata. In Persia it may so infest villages that the inhabitants may be driven out of it. FRAMBCESIA TROPICA (YAWS). DEFINITION. A tropical, specific, infectious and contagious disease due to the Treponema pertenuis, characterized by a yellow-tipped, granulomatous eruption. DISTRIBUTION. Originally it was purely an African disease, now it is widely spread. 22 DISEASES DUE TO PROTOZOA Africa. — Tripoli, Sudan, ^^>st Coast, Congfo State, Angola, Uganda, Rhodesia and Madagascar. Asia. — Malay Peninsular, Assam, Upper Burmah. Siani, Java, Batavia, Philippines and Ceylon. In Ceylon the average admitted per annum over lo years was 3,500. America. — West Indies, British Guiana, \>nezuela, Colombia, Brazil. Some of the Southern United States. Australia.— North Australia, Samoa, New Hebrides, Xew Cale- donia, Fiji, New Zealand and Tasmania. THE CAUSATIVE AGENT. The organism is a spirillum, the Treponema perlenuis (Castellani, I905)> 18 to 20 /J, long, with six to twentv fine uniform coils as shown by Leishman's stain (for five minutes, tlien with water admixed and stained for one to four hours). It is more difficult to stain than T. pallidum; the difference between the two must be based on biological tests. Its presence is constant in the primary lesion or '" mother yaw " and in the un- broken papules of the general eruption. It is also found in the spleen, lymphatic glands and bone marrow. It has not yet been seen in the blood, but its presence is certain, because when monkeys are injected with blood from an infective person it will develop typical yaw lesions. It has not been found in the C.l^. fluid or the tertiary lesions. Treponema fericuiic. (After Castellani and Chalmers.) Multiple infection of the ulcers is very speedy HISTOPATHOLOGY. The surface epithelium is greatly thickened over the site of the papules. The corium is the site of a marked oedema. There is an infiltration by millions of plasma cells; as a matter of fact, there is nothing else (Macleod). There is no perivascular mononuclear infiltration as in Syphilis, or any endothelial proliferation in the vessel walls. Giant cells are absent, but they are present in syphilitic lesions. A well-marked hyperkeratosis is seen. The parasite is chiefly found in the epithelial layers (after Leish- man's stain). FRAMBCESIA TROPICA 23 SYMPTOMATOLOGY. ■ The symptoms last six to twelve months, frequently longer. Three stages have been described : — The Primary Stage. — The primary lesion or mother yaw. The Secondary Stage. — The characteristic g'eneral granulomatous eruption. The Tertiary Stage. — The deep-seated ulcerations and gummatous- like nodules. These divisions are very arbitrary. INCUBATION. This is from two to nineteen weeks, but may be absent. PRODROMATA. Malaise, rheumatoid pains, headache and irregular temperature, but these may be absent. THE PRIMARY STAGE. The primary lesion occurs at the seat of inoculation, and is nearly always extragenital on the mammas or hip. At first there is a papule the size of a split pea, in seven days it becomes moist, develops a yellow crust, other smaller ones coalescing with it. The crust breaks down, and an ulcer remains with clean-cut edges and a granulating base. This may heal, leaving a white, later, pigmented scar, or it may become a bare granulomatous mass. It is often painful at first, but is never indurated. The proximal glands may be enlarged, but do not suppurate. This mother yaw may develop on an old ulcer, insect bite or wound. The smallest abrasion is sufficient to afford an entrance to the virus. The mother yaw is usually still present when the secondary eruption appears. The duration of the primarv yaw is a few weeks to a few months. THE SECONDARY STAGE. From one to three months after the appearance of the primary lesion there may be malaise, headache, pains in the bones, joints and muscles. Pin-head papu^les then appear, commonl}- on the limbs and face, but frecjuentlv over the whole body; these soon show a yellow crust. Some disappear, others coalesce, and others increase in size, forming large nodular masses. The vellow crusts conceal a yellowish fungoid granular mass secreting a thin, slightly purulent fluid. These ulcerations often form rings about the mouth and anus, enclosing good skin. After several months the secondary eruption diminishes and hyper- keratosis sets in, when the papules become hard and warty. 24 DISEASES DUE TO PROTOZOA Most of the lesions usually dry up within six months (three to six months in children) and disappear. In some cases the lesions may persist for years, in other cases the eruption may reappear every few months. Each granuloma lasts about two months. The ofifensive sour odour given off is probably due to the secondary infection. The eruption is seldom painful except when it attacks the palms of the hands and soles of the feet, when the pain may be considerable. The eruption may attack the margins of the nails, when the latter may become hard, brittle, thick, and finallv be shed. White patches may peel off the palms and soles, thus simulating syphilitic psoriasis. The centre of the papules may fall out, leaving a pitted appearance which may persist for years. Fever is common and is intermittent or remittent in type, but it only occurs prior to the secondary eruption. The cervical and inguinal lymphatic glands often enlarge, become hard, but do not suppurate. Joints sometimes become acutely painful and swollen simulating rheumatism, but sodium salicylates are useless. As a rule no fever accompanies this condition. Periostitis is common and often affects the digital phalanges. Contractures of the flexors of the forearm may become permanent. Neuritis and neuralgia pains occur frecjuentlv. Hyperidrosis is often limited to the face, hands and feet. Anaemia is common but is not severe, from three to four millions. THE TERTIARY STAGE. This may not develop ; some denv its existence altogether. Daniels affirms it in Fiji cases. Gummatous nodules and deep ulcerations may follow the secondary eruption after several years. On the other hand, they may not ensue at all. When the skin is affected the ulcers are rounded or irregular in outline, with very thick and undermined edges and a granulating base. There may be painful nodes under the periosteum of the ribs or sternum. vSome cases show a chronic periostitis which alters the shape of the bones. Bahr has described acute and chronic periostitis, osteitis, epiphysitis, synovitis, ulceration and gangosa. There may be ulcerations about the nasal bones resulting in rhinopharyngitis mutilans. Internal affections have not yet been described. FRAMBCESIA TROPICA Late Manifestations. Harper, in Fiji, where syphilis is said to be absent, affirms that tabes, general paralysis, aneurism and gangosa are late manifestations of yaws. COMMUNICABILITY. The disease is not hereditary. Two-thirds of the patients get it before puberty. Parents are infected from their children more than children from their parents, as a result of the child suckling, when the mother will have the primary yaw on the nipple or breast and as a result of the child being carried astride the hip, when the primary yaw will appear in that position. Infection is by direct contact; a damaged surface is necessary. Insects may carry the disease, for they eagerly crowd on the open sores and suck the secretion which may be deposited later upon the damaged skins of other people (Robertson). The mortality is low, 2*5 per cent, in treated cases, but the working capacity is much reduced. Immunity is usually afforded after the first attack. The habits of the people predispose them to the disease, the hand- ing round of chopsticks and water-pipes from mouth to mouth and the employment of sleeping mats common to all. -'6 DISEASES DUE TO PROTOZOA DIAGNOSIS. From Syphilis. — Syphilitic patients may contract it and the reverse. Monkeys inoculated with yaws do not acquire immunity against syphilis. Syphilis is worldwide in its distribution, hut yaws is limited to certain tropical regions. In Samoa, syphilis was unknown prior to 1880, but yaws has been endemic there ever since the people have been known. In British Guiana yaws has recently disappeared, but svphilis remains (Daniels). The primary Icsicm is usually extragenital in \-aws. Pruritis is usually well-marked. The eruption is nearly always papular, becoming granulomatous. It is not hereditary. There is no thickening of the blood-vessel walls so characteristic in syphilis. There is a marked diffuse plasma cell infiltration of the granulomata. Giant cells are absent in yaws but present in svphilis. The consensus of opinion goes to show that yaws is not identical with syphilis, although the morphological similarity between the causal agents of both diseases is a very strong one. The same argument applies to Tuberculosis and Leprosy. From Verruga Peruviana. — This disease is limited to certain valleys of the Andes at an elevation of 3 feet to 10,000 feet. It has a high mortality, 30 per cent, to 40 per cent. It has a severe fever of long duration. The eruption attacks the mucous membrane, which bleeds readily. TREATMENT. Salvarsan, neosalvarsan, galyl and kindred preparations act very quickly, but they may fail to effect a cure in old tertiary cases. Neo- salvarsan is better than salvarsan because — It dissolves more readily in water ; It gives a neutral reaction ; It is less toxic and better tolerated ; It can be given intramuscularly and intravenously. The average single dose for men is o"6 — 0*75 grm. ,, ,, ,, women, 0*45 — o"6 grm. ,, ,, ,, children, 0-15— 0-3 grm. More than o'q grm. should not be given in any case. Intravenously. 25 c.c. of freshly distilled water are required for each o"i5 grm. Some give neosalvarsan and galyl concentrated, such as when THE DYSENTERIES 27 o"45 — o"6 gmi. is dissolved in 10 c.c. of sterile distilled water. 075— o'9 M - 15 M ,, „ >, The median basilic vein is usually chosen. Intramuscularly. Inject into the buttocks 5 c.c. of a ^ per cent, solution of novocain. Leave the cannula in situ, and after a few minutes inject the neo- salvarsan through it. For each o'i5 grm. use 3 c.c. of freshJN- distilled water in making the solution. Doses are prepared in sealed tubes containing o'i5, 0*3, 0*45, o'6, 075 and o'9 grm. Add the contents of the sealed tube to a sterile saline solution o'4 per cent, at room temperature. Well-boiled sterile tap water may be used. Inject immediately and aseptically at a temperature not above 680— 720 p. Sufficient should not be prepared for several patients at the same time. Neosalvarsan must not be reheated. If any remains over it should be thrown jvvay. Galyl has given excellent results in the writer's experience. Its low toxicity, reduced price and equal efficacy compared with salvarsan are points to be appreciated. Intravenous treatment always gives the best results. Give two injections eight days apart. Potassium iodides can be given in large doses, I'o — 2*0 grm. thrice daily, omitted one w^eek in six. Continue the treatment for several months after the disease has cleared up. Mercury is useless. 16 c.c. of serum of yaw patients already treated with salvarsan has efficient curative properties. Boiling does not reduce its power. The ulcers and crusts can be washed wath perchloride of mercury to take awav the smell and to allav the itching. They may then be dusted with iodoform. Protargol ointment 20 per cent, has been used for ulcerative lesions. THE DYSENTERIES. The dysenteries include a group of diseases manifesting abdominal pain, tenesmus, small, frequent, blood-mucous stools, ultimate emaciation, and pyrexia in the bacterial variety. HISTORY. 3,000 B.C. Hindu records carry us back to this time when dysentery was divided into acute and chronic varieties. 28 DISEASES DUE TO PROTOZOA The Hindu surgeon, Sushrula, wrote lliree to four centuries B.C. that : — " He falls an easy victim to internal and external diseases who drinks of, or bathes in, a pool of water which is full of poisonous ■worms, or is saturated with urine, or fc'ocal matter, or is defiled with the germs of vermin or decomposed animal organisms, or is covered over with the growth of aquatic plants, or is strewn over with withered and decomposed leaves, or which in anv ^^•a\• is rendered poisonous and rontaminated, as well as he who drinks and kvUlies in the freshlv collected water of a pool or reservoir during the rains." Hippocrates seems to have introduced the term " dysentery " and to have dififerentiated it from diarrhoea. Most ancient writers of the Near East were acquainted with it. 534 A.D. there was an epidemic of dysentery in France. 820. It occurred as an epidemic in Hungary. 1083-1113. It was in Germany in epidemic form, and in 13 16 it visited England as an epidemic. Wars, famine and foul drinking water were the chief allies of the various epidemics. 1 2 16. King John died from it. Edward I (1307) and Sir Francis Drake (1595) both were attacked by it a few days before their deaths. 141 1. The military camp at Bordeaux lost 14,000 men by it. 1538. The first European pandemic took place, which was followed by at least six others some time later. Some of these pandemics lasted for three years. 1655. Cromwell's failure to take St. Domingo was due to dvsenterv. There were 1,700 deaths during the three weeks of the conflict among the troops and islanders. The disease decimated the same troops when they took Jamaica from the Spanish. 1870. The Franco-German War lost 2,380 deaths from dysenter\-. 1859. The living amoebcC were found in the faeces at Prague bv Lambl. 1873. Losch at St. Petersburg found and described for the first time the amoeba when he called it "Amoeba coli," an organism now believed to have been the Entamoeba tetragena in that particular case. 1883. Koch differentiated the two main types of dysentery, amoebic and bacillary. 1893. Kruse and Pasrjuale differentiated the two types of ama?ba>, the harmless coli and the pathogenic tetragena. 1894. Japan had 38,094 deaths from the disease during the land campaign with China. They lost three from disease to one from Avounds. In the Russian War these figures were reversed. THE DYSENTERIES 29 In 1897 they lost 22,300 from the same disease. 1899-1902. In the South African Campaign 1,342 died from dysentery. 1900. In India the deaths from bowel complaints reached nearly half a million (Hirsch). In the American Civil War the Federals lost 37,794 of their troops from dysentery and diarrhoea. CLASSIFICATION. (i) Bacterial, caused by : — B. dysenteriai of Shiga. (See section on Diseases due ta Bacteriology.) B. dysenterias of Flexner. (See section on Diseases due tO; Bacteriology.) B. pvoc\-aneus. (See section on Diseases due to Bacteriology.) and kindred organisms. (2) Verminous, caused by : — Schistosoma japonicum. (See section on Diseases due ta Helminths.) Schistosoma haematobium. Qisophagostomum brumpti. Faciolopsis buski. Gastrodiscus hominis. (3) Protozoal, caused by : — Amoeba (amoebic). Balantidium (ciliar). Kala-azar (Leishmanic). (See article on Kala-azar.) Malaria (Laveranic). (See article on Malaria.) (4) Pseudo-dysenteries. (]\Iost common in temperate climates.) These manifest diarrhoea, blood-mucous stools, abdominal. pain and tenesmus. The causes are : — Intestinal tuberculosis. Intestinal cancer and polypi. Inflamed internal haemorrhoids, Gummata of rectum, Intussusception, Errors of diet, e.g., small fish bones eaten by natives,. ptomaines, e.g., ricin, excreta of locusts in water (Prout). Deeks classifies the Dysenteries of Ancon Hospital thus : — (i) Amoebic dysentery, caused by E. histolytica of Schaudinn.. (2) ,, ,, ,, E. tetragena of \^iereck. 30 DISEASES DUE TO PROTOZOA (3) Bacillary dysenteiy, caused by Shiga's, Flexner's and allied bacilli. (4) I^ilharzial (5) Balantidial (6) Malarial (7) Tuberculous M >> »> (8) Nephritic Schistosoma mansoni. Balantidium coli. The malarial parasite. Tubercle bacilli of Koch in the intestinal ulcers, associated with acute diffuse nephritis or secondary to chronic nephritis with an acute process superadded. (9) Diphtheric colitis, a very fatal form. (10) Dysentery in the course of pellagra. (11) ,, caused by the ingestion of decompcjsing meats or fish. (12) ,, secondary to cardiac or hepatic disease. (13) Clinical dysentery, often climatic, when no microscopic or cultural findings are successful. AMCEBIC DYSENTERY. DEFINITION. An acute or chronic specific disease of the intestine caused by Entamoeba tetragena, sometimes accompanied by E. coli, which is said to be non-pathogenic. The disease is generally insidious in onset with a tendency to chronicity ; relapses are common; there is liability to liver abscess. It may concur with other dvsenteries. DISTRIBUTION. In Africa, Asia, America, Europe, China, India, Russia, Germany, in short, throughout the tropical world and frequently in the temperate zone. THE PARASITE. This is the E, tetragena, but it is not unlike the E. coli on superficial observation. The following points will assist in the description and differentiation. Jt. tetragena cysts Size 8 to 30 ^ Shape Spherical, amoiboid processes sometimes oval Colour Greenish Protoplasm Ectoplasm tough for boring purposes. Ecto- and endo- plasm easily distinguished. Ectoplasm refractile E. coli cysts 10 to 40 ;U Spherical, when resting Opaque : greyish Ecto- and endoplasm not easily distinguished. Ectoplasm not refractile, homogeneous THE DYSENTERIES— AMCEBIC Pseudopodia Vacuoles ... Nucleus Chromidian bodies ■Contents ... Motility Multiplication Pathogenicity It. tetrageiia cysts Large and easily distinguished. Consists of ecto- and endo- plasm Many Often absent, when present its structure is hidden. Nuclear nien)brane not well defined. Changes position markedly. Never more than four nuclei — hence " tetragena" There is little chromatin Erythrocytes, bacteria, pus cells, crystals Great progressive motility In intestine by fission and bud- ding. Buds small, 4jU with two nuclei. (^*n hard faeces and outside body resistant spores are formed without encystment. These develop when ingested. Pathogenic, penetrates the tissues and often causes liver abscess E. coll cysts Hard to distinguish Entirely ectoplasm Never more than one. May be absent Almost always present, with well defined nuclear men-.- brane and other structures. When organism moves, nu- cleus retains its relative position. May be up to eight nuclei There is much chromatin Rarely cells or organisms Motility limited In intestine by binary fission and multiple fission into eight amoebulac. These are set free when ingested Never pathogenic and never seen penetrating the tissues. Never causes liver abscess. They are limited to the large intestine and caecum. LIFE-HISTORY. The E. tetragena reproduces in tliree ways : — (i) By binary fission, discovered bv Schaudinn. The nucleus divides by amitosis into two, and then the cytoplasm splits into two ecjual daughter cells. (2) By gemmation. — Found by Schaudinn to be more frequent than binary fission. The nucleus divides by amitosis into two or more daughter nuclei with a portion of the cytoplasm, which then separates off from the mother cell, the daughter cells being the smaller. (3) By spore formation. — The chromatin becomes diffused, collects around the periphery, the nucleus disappearing. The ecto- plasm forms into small knob-like processes, each containing several chromidia. These become separated off and are surrounded with a yellowish-brown envelope, forming spores ready for infecting a new host (Schaudinn). These are surrounded by a cyst wall which is broken down when ingested and the eater infected. These E. tetragena are found in the faeces, intestinal contents, debris from dysenteric ulcers, liver abscesses, mucosa and submucosa of intestinal wall. On the warm stage th^y show active amoeboid movement. The cyst resists drying. 3-^ DISEASES DUE TO PROTO'ZOA Wenyon has reproduced the disease in cats, but if it is commonly present in animals is not known. It should not be forgotten that the drv spores can be carried by flies and wind (Vedder). Some afifirm that the presence of intestinal bacteria, e.g., paracolon bacillus, is necessary for the growth of the amoebae (Lesage). Flies are blamed as mechanical carriers of the parasite from faeces to food (Wen3'on). PATHOLOGY. Microscopic. — The spores enter the body with drinking water and food, producing young amoebie in the large bowel. These enter the Entamaba colt : life cycle, a — <;, stages in binary fission : A — Z), schizogony, with formation of eight merozoites ; 2 — lo, cyst formation or sporogony, with formation of eight nucleate cysts. (After Castellani and Chalmers.) mucosae by Lieberkiihn's follicles, entering the lymphatics, and pass- ing to the submucosa, they feed upon the tissue cells and erythrocytes of the blood. They may destroy the tissue and enter the tributaries of the portal vein or branches of the mesenteric artery, sometimes causing thrombosis. They find their way to the liver, causing hepatitis and liver abscess in 15 per cent, of cases. Patches of the mucosa become oedematous and infiltrated bv small THE DYSENTERIES— AMCEBIC 32> D9£,- I I t'>'/;;/', >•• /» lis c
  • - W c 'i c •.2 5 . — . eao u o "^ 3 U! ''^ 2 '5 — u 1) C ~ ■- c >> o . T '-5 «« ±: M i-, ^^ ii •-J — 3 rt O . D The liver is fatty, perhaps congested ; there may be one or more abscesses. For details, see article on Liver Abscess. SYMPTOMATOLOGY. Acute amoebic dysentery. Onset is usually sudden, pain in the lower abdomen often severe, much griping and straining at stool, stools up to thirty per diem with THE DYSENTERIES— AMCEBIC 37 Eniamaba histolytica in tissue. Section of submucosa of colon, fixed in corrosive sublimate and alcohol, and stained with nigrosin. Three entamoeba may be seen following each other in a tunnel which the leader is excavating. E, Entamoeba ; G, glandular tissue (disintegrating) ; Z, sniall cell infiltration. X 350. Entamceba histolytica in mucosa of colon. Invasion of the crypts of Lieberkiihn from the interglandular tissue, and subsequent destruction of epithelium by the organisms. E, Entamoeba ; Z, small-cell infiltration ; B, blood corpuscles and debris, x 300. (After Dopter.) blood and mucus, leucocytes, amoebae, bacteria, Charcot-Leyden crystals and bits of tissue. Anorexia, moist furred tongue, sometimes nausea and vomiting. 38 DISEASES DUE TO PROTOZOA Dyspepsia, pain along line of large gut. Pulse and respirations quickened. Red cells diminished, cytes and eosinophiles increased. leuco- Section of intestine from a case of amcebic dysentery, showing a typical " ulcer of Harris." X 45- iifj^^^i Section of small amoebic abscess, in which the pus pushed through the muscular tissue, and collected beneath the serous coat of the peritoneum. X 85. Urine diminished with some albumin and casts usually. Remittent fever may be present or absent. Normal temperature, absence of pain and tenderness after they have been manifested may indicate : Recovery, haemorrhage, or gangrene. The condition of the stools will indicate if the condition is improving. THE DYSENTERIES— AMCBBIC 39 Death ma}- result in seven to ten days from exhaustion, perforation, peritonitis and haemorrhage. Chronic amoebic dysentery. This folloAvs the acute, or it may be insidious in onset not preceded Experimentally infected cat's colon. Under the higher magnification, the glands of Lieberkiihn are seen to be full of entamoeba, which have destroyed most of the epithelium, and are traversing the basement membrana. x 350. (After Jiirgens.) En/aviaba histolytica. Organisms in dysenteric mucus. X 400. The granular piotoplasm occupies almost the entire cell, and is distinguished from the ectoplasm only by a slight difference in shading. by an acute attack ; there is diarrhoea, with occasional abdominal pain and passage of fc-eculent material with much mucus and perhaps streaked with blood. In between attacks there may be constipation. Stools, which are often more frequent at night, are from twelve to four- 40 DISEASES DUE TO PROTOZOA Amoebic suppuration of the brain. Section of a minute abscess. The cavity contains numerous entamcebse and pus corpuscles. The nuclei of both are deeply stained. (After Legrand and Dopter.) x 300. Balantidium coli. a, nucleus; ^.vacuole; c, peristome;^, bolus of food. (After Leuckart.) n Balantidium coli, free and encysted ; a, anus or cytopyge ; ;/, macronucleus ; b, bolus of food, (After Casagrandi and Barbagallo.) Balantidium coli. a. Natural condition ; b, reproduction by binary fission ; c, reproduction by sexual conjugation. THE DYSENTERIES— AMCEBIC 41 teen per diem. The condition may persist for years, resulting in marl-ced emaciation. Large offensive sloughs may be passed at any time. The cysts are responsible for the spread of infection, hence carriers are a danger to a community. Certain carriers manifest no symptoms. Before a naked-eye examination of the stools they should always be Avashed. Errors in diet can be more readily detected and corrected by this means. The Amoeba minuta lives on the surface of the mucous membrane, but is capable of maintaining the infection. After an acute attack caused by A. tetragena the A. minuta may lead to a relapse of the acute condition, but by itself alone it is doubtful if it causes any symptoms. One must not forget that the amoebse are not confined to the bowel. Urinary amocbiasis is not infrequent in Indians and other Asiatic races. Because of the possible widespread distribution of the amoebae in the human body some have used the term Amoebiasis in preference to Amoebic Dysentery. The stools should always be washed under the tap when one is searching for cysts, and in all dysenteric cases it should be done systematically with every stool. The washing should be continued until all traces of faecal matter have disappeared. This method enables the physician to differentiate the sloughs and mucus. The diet can also be controlled and any undesirable ingested foods detected. It is often necessary to concentrate the cysts in doubtful cases. The method is as follows : — (i) Shake up for half an hour about one gram of faces with 300 c.c. of normal saline until the fa?cal mass is disintegrated and an emulsion is formed. (2) Pour it into a separating funnel, and shake for half a minute with one-twentieth of its volume of ether or methylated spirits. The facal matter absorbs ether and becomes lighter than the water. Cysts are not aft'ected by the ether and remain at the bottom in the saline. (3) Draw off the saline from the separating funnel and centrifuge it for several minutes. The bottom of the tube should contain the cysts in about fifteen times more concentration than the ordinary faeces (Cropper and Row). Colonel Wenyon has shown that the mobile stage of the pathogenic amoeba is not infectious by the mouth. Indeed, "the cystic phase is the sole cause of transmission," and these cysts are able, under favour- able circumstances, to live for at least a month outside the body. COMPLICATIONS. Hepatitis, liver abscess, gangrene of bowel, peritonitis, haemorrhage, stenosis of sigmoid, abscesses in other parts. 42 DISEASES DUE TO PROTOZOA DIAGNOSIS. From Bacterial Dysentery by its chronic course, rare pyrexia, absence of toxic symptoms, complication of liver abscess and the iinding- of the amcx^bcU in the stools. When examining the stools for amoebie a little methylene blue \vill stain the pus and epithelial cells, but not the amoebae, thus facilitating their detection and examination. It is not important in practice to diagnose A. tetragena from A. coli, if one employs the rule that if the symptoms of dysentery are present and amoebae are seen in the stools treat as for amoebic dysentery. Wenyon suggests that the stool should be examined \vith a little iodine tincture, so that the nuclei may be well seen with an oil immer- sion and No. 2 eyepiece, the condenser slightly lowered to reduce the light. Amcebic Bacillary Nearly always chronic in its course Nearly always acute Pyrexia rare Pyrexia common Toxic symptoms absent or late when no Toxic symptoms usually present liver abscess Liver abscess in 15 per cent, of cases Never liver abscess, unless multiple and small Small intestine frequently attacked Nearly always confined to the large intestine Amoebae found in the stools Dysentery bacilli found in the stools From Sub-tertian malarial dysentery hv the absence of malarial parasites the presence of fever and its not yielding to quinine treatment. From Ulcerative colitis and Hcemorrhagic typhoid by high fever, prostration, pain, violent delirium and the absence of entamocb^e. The diagnosis is often difficult. From Helminthic infectio7is by finding the causative parasites. From hitestinal tuberculosis bv marked tenderness in the cascal region rather than over the sigmoid flexure and the absence of parasites. From Malignant disease of the sigmoid and rectum by the severe tenesmus, increasing difficulty to pass large-formed stools, the age of the patient and the absence of parasites. TREATMENT. Absolute rest in bed. Relieve griping bv morphia, hypodermically, also by enemata or suppository. Give castor oil half to one ounce (15-30 grm.). Emetine hydrochloride is a specific, half a grain (0*03 cm.) dis- solved in normal saline, given twice daily until 12 grains (0*75 cm.) have been given. It can be administered hypodermically : sterile tubes of the drug can be obtained ready for use; it may be given orally as " alcresta " ipecacuanha, ijl grains (D"09 cm.) of emetine can be given THE DYSENTERIES— AMCEBIC 43 by the mouth per diem in this way. It can also be given inlravenously, o'lo grm. dissolved in lo c.c. of saline daily. 10-20 per cent, of cases are not cured by emetine. Emetine bismuth iodide in gelatine capsules, one grain (o"o6 cm.) thrice daily per os until 36 grains have been given, has now superseded the emetine hydrochloride treatment. It has cured '' emetine-resistant " cases. There are several good alternative treatments, e.g., tincture of opium, 15 minims, followed in fifteen minutes by ipecacuanha, 10-20 grains in cachet or pill, twice daily. The best Brazilian ipecacuanha should be used, as it contains 72 per cent, of emetine. In the chronic stages, use daily intestinal irrigations of quinine bihydrochloride, 1-5,000 to 1-1,000, ^-^l litres slowl}' injected through a well-vaselined rectal rubber tube. Tannic acid is good, 5-1,000. Also protagol, 1-500. These could be preceded by a morphia suppository half an hour before. Later a bismuth mixture could be given, followed by a tonic. It is a good practice to give small doses of emetine later to prevent relapses. There could, of course, be a combined treatment of emetine and ipecacuanha. Decks strongly advocates the bismuth-milk treatment as follows : — Rest to increase resistance and diminish bowel movement. Generous milk diet — it is absorbed before reaching the large bowel. Saline or water irrigation thrice daily to wash away toxic products. Bismuth subnitrate, grains 180, a heaped teaspoonful, mechanically suspended in a tumbler of water; effervescent, three hourly, day and night in severe cases, reduced as the patient improves. When the stools are few and the tongue clean give it thrice daily. The bismuth salt locks up the free and the nuclear sulphur of the bacteria in the intestine. It destroys certain organisms and influences others. Entamoeba show early degenerative changes (James), become vacuolated, swollen and fragmented. The characteristic faecal odour disappears. The entamoeba usually disappear after the fourth day, no matter how serious the condition. Too much opium favours retention of toxic products that irritate the normal mucous membrane and interfere \\illi (he production of enzymes and hinder digestion. C^costomy in selected cases of emaciation and exhaustion (Herrick) should be done. It prevents food residue from reaching the ulcerated colon, admits of better irrigation of the bowel, and makes possible a more varied and generous diet ; but, on the other hand, convalescence is lengthened and a restorative operation is necessary later. 44 DISEASES DUE TO PROTOZOA Sir Patrick Manson recommends simaruba officinalis as follows : — Simaruba bark ... ... ... ... ... Grm. 15 Pomegranate fruit rind ... ... ... ... ,, 15 Gum Arabic ,, 15 Add water to one litre and boil to half its bulk. Give one ounce (30 grm.) thrice daily. Dapter suggests a creosote rectal wash, i — 100, twice daily. He maintains that the creosote is absorbed, and acts upon the amoebae in the tissues and in the localities where other drugs have failed to reach them. The administration of sulphates at the same time as other treatment will assist in washing out the bowel, but patients must not be exhausted by their prolonged use. A dry but varied diet is most generally useful. Men, dogs and cats act as carriers without obvious symptoms, and should be treated pro bono publico. Remark. — The Entamoeba tetragena can cause a serious cystitis of the urinary bladder quite apart from any dysenteric affection (Wright). CILIAR DYSENTERY. (i) Balantidium coli (sometimes B. minutum) may cause trouble- some intestinal disturbances, such as occasional, remittent or persistent diarrhoea, in which the parasites can be found. Blood and mucus are present in all the severe cases. Peritonitis may occur with or without perforation. Extensive ulceration is found in fatal cases, most marked near the rectum, and less so in the direction of the caecum. Sometimes there is vomiting, with oedema of the face and ex- tremities. It is chiefly confined to the large intestine. The diagnosis can only be made by the microscope. There is no specific treatment. The mortality is about 30 per cent. It is most common in the Philippines, Japan and Europe. THE PARASITE. It is an oval-shaped, large, ciliated infusorian, 30 — 200 fx x 20 — 70 ju,. It reproduces by division, budding and conjugation. It may lose its cilia and become encysted. It is a common parasite of the pig. It is very active in liquid human stools. It has been found post-mortem in the exudate, follicles, ulcers, muscular coat, blood-vessels and lymphatics of the intestine. The method of infection is unknown. THE DYSENTERIES—CILIAR 45 Balantidium coli. Living forms in the dejecta of Balantidian dysentery. ;.» ».-%:. ■^. v.'..-:*.! rezf^zt^ Balantidium coli. Invasion of the wall of the sigmoid flexure in a case of Balantidian dysentery. A, Mucus ; B, glandular infiltration and destruction ; C, parasites in the connective tissue of the submucosa, with infiltration of small cells. (After Dopter.) 46 DISEASES DUE TO PROTOZOA Balantidium con. Parasites in a lymph space of the submucosa. (AftcrDopler.) Balantidiuin tninnttifii. P, Peristome ; A'', nucleus ; I\I, micro-nucleus ; V, vacuole. (After Schaudinn.) TREATMENT. Castor oil, salines, intestinal irrigation \\itli tannic acid or cjiiinine. Emetine and ipecacuanha can be tried. Methylene blue has been recommended, rectal injections, and by the mouth. (2) Laniblia intestinalis is probably pathogenic, attacking prin- cipally the small intestine. It is common in India. The tissues are not invaded, but one may have a chronic recurrent diarrhoea with abundant mucus, with bile or blood stains. There are usually intervals of relief between attacks with constipation. The parasite, a split pear-shaped, double nucleated, protozoon with a sucking disc, can be found in the diarrhoea excretions. The disease is chronic and may last thirty years. When searching for the parasite one should note the two flagella at the (ail end. There are also three other pairs from the central nuclei. There are two nuclei, one on either side of the longitudinal dividing line; its aspect is not unlike that of a face. The parasite, about 12 — 18 yu long, soon dies on leaving the body, but it is very persistent in the host. Lamblia is a common parasite in rats and mice, in which it causes an enteritis. These rodents probably form a reservoir of infection for THE DYSENTERIES— CI LIAR 47 Lainhlia intestinalis. A, ventral view ; B, side view ; N, one of the two nuclei ; ax, axostyles ; fl'^,fi'',Jl^,P, the four pairs of flagella ; s, sucker-like depressed area on the ventral surface: jir, bodies of unknown function. (After Wenyon.) man. The cysts have been found in the fajces of the common house fly, which probably acts as an insect porter (Bahr). TREATMENT. Free purgation and intestinal antiseptics. Enemata are not much use for the small intestine. Methylene blue can be tried, i — 2 grains, with or without liquid paraffin, ;} ounce, thrice daily. Beta-naphthol has been tried. (3) Trichomonas intcstinalis is the common intestinal flagellate in man which lives in the large intestine and ca?cum. It is a large pear- shaped bod}' with three free flagella and one attached to the undulating membrane. Its movements are very rapid, but a sixth objective will reveal its characters. It will survive outside the bodv for days. Some assert that it is harmless, being found usually where other organisms have deranged the intestine. Encysted forms have not been proved. (4) Tetramitis mcsn'ili has been blamed for intestinal irritation, followed by diarrhoea. It somewhat resembles the trichomonas, but the latter has an undulating membrane and no large cytostome like the former. It dies in a few hours when passed in the f^ces, while tricho- monas persists for days. It may not be pathogenic. 48 DISEASES DUE TO PROTOZOA (5) Less well known causative ciliar parasites are : — Colpoda ciscullus. Nyctotherus faba, „ giganteus. Cercomonas, Bodo, Prowazekia are rare. Each of ihem possess flagella from the blunt end of organism, but they cannot be seen until a few days after the faeces have been passed. They are not pathogenic. They all probably have an amoeboid stage. (6) Coccidia, Genus Isospora, have been found in faeces of patients from Gallipoli, and are now regarded as having some pathogenic significance in man. Little is yet known of them, except in animals and birds. LIVER ABSCESS. INCIDENCE. In India the native soldiers are seventeen times less liable to hepatitis than the European soldier, and twenty-five times less liable to liver abscess. VARIETIES. Single : These are tropical in 75 per cent, of cases, and are due to amoebae, ascarides and gallstones. Multiple : Usually pyasmic, sometimes coccidia. POSITION (Cantlie). Supra-hepatic : The pus lies between the layers of the suspensory ligament; is seldom associated with dysentery; the pus is usually sterile. Intra-hepatic : Usually amoebic; the pus is always infected. Sub-hepatic : Rare, and when present is not dysenteric. CAUSATION. Traumatism, chiefly pyogenic cocci. Gallstones, chiefly B. coli communis. Parasites, amoebae, ascarides, hydatids, coccidia, distoma rare. Direct extension, from right empyasma, peritonitis, right peri- nephritis. Typhoid, along the bile ducts from the intestine or by pylephlebitis, or directly from a focus of suppuration. Pyaemic, along the portal vein after dysentery, gastric or duodenal ulcers, appendicitis, abscess of spleen or pancreas, after treatment for haemorrhoids, sepsis of umbilical cord, along the hepatic artery, after septic injuries of the cranium, otitis media, ulcerative endocarditis and septic diseases of the lungs. LIVER ABSCESS 49 c4 c •o u 50 DISEASES DUE TO PROTOZOA AMCEBIC ABSCESS. HISTORY. 21 per cent, of dysenteric autopsies in various tropical countries had liver abscess. 35 per cent, of European soldiers in India who died from dysentery had liver abscess. 84*4 per cent, of the patients at the Seamen's Hospital who had liver abscess revealed at the post-mortem evidence of dysentery. Liver abscess is more common in Europeans than natives and in males than females. Waring savs that 65 per cent, of liver abscess cases were alcoholics. The disease is more common between the ages of 20 and 40, but may occur at any age. In 90 per cent, of cases the organism is associated with or derived from dysenteric processes in the colon. Liver abscess was operated upon in the days of Hippocrates. PATHOLOGY. The abscess, which is usually single, is most frequently in the right lobe of the liver. It is so frequently in the right lobe because the patient is in bed, and the right lobe being heavier than the left lies lower, and the amoebas coming along the portal vein are assisted by gravity to affect the lower or right lobe. No' matter how large the abscess may be it never crosses over to the other side, and in this it simulates hydatids and malignant growths. There is no anastamosis or communication whatever between the vessels (jf the two sides; injection has proved this. There are really two livers arising from two distinct buds from the gut and the gall- bladder lies between them (Cantlie). An abscess may occupy half the liver, and the patient recover because the other half takes on the work, as in the case when one kidney is removed. There is no doubt that the whole liver is enlarged and congested. The right lower lobe of the lung is congested. The abscess wall is thick, firm, ragged, and is made up of three layers : — (i) The outer layer is of hyper^emic liver tissue with some con- nective tissue. In some cases a fibrous capsule may be formed from it. (2) The middle layer is of brownish red friable liver tissue. (3) The inner layer consists of grey necrosed tissue containing amoebae and pus cells, the latter less frequently. There is no lining membrane. The contents of the abscess consist of a viscid chocolate-coloured AMCEBIC ABSCESS 51 pus, with red blood here and yellow mucus there, while a little green bile may add to the variety of colour. The pus is not readily taken up by the dressing and has a peculiar smell. The pus is usually sterile. Under the microscope can be seen red blood cells, broken down liver tissue, large, granular, pigmented, spherical cells, leucocytes, debris, oil globules, h^ematoidin crystals, amceb^e, and very rarely pyogenic cocci. Amoebae are best seen four days after the operation coming through the drainage tube. They persist until the abscess has healed (Manson). The necrosis is thought to be due to the toxic action of the E. tetragena. SYMPTOMATOLOGY. There is nearly always a history of dysentery, but amoebic diarrhoea is not uncommon. Rogers states that 30 per cent, of his cases gave no history of dysentery, 14 per cent, of no bowel disturb- ance, but 98 per cent, of them revealed ulceration and scarring post mortem. There is chill, headache, foul tongue, loss of appetite, languor and depression. Weight and fulness in the right hypochondrium, sharp stabbing pain often affecting the right shoulder and arm from the phrenic nerve and the fourth cervical to the brachial plexus. Cough, according to the extent of the irritation of the diaphragm and pleun-e; there is often dyspnoea due to the base of the lung being affected. Sweats at night, earthy tint of skin, emaciation. Breathing rapid and shallow, chiefly on the right side, and thoracic. Pulse, 80 — 100; hands and feet cold. Rigors sometimes. Right rectus rigid; the left is not so. Pain on palpation. The whole right side bulges, and the intercostal spaces are obliterated. The liver dulness is higher than normal and arched abDve. It is also lower than normal. Pleuritic friction may be heard. The body is often bent to the right side and the right leg flexed. Cutaneous oedema of the chest wall is common, but oedema of the feet and ascites are rare. Vomiting may occur from gastric irritation due to pressure. Occasionally one sees varicosity of the epigastric and h^emorrhoidal veins. Jaundice is not constant, and is but slight. There is leucocytosis, the polymorphs going up to 74 — 87 per cent. Basal pneumonia of the right lung alone in a dysenterv patient should arouse suspicions. 52 DISEASES DUE TO PROTOZOA DIAGNOSIS. From Hepatitis by : — A definite epigastric swelling compatible with liver abscess, X-ray examination and surgical exploration. The trouble is not progressive, but often intermittent. Chronic malaria with hepatitis may be troublesome, but the spleen also \\ill be enlarged considerably. Tropical liver or febrile congestion is due to diet, alcohol, &c. Intermittent hepatic fever due to infective cholangitis gives a history of cholelithiasis. Syphilitic gummata by history, \\'assermann and drug reaction. Enteric, uncomplicated, shows a leucop^enia. Undulant fever, Kala-azar and Tuberculosis the same. An excess of mononuclear leucocytes is not common in liver abscess, but there is a constant excess of polymorphs, 75 — 80 per cent. Double infections are common. Drugs will sometimes help, as Cjuinine in malaria and emetine in dysenteric abscess. The stools should always be examined for amo?bai. TERMINATION. The abscess may run lis course in from three weeks to three nionihs. It ma\' burst and refill or encyst and give rise to no more symptoms. 28 per cent, rupture spontaneously, and usually into the lung, peri- toneum or pleui'cC. There ma}' be 5 — 10 ounces of ]3u.s couglied up in twenty-four hours. Recovery may ensue or sudden h^emoptosis result. The pus coughed up or vomited from the stomach may cease and recover\- take place, or the whole series of symptoms may be repeated. When there is spontaneous rupture the possible positions are as follows : — Into the abdomen or intestine; here the pus causes the intestines to become matted together, but the pus is sterile. This condition should never be operated upon; the pus will be absorbed. A^^hen into the intestine the pus is passed per anum and usually missed. When it passes into the peritoneum a fatal peritonitis has been caused. Into the stomach when the pus is vomited. Into the pleura, rare; causes empvema. Into the lung, may bog its base, give rise to signs of pleurisy, expectoration of pus and blood; 70 per cent, recover (Groves). Into the pericardium, when it is rapidl}' fatal. Into the inferior vena cava, rapidly fatal. Into the gall-bladder, when the pus is passed ])er anum with possible recovery. Externally, by the skin, when the prognosis is at its best. AMCEBIC ABSCESS 53 The pus may pass between the two la)'ers of the Hgamentum puhnonis and here penetrate the bronchus, but it never passes from the lung tissue into the bronchus (CantHe). The pus is then like anchovy sauce. The mortality of Liver Abscess is always high, 50 — 80 per cent. In Algiers, 80 per cent. In the Indian Army, 57*7 per cent. TREATMENT. Liver abscess can often be prevented if, when there are signs and symptoms of hepatitis, treatment is adopted as for amoebic dysentery. When the abscess has once formed operation is the only thing. The starvation diet before operation should not be observed in these cases. From two to three hours before give a very nutritious and easily digestible meal, well sweetened. It prevents some of the evil effects of the chloroform poisoning dependent upon the state of ihe liver (Cantlie). Always give a general anaesthetic. Insert the needle to diagnose correctly. If pus, then operate. When the pus is in the left half of the liver, which is verv rare, do not explore with a needle, nor use a trocar and cannula, but cut down and evacuate the pus in the ordinary Avay. In mapping out the liver before operating remember : — That the left margin of the liver does not coincide with the right costal margin. In a tall man it is normally above, and in a short, stout man below the costal margin, as the ribs pass out\\ards more transversely. To get the lower border for that particular patient place the patient's hand (right) with the upper border at the articulation of the sternum with the ensiform cartilage and draw a line along its lower border; this is the normal lower border line of his liver. Each inch below this line means one pound of liver extra, and this is serious (Cantlie). Examine for an egg-shaped swelling along the upper border between the right nipple and the sternum. Remember that the pleura comes to within three fingers breadth of the lower costal margin and the lung to five fingers breadth. When needling, it does not matter if the pleura is penetrated. Even if the base of the lung is pierced it is not of importance, as this is congested, doing no work, and the puncture will relieve the tension. Bleeding from the hepatic veins is good; it relieves congestion and affords comfort even if no abscess is found. The portal vein has never been entered. The vena cava is 4I inches away from any part of the surface of a 54 DISEASES DUE TO PROTOZOA normal chest, so that a needle of 3I inches in length can do no harm in any case. Do not insert the needle where the liver overlaps the stomach. Do not forget that one lobe may be enlarged by overwork becau.se the other is atrophied. It is possible to miss the abscess after six punctures. Always incise the skin first, then use the needle, or a piece of skin may block the needle. Never aim at the vena cava each time as some areas are thus missed. To evacuate the pus a special trocar and cannula are required, that is, when the abscess is in the right half of the liver; the cannula should be 3J inches long; the vena cava is 4J inches distant from the surface. Push the cannula off the trocar when the end is inserted in the liver, and the liver cells are by this means pushed aside and not cut. Do not wash the abscess cavity out with carbolic; it coagulates the blood and causes it to resemble pus. Remove the ribs below the pleura, if necessary, and put in a tube. This tube can be of greater diameter than the cannula and inserted by stretching it upon a special rod, which is then inserted down the cannula, the cannula withdrawn, the rod liberated from the rubber tube by an appliance and withdrawn, leaving the tube in situ, exer- cising pressure upon the surrounding liver cells and preventing pus from leaking into the pleural cavity. Haemorrhage is also thus pre- vented. Do not evacuate all the pus before the tube is inserted or the abscess cavity will collapse, and there will not be a cavity in which to insert the rubber tube. The after-treatment is all-important. Drain the abscess by syphoning. Attach to the rubber tube a glass tube, and to this a rubber tube passing to a bucket by the bedside. If the syphon action is excessive blood may come ; then raise the bucket on to a stool, then a chair, then on to the bed, and so reduce the suction until the desired effect has been obtained. Give emetine at the same time as for amoebic dysentery. Retain the tube in position for two to^ ten weeks, shortened from time to time as required, keep it in until the bile comes or the pus has all been evacuated. Then remove the syphon tube, and shorten the rubber tube as the liver pushes it out. When bed sores arise turn the patient on to his side. If the fever still remains there are more abscesses or the drainage has been insufficient. If the abscess is aseptic, irrigate dailv with c}uinine i — 1,000, but remember that such fluids with flocculi of pus may enter the open mouths of the hepatic veins and may prove rapidly fatal. Patients treated for Liver Abscess should never return to the tropics. TROPICAL LIVER 55 Operation has reduced the mortality to 32 per cent. Canthe had 115 recoveries with 27 deaths. Some aspirate the abscess and inject c^uinine bihydrochloride, 0-50 grm. to the litre (Rogers and Wilson). Quinine kills the amoebae on the abscess wall, and the pus becomes less copious and almost serous as long as it is sterile. Change the dressing at least twice daily; the pus tends to run by the side rather than into the dressing. Failure of this treatment is due to : — (i) A secondary abscess which may burst into the first cavity. (2) Septic infection. Culture the pus organisms. (3) Insufficient emetine. (4) Intercurrent disease, e.g., enteric fever, &c. TROPICAL LIVER. This is a distinctive disease affecting Europeans residing in the tropics. It is more prevalent generally during the early years of residence. The foul tongue, painful liver, earthy skin, and irritable temper of such affections are well known. The liver functions are adversely affected by heat, food, alcohol, malaria, abuse of exercise, congestion and inflammation. TREATMENT (Rogers). Absolute rest in bed. External applications, such as hot fomentations on oleate of iodine. Internal medication, e.g., salicylate of sodium, ammon. chloride, sodium sulphate, pot. iodide, ipecacuanha. Also calomel, blue pill, soda and phenalgin, followed by a saline purge. Ipecacuanha is most useful if there is hepatitis. Give it in large doses on an empty stomach, 20 — 40 grains at night, preceded by chloral, 20 grains. Ipecacuanha in keratine capsules does not act until it has reached the intestine, and hence is to be recommended. THE LEISHMANIASES. These will be considered under the following heads : — (i) Kala-azar. (2) Infantile kala-azar. (3) Dermal Leishmaniasis (Oriental sore). (4) Naso-oral and Oro-phalangeal Leishmaniasis. (5) Canine Leishmaniasis. (6) Pseudo-kala-azar (Tropical febrile splenomegaly). 56 DISEASES DUE TO PROTOZOA Kala-azar. DEFINITION. A chronic, specific, infective, febrile disease, caused by Leishmania donovani ; characterized by irregular fever, enlargement of the spleen and liver, emaciation and anaemia, frequent hyperpigmentation of the skin, and accompanied by a heavy mortality. HISTORY. 1869. It was noticed by British officers in India, decimating and, in some instances, depopulating numerous districts of the Garo Hills. The Garos called it " kala-azar," or the black fever, 1875. It became epidemic with a very heavy mortality. 1882. The first account of it was published by Clarke. 1889. It spread to Assam along the lines of communication. 1900. Sir William Leishman found the parasite in the spleen of a soldier at Xetley, but he did not publish it until 1903, in which vear Donovan found the parasite by splenic puncture during life. 1907. Patton found the parasite in the leucocytes of the peripheral blood, also that it became flagellated in the alimentary canal of bugs. DISTRIBUTION. It is endemic, and may become epidemic in East India, Assam, Madras and Calcutta. It is present in Arabia, Ceylon, Burma, Indo- China, China, the Yangtse valley, Sudan, Egypt, Tunis, Algeria, Sicily and Portugal. The Indian epidemic began in the Lower Bengal at the foot of the Garo Hills, slowly advancing up the valley of the Bramaputra, travel- ling 100 miles in seven years. ■It followed the lines of intercourse, attacking first the larger stations. Isolated villages seemed to escape. As it spread into new villages ahead it died out in those first attacked. It seemed to cling to a place for about six years, and then died out without apparent cause. A house would appear to retain the infection for months. The disease terrorized the natives, those afiflicted were expelled from their villages, made semi-drunken, and taken into the bush to be destroyed. There have been sporadic cases in other parts difficult to account for, although they seemed to be typical cases of Kala-azar. AETIOLOGY. The disease is spread by Leishmania donovani. The carrier blamed by Donovan is a Conorhinus. The predisposing causes are explained by the habits of bugs thus : — • LEISHMA NIA SIS—KA LA -A ZA R 57 An epidemic will travel slowly along lines of human commimication, It runs in families, the children suffering most. The poorer sections of the community are affected most. The dwelling becomes infected and will infect those close to it. Neither sex nor season has anv influence. WM. kx A 4ff ^ '■ is Leishmania donovani. i, Free forms, each with nucleus and rod-shaped blepharo- plast (after Christopheis) ; 2, endothelial cell and leucocytes containing parasites (after Christophers) ; j, capillary in the liver showing endothelial cells containing parasites (after Christophers) ; 4, two parasites escaping from a leucocyte in the alimentary canal of the bug (after Patton) ; 5, further development in bug (after Patten) ; 6, young flaggellate forms in bug (after Patton) ; 7-//, culture forms (after Leishman) ; 7, 8, g, show development of flagellum. THE PARASITE. The l^eishman-Donovan " body " is a small ovoid or roundish organism, 2 — 4 /i in diameter; when stained it shows two lilac- coloured chromatin masses of unequal size enclosed in a c_ytoplasm of a bluish tint. The larger mass is the nucleus, oval and centrally placed in the 58 DISEASES DUE TO PROTOZOA resting stage, elongated, and situated peripherally in the pre-division stage. The smaller mass is the muco-nucleus or blepharoplast, a short rod, perpendicular or at a tangent to the nucleus. The parasite multiplies by simple fission, the nuclear masses always elongating and dividing before the protoplasm. The parasites are almost always intracellular in man. Their growth and multiplication within the cell causes the cell to enlarge and disrupt ; these parasites set free enter other endothelial cells or are engulfed by leucocytes in which they may be seen in the peripheral circulation. Clusters of them may be seen, 50 — 200, in a structureless matrix debris of the host cells. In cultures the parasite enlarges rapidly, becomes elongated, and acquires a flagellum at its rounded end acquired from the blepharoplast, the whole measuring 12 — 20 /x in length. Attempts to transmit the parasite to vertebrates have failed. The parasite can be cultured from the blood, even during apyrexial periods, on N.N.N, media. Ten or twelve tubes of this media should be inoculated, otherwise parasites, if scanty, may not be secured. Eight out of ten tubes may be negative. It is the flagellate form of the parasite that develops in the cultures (Cornwall and Menon). Run a few drops of finger blood into 15 — 20 c.c. of citrated saline solution, centrifuge it, inoculate N.N.N, media with the deposit of corpuscles. Donovan believes that a biting insect carries it to man, while Manson suggests that insects might deposit it upon (he wounded and abraded surfaces of man. Once in the body it enters an endothelial cell of a capillary blood- vessel or lymphatic, and therein grows and multiplies until up to 220 may be seen in one cell (Leishman). The liver, spleen, bone marrow and hmphatic glands may be thus affected, less so the pancreas, kidneys, suprarenals, testicles and lungs. The enclosing cell ruptures, the liberated parasites are taken up by leucocytes, polymorphonuclears, mononuclears, and rarely eosino- philes, as a result of which process the parasites appear in the peripheral circulation, especially if a diarrhoea due to intestinal ulcers increases the polvmorphonuclears. The further development takes place in ihe bug, but ihe complete life-cycle has still to be ascertained. INCUBATION. Not yet ascertained. One case was under ten days. It is generalh' considered lo be from (liree ^\•epK's lo sp\eral months. LEISHMA NIA SIS—KA LA -A ZA R 59 SYMPTOMS. Onset is often by rigor, which may recur daily. Initial fever is irregular, high, intermittent (jr continuous, showing a double remission daily on a four-hourly chart. Vomiting is not infrequent. Less frequently there are gastro-intestinal disturbances, or in some instances the onset is insidious. Secondary low fever is chronic in its course, continues from two to six weeks, then gradually declines. The spleen and liver enlarge, may be painful and tender. Then there is an apyrexial period, or a very mild fever. Profuse sweats are common. Rigors are now rare. Apyrexia and pyrexia mav now alternate. The anaemia increases. Cachexia is now manifest. There are : asthenia, wasting of muscle with protrusion of abdomen. The ribs show, the extremities are thin, TIME M E M E l\ /I E M E W z M E M E M E M E M E M E M E M E M E 104 103 1 02 1 01 1 OO 9 9 96 97 M X / ^ % t A A \i / V i rf fy A rt / \ t A Y \ N A A n J V J V I \ A A r\ ' V V V \, ,* V V r \ V /•v 7 V v Kala-azar. Undulating type. cheeks sunken, nose sharp and ankles puffy. There may be oedema of the legs and ascites. The skin becomes an earthy grey colour. The hair becomes dull, dry, brittle, and may fall out. Epistaxis and bleeding from the gums are not uncommon. The spleen may nearly reach the pelvis, but the liver is not so much enlarged. Diarrhoea and dysenteric attacks are common. Haemorrhages may occur from anywhere — nose, gums, stomach, bowels, or under the skin. There may be a papular eruption about the thighs. Ulcers may form. TERMINATION. The disease goes on for months or years, average twelve to eighteen months. 4 per cent, improve slowly, 96 per cent, die of asthenia or some intercurrent disease (Rogers). 6o DISEASES DUE TO PROTOZOA Dysentery carries ofif about 90 per cent, of them, then comes phthisis and pneumonia. Usually the tongue is normal and the digestion good. THE BLOOD. The parasites may be found in the peripheral circulation. There is marked anaemia, 4 — 2,500,000 reds per cm. (Rogers). Mb. is reduced in proportion. The colour index is normal. There is marked leucopaenia, 2,000 or less. Polymorphonuclears and eosinophiles are reduced. Mononuclears and lymphocytes are increased. The reduced pohs probably predispose to bacterial invasion. Coagulability is decreased; exploratory^ punctures may set up a fatal haemorrhage. The whites to reds varv from i to 2,000, i to 4,000 reds instead of I to 625. DIAGNOSIS. An irregular chronic fever with a very enlarged spleen and a relative mononuclear leucocytosis is probably Kala-azar, but one must find the Leishman-Donovan body to be certain. Centrifuge the blood for the leucocytes. To puncture the spleen is dangerous, but is practised at times. Some artificially excite bullcC for the leucocytes. A blood examination will exclude a leukaemia. The double dailv remission of fever is important. Banti's disease is sometimes troublesome; the microscope only will exclude it. PROGNOSIS. This is always bad. Moderate estimates state that 70 per cent, die who have had treatment, and 96 per cent, without it. The increase of the polys is a good sign. Better results may be obtained by tartar emetic, intravenously and in strong doses. The writer suggests Injectio antimonii oxide. MORBID ANATOMY. The body is emaciated. There is marked muscular atrophy. There is some oedema present. The spleen is much enlarged, it is firm, deep red in colour, the capsule thickened and congested throughout. Many parasites may be seen. The spleen sometimes weighs 80 ounces. The liver is somewhat enlarged, the intra-lobular arteries are dilated, they contain macrophag"es full of parasites, the liver cells are LEISHMANIASIS— INFANTILE KALA-AZAR 6i atrophied and degenerated. Sometimes the cirrhosis is severe and no parasites are seen. There may be ulcerations of the sl and I4<5, formation of microgametes ; i3rt and 14a, maturation of the macrogametes ; 15/', microgamete ; 16, fertilization ; 17, ookinete; 18, ookinete in the walls of the stomach; 19, penetration of the epithelium of ihe stomach; 20—25, stages of sporogony on the outer suiface of the intestinal wall ; 26, migration of the sporozoites to the salivary gland ; 27, salivary gland with sporozoites. 76 DISEASES DUE TO PROTOZOA sanguinis, the pigment being liberated at the same time is then taken up bv phagocytes, Avhich may also destroy many spherules. The spherules which have escaped the phagocytes attack and enter new red cells. The young parasite now shows active amoeboid movements, shoots out long, retracting, slender pseudopodia, growing as it feeds upon the haemoglobin, converting the latter into parasites, protoplasm and iKemozoin particles. The movements gradually cease and spherules are formed, completing the cycle. The ha?mozoin particles show a Brownian movement, otherwise the particles are now passive. The voung parasite contains nucleus and nucleolus, which break down and become diffused in the protoplasm, only to reappear as small scattered nucleoli around which the parasite segments itself. As long as the nucleus remains entire the h^emozoin is situated at the periphery ; when the nucleus becomes segmented the h^emozoin becomes central. These facts are not sufficient to describe the latency of the parasites in the body, and their recurrence causing later a typical attack of the fever. It is known that good powers of resistance and quinine favour latencv, but that reduced resistance discourages it. EXTRACORPOREAL OR MOSQUITO CYCLE. When fresh mounted malarial blood is watched under a microscope, for ten to thirty minutes certain parasites may be seen to throw out long slender processes, one to six, giving the cell a cuttle-fish-like appearance. These flagella, or more correctly microgametes, act like spermatozoa, since this is the male form. These vigorous filaments, four to six times as long as the diameter of the body of the cell, break away, swim free in the liquor sanguinis, and are lost to sight. These flagellated cells are derived from crescent bodies and other large parasites just prior to the concentration of h^emazoin and seg- mentation. Such bodies are only formed seven to ten days after the onset of acute malarial symptoms. These cells may not be numerous, but thev persist after all other forms of the parasite have disappeared, and mav be seen from one to six weeks after all clinical symptoms have cleared up. After this time they may gradually disappear. These crescents are not affected by quinine. Thompson has shown that gametes as individuals do not persist, but that there is an asexual cycle which produces the gametes from time to time. The individual gametes do not live very long in the peripheral circulation, probably about ten da}s ; if they persist after that time it is because the asexual cycle has not been killed. Hence, when gametes can be found relapse is always possible and probable. Others agree with Thompson in this. The severity of the infection does not account for the relapses; the mildest quartan will relapse time after time (James). MALARIA yy Ouinine eiven b\' the mouth verv often does not e^^ldicate the asexual cvcle in the marrow and spleen; the residual parasites become immune; the longer the asexual cycle persists, the easier it acquires immunity against the drug, consequently large doses must be given to eradicate the disease. The crescent body of subtertian malarial infections exhibits no amoeboid movements, has a very crescentic shape, contains needle- shaped h^emozoin particles somewhat centrally placed, and shows a thin circular outline of the damaged red cell outside it. Rarely twin crescents may be seen within one red cell. These cell membranes are better made out in stained specimens. When the crescent is young the hiemozoin particles are scattered. When the crescent is mature the ha^mozoin particles are concentric. \\^hen the crescent is effete the protoplasm shows vacuolation, e.g., degeneration. ■ The hiemozoin can be dissolved by weak solutions of ammonia. in the male the protoplasm is hyaline and the ha?mozoin loosely arranged ; the protoplasm stains more deeply ; the nucleus is larger. In the female the protoplasm is faintly granular, the ha?mozoin more concentrated and centrally placed. The protoplasm stains faintly, the nucleus smaller. llie early forms seen in the spleen and bone marrow about the fourth day of a subtertian malarial attack are rarely seen in the peripheral blood until they are mature, which is about seven davs later. Some of the crescents outside the body become oval or spherical and throw off microgametes like the large spherical parasite; the remaining central portion breaking up is carried awav bv phagocvtes when the microgametes have become separated. Just before the filaments are thrown out the agitation of the hyaline sphere becomes intense. These are the male sex cells. The granular spheres do not give off these filaments or micro- gametes because they are the female sex cells. In the parasites other than the subtertian ones the large spherical parasites act in a similar way, with the exception that they are never crescent-shaped. Ross has shown that the blood must come in contact with the air for these changes to take place in the male sex cells. Adding a little moisture will hasten the process. Both of these factors, air and moisture, can be added by gently breathing on the slide before adjust- ing the cover slip, the male sex cells of course being mature. THROUGH THE ANOPHELIN^E. When mature crescents are taken up by some of the Anophelina?, they become transformed into male or female sex cells, the filaments 78 DISEASES DUE TO PROTOZOA of the male cell break up, one filament bulls and bores its way into the granular or female sex cell. Where this iilament or microgamete disappears inlo the female cell a small minute papilla is thrown out to meet the oncoming microgamete. No second filament can enter, no matter how energetical Iv it attacks the impregnated cell. Later this cell becomes oval, elongated lanceolate, and finally a vermicular form, the a h c d e Stages of development of peinicious or malignant terlian pirasi'es in the intestine of Anopheles maadipennis. (After Grassi.) a, macrogametocyte (crcsceni) still attached to human blood ci'fpuscles; b, macrogametocyte (sphere) half an hour after ingestion by ihe musquiio ; c, microgametoc>te (crescent) attached to the blood corpuscle ; d, microgametocyte (sphere) half an hour after ingestion ; the nucleus has divided several times ; e, micrugametes attached to the residual body (polymitus stage). anterior end becomes pointed and hyaline, the posterior end broad and granular as a result of the presence of the hiemozoin. The vermiculc then moves about, and is now called the Ookinet. This can pass through a red or white cell. The ookinet now passes through the wall of the mosquito's stomach and the delicate basement mem- brane of the stomach wall, and lodges amongst the longitudinal and i:^* ^m-| Ookinete of the malignant tertian parasite in the stnmsich of ^/top/ie/es macu/ipe/i>ir's, thuiyAwo hours after ingestion of blood. (After Grassi.) transverse muscle fibres between the inner membrane and the outer- coat of the stomach wall. Here it grows for a few days, becomes spherical, accjuires a capsule, and by its increasing size bulges inwards the stomach wall, it is now an Oocyst. Spherical daughter cells are formed within it. Around these numerous spindle-shaped nucleated bodies are formed, giving it the appearance of an apple studded with needles. The spherules disappear and the spindles remain loose in the capsule, and are now known as sporosoites. In about one week ihe capsule ruptures and discharges its contents into the body cavity MALARIA 79 of the mosquito, leaving there probably by the blood, and ultimately reaching the three lobed salivary glands which communicate with the base of the proboscis by means of a long duct. The parasites may be seen in the cells of the salivary glands and in the ducts. The parasite is now ready to enter man when the mosquito bites him. SUMMARY OF COMPLETE LIFE-CYCLE. Sporozoites enter human blood corpuscles, where they exhaust the Hb., form pigment, become mature, and develop into either — (i) Schisonts, which are the segmented and rosette forms. . Section of the stomach of an The hfemozom concentrates, mero- Anopheles, wiih cysts (oocysts) zoites form, burst the red cell and ofthe malignant tenian parasite, (After Grassi.) enter fresh ones, only to begin again the endogenous life-cvcle. This is k'nown as the asexual stage of schizogony. (2) Gaiuetes. These are crescents in the subtertian form, spherical bodies in the ter- tian and quartan forms. There are male and female sexual cells, which become dififerentiated in the mos- quito. Microgametes break ofif from the male and im- pregnate tb.e female cell or macrogamete. This impreg- nated female is now the ay got e It begins to move and is now an ookinet. It rests in tiie stomach wall, forms a capsule, and is now an oocyst. It divides into daughter cells and residua' Four dififerent sporulation stages of malarial parasites from Anoplieles tiiacu/ipeittiis, much magnified, a-c, of the malignant tertian parasite ; a, four lo fcur and a half days afier sucking ; b and c, five to six days after suck- ing ; d, of the tertian parasite, eight days after sucking. (After Grassi.) bodies. The daughter cells produce around themselves needle-like bodies, perhaps io,ooa in one cysf, which become sporosoites. The oocyst ruptures, the sporozoites reach the bod\- cavitv, and ultimately the salivary glands, and are injected into man along the proboscis. These become schizonts in his blood, and renew the endogenous cycle of sporogony. It is suggested, but not proved, that the mosquito mav live in ■8o DISEASES DUE TO PROTOZOA A-ertebrates other than man, or probably the mosquito may infect its own eggs, and thus hand down the infection without tlie human element being present. This has not been demonstrated. CHARACTERISTICS OF THE MALARIAL PARASITES. (Alodihed after Manson and Mannaberg.) For brevity in this statement " O " will mean Quartan, " T " Tertian, and " S-T " Subtertian. DURATION OF DEVELOPMENT. O. 72 hours. T. 48 hours. S-T. 36 to 48 hours. MOVEMENT. Q. Slight movement in the immature forms. T. Active amoeboid movement in the immature forms and also in the middle-aged forms. S-T, Active movement; remains present in the pigmented stage. H^EMOZOIN. O. Coarse grains; little or no movement. T. F"iner grains in immature forms; often in the larger actively swarming. MAXIMUM SIZE. Q. The size of a red blood corpuscle. T. Ditto, sometimes a little larger. S-T. Half to two-thirds the size of a red cell, FORM OF SEGMENTATION. O. Daisy form; the single spores roughish, \\\\.\\ distinct nucleolus, T, Sunflower or grape-like spores, single, round, small, nucleolus rarely seen. S-T. Irregular heaps. NUMBER OF MEROZOITES. Q, 6-12. T. 15-20, often less. S-T. 10-12, rarely 15-16, FORM OF GAMETOCYTE. O. A sphere. T. A sphere. S-T. A crescent. MALARIA 8i ALTERATIONS IN INFECTED BLOOD CORPUSCLES. Q. The red blood corpuscles are little discoloured, and are not materially altered in size ; some appear smaller. T. The red corpuscles are often hypertrophied and have lost colour, it may be completely. Schijfifner's dots in deeply stained specimens. S-T. The red blood corpuscles shrink frequently ; they are dark, or may be perfectly colourless. RELATIVE NUMBER OF PARASITES SEEN IN PERIPHERAL AND VISCERAL BLOOD. Q. Parasites seen in peripheral circulation throughout the whole cycle, and in as great numbers as in visceral blood. T. Parasites seen in peripheral blood throughout the whole cycle, but not in such large numbers in visceral blood. S-T. An enormously greater number of parasites present in internal organs as compared with peripheral blood. The latter part of the cycle takes place in internal organs only. INFLUENCE OF QUININE. Q. Causes disappearance of parasites readily. T. Ditto. S-T. Causes disappearance of parasites less readily. LIABILITY OF RECURRENCE OF PARASITE AFTER LEAVING INFECTIVE REGIONS. Q. Liability persists for a very long period. T. Liability persists for a long period. S-T. After a few months less liability to recurrence. THE MOSQUITO. It does not follow that if there are Anophelin^e that there is malarial fever, e.g., England, Epping Forest in particular, harbours many of these mosquitoes, but there is no malaria in consequence because the parasite is absent. Again, if there are none of these mosquitoes there cannot be any new cases of malaria if the parasite is brought in bv carriers. If there is an attack of malarial fever where there are no mosquitoes it is because the patient has been previously bitten elsewhere. For example, cases have arisen after weeks at sea owing to the climatic changes reducing the resistance of the patient and giving the parasites, lying in the spleen probabl}-, a new opportunity to do mischief. Where mosquitoes exist the temperature must be favourable for rhe 6 82 DISEASES DUE TO PROTOZOA development of the parasitic oocyst in the body of the mosquito. If it is below i5°-i6° C. no further development is said to take place. L. malarias is said to require the highest temperature, P. vivax the lowest, and P. malarise will develop at low or medium temperatures. These differences may account for the unequal distribution of the parasites and for their lesser danger in sub-tropical and temperate climates. For details of the habits, &c., of mosquitoes, see article at the end of the present one. MAN. Man is the third essential factor for the spread of malaria ; without him, as far as is known, malaria cannot exist. The native population in the tropics forms the great reservoir of parasites, but Europeans may also carry large numbers of gametocytes. A new district should always be investigated with regard to malaria and the following facts ascertained : — (i) The diagnosis of the causative parasite. (2) The population of the area under consideration. (3) The average number of infected persons, ascertained by the spleen rate. (4) The average number of persons having gametocytes in the blood. (5) The species of Anophelinse and their breeding places. (6) The species which carry the parasite. (7) The species in which the parasite is found. (8) The number of Anophelines in the infected area. DISTRIBUTION AND CLIMATOLOGY. Malaria is most prevalent in the region of the Equator, 63° N. — ■ Regions that were once deadly may become salubrious, e.g., England, Germany, Austria-Hungary. On the contrary, countries once free may become infected, e.g., Mauritius, which was said to be infected during the sixties of last century by the introduction of carry- ing mosquitoes (Ross). The West Coast of Africa, from Senegal to the Congo, is perhaps the worst malarial country in the world. India is heavily infected, especially about the swampy lands at the foot of the Himalayas. It is also found in the following countries : Borneo, Arabia, Syria, Siam, China, Western Australia, New Guinea, Solomon Islands, Bismarck Archipelago, Central America, West Indies, Mexican Gulf, the north of South America, Brazil, Paraguay, Bolivia, Colombia, MALARIA 83 Peru, Chili, many of the Southern States of Xorth America, Russia, Italy, Greece, Turkey, Austria-Hungary, Southern France, even amongst the soldiers of the present War. In Switzerland, along the Rhine in Germany. Some parts of Sweden. For malarial epidemics there must be malarial parasites, carrying mosquitoes, man, heat and moisture. High altitudes and strong winds diminish its prevalence. Malaria does not exist in : — The Seychelles, Indian Ocean, Fiji, Society and Friendly Islands, Southern Pacific, Barbados and St. Helena in the Atlantic. Where malaria is prevalent children tend to become immune about the twelfth year (Ross). PATHOLOGY. The febrile phenomena are explained b}- various malarial products : — (i) Toxins that act on the heart controlling centre. (2) Haemolytic toxins. (3) Toxins acting on the innervation. Blood serum taken before a rigor and passed through a Berkefeld filter will, when injected into a healthy man, cause a febrile paroxysm resembling malaria (Daniels). The heat output during the cold stage of an attack is diminished, but the causative metabolic changes are but little known. The urine is increased during this stage, probably due to the con- traction of cutaneous vessels and increased B.P. internally. The specific gravity is raised as a result of the increased metabolism caused by the toxins. The colour is dark and the acidity increased. Nitrogen is in excess owing to urea. The salts are all increased, except phosphates, which are diminished during an attack, and increased during the intermission, therefore phosphoric acid is retained during the attack. The excretion of iron is increased in the h^mozoin and hasmosiderin. The increase commences just after the attack. There may be a considerable quantity of urobilin excreted, and the indigo blue may be increased. To test for urobilin : — Add to urine equal parts of ZnSo4 solution (ZnSo4 10, absolute alcohol, 90). Shake the mixture. Add a few drops of lugol, stir and filter. Fluorescence equals urobilin. The diazo reaction is present in 5*5 per cent, of cases. During the intermission the quantity of urine is diminished, but the nitrogen keeps up. During convalescence there is polyuria with low specific gravity, especially in subtertian cases. 84 DISEASES DUE TO PROTOZOA The jcBces show increased excretion of bile and iron, both from blood destruction. Stercobilin is increased. The sweat has a peculiar odour and is toxic to rabbits. Goose skin may be caused by some malarial toxin acting on un- striped muscle, affecting the erector pilorum. Hcemozoin is the black dust-like grains of pigment formed from haemoglobin and distributed over the body after the rupture of the red cells. Phagocytes remove it to the connective tissue, e.g., the liver and spleen. It is soluble in alkalies, entirely and rapidly in ammonium sulphide, but not in water, alcohol or acids. It contains an organic compound of iron which will not give the Berlin blue re- action. Eventually it disappears from the body, but how is not known . It is peculiar to diseases caused by malarial parasites except melanotic tumours, but in the latter instances it is never seen in the blood-vessels. Intravascular black pigment is pathognomonic of malaria. It is most abundant in the splenic vein and lymphatic glands at the hilum of the liver. HcBmosiderin is a yellow pigment found as yellow granules in the parenchyma cells of the liver, spleen, kidneys, pancreas, bone-marrow, capillary epithelium, and less frequently in the leucocytes. It contains an inorganic compound of iron which gives the Berlin blue reaction (ammonium sulphide and double cyanide of iron and potassium). It is insoluble in alkalies, acids and alcohol (Manson). It is not peculiar to malarial diseases, but may occur in any where there has been marked blood destruction, as in haemoglobinuria, pernicious ana&mia, extensive burns and toxic poisoning by such agents as potassium chlorate and pyrogallic acid. The liver converts the free haemoglobin into bile pigment, which, when in excess, overflows, as it were, causing bilious diarrhoea and vomiting; consequently polycholia is a constant feature of malaria. The yellow tinging of the skin and sclerae may be due to free hemo- globin and not to cholasmia as a result of bile absorption as once commonly believed (Manson). This yellow pigment is probably pre- cipitated haemoglobin, stored up and waiting to be worked off by a busy liver. Should the haemoglobin go beyond this it overflows, and then we have haemoglobinuria. The red cells. — The body (150 lbs.) contains about 25,000,000,000,000 red cells. To examine all these under the microscope at the quickest rate would take over 1,000 years (Ross). In severe infections 12 per cent, are infected, i.e., 2,000,000,000,000. If only I in 100,000 corpuscles are infected, i.e., 250,000,000, there will be but little manifested of the disease (Ross). MALARIA 85 Daniels says that 600,000,000 red cells could be infected without the victim having " fever." It has been estimated that 300,000,000 are required to produce each degree F. rise in the body temperature due to a malarial attack. Anything under this number has been called " latent malaria." The different pictures caused by the various malarial parasites will be given in a table later. The marked blood destruction during an attack, especially in the subtertian variety, is considerable, but it is made up very quickly during the intermission, so that the number of red cells may be almost normal by the time of the second paroxysm in tertian and quartan cases. Unafifected red cells become pale, vary in shape (poikilocy- tosis), sometimes with megaloblasts (polychromatophilia), basic and granular degeneration with normoblasts. OligocythcBmia is always present. If i per cent, of the red cells is attacked and contains a parasite, we should expect a reduction of I per cent, of total red cells. If every twentieth cell, then 5 per cent, of the total destroyed, and so on, but it is not so. Only after one paroxysm of fever the drop may be from 5 per cent, to 10 per cent., and after some one pernicious attack I- to one million per c.c. of blood will be destroyed, and if the pernicious attacks continue the count may be about one million instead of 5|- millions. The Hb. value of the remaining corpuscles goes doMm 10 per cent., 20 per cent, to 50 per cent, below normal. The volume of blood is also diminished as demonstrated post mortem . The venous system, apart from that of the portal system, spleen and liver, may be markedly empty. Blood may not flow freely from the pricked finger. The writer's blood during a pernicious attack in Colombia was so viscid and blackish that hcemocvtometer pipettes were repeatedly blocked and no count could be made. Anaemia during first attacks is marked, but rapidly replaced. Anaemia during the following attack is less marked and less rapidlv replaced . The white cells. The leucocytes are at first increased during the rigor, 8,000 to 30,000 in some cases, but thev markedly diminish, causing a leucopsenia with a ratio of i — 500 or 600. In pernicious malaria there may be leucocytosis. Mononuclears are more marked during the leucopasnia, and persist for some time after the fever has subsided. It is a useful factor for diagnosis when the patient is seen after the attack. The increase is relative and absolute; 15 per cent, increase suggests malaria. It is also present in other protozoal infections. 86 DISEASES DUE TO PROTOZOA Phagocytosis is carried on more by the large mononuclear elements and transitional leucocytes than by the polys. A phagocyte may engulf a red cell and its contained parasite. Vacuolization and a reduced staining power have been noticed. Myelocytes have sometimes been found in subtertian cases (Da' Costa). MORBID ANATOMY. (i) In acute vialaria of P. malarice. The parasite does not especially accumulate in any one organ. The spleen is enlarged, not soft or very melanotic. The liver and bone-marrow may be markedly melanotic. There are parasites in the spleen and the blood, but not in the brain. (2) In acute malaria of P. vivax. Death may be caused in rare cases by coma, hsemoglobinuria with pigmentation of the bone-marrow, spleen and liver. The spleen is enlarged. Its contained blood shows large numbers of parasites. The kidneys and colon are inflamed. The endothelial cells of the brain are swollen and contain pigment (Ewing). (3) In the acute malaria of L. malarice. The organ chosen for sporulation suffers most, and produces the symptoms giving the character of that particular type of the disease. The organ attacked principally may be the brain, intestine, heart or pancreas. Macroscopic. The body is pale, yellowish in white races; the heart muscle pale and flabby; ecchymoses sometimes in the epi- and endo-cardium. The lungs may be normal or congested, rarely sclerosed. The liver is enlarged, dark brown to slate colour on section, soft and congested. The gall-bladder is full of dark bile. The spleen is enlarged, capsule tense; on section, deep brown to black in colour. The stomach and intestines are not affected, except in choleraic forms, when the mucous membrane is congested (except about Peyer's patches and the solitary glands) with blood-stained contents, flakes of mucous and dark pigmentation due to h^mozoin readilv demonstrated by the microscope. The lymphatic glands are swollen. The pancreas is normal or in a condition of hcemorrhagic pan- creatitis. The suprarenals are congested. The kidneys are normal or congested, with punctiform haemorrhages in the pelvis, and cloudy swelling in the parenchyma. MALARIA Sy The bone-marrow is hypercemic and chocolate-brown in colour. The brain is normal, or in the cerebral type of the disease one finds oedema, hyper^emia of leptomeninges; broM'n or black pigmenta- tion of cortex and punctiform haemorrhages in the white matter under the cortex. The spinal canal is similar to the brain. The retina may show numerous haemorrhages. Microscopic. Parasites are found in the blood of the heart, spleen, bone-marrow, capillaries of brain, intestine, pancreas, &c., but the types are not differentiated clearly after death. They shrink considerably. The mononuclears show pigment granules. The polys show phagocytosis in a small degree. Macrophages rnay be seen from the internal organs containing parasites and red cells. The heart muscle is loaded with hasmosiderin and the capillaries with parasites. The lungs contain parasites in all stages of development with pig- mented macrophages and leucocytes. The pneumococcus is always present, and perhaps forms a double infection. The capillaries of the liver are enlarged and swollen by the endo- thelial cells loaded with pigment, and filled with blood cells containing parasites and leucocytes with pigment. The perivascular h-mphatics are swollen. The liver cells are compressed between dilated capillaries and contain hasmosiderin ar.:l bile pigment. Rarelv there are localized patches of necrosis. The portal canals are infiltrated with red cells containing parasites. The red cells of the spleen show schizonts and crescents. The leucocytes and macrophages show pigment. The kidneys show pigmentation of the capillarv walls of the glomeruli. Parasites are rare here, but plentiful between the tubules. Phagocytes with pigment and parasites are not uncommonlv seen here. The cells of the glomeruli degenerate and are cast off into the capsule; the epithelial cells of the convoluted tubules degenerate and are cast off into the lumen. The suprarenals show irregular areas of vasodilatation, full of red cells, many of which contain parasites. The same may be said of the capillaries of the abdominal fat. The bone-marrow is chocolate-coloured in the small bones and brownish red in the long ones. It is soft, diffluent, contains sporu- lating parasites and crescents. The brain in cerebral cases has the capillaries full of sporulating parasites, mononuclear elements, macrophages containing dead para- 88 DISEASES DUE TO PROTOZOA sites. Nissl's bodies may be damaged and disappear or degenerate only. There may be degeneration of the neurofibrils. The puncti- form haemorrhages are due to the diapedesis of apparently normal red cells. (4) In the chronic malaria of P. vivax. (There are no records of post-mortem findings in chronic malaria due to P. malarise.) Those of P. vivax are ; — Enlarged spleen, which is firm, dark, containing parasites and pigment in the endothelial cells about the Malpighian bodies. Some haemosiderin. The liver revealed nothing macroscopical, but microscopically pig- ment could be seen collected in the large intracellular masses in the portal canals. The macrophages contained pigment. The bone-marrow was slightly pigmented, showing a few endo- thelial cells with black pigment. In one case (Ewing) the patient was ill for twelve months, and died from endocarditis three months after the last malarial attack. (5) In chronic malaria due to L. malarice. The spleen, liver and bone-marrow are the parts always affected. Spleen, enlarged, firm, slaty colour, depending upon the amount of contained pigment, signs of old perisplenitis, e.g., thickened cap- sule; Malpighian bodies stand out boldly, as they are enlarged and non-pigmented. The capillaries are dilated, and are separated by splenic pulp or connective tissue containing giant cells. The pigment may be scattered diffusely, but is generally collected around follicles or extracellular, and contained in lymphatics of arterioles or septa. Liver, large, hard, pigment not always present, seen at times gathered around the periphery of lobules; later the pigment is peri- vascular and finally disappears. The capillaries or lymph spaces are dilated, and by their pressure cause atrophy of the liver cells; the hepatic cells may be seen repairing the damage done. Bone marrow, usually pigmented and of a chocolate colour in the small bones, reddish in the long ones. The change of colour is due to replacement of the fat by vascular tissue. (6) In malarial cachexia. It may follow a few acute attacks, or more commonly coma as a sequel to chronic malaria. Anemia is marked. Oedema of the ankles and abdomen frequent. The spleen is enormously enlarged, the liver also. The bone-marrow is yellow, sclerotic or gelatinous. MALARIA 89 Parasites may be found or may be absent. Sometimes there are amyloid changes in the kidneys with parenchy- matous nephritis, associated more rarely with amyloid changes in the intestine, spleen and liver. SYMPTOMATOLOGY. A typical febrile malarial attack. In all types of malarial fever there are definite attacks every twenty- four, forty-eight, or seventy-two hours. Each attack has four stages, followed by an interval of apyrexia. (i) Premonitory stage. This is sometimes absent. When present it lasts from a few hours to a few days. There are : Lassitude, aching of bones, headache, anorexia, yawn- ing, sometimes vomiting. Two-thirds of actual agues take place between midnight and mid- day, most other febrile diseases from midday to midnight (Manson). (2) Cold stage. This lasts about an hour. Teeth chatter, patient shivers and shakes from head to foot. Wraps himself in blankets to keep himself warm. Vomiting may be distressing. The features are drawn and the skin blue, but the body temperature may be several degrees above normal and rapidly rising. The urine is abundant and passed frequently. Urea is increased Young children may have convulsions. Then follows the — (3) Hot stage. This lasts four hours. There are waves of warmth, intense heat. Blankets are thrown off; there is a desire for more air. The face is flushed, pulse rapid, full and bounding. Headache intense, vomiting frequent, respirations hurried. Conjunctivae injected, sometimes erythematous rash. Skin dry and burning. Body temperature 40'6° C. — 41 '0° C. (104O— 106° F.). Urine scanty, loaded with urea and chlorides. Phosphates diminished. Bile pigment present in urine. Then follows the — (4) Sweating stage. This last from two to four hours. There is profuse perspiration, clothes and bedding are soaked. 90 DISEASES DUE TO PROTOZOA Fever rapidly declines. The urine is as in the hot stage. Distressing symptoms abate, relief comes, patient sleeps readily. Temperature may fall to normal or sub-normal. Apart from weakness the patient feels well. The whole attack lasts from six to ten hours, but may vary much. A similar attack takes place one, two or three days later, unless quinine is given in the interval. The spleen enlarges temporarily, but remains slightly larger after each attack. In frequent attacks the spleen may be enlarged enor- mously, permanently and accompanied by a cachectic state. The most pernicious fevers, so common in Africa, are most atypical ; the patient may reach a serious condition before a doctor is consulted. The rise of temperature is caused by the discharge of malarial toxin, when the red cells rupture, and not because of the parasites being liberated in the serum. Between attacks the young parasites are grow- ing to maturity in fresh red cells to cause another rise of temperature, when the latter are ruptured. There are continued and remittent types of malarial fevers, when parasites of all stages may be met with in the red cells. CLASSIFICATION. Acute Malaria. 13 . ^ , j Simple, Triple, ^ ■^ I Double, Mixed, D . T, ,. ( Simple. Double, Benign leniaii. ... \ ^ ^ . , ,. ** ] Irregular subcontmuous, Malignant or Simplf^, Siihtertian. Double, (Crescents.) Irregular, -to" Do not form crescents. Remittent, typhoid. adynamic. bilious. Pernicious with general symptoms, e.g., Algide, Diaphoretic, Hemorrhagic, Scarlatiniform. Pernicious with local symptoms, e.g.. Cardiac, Pulmonary. Pulmonic, Pleuritic. Gastrointestinal, Choleraic, Dysenteric, Haemorrhagic pancreatitis, Peritonitic. MALARIA Cerebrospinal, Comatose, Hyperpyrexia, Delirious, Tetanic, Eclamptic, Meningitic, Hemiplegic, Amblyopic, Bulbar, Cerebellar. Chronic Malaria. Cachexia. CLINICAL VARIETIES. Sitnple Quartan Fever (Benign). The parasite is P. malariag. Its cycle is seventy-two hours. 91 rVlMCl«|e|Mlt|ir j-MiM£j]CMCMtUtMtMllMtl Double quartan. of parasite present. There is a daily fever. The condition is diagnosed by the microscope only. The rises of temperature may be unequal for each family of parasites present, but when there are other varieties of malarial parasites the condition is known as a mixed one, and greater differences of temperature variation may be noticed. Major Donovan records one case in which he found the three varieties of malarial parasites. This seems to favour Laveran's view that the malarial parasites constitute a single species with three varieties, a view not widely held. Simple Benign Tertian Fever. The parasite is P. vivax. The cycle is forty-eight hours. The very young form is indistinguishable from that of the quartan, but later one sees — Much more amoeboid movement. MALARIA 93 The change of form and position of the parasite in the corpuscle from time to time. That it pushes out and retracts pseudopodia. The movement is suspended when the concentration of haemozoin is accomplished. The haemozoin particles are finer than cjuartan and have more active and incessant movement. There is hypertrophy and marked decolorization of the invaded red cell, which may be twice its normal size. The rim of haemoglobin becomes almost colourless. With deep Leishman's stain the Hb. shows chromatophile dots, TIME M E M e: a A Z M Z t, A E M E M E M E M E M Tl M E M E M E f' 105 10"* I03 J02 101 lOO 99 98 97 I \ 1 i [ ^ \ \ 1 i , N \ 1 \ ^ V ^J V "^ V V •A s J V "* * V >r- -v >«' ^ Simple benign tertian. " Schiifner's " dots, which are not shown by quartan or sub-tertian parasites. The segmented body has sixteen to twenty spherules, like a cluster of grapes and not daisy fashion. One or two particles of pigment can be seen among the spherules. These latter are smaller, smoother and rounder than those of the quartan, The segmented parasite is called a " rosette " body. As in the quartan the gametocyte is a spherical body, but much larger than the quartan. This parasite is the commonest, and occurs in tropical and tem- perate climates. The fever resembles that of the quartan type. Spontaneous cure is more likely than in the quartan type. The resulting anaemia is more readily recovered from than that of quartan malaria. Double Benign Tertian Fever. This is the same as the above, but there are two families of parasites maturing on different days. The two attacks may not be equal in severity. 94 DISEASES DUE TO PROTOZOA Irregular Sub continuous Benign Tertian Fever. Parasites may mature at different times of the same day, thus pro- ducing a somewhat continuous fever with remission and exacerbations. In this respect it may resemble subtertian fever. Irregularities may also be caused by a mixed infection of other types of malarial parasites. Simple Subtertian Malarial Fever. The parasite is Laverania malarise. The cycle is probably twenty-four to forty-eight hours. These are crescent-forming, and all are malignant. The subtertian parasite is much smaller than the tertian or quartan, occupying as it does half to three-quarters of the red cell. The early unpigmented stage is difficult to see. The amoeboid movements are very active at first. TIME M E . M E . M E M i : M E M E M E M E M E F° 105 1 04 103 I02 1 1 1 GO 99 96 97 I 1 \ 1 ' > A \ A V \^ V^J V V '\ N, r -% / r V V Double tertian. The parasite settles down later and forms small colourless rings. Multiple infection of individual cells is common, much more than in other types, owing perhaps to the enormous number present at the same time. The invaded corpuscle seems to be filtered out by the capillaries and small arteries of the deeper viscera and bone-marrow ; hence few are seen in the peripheral blood. The segmented form is very rarely seen in the blood. It has ten to twelve segments. The invaded cells shrink, become darker, sometimes crenated or folded, when they are known as " brassy " bodies, when the parasites may be made out as small minute pale rings. The gametocyte is crescent-shaped, and in this is unique. A week may elapse after the small intracorpuscular parasites have been seen before crescents are formed, probably not until the pabulum has been exhausted by swarms of endogenous parasites, so that the Essentials of Tropical Medicine. Tertian Malarial Parasite. (Weight's Stain.) (From Webster's Diagnostic Methods.) Estwo- Autumnal Parasite. (Wright's Stain.) (From Webst er s Diagnostic Methods.) MALARIA 95 crescent provides for life and growth elsewhere, e.g., in the mosquito. These persist in the circulation, in spite of heroic quinine treatment, from two to six weeks, after all other parasites have disappeared. Subteitian malaria. Periodicity still definite. TIME A.M P M. A M PM. A.M. PM A M. P M A M. P M. A M RM. a.m|p.m| F° 103 1 02 1 1 1 OO 99 98 97 96 n , 1^ \. /^ r ]/ \ n \ Y r ' \ w \ \ r hi \ V I \ / V \ V J i \ r A V \ / w \ V M \ 11 \ Subtertian malaria. Periodicity indefinite. TIME M E M E M E M E M E M E M £ 1 O 4 1 03 102 1 1 1 OO 99 98 97 A A 1 r A A / / \ V. ^ -V w VI ^ I A- V Subtertian malaria (untreated). Slight fever only. No definite periodicity. Diagnosis based on blood examination. TIME AM. P.M A.M. PM A M. P.M A.M P.M. I06 105 1 O-T 1 03 1 02 1 O 1 1 00 99 98 97 A, 1 \ V / ^ , 1 / \ \ w \ V 1/ \ • \ \ \ \ ^.. yN s/ Severe subtertian malaria (treated). Quinine given very early may stop their formation, but later it has no effect upon them. The presence of crescents is usually marked with cachexia. It is common in all tropical regions. In the sub-tropics it occurs 96 DISEASES DUE TO PROTOZOA in the late summer and late autumn, and hence is called " aestivo- autumnal " fever. It has been noted that crescents can rarely be found in the African subtertian fevers, but when these patients get to Europe the parasites can more frequently be found (Manson). The fevers produced by the subtertian parasite are very irregular, the rigor is less marked, the pyrexial stage more prolonged, while vomiting, body pains, intestinal disturbances and depression are more marked. Relapses are much more frequent. There may be a false crisis preceding the true one. There is a rapid destruction of corpuscles, followed by a marked cachexia. Grave symptoms may arise at any time. Double Subtertian Fever. This is caused by two broods of the Laverania malarise parasite, and has symptoms in common with the preceding form. Irregular Subtertian Fever. This is caused by several broods of L. malarise sporulating at different times, causing an irregular fever. It is common on the West Coast of Africa. Remittent Subtertian Fever. An ordinary attack may be prolonged or two attacks may be con- tinuous, the second commencing before the first has concluded. These may be serious at any time or may become pernicious. There may be sleeplessness, restlessness or delirium. The liver and spleen are enlarged and tender. There is slight dilatation of the right side of the heart. Unless drastically treated the fever may resemble — (i) Typhoid fever in its clinical manifestations, with low delirium, prostration, dry tongue, liver and spleen much enlarged, and melan^mia; (2) Bilious fever, with vomiting, diarrhoea, constipation, jaundice, due probably to the absorption of modified haemoglobin, e.g., haema- phein ; the liver is much enlarged. There is much blood destruction, much bile formation, and sometimes coma and death. (3) Adynamic fever, with tendency to haemorrhages, local gangrene, hasmoglobinuria, great weakness, nervous depression, muscular and cardiac debility, profound and rapid blood deterioration, icterus, leucocytosis and melanagmia. The hasmoglobinuria must be differentiated from blackwater fever proper. The former complicates a subtertian attack. It has been shown that L. malaria produces an haemolysin in such quantities that it cannot be kept in check by the anti-h^molysin, which results in dissolved blood being excreted by the kidneys. Jaundice is more rare in this condition than in ordinary blackwater fever. MALARIA 97 PERNICIOUS SUBTERTIAN FEVER. This ivpe is caused by certain viscera being selected by the parasite for sporiilation. The consequent symptoms have local as well as general manifestations owing to that particular viscus being affected not onl\- by the toxins, but because of its impaired nutrition, for the capillaries may be completely blocked by parasites, red cells, swollen endothelial cells, leucocytes loaded with pigment, free pigment and merozoites. These fevers are accompanied by a high mortality. We shall now deal with them seriatim. (i) Algid Pernicious Subtertian Fever. The condition of collapse is marked, e.g., sharp nose, sunken cheeks, lips and extremities cyanotic, i he pulse is small, soft, frequent. Respirations are laboured. The skin is cold and clammy. There is severe thirst. The patient may die in a few hours. (2) Diaphoretic P.S.F. The sweating of the fourth stage is excessive, a pool of per- spiration may fall on the floor beneath the bed. Exhaustion and collapse may follow. (3) Hccmorrhagic P.S.F. There may be haemorrhages from the skin, mucous membrane of the bronchi, intestines, stomach, or generative organs during the attack, but not during the intermission. A grave anaemia may follow with : thready pulse, coma, delirium, convulsions and death. This variety is rare. (4) Scarlatinijorm P.S.F. There is a diffuse scarlatiniform rash with desquamation of the horny layer and erythema of the fauces. A typhoidal state may carry off the patient, (5) Cerebrospinal P.S.F. The symptomatic manifestations may resemble : — (a) Coma. — There is a sharp onset, with weakness, sleepiness, headache, disturbance of vision, stupor or delirium, ending in coma. The pupils may be contracted. The speech is scanning in character. There may be haemor- rhages under the skin and into the retina. The urine and motions may be passed involuntarily. The heart is dilated, pulse slow, becomes quick and thready before death. In fatal cases, the tongue becomes dry and the patient colder and colder. 98 DISEASES DUE TO PROTOZOA There may be improvement for tAventy-four hours with relapse and death. Some cases recover. (b) Hyperpyrexia. — The temperature may rise to 107° — 108° F. There may be brief mania, followed by muttering delirium, unconsciousness, coma and death in one or a few hours. It is due to embolism by malarial parasites, swollen cells, debris, &c., blocking the capillaries supplying the thermic centre. (c) Delirium. — There may be delirium with sudden onset, followed by exhaustion, coma and death. All are fatal. The fever is usually high. It may be mistaken for thermic fever. (d) Tetanus. — Some delirious patients may show trismus, con- traction of limbs, opisthotonos, retraction of abdomen, and conjugate deviation of the eyes. There may be recovery or death with hyperpyrexia. (e) Eclampsia. — Children may have convulsions, stupor, coma and death. (/) Meningitis. — It occurs in young persons and children. There are : vomiting, slow pulse, headache, retraction of head, rigidity of neck, convulsions, hyperc'esthesia, fever, irregular pulse, coma and death. (g) Hemiplegia. — There may be all ihe signs and svmptoms of hemiplegia with paralyses. There may be aphasia, often resulting in permanent psychical disturbances, loss of memory, &c. This is due to the blocking of the capillaries supplying Broca's convolution (embolism). (h) Amblyopia. — Blindness is sometimes complained of, is usually only temporary lasting for several davs, but in some cases it persists, when there may be found optic neuritis, peripapillary oedema, extravasation of leucocytes, plugging of retinal or choroidal vessels bv parasites, pig- ment, leucocytes and consequent multiple haemorrhages in the fundus (Poncet). In quinine amblyopia (see p. 524) there is retinal anccmia due to toxic spasm of the arterioles and the amblyopia is more persistent. The discs are white and the vessels shrunken, while no inflammator}^ symptoms are present. In the malarial condition one eye only mav be affected, and the condition may clear up quickly under quinine treat- ment. The pupils react to light, but they do not react in quinine amblyopia. (i) Bulbar. — There is difficulty of speech and deglutition with MALARIA 99 facial paralysis or paresis, increased tendon reflexes, ataxia and vomiting. (y) Cerebellar. — There is cerebellar ataxia, severe headache, vomiting, &c. (6) Gastrointeslinal P.S.F. The symptoms may resemble — (a) Cholera. — There is vomiting, abdominal pain, severe diarrhoea, the stools are loose, profuse and numerous, pain- ful cramps of legs. Collapse may ensue with sunken eyes, cyanosis, clammy skin, hiccough, severe thirst, scanty urine, delirium, coma and death. Occasionally a case recovers. The condition may be mistaken easily for true cholera, but the stools usually contain some bile (not rice water-like). The blood also will show indications of malaria. This manifestation is seen in the Punjab. =5e Parasites in capillary from intestine. (6) Dysentery. — The fever is usually high. The stools contain blood and mucus tinged with bile. There is great distress and prostration. The pulse is small and rapid- Quinine may result in rapid recovery. (c) HcEmorrhagic Pancreatitis. The diagnosis is made after death. It is seen in Ceylon. There is an acute onset with epigastric pain. There may be signs of partial intestinal obstruction with marked collapse. ((/) Peritonitis. — This may be simulated when the suprarenal glands are affected in particular. (7) Cardiac P.S.F. The right heart is enlarged, there is severe cardiac pain, and vomiting of blood. TOO DISEASES DUE TO PROTOZOA The patient passes into an algid condition and dies. The capillaries of the heart may contain blood in a condition of stasis which may cause the death of the patient, especially in those with fatty heart and pericardial adhesions. Chronic alcoholic subjects and beriberi victims run grave risks in exposing themselves to malarial infection (Daniels). '^^&&. «« « ©^;.,^^t|V % .* % Parasites in capillaries of pancreas. (8) Pulmonary P.S.F. Resembling — (a) Pneumonia. — There is blood expectoration, in the red cells of which are seen malarial parasites. There is dyspnoea and cough. The symptoms are worse during the fever than during the remission. The blood is usually full of the parasites. The pneumococcus complicating the fever may be the cause of this manifestation. (b) Pleurisy. — There is sharp pricking pain, dry cough, friction sounds, which are worse during the febrile attack. Apart from all these varieties of subtertian manifestations, the testicles may be selected as the point of attack with the corresponding symptoms. The appendix may also be chosen with its symptoms. Dry gangrene of the feet and legs may be caused, malarial end- arteritis (Tomaselli). MALARIA loi CHRONIC MALARIA. The causative organism is usually Laverania malari^e, but either of the malarial parasites may cause it. The numerous symptoms are often slight but frequent. There are : — Repeated small fevers, enlargement of spleen and liver, pigmenta- tion of skin and mucosae, oedema of feet, anaemia which is often marked, haemorrhages which make operations dangerous, multiple neuritis, skin eruptions, sinovitis, palpitation, dizziness, bronchial and intestinal disturbances, morning diarrhoea, fleeting pneumonias and headaches. Sometimes the fevers are absent, such not being necessary for the condition. The spleen may become enormous in size, firm but painless. It is very friable, and may be ruptured by slight blows or even spon- taneously. Vigorous games and corporal punishment should be withheld from such. The liver enlarges from chronic hepatitis. There is hypertrophy of the intralobular connective tissue which leads to hypertrophic or atrophic cirrhosis. This incurable condition leads to portal obstruction and ascites. The h^emosiderin may be in blocks as large as blood corpuscles. The term " Siderosis " is then applied to this condition. The secondary anaemia may be profound with loss of red cells, and Hb., with a large increase of the mononuclear elements. Abortion and sterility are common effects of this anaemia. The condition described above is known as " Malarial cachexia.** If the acute conditions were adequately treated with quinine this condition could hardly arise. Unfortunately malarial relapses are exceedingly common even when quinine has been administered and without reinfection. Some of the parasites, lying dormant, wake up later and cause a relapse for some unknown reason, unless it is because the resistance of the patient is diminished at that time. Recurrences may often occur after several years. Malarial parasites have been found in the blood four years after leaving a malarious district. Apparent recurrences in malarial districts are usually re- infections. Latent malaria is a term given to a condition when malarial parasites are found in the blood and there are no symptoms present. The parasite is usually of the subtertian variety. Masked malaria is a term used when there may be neuralgias, 102 DISEASES DUE TO PROTOZOA cerebral abscess, chronic diarrhoea, &c., when the malarial parasite is found, and the condition clears up on the administration of quinine. Congenital inalaria is doubted, but one case is on record where a malarial mother gave birth to a child, in the umbilical cord of which parasites were found. After death they were also found in the heart blood. The parasites were identical with those in the maternal blood and the placenta. Bignami and others have failed to find parasites in similar cases. Juvenile malaria, when chronic, causes stunted growth and retarded puberty. SEQUELiE AND COMPLICATIONS. The sequels, such as neuritis, neuralgia, anaemia, cirrhosis of the liver and of the spleen, with traumatic rupture of the same, have already been mentioned, but to these may be added mental modi- fication, insanity, tinnitus aurium, vertigo, deafness, anosmia and loss of taste. Malaria may be complicated by — Typhoid fever, to which condition the term of typho-malaria has been applied. There is no hybrid or distinct disease, but the one complicating the other, there being two distinct causative organisms present. Amoebic dysentery may be present, but one must not forget that malaria itself can cause dysentery. Lobar pneumonia is not uncornmon. The low form in chronic malaria is of a deadly type. The possibility of a malarial pneumonia has not yet been decided. Nephritis may be present and is due to irritation by the malarial toxins. It is common in children (Daniels). DIAGNOSIS. Decide positively and treat accordingly if : — (i) The fever has a typical quartan or tertian periodicity. (2) When malarial parasites are found in the blood. (3) When hasmozoin is found in mononuclear leucocytes. Spleen puncture for diagnosis is not devoid of risk. A quartan or benign tertian will yield to quinine within four days, but not necessarily so a subtertian attack. One must differentiate malaria from : — Typhoid Fever, Insolation, Liver Abscess, Kala-azar, Undulant Fever, Influenza, Yellow Fever, Dengue, and Seven-day Fever. A mononuclear increase in a differential blood count is useful, but it may indicate a past malarial attack or pneumonia, sepsis, or an acute MALARIA 103 hepatitis. The latter will mask it by producing an increase of other leucocytes. Children commonly have mononuclear increase without any disease (Daniels). PROGNOSIS. The mortality amongst natives is usually low. In Europeans resident in the tropics it is high, Africa in particular. Simple tertian and quartan parasites give the best prognosis. Subtertian is always grave; pernicious symptoms deadly. People unable to take quinine should not be allowed to reside in the tropics, e.g., malarial countries. Complications always make the outlook more serious, especially typhoid fever and pneumonia. Syphilis in a malarial patient will not vield to anti-syphilitic treat- ment until the malaria has been cleared up. Ross gives us the following interesting figures for India : — The mortality is 5 per 1,000 living, or 1,150,000 per annum. It is greater than the mortality of cholera and dysentery combined. A quarter to one-half of all tropical sickness is due to malaria. Malaria tends to abound in the most fertile countries, hence very malarial countries cannot be prosperous. TREATMENT. For the patient to " fight the fever " himself by his own will-power is a marked error of judgment, and an unjustifiable risk for the patient to take. The indications are : — (i) To kill the parasites. (2) To aid the excretion of the toxins. (3) To relieve the symptoms of the patient. Quinine is a specific if the right kind is given and a sufficient quantity used. Quinine is slightly cumulative; the maximum is eliminated in four to twelve hours, nearly all of it in thirty-six hours. It can be recovered from the urine within fifteen minutes from its administration. The sulphate is soluble i in 800 of water and must be dissolved in mineral acids. It is the cheapest kind, but is not to be recommended. In the early days of quinine treatment, when the Chinese patients of Sir Patrick Manson passed the quinine given as the sulphate in pills, the pills were collected by Chinese physicians, washed, and sold again to fever patients. The hydrochloride is soluble i in 40. The bisulphate is soluble i in 11. The bihydrochloride is soluble i in i. 104 DISEASES DUE TO PROTOZOA The bihydrobromide is readily soluble in water, and is given to those with deafness or headache or idiosyncrasy towards quinine. Quinine valerianate is given to nervous people. / Quinine ^ anna te is not so bitter and can be made up chocolate- coated for children. I Euquinine is very expensive. It is useful for women and children. Solubility and Equivalent Value of Salts of Quinine (after Manson). Amount equiv- Name of salt rercriu alkaloid in the salt Solubility in water a) eni in value one of quin- to sulphate Sulphate 73-5 P er cent. In 800 parts roo Hydrochloride 8r« ,, 40 5> •90 Bihydrochloride 72-0 ,, I n ro2 Hydiobroniide 76-6 ,, 45 1) •96 Bihydrobromide ... 6o'o ,, . . . 7 5' "•23 Bisulphate ... 591 ,, 1 1 n 1-24 Phosphate ... ... 76.2 ,, 420 )' •96 Lactate ... 78-2 T1 . . . 10 )' •94 Salicylate 701 1) . . . 225 11 1-05 Hydrochloi o-sulphate 74-3 ,, . .. 2 )1 ■99 Valerianate ... 73-0 11 . . . 1 10 )) roi Arseniate 69-4 ,, ... slightly ro6 Tannate 20'0 )» ... )) 3-67 If ingested quinine, especially the sulphates, are not dissolved by the acid gastric juices of the stomach it is probably not dissolved at all, as this is not permitted by the alkaline juices of the intestines. Such quinine is then excreted practically unchanged. In small doses quinine is a vascular tonic, but in large doses it is a cardiac depressant. Most of it is oxidized in the tissues. The kidney excretes it as quinine dihydroxyl. It may cause cerebral congestion, manifesting itself as tinnitus, deafness, headaches, &c. It may cause constriction of the retinal arteries, followed by temporary amblvopia or degeneration of the retinal ganglion cells, followed by permanent amblyopia. \^arious kinds of eruptions have been reported from the use of quinine. Ten grains of quinine bihydrobromide contains bromine equal to that in 3 grains of pot. brom., hence if this quinine is used prophy- lactically for long periods mental depression may be expected from the quinine and bromide. MODE OF ADMINISTRATION. Under all circumstances it is best given after food, as then there is more gastric juice, the acidity of which facilitates its solubilitv. (i) By the mouth. The bisulphate or bihydrochloride are to be recommended if the expense is not a consideration. They can be taken as powders, .MALARIA 10 :) solutions, capsules, cachets, tabloids, tablets, or pills. They may be plain, sugar, or chocolate-coated. The sugar-coated ones are not to be recommended unless they can be used quickly, as the sugar hardens in the tropics and hinders the solution of the drug. In some cases it is useful, as it can be given to patients unknown to them. Tablets or tabloids are compact and most useful for work involving much transport. For hospital use the sulphate, dissolved in mineral acids and flavoured, is cheapest. Many tropical residents take 5 grains daily as a prophylactic, or 15 grains (i grm.) twice weekly. A regular habit is to be encouraged. For malarial attacks, 5-10 and even 20 grains t.d.s. has been taken. Darling recommends heroic does; such were absolutely necessary in the writer's experience when in Colombia. One should wait until the temperature has begun to fall before administering the quinine, except in chronic cases, because the head- ache is increased, and the quinine cannot kill the young parasites until the red cells enclosing them are ruptured. When headaches and tinnitus aurium are common, pot. brom., 5-10 grains, or dilute hydrobromic acid should be administered with each large dose of quinine. In old Blackwater cases one should proceed carefully with J-grain doses. If the fever is not being mastered, inhalation of amyl nitrite may dislodge the parasites from the capillaries so' that the quinine can get at them. Children stand quinine well by the mouth. They must have sufificient, say a child under one year, from J-iJ grains six times daily. A child aged 3-10 years old 2-^ grains six times daily. After fever in adults give 15 grains (i grm.) daily for a week, then 10 grains for two weeks, followed by 5-10 grains for a month. Iron and arsenic should be given. In patients with weak hearts digitalis should be given. (2) By the rectum. Useful in gastric disturbance. One should double the ordinary doses one would give by the mouth, say 20-30 grains, in 10-12 ounces of water or warm saline. The writer when in extremis received 40 grains at night, followed by 40 grains the next morning. This method is most useful for comatose patients. Use a large catheter attached to a glass syringe or rubber tube with funnel. Give it slowly. Continue by the mouth as soon as possible. (3) By the muscle. Subcutaneous injections should be abandoned. The writer has a io6 DISEASES DUE TO PROTOZOA scar resulting from a subcutaneous injection of quinine the size of half-a-crown tliat he will carry to the grave. The necrotic ulcer required four months to heal. Intramuscular injections are useful when there are gastric disturb- ances and serious subtertian attacks. Painful spots may remain for months at the point of each injection. I have seen a case of wrist drop following an injection of quinine in the upper arm, the needle having penetrated the musculo-spirial nerve, not to mention the consequent necrosis caused by the quinine itself. One of my patients had been previously treated by quinine injections in both buttocks (even when there had not been any vomiting), and had been partially paralysed in both legs owing to permanent damage having been done to both sciatic nerves. For intramuscular injections the bihvdrochloride should be dissolved in normal sterile saline solution, lo grm. of quinine in lo grm. of saline, given i-ioth at a time (Bacelli). Giemsa's formula is not supposed to be painful in administration. Quinine hydrochloride lo grm Aquas destill i8 „ Ethylurethane 5 ,. Give aV for each injection. Hermetically sealed vials can be purchased readv for use. The gluteal region is chosen usually for the injection along a line drawn from the posterior-iliac spine to the ischial tuberosity. It is doubtful if intramuscular injections are sufficiently rapid in their action for severe and acute cases. There is always some local damage done and absorption would be slow in consequence, during the process of which the patient might die. (4) In the vein. In pernicious cases no time can be lost, hence the intravenous method has its uses. An injection of ether should precede that of the quinine if the pulse is bad. A superficial vein about the elbow should be chosen. 15 grains (roo grm.) should be given at a time, well diluted in 20 c.c. of saline, and injected slowly. It should be repeated if necessary, but after the first injection there may be sufficient recovery to continue quinine treatment by the mouth. Quinine should be given with care in pregnancy as it may cause abortion, but untreated malarial attacks are more likely to produce it. The administration of Cjuinine may precipitate an attack of haemoglobinuria. 5 grains has caused this (Sandwith). Fever cases, during the acute attack, must have — Rest in bed, light diet, blankets for cold stage, hot bottles, hot MALARIA 107 drinks to acid perspiration. In hot stage, vinegar or its equivalent to the forehead ; for headache, aspirin can be used but in severe cases heart failure may be caused by it. Caffeine is good in small doses, 2-3 grains. In the sweating stage remove all blankets, damp clothing and bedding, then administer tepid sponging, iced soda water, &c. For — Vomiting: iced champagne; mustard leaf to pit of stomach; chloro- form and morphine mixture, stomach lavage. Hiccough : mustard leaf, codeine, morphia. Cough: codeine and morphia. Constipation : calomel, 1-3 grains, followed by saline. Hyperpyrexia: cold sponging, cold packing, cold baths, cold enemata. If the temperature is kept within limits for a few hours the quinine will have a chance to act. Algidity: salines given hypodermically, intramuscularly, intra- venouslv or per rectum. Warm applications to body, oxygen inhala- tions, ether and strychnine. Hcrmorrhages : calcium lactate, adrenalin, salines. Big spleen : counter-irritants, saline aperients, quinine, iron and arsenic. Convalescence : Give quinine for three months, iron and arsenic for two months. If the attack has been very serious send patient to a cool climate. PROPHYLAXIS. It is most essential that all the scientific methods of prophylaxis should be carried out. By them the death-rate, case incidence, illness and mortality from complications, as well as the disease and the expense to employers of labour, are enormously decreased. The work of Colonel Gorgas and his Sanitary Staff at Panama for the abolition of Yellow Fever and the enormous decrease of Malaria is too well known to be repeated here. This work was made possible by the sanitarian. The monev spent in such work is insignificant when compared with the work achieved and the lives saved. Prophylactic measures against Malaria may be summarized under two heads : — (i) Protection against mosquito bites. (2) Mosquito reduction. These will now be dealt with. (A) PROTECTION AGAINST MOSQUITO BITES. (i) Mosquito nets must be used invariably, twenty-five strands to the inch, which will keep out the Simulid^ also. The nets should be tucked under the mattress and not allowed to fall looselv on the floor. io8 DISEASES DUE TO PROTOZOA It should be kept in good repair. Each net will last one year in travel, and about two years stationary. When the strands are becoming rotten the nets should be destroyed. A net with small holes or not tucked under the mattress is worse than not having one at all. (2) Portable mosquito-proof rooms could be used, and are extremely useful for doing night work or reading in mosquito districts. They are essential in some districts when one wishes to work in peace during the daytime when flies are a pest. (3) Fixed mosquito-proof rooms can be used which are more stable for permanent residence. Copper gauze wire can be used fixed to timbers. Portable ones on frames are also made with copper wire, but they are subject to much damage in constant transit. Some steamers trading between Liverpool and the Amazon are now- screened against mosquitoes. The sea air may be injurious to the copper gauze. (4) Mosquito proofing of windows and doors excludes flies, moths, glare of the sun, damp exhalation after heavy tropical showers, and allows the breeze to enter unimpeded. Mosquito wire is of tinned iron, copper or brass, the prices being as two is to three. (5) Mosquito proofing of verandahs. This is more expensive, but in selected cases gives good results. It obscures light and seems to retain the heat. (6) Hands and feet can be protected by mosquito boots, gloves, &c. (7) Medicine. All exposed to mosquito bites should take 5 grains of quinine daily. To keep off mosquitoes employ eucalyptus, petro- leum, camphor bags about neck, &c. Natives like the mixture of "Camber-green oil," with which they paint their bodies. It is made up of Citronella oil, i|; Kerosene, i ; Cocoanut oil, 2. (8) Constant movement will prevent mosquitoes from settling nearly as frequently as they otherwise would. (9) Fans and punkas. These creating a breeze are useful in houses or on verandahs. They can be driven by hand or electricity. (B) MOSQUITO REDUCTION. (i) By killing adults in houses with a small hand net. (2) Fumigation for the same purpose. This method is much used in Italy and the States. Sulphur is generally used. ^- Powdered sulphur, 2 lbs. per 1,000 cub. feet. Moisten with methylated spirits. Place in shallow pan, supported on brick, in a large flat basin of water in a sealed room. Leave for three hours after ignited, and then ventilate room well. Pyrethrum powder may also be used, 3 lbs. per 1,000 cub. ft. Sulphur affects brass work and steel goods. MALARIA 109 Camphor and carbolic acid can be used, equal parts, 4 ounces dis- solved bv gentle heat, per 1,000 cub. ft. Only about half an hour is required. (3) By natural enemies, e.g., bats, birds, lizards, dragon flies, fishes as Girardinus poeciloides (millions), tadpoles. All such should be bred and protected. Such means, however, are not always best. 1 1 mav be much cheaper and better to remove the water altogether than to maintain " natural enemies." (4) Dealing with the larvae. — All small receptacles for water should be removed or filled with lime or given a surface film of kerosene, if such are used for table legs to keep away ants, &c. Larger quantities of water and small streams can be covered with a thin surface film of crude kerosene which does not permit the larvae to reach the surface for air. It requires half an ounce per square yard ever}' seven days to be effective. Wherever possible destroy and do not treat mosquito breeding places. Small pools should certainly be drained. Holes in rocks and trees should be filled with rubble and cement. Plants which breed them, as pineapples, bananas, &c., should be removed from near dwell- ings. Culicines breed in palm trees and sugar cane. Larvicides, such as copper sulphate, &c., can be used in water, which rapidly kills ofT the larvae, but it becomes poisonous for other animals. (5) Screening of breeding places is sometimes necessary, such as of water tubs, wells, cesspits, &c. Cattle should be watered at certain parts only and the hoof impressions levelled. (6) Drainage. — Open channels should be cut in the soil and con- creted. Drains could be of stone and gravel. Local material available will help one to decide. The subsoil should be drained by pipes. As much as possible of the surrounding land should be suitably cultivated. (7) Trees and bush. — Eucalyptus trees are not worth while. Many .trees should not be allowed to remain near to houses as they attract and give out moisture, exclude breeze and increase heat. All bush and undergrowth Avithin 200 yards of all villages, houses and dwellings and all grass within this area above 12 inches in height should be cut down. A mosquito will not be able to cross such a zone without destruction by sun or wind. (8) Houses should be built several feet above the ground, upon sites high and dry, well away from coolie lines and native villages. Houses should be lofty — of stone, if possible, or brick — with good light and ventilation, which mosquitoes do not like. Whitened walls are good. Curtains and fancy decorations are bad. As to the height of the site, one may remember that the temperature of the air tends to fall 1° F. every 300 feet above sea-level. Malaria no DISEASES DUE TO PROTOZOA tends to diminish at 500 — 1,000 feet high, but under suitable conditions it may be found 5,000 feet high. (9) Rice should not be cultivated within five miles of towns in Italy because of the swampy nature of the ground. In India, however, where this law would mean famines it could not be enforced. Professor Pearson has worked out an interesting point on mosquito reduction. Me affirms that if moscjuito propagation is suppressed within the circular area of a mile — The mosquito density at the centre will be 3 per cent. At a quarter of a mile from the centre 18 per cent. At the periphery 75 per cent, of the density surrounding that area. Sir Ronald Ross's work at Ismailia reduced malarial cases from 1,551 in 1902 to 37 in 1905, the latter being all relapses. The cost of the work was 2 — 3 francs per head of the population. Every malarial district before being opened up should be systematic- ally surveyed with regard to malarial propagation, and the work commenced at once on given lines. Celli has shown us some interesting figures on the Relative Values of Malarial Prophylaxis. Protection Quinine and Method of prophylaxis None Qjinine alone from mosquito protection alone from mosquito Percentage of infection ... 33 ... 20 ... 2*5 ... 175 Hence quinine alone will prevent 13 per cent, of cases, and Quinine plus mosquito protection will prevent 3r25 per cent, of cases. FOR NEW INFECTIONS ARE REQUIRED:— (i) That an infected person with gametocytes is living in or near to the locality. (2) That an Anopheles, capable of carrying" such gametocytes,. sucks up sufficient blood from the infected person. (3) That this mosquito lives for a week or more under suitable conditions. (4) That it then bites a person non-immune and not protected by quinine. (5) Infected persons and carrying flies must be sufficientlv numerous. If there are many flies and few infected persons the chances of becoming infected are greater than if there were few flies and many infected persons. The following facts may be of interest : — Spleen Rate. Within 300 yards of jungle, undrained, it was 47 per cent. THE MALARIAL MOSQUITO iii Within i,ooo yards it diminished to 2*6 per cent. (Watson). At the edge it was 59 per cent. Fry found it to be 2s per cent, at 200 yards away and nil at one mile distance. Mosquitoes fly readily for a Cjuarter of a mile, but half a mile appears to be beyond the normal distance of flight. A gentle breeze will carry them a distance of one and a half miles. 100,000 mosquitoes per 100 yards square was once worked out to be an average number present. Anopheles are not hungry for twelve to twenty-four hours after being hatched out or after laying eggs. On an average only one out of forty-eight of all females ever have the chance of carrying malaria even in a malarial district (Ross). The cost of a new hospital wOuld often suffice to prevent more cases of sickness than are treated in it, and the cost of invaliding would often suffice to prevent the disease which caused it. THE MALARIAL MOSOUITO. The knowledge of these mosquitoes is so extensive that special works must be consulted for details. A resume only of the outstanding facts can be attempted here. The four great families of the Xematocera, order Diptera, which are of interest to the medical officer are the — (i) Culicidas, or mosquitoes. (2) Psychodidfe or moth-like midges, containing the notorious Phlebotomus. (3) Chironomid^e, or midges. (4) Simulidi^e, all the species of which are extremely bloodthirsty. FAMILY CULICIDiE. They are distinguished from the midge-like flies by : — (i) The venation. The costal vein runs all round the edge of the wing. ,, first vein is very long. ,, second bifurcates. ,, third is very short and goes off the second at right angles. ij fourth both bifurcate. ,, fifth ,, sixth is simple and short. (2) The close fringe of scales on the posterior border of the wings. 112 DISEASES DUE TO PROTOZOA (3) The projecliiiij;- proboscis of extraordinary length. There are two sub-families : (a) Corethrinae. (b) Culicinc'e. SUB-FAMILY CULICIN^. Genus Anopheles. The Sub-genera are important :-■• Anopheles (sensus restrictu). Mvzorhynchus. Arribalzagia. Christ3^a. ]\Iyzom}ia. Pyretophorus. Nyssorhvnchus. Neocellia. Cellia. Chagasia. All known carriers are included in the Genus Anopheles, of which there are about 100 species universally distributed, but chiefly in the Tropics. Every medical ofBcer should examine the stomach and salivary glands of mosquitoes caught in his district for malarial parasites in order to ascertain the species prevalent there. For the dissection of mosquitoes, see p. 637. The known malarial carriers in the dififerent countries are : — (After Alcock.) IN EUROPE. Anopheles maculipennis. ,, bifurcatus. ,, (" Pyretophorus ") superpictus. ,, (Myzorhynchus) pseudopictus. IN SOUTHERN ASIA. Anopheles (Myzomyia) lis'.onii. ,, ,, culicifacies. ,, (Myzorhynchus) barbirostris. ,, ,, sinensis. ,, (Nyssorhynchus) fuligiosus. ,, ,, theobaldii. ,, (" Neocellia ") stephansii. ,, ,, willmorii. IN TROPICAL AFRICA. Anopheles (Myzomyia) funestus. ,, (" Pyretophorus ") costalis. THE MALARIAL MOSQUITO 113 Anoplieles (Myzorhynchus) maurilanus. ,, ,, paludis. IN AUSTRALIA. Anopheles (Nyssorhynchus) annulipes. IN NORTH AMERICA. Anopheles maculipennis. ,, bifurcatus. IN TROPICAL AMERICA. Anopheles (Myzomyia) lutzii. ,, (" CelHa ") argyrotarsus. • ... IN THE UNITED STATES (Von Ezdorf). Anopheles allumanus. ,, argyrotarsus. ,, crucians. ,, intermedium. ,, quadrimaculatus. ,, pseudomaculipes. ,, pseudomaculipennis. ,, tarsimaculata. The following species are known to carry the larvcs of Filaria bancrofti : — Anopheles maculipennis. ,, (Myzomyia) rossii. ,, (Myzorhvnchus) nigerrimus. ,, ,, mmutus. ,, (Mvzomyia) funes(us. (" Pyretophorus ") costalis. ' The Malarial parasite also. ,, {" Cellia ") argyrotarsus. ) SUMMARY OF FACTS RELATING TO THE ANOPHELES {ai'0)(f)6\i']s =^ unprofitable, harmful). CULICIDiE. Adults. — The head is small, hemispherical, has a distinct neck, brown cheeks covered with scales, used for differentiation of species. Eyes reniform ; no coelli. Antennae long, slender, 14-15 segments, first globose; others carry whorls of hairs, wispy in female, thick and bottle-brush-like in male. Labium, in the majority, is long and slender, covered with scales ; ends in pair of small stiflfish labella, bent when piercing. Maxillary palps, covered with scales, show specific and sexual 8 114 DISEASES DUE TO PROTOZOA I, Culicine, male; 2, Culicine, female; 3, Anopheline, mile ; 4, Anopheline, ''female. THE MALARIAL MOSQUITO 115 differentiation; may be longer than proboscis; clubbed in male Anopheles. The parts ensheathed in proboscis are long, slender, piercing organs except in the Corethrin^e, consisting of : — Proboscis Antennae PaTpi ' Eyes'' Occiput ~" Protlnoracic lobes Mesothorax-""' ^ Scuteilum — Mcto thorax orMctaootuiD First abdomin'oL segment Abdomen Eosal lobes of Q .. , ., , + Male genitalia Basal lobes Clasper. proboscis Palpi Antennae. Basal lobes ofantennae Prons Vertex Eyes Occiput Nape v-^^- tarsal ungues ^4^ Diagram showing the structure of a typical mosquito. (Theobald.) (i) A Stout-pointed epipharynx, grooved ventrally. (2) A slender hypopharvnx, which is itself an efferent tube for the saliva; forms when applied to the epipharynx a groove known as the afferent suctorial tube. ii6 DISEASES DUE TO PROTOZOA (3) A pair of slender mandibles expanded and very finely serrated at the tip. (Absent in the males.) (4) A similar pair of maxilUe coarsely serrared ar tip. (Absent in the males.) Sometimes the mouth parts of the males, which only live on juices, appear to consist solely of the epipharynx and labium Photographs of living mosquitoes, C. impellcns. Walk.). Above $ and J in profile ;_in the middle ventral aspects of the same; and beneath J and J dorsal views. About twice natural size. Thorax is covered with scales or hairs. Scutellum is narrow, not lobed in .Anopheles, and is overlapped by the menatonum, which is bare. Abdomen is long, narrow, scales or hairs, nine segments, last bilobed, complicated in the male with a pair of chitinous clasping hooks. The wings are as described above; all the veins are clad with scales, lanceolate in shape for Anopheles. THE MALARIAL MOSQUITO 117 The halteres (balancers) are plainly visible. The legs are long, slender; fifth segment carries pair of claws. In order to spot the male from the female readily use the antennas as the chief guide. -^iSPEajStev 8 9 Various forms of Mosquito Eggs. — (l) Egg-boat of Ciilex, seen from above; (2) the same, side view (after Sambon) ; (3) separate Cities eggs; (4) eggs of Panoplites (after Daniels); (5) ^gg^ "^f Stegomyia ; (6) the same more highly magnified (after Theobald) ; (7) groups of Attophales eggs, as they float on the water (after Sambon) ; (8) egg of Anopheles maculipennis, showing lateral floats, seen from above, ;< 30 diams. ; (9) the same, viewed laterally (after Nuttall). a, eggs of Culex ; b^ b'^, eggs of Anopheles ; c, egg of Stegomyia ; d, egg of Teeniorhynchus ; e, egg of Psorophora. For the differentiation of species see a special work. Eggs. — These are laid on the surface of the water — If as a sheet of jelly-like frog's spawn they are of the Corethra. ii8 DISEASES DUE TO PROTOZOA Breathing apertures The anterior parts are shown in the prone position and the hinder ends in profile, owing to the body being twisted by the pressure of the cover-glass. (Anopheles rossii, Giles ; larva) Breathing tube (Culex impellens, Walker ; larva) Palpi Palpi Male Female Anooheles G. M. Giles, de nat. dec. Male r Culex Femcle THE MALARIAL MOSQUITO 119 If in groups or rafts they are of the Culex. If singly they are of the Anopheles. Each Qgg is oval, one end blunter than the other, with a pigmented chitinous shell. It has a very fine external membrane which facilitates the floating of the eggs. They hatch in twenty-four hours in a hot tropical season. Larvce. — All must live in water and can be found in collections almost anywhere, even in sea water, but not as a rule in rivers where the current is strong. They are very active, and live principally on algag and similar vegetable matter. The head is a rounded chitinous capsule with well-developed appendages. The eyes are irregular masses of pigment in the younger, and distinctly faceted in the older ones. The antennae are long. The clypeus is prominent, to which are attached the " mouth- brushes," which have a rotatory motion to sweep food to the mouth. The thorax has three segments, distinguished from the abdomen only by an arrangement of hairs, which are in tufts, single-branched or feathered. The abdomen is elongate, soft, with nine segments sometimes beset with stiff hairs like the woolly-bear caterpillar, but usually hairs are lateral and on the free edge of the last segment. On the dorsum of the eighth segment the breathing organs open by two independent orifices in Anopheles, or one breathing tube of varying length in others. This latter has a valve and carries spines. The intestine opens at the free end of the ninth segment, which carries bunches or whisks of hairs and four tapering tracheal gills. In repose some larvae hang with the head downwards with the tip of the breathing tube at the surface for air, but the larva? of the Anopheles groups lie horizontally to the surface. Larvas become fully grown in about one week, but in cold climates may remain unchanged during the winter. They moult several times and feed continuously. Pupa. — They must live in water. They are active, but do not feed. In appearance thev are like tiny lobsters. The head and thorax form one mass. Two ear-like breathing trumpets come from the back of the head mass for breathing. The curved abdominal ninth segment ends in a pair of large blade- like fins. On the first segment there are two tufts of hairs, fan-like, to catch 120 DISEASES DUE TO PROTOZOA the surface film and to bring the pupa into a good position for breathing. The pupa matures in two days in hot weather. When the adult is about to emerge the pupa straightens its back, the skin of the cephalothorax bursts along the back, out of which opening the adult appears. It rests for a few minutes and then flies away . Vn^pa. oi Anopheles niaculitennis, Meig. Enlarged. (After Grassi.) Soon after a female is hatched it probablv becomes fertilized; some maintain that it takes blood first; oviposition follows the blood meal, and takes place in the earlv morning. The time of development is (average) : — Egg stage Larval ,, Pupal ,, I to 7 „ •7 i8 days lo to 24 days, or longer BIONOMICS. The imago emerges from the pupa during the late afternoon when the female is ready for fertilizing the male. The latter sex usually predominates numerically. The female alone bites man and animals in order to obtain blood, which forms rich food for the eggs, but much more rarely they will feed on juices, the Culicinie more than the Anophelinaj. The mouth parts of the female alone are adapted for piercing. It is during this act that malarial sporozoites are injected into the THE MALARIAL MOSQUITO 121 human bodv from the infected mosquitoes. They pass down the hypopharynx or salivary tube, while blood and malarial "gametes pass up the labial tube to the mouth. They feed mostly at night, but may do so at any time of the day. Thev become blown out with blood, then retire to digest it. Next morning the female Hies to the nearest water to lay her eggs; she ma_y travel half a mile for this if it is necessary. The Anopheles prefer clean water with weeds, the Culicina^ any kind. The Anopheles eggs may be found in the back-eddies of streams, margins of lakes, large wells, puddles, in broken bottles, shells, holes of rocks and trees, and in plants like bamboos, pineapples, &c. At night the female seeks blood again. The larvffi are cannibals, living on each other as well as on algse. These larv^ must be attacked by the medical officer everywhere, or he can only protect himself with nets and drugs. In the dry season mosquito-larvaj can ^estivate and wait for more suitable conditions. The adult lives for about four weeks, not counting hibernating periods. One adult mosquito can give off 200,000,000 in four months (Ficalbi). Adults may be transported great distances in ships, railway carriages, but it is by accident and not by choice. The mosquito engorges herself with blood in one minute. She begins to secrete the liquor sanguinis almost at once, this being the refuse of digestion. The peculiar buzzing noise so well known to tropical residents is due to the vibration of its proboscis, and has no relation to the wing movements (Darling). Darling affirms that Anopheline females will suck blood at any time and do not wait for fecundation. Ross says that the female sucks blood after fecundation, also that the male only lives for a few days. Darling says that the male lives fifteen to nineteen days, e.g., as long as the female when suitable food is available, such as sliced banana, &c. Mosquitoes are not confined in their attacks for blood upon man, for they are known to attack invertebrates, e.g., insects, and also young fish. Possibly a quarter of the total number of anopheles may succeed in biting human beings once. A third of these may live for a further ten days, of which only a quarter may succeed in biting again. 122 DISEASES DUE TO PROTOZOA That is, only one out of every forty-eight mosquitoes can ever have a chance of carrying malarial parasites (Ross). The Mansoni titillans has now been found to be the most numerous of all mosquitoes in the Panama Canal Zone. It has habits which enable it to escape both in the larval and pupal stage all larvicidal efforts, as these stages are passed beneath the water. This is rendered possible by breathing tubes being adapted for piercing the rootlets of the Pistia stratiotes and thus obtaining their supply of oxygen. The roots are sometimes several feet long, and to these the larvas are attached. Xot all plants, however, contain them, other conditions being necessary. The adult mosquito has long been known in the Canal Zone, but the larvce and pup^e have not before been found. TRYPANOSOMIASIS. (i) African Trypanosomiasis. (2) South American Trypanosomiasis. (3) Notes on Mammalian Trypanosomiasis. AFRICAN TRYPANOSOMIASIS. DEFINITION. An acute specific infection caused by : — (i) Trypanosome gambiense, carried by Glossina palpalis. (2) Trypanosome rhodesiense, cari-ied by Glossina morsitans. Other species of trypanosomes may cause the disease. The morbid manifestations are : irregular chronic fever, fleeting skin eruptions, local oedema, adenitis, physical and mental lethargy, mania, eye lesions, tenderness of muscles and bones. HISTORY. The '* surra " of India has been ascribed to the bites of certain blood-sucking flies by the natives from time immemorial. 1724. John Atkins in "The Navy Surgeon " described the sleep- ing distemper common among the negroes of the Guinea Coast, seen by him in 1721, but not published until 1724. 1803. Winterbottom described it as he saw it on the West Coast near Sierra Leone. Slave dealers would not buy slaves with enlarged cervical glands. 1846. Trypanosomes first found in fishes. 1879. Lewis found the rat trypanosome (T. lewisi) in Bombay. 1880. Evans found the T. evansi in horses of India at Madras. AFRICAN TRYPANOSOMIASIS 123 1849. Clarke saw trypanosomiasis on ihe Gold Coast. 1869. Guerin found it in Martinique in the negro slaves imported from Africa. 1890. Nepveu found the trypanosome in the blood of man in Algeria while searching for malaria. This was the first time it had been found in man, and it was accidental (Manson). Its significance was not then known. 1891. The first case was brought to London under Sir Stephen Mackenzie. 1895. Bruce showed that " nagana " was due to T. brucei. 1900. Two human cases were brought to London under Sir Patrick Manson. The morbid anatomy of these cases was studied in detail by Dr. Mott. . 1901. Ford and Dutton found T. gambiense in the blood of patients on the Gambia. 1902 and 3. Castellani found trypanosomes in the cerebrospinal fluid of patients in Uganda. 1903. Sir David Bruce and Nabarro showed that Trypanosomiasis was spread by Glossina palpalis, an hypothesis alreadv formed by Sambon and Brompt on epidemiological grounds. 1905. Thomas introduced " atoxyl " for treatment. 1907. A bureau was founded in London for the studv of the disease. Ehrlich found that trypanosomes mav become atoxvl- resistant. Plimmer and Thomas introduced tartar emetic associated with atoxyl for treatment. 1910. Stephens and Fantham created a new species, e.g., T. rhodesiense. 191 2. Kinghorn and York showed that G. morsitans was a trans- mitting agent for T. rhodesiense. Livingstone (1841-1873) gave arsenic to horses for nagana. Manson had used liquor arsenicalis. DISTRIBUTION. It was first noticed on the West Coast of vSierra Leone. It was imported from this endemic centre to the West Indies from time to time, where it soon died out. In 1882 it existed from Senegal to Loando and the islands of the Gulf of Guinea. It was much wider spread at this time, but it was not known to civilization. In 1898 it was known on the Upper Niger. Tlje disease was probablv spread in Africa as follows : — In 1886 vStanlev took some Congolese natives across Africa to the Victoria Nile. Some of these natives settled to the west of Lake Albert 124 DISEASES DUE TO PROTOZOA Nyanza and in Uganda. There is little doubt that men of Stanley's expedition and Emin Pasha's followers carried the disease with them across Africa into Busoga and Uganda. The former place was known to be infected in 1896, and the latter extensively infected by 1900. The western shores of Victoria Nyanza were found infected in 1901 ; the eastern shores and German East -Africa in 1902 ; Button and Todd found ii widelv disseminated in the Congo Stale 1904-1905, spreading along trade routes. These writers stated that the disease would spread into Eastern Rhodesia, which has since come true. It has spread upwards from Uganda to Wadelai on the Victoria Xile since 1904, and had invaded the Lado before 1908. It was recognized in the Sudan, Bahr-el-Ghazal province, in 1909. Its present boundaries (1919) are : — On the West Coast from St. Louis in Senegal to Mossamedes in Angola, up to Timbuctoo on the Niger, throughout the Congo into Uganda, Rhodesia, Southern Nyasaland and Portuguese East Africa. From Uganda and Busera southwards to German East Africa and Lake Tanganyika, and northwards to the Bahr-el-Ghazal province. It may spread to Arabia as tsetse flies exist there. Of course it may also spread to co-existing lands wherever tsetse flies prevail. AETIOLOGY. The known causative organisms are T. gambiense, 1902, and T. rhodesiense, 1910. The L'^ganda strains may differ from the others, an hypothesis suggested by the difiference of its virulence. The trypanosomes of animal trypanosomiasis may cause it. Pro- fessor Lanfranchi, who has never left Europe, was accidentally infected with a supposed laboratory strain of T. brucei, causing irregular febrile attacks, general debility, and large patches of cutaneous tvdema over a period of two years. T. gambiense probably lives in antelopes chiefly. T. rhodesiense in hartebeest, waterhogs and domestic pigs. These animals and man form the reservoir from which man is infected. It is not known if Glossinae infect their eggs. Trypanosomes are known to develop more rapidly at high tem- peratures. The trvpanosomes are injected at the same time as the Glossina palpalis and morsitans suck blood. Koch has suggested that it may be also transmitted by sexual intercourse. Some authorities blame mosquitoes also. AFRICAN TRVPANOSOMIASIS 125 iMinchin considers that encysted forms from fly dropjDings may be ingested and cause infection. It is fairly conclusive that Tabanides convey it mechanically from beast to beast in herds of cattle. Race does not affect infection. Occupation predisposes in so far as there may be exposure to the flies near their breeding- places or cover areas. Hence those working along the shores of rivers and lakes of infected regions are exposed to the bites of infected Glossinaj, usually palpalis, while porters marching through the bush are exposed to the bites of G. morsitans. THE PARASITE. As seen in Jrcsli bluod the trypanosome is an active wriggling organism with a laterally compressed spindle-shaped body, provided with a delicate undulating membrane. Fringing the dorsal edge of the trypanosome and terminating in a free whip-like filament is the flagellum. Stained specimens show a nucleus, somewhat central, and a minute deeply staining chromatic mass, the blepharoplast, which is nearer to one pole, e.g., the thicker or aflagellum or anterior end of the organism. Near to the blepharoplast is a small non- staining area, viz., the vacuole. The thickened free border of the undulating membrane springs from the blepharoplast at one end, and is continued as the flagellum at the other. In some places the cytoplasm is homogeneous, while in others it is faintly granular when stained. There is great diversion in the dimensions of the parasite in body, nucleus and flagellum. Multiplication is bv longitudinal division, commencing at the blepharoplast, which elongates and then divides. This is followed by the duplication of the thickened margin of the undulating membrane and longitudinal division of the whole body. The flagellum does not divide. The complete separation of the two halves along the posterior border does not take place until the new flagellum has been formed. When separation takes place it is postero-anteriorly. Sexual differences have not been decided upon. Trypanosoma gaiiibiense. (After Dutton.) 1,700. 126 DISEASES DUE TO PROTOZOA HABITAT. Parasites occur in the blood, lymphatic glands, cerebrospinal fluid and probably in the fluid of the serous cavities, which facts point to the lymphatic system as being the most important habitat. It may be very difificult to find the parasites in the peripheral blood. When present they may be more readily found during a febrile attack. T. gambiense has not yet been cultivated on artificial media, but it can be readily communicated to monkeys, dogs, rats, guinea-pigs and other animals. The rat trypanosome, T. lewisi, has been cultivated through many generations. During adverse conditions, such as increasing scarcity of nutri- ment, lowering of temperature, addition of chemical solutions and the influx of sera from non-susceptible animals, the trypanosomes tend to agglutinate, e.g., to congregate in bunches, with their extremities (anterior) directed towards the centre. One bunch may contain loo individuals. The parasites mav disperse again, apparently unaltered and uninjured. In cultures, trypanosomes may assume a spherical form and lose their flagellum. The time required for the trypanosome to remain in the fly before transmitting the infection is probably 20 — 47 days (Manson). CLASSIFICATION. (After Bruce, Lectures before Royal College of Physicians, 1915.) Classification is based upon : — (i) Morphology. (2) Pathogenic action of animals. ^ (3) Mode of development in tsetse flies. Cultivation is of no assistance at present. Inoculation experiments and serum diagnosis are not helpful for diagnosis on the field. (i) Morphology. In fresh films one ascertains the general appearance of the trvpano- somes and the kind of movement. Some vibrate about one spot, others hurl themselves about the field with great power and velocity. Stained specimens give more exact details as to length, breadth, cell contents, nucleus, micronucleus, undulating membranes and flagellum. (2) Pathogenic action on animals. The passage of a trypanosome through a series of animals of the same species exalts their virulence towards that animal, e.g., the wild strain of the nagana trypanosome which kills a rat in 20 — 30 days, but AFRICAN TRYPANOSOMIASIS 127 if passed through rats for many generations the rat will be killed by them in two days. The passage of trypanosomes through dififerent species will lower their virulence, e.g., some wild trypanosomes will kill monkeys in a few days, but if passed first through a goat, an attempt to infect the monkey fails, hence its passage through the goat lowers die virulence of trypanosomes for monkeys. Care is necessary in adopting this as a means of differentiation. It has been observed that — T. brucei is more virulent for laboratory animals than T. gam- biense. Some are deadly to horses and cattle, and are harmless to dogs, monkeys and rabbits. Others show a preference for domestic pigs. (3) Mode of Development in Tsetse Flies. All the trypanosomes pathogenic to man and domestic animals in Africa, with the exception of two northern species, pass through a specific cycle of development in the tsetse flies. The mode of develop- ment in the tsetse is different for different species, and this feature may be used for differentiation. North African species have not been found capable of developing in tsetse. It may be that from disuse they have lost the faculty, if ever they had it. CENTRAL AFRICAN PATHOGENIC TRYPANOSOMES. Group (A): Trypanosome Brucei Group. Synonyms : T. rhodesiense, T. ugand^e. The question of identity of T. rhodesiense and T. brucei is still sub judice. The differentiation of the groups is according to the development of the trypanosome in the tsetse. The microscope will decide to which group the trypanosomes will belong. General features of all in this group. All are more or less polymorphic. They vary much in size and shape. The cytoplasm contains numerous dark-staining granules. The kinetonucleus is small and situated at some distance from the posterior extremity. The undulating membrane is well developed and has bold folds. They affect many species of animals, including man, cattle, horses, dogs, &c. T. brucei and T. gambiense develop in the tsetse in the same wa}-, at first in the intestine, then in the salivary glands. There they com- pletely develop into infective forms. No other group invades the salivary glands. (i) Trypanosoma brucei. 128 DISEASES DUE TO I'KOTOZOA U is ihe must widely disl-ribuled pathogenic irypanosome of Central Africa. It causes nagana amongst domestic animals. In Nyasaland it causes trypanosomiasis in man. It is rapidly fatal to man and domestic animals. It is carried by the Glossinae morsitans and pallidiijes. (2) T. gambiense. Synonym : T. nigeriense. It causes trypanosomiasis in man. Cattle and antelopes form the reservoir for the virus without causing symptoms in them. This trypanosome is less fatal to man than T. rhodesiense. vSome recover. It is carried by the G. palpalis. (3) T. evansi. Synonym : T. soudanense. It causes surra in horses and mules, camels and cattle in India, Philippines, Mauritius, North Africa, &c. It is transmitted by the bites of fleas, flies and ( ?) b\- eating infected meat. (4) r. equiperdum. It causes dourine or mal de coit in horses in Europe, India, Xorth America and North Africa. It is spread by coitus. It is always fatal from two to eighteen months. Group (B): Trypanosoma Pecorum Group. General features of all in this group : — All are small and monomorphic. The cytoplasm is non-granular. The kinetonucleus is prominent, sub-terminal, and often seems to project beyond the margin. The undulating membrane is fairly well developed. Development begins in the intestine, and later passes to the proboscis and salivary duct or hypopharynx, where they complete their development and beco)ue infective. (i) T. pecorum. Synonyms : T. confusum, T. nanum. It causes an important trypanosomiasis in cattle. It is carried bv T. morsitans, in which its development takes place. It is also carried mechanically by Tabanidfe (?). (2) T. simice. Synonym : T. ignotum. It rapidly kills domestic pigs. AFRICAN TRYPANOSOMIASIS 129 Its flagellum is uncertain. Its reservoir is the warthog". Group (C): Trypanosoma Vivax Group. General features of all in this group: — They are monomorphic. Their movements are extremely rapid. Their posterior extremity is enlarged. The cytoplasm is clear and hyaline. The kinetonucleus is large and terminal. The undulating membrane is but little developed and simple. The trypanosome only affects horses, cattle, goats and sheep. It does not affect dogs, rabbits and pigs. Development begins in the labial cavity of the proboscis, later in the salivary duct or hypopharynx. No part takes place in the intestinal tract. Trypanosoma bmcei in division, n, nucleus ; bl, blepbaroplast ; /, flagellum. x 2,000. (After Laveran and Mesnil.) (i) T. vivax. Synonym : T. cazalboui. It is very active. It is widely distributed. It attacks horses, cattle, sheep and goats only. It is fatal to cattle in Uganda. (2) T. caprce. It affects cattle, sheep and goats only. It is more heavily built than the above. It is found in Nyasaland and L. Tanganyika only. (3) T. uniforme. It is as T. vivax, but smaller. It is only found in Uganda. 9 130 DISEASES DUE TO PROTOZOA These trypanosomes will now be dealt with a little more in detail. T. hrucci (rhodesiense). History. It causes nai^^ana in domestic animals. It causes Trypanosomiasis in man of a virulent type. It was the first pathogenic trypanosome discovered in Central' or South .Africa. Jl was found by Sir David Bruce in North Zululand, 1895. Stephens, in 1909, was examining a supposed gambiense at Liver- pool when he noticed different characters to those expected, hence he called it T. rhodesiense. The parasite was obtained from a patient who had been resident in Northern Rhodesia and was suffering from Trypanosomiasis. In this way the Congo and the Rhodesian types of the disease were differentiated for the first time. It lias been decided for the present that T. brucei and T. rhodesiense are identical. Distribution. T. brucei and nagana are widely distributed from the Sudan on the north to Zululand on the south, from Gambia on the west to Zanzibar on the east. It may be that the T. togolense of Togoland and the T. ugandas of Uganda are the same species. Morphology. In the T. brucei there is a greater diversity of shape than is found among species of other groups; the short, stumpy forms have no free flagellum, while the long forms are slender and have a well-marked free flagellum. They are actively motile, but do not move far from one place. The protoplasm of many trypanosomes show granules, especially at the anterior end. The nucleus is oval in the slender and round in the stumpy forms. It is frequently placed far back in (he bod\' of the organism, more so in the short forms. The kinetonucleus is small, round, and about 1*4 — 2 ^ from the posterior extremity. The flagellum averages 5"8 jj,, bul is absent in stinnpy forms. Animal Susceptibility . It attacks man, horses, mules, donkeys, oxen, goats, sheep, monkeys and dogs. Birds, crocodiles, lizards and frogs are not affected by it. One trypanosome may begin the infection as well as a thousand. Infection can take place very easily through the skin; the slightest puncture or scratch suffices. Infection probably takes place also through the mucous membrane, l^ndoubtedh' infection is most frequently by the tsetse bite. AFRICAN TRYPANOSOMIASIS 131 The disease runs a fairly rapid course in man, killing him in three to four months. Horses, donkeys and mules die in about thirty-eight days. In the ox it is more chronic and some recover. It is fatal to horses as in man. No case infected has been known to recoA^er, and remain free from the disease for a year. Goats, sheep, monkeys, dogs, rabbits, guinea-pigs and rats nearly all die. Amongst these animals, three recovered out of 318 infected. It is highly probable that the Trypanosome of man in Nyasaland and of nagana are not separate species. Carriers. Glossina morsitans and pallidipes are the carriers of nagana. About one per 500 of tsetses are infected with the trypanosome. The infected tsetses are equally numerous all the year round. If man is bitten bv one tsetse in the nagana area it is 500 to i against his taking the disease. For its development in the tsetse see the development of T. gam- biense, which is identical with T. brucei in this respect. Reservoir. The big game of the fly country are very heavily infected, more than ;^2 per cent. These form the reservoir. The other trypanosome species pathogenic to domestic animals were found as follows : T. pecorum, i4"4 per cent.; T. simiae, I'y per cent.; T. capra), iri per cent, of all the game examined. Conse- quently all such game should be exterminated (Bruce) in those areas. T. gambiense. History. It was first seen in the blood of man in 1901. It was found by Dr. Ford and described by Dr. Dutton, but it was not then associated with Trypanosomiasis. The next year Dutton and Todd were sent out to investigate the trypanosome at Bathurst. They reported that in their opinion the blacks were immune to the disease, but that they acted as reservoirs for the more susceptible whites. The real danger was ascertained by the Royal Society Commission in Uganda, 1903. Distribution . North. — From St. Louis, at the mouth of the River Senegal, to the Bahr-el-Ghazal district in the Egyptian Soudan. East. — Down to the eastern shore of Victoria Nyanza. South.- — To the southern end of Lake Tanganyika, the River Luapula in Northern Rhodesia, and Donguela in Portuguese West Africa. J.;}2 DISEASES DUE TO PROTOZOA Morphology. It much resembles the nagana parasite. There is great variation between the long and short forms, but among the short forms there is an absence of the blunt-ended ones. The protoplasm contains many chromatin granules. There are no posterior nuclear forms. The kineto nucleus is small, round, from r8 — I'l ^ from the posterior extremity. The undulating membrane is well developed and has bold folds. The tlagellum is long and free, except in the short forms, where it is absent. The length of the organism is about the same as the T. brucei. No difference can be ascertained by the microscope in blood pre- parations between T. gambiense and T. brucei. 3 f .'^ Trypanosoma gambiense. Development in vertebrate host, a, long, slender, /', intermediate and c, short, stumpy forms, found in the blood : d, e, /, non-flagellate, latent forms from internal organs, x 2,000. (Original. From preparations by Fantham.) Animal Siisccpiibility. Tt is difficult to infect experimental animals from infected human blood, and in this it differs much from T. brucei. The rat is the least refractory, but its virulence can be increased by passing it through several of the same species. The virulence of both these trypanosomes is illustrated by the table below : — Monkey Dog Guinea-pig White rat T. gambiense 159 96 264 137 T. brucei 26 34 67 30 hence T. gambiense is much more chronic than T. brucei, and this test is best for the differentiation of the species. AFRICAN TRYPANOSOMIASIS 133 Carriers. The Glossina palpalis. It inhabits wooded shores of rivers and lakes. Although the shores of Lake Victoria Nyanza, the banks of the Nile and other rivers swarmed with these tsetses before 1898, they only became infected with trypanosomes about this time. Consequently one concludes that the infection was brought by Emir Pasha's men from the Belgian Congo. Thirty per cent, of the natives working for the Government (one month yearly, at Entebbe in Ugand^ in lieu of hut tax) were infected with these trypanosomes in 1903. The hut-tax labourers were removed from the lake shores, and one year later the flies infected with this parasite fell from 11 '2 per 1,000 to i'2 per 1,000. In 191 2, as the lake shores became more deserted, it had fallen to o'i4 per 1,000. Hence man in the A'icinity means more flies infected. A fly may remain infective for several months. Man is bv no means the only source of the virus. Tsetses can convey the infection for some fifty days after the fly has fed on an infected animal (Kleine). An infected flv mav and does infect susceptible creatures bitten on the first bite. Cycle of Development. The cvcle of development of the T. gambiense in the G. palpalis is as follows : — Laboratory flies when fed on infected animals become infective in an average of thirty-six days, extremes twenty-seven to fifty-three days. Of those tsetses allowed to feed on infective animals, only o'5o per cent, become infective. When in test-tubes the trypanosomes seem to die off, but after twenty davs a resistant strain appears which soon multiplies by myriads. Manv flies become infected, but few become infective, e.g., try- panosomes partially develop in many, but go on to completion in but few tsetses. It was found that 2 per cent, became infected, but only o"5 per cent, infective. For the first three to four days after the Glossina^ have fed on infected blood, trypanosomes are found in all, these being the try- panosomes originally ingested with the blood. In six to seven days, when digestion is completed, most have disappeared from the tsetse, except in from 2 per cent, to 8 per cent, of those infected. In the remainder, say about 5 per cent., the trypanosomes develop, increase, and fill the whole of the gut, fore, mid and hind gut, with swarms of multiplication forms. 134 DISEASES DUE TO PROTOZOA This infection may continue for the rest of the life of the fly. One case retained its infection for ninety-six days, but some lose their infectivitv and become harmless. Trypanosomes are never found in the proboscis except immediately after a meal. The greatest development is found in the fore, mid and hind gut, first degenerate blood forms, then comes a dominant type, a long, broad form with a narrow, simple, undulating membrane and a very short flagellum, if one at all. This appears to rise from a pink- coloured body near the kineto nucleus, a condition or phase never seen in ordinary blood trypanosomes. There are masses of these at all times in all parts of the gut. When the blood supply runs low these degenerate and disappear. When there is fresh blood supply they multiply and increase at an astounding rate, hence there are at the same time trypanosomes in all phases of their development which beggars description. Trypanosomes appear in the salivary glands on the twenty-fifth day and remain present there. They arrive there b}' way of the proboscis and salivary duct or hypopharynx. Trypanosomes have never been found in the body cavity. As soon as the trypanosomes reach the salivary gland they revert to the original blood forms and become infective. Conclusions. Trypanosomes taken into the alimentary canal of tsetse flies retain their shape and infectivitv for some eighteen hours. They then degenerate and lose their power of infectivity. Thev disappear in the majority of cases within five to six days. In a small percentage of flies, the female and the male, the try- panosomes retain their position, multiply, swarm in the gut, but do not resemble the original trypanosomes. After some twenty days the trypanosomes reach the salivary gland, resume their original blood form, and regain their infectivity. Reservoir. When men were numerous about the shores of Lake Victoria Nyanza, 20 per cent, to 50 per cent, of the natives were infected. (The epidemic there has since died out.) Months after the natives had been removed the flies were still infective. Animals were then suspected and examined. Cattle were found heavily infected, but showed no sign of the disease, but healthv susceptible animals could be infected from them by tsetses. The same can be said of antelopes. Animals not showing the trypanosomes microscopically would infect susceptible animals. Five years after the removal of the population from about certain parts of the shores of Lake Xvanza antelopes were still carrying AFRICAN TRYPANOSOMIASIS 135 infective trypanosomes. Should tliis district become repopulated the epidemic undoubtedly would come back again. Groups (B) and (C). None of these attacks man, hence little will be said about them. Group (B). T. pecorum. Morphology. It causes the most important trypanosome disease of domestic animals in Central Africa. It is the smallest of all pathogenic trypanosomes, being 9 — 18 /a long. It is short and stout. The contents of the cell are homogeneous. The nucleus is oval and centrally placed. The kineto nucleus is small, round, situated towards the posterior extremity, and may appear to project beneath the edge of the organism. The undulating membrane is simple. There is no free f^agellum. Pathogenicity. It is a disease of herds, horses, donkeys, oxen, goats, sheep and pigs. Some attacked recover. It readily loses its virulence by passage through certain other animals. If a trypanosome, infective to the monkey or dog, &c., passes through a goat, it loses its power of infectivity for the monkey and dog, &c. T. nanum is really a strain of T. pecorum. It is not so rapidly fatal to horses, donkeys and mules. In Nyasaland two-thirds of the cattle were lost and seven-eighths of the goats. Carriers. The Glossina morsitans. The Tabanidae. 4'6 per 1,000 tsetses were infected by the T. pecorum. Once a herd is infected, then ordinarv cattle or buffalo flies — the Tabanidae, may spread it. These flies come and go in swarms, during which visits they are real pests to cattle. The cattle feed at the hottest time of the day and crowd for self- protection, hence conditions are very favourable for mechanical trans- mission. When diseased members of a herd are removed, the disease seems to cease when the Tabanidae and not the Glossina morsitans are present. Between 1908-1913 some 2,500 to 3,000 head of cattle died in the Barotse Reserve in Northern Rhodesia, though no Glossina morsitans was present. The mortality begins in February and ceases in June each year. 136 DISEASES DUE TO PROTOZOA Development. At first this takes place in the gut of the tsetse, then in the labial cavity of the proboscis, later in the salivary duct, but, be it noted, not in the salivary gland. In the salivary duct it reverts to its original form and becomes infective. The cycle requires nineteen to fifty-three days for the development of infectivity. The intestinal forms cannot be distinguished from other intestinal developmental forms of pathogenic trypanosomes. Thousands of infective forms can be obtained by a biting fly attempting to bite one's finger through a watch glass, when the saliva will reveal them. Reservoir. I4'4 per cent, of animals examined were infected. These were : — Eland, 60 per cent. ; Koodoo, 66 per cent. ; Bush buck, 70 per cent. ; Bufifalo, 22 per cent. T. brucei were not found in any of the animals examined. T. simian. This is very virulent towards monkeys and domestic pigs, killing them in a few days. It is harmless to oxen, antelopes, dogs and smaller experimental animals. It affects goats and sheep. It is like T. pecorum, in that its virulence soon becomes modified. The warthog is the onlv member of wild game yet found to harbour it. 10 per cent, of the thirtv examined were found to be infected. The trypanosome is 14-24 jit long. The long undulating body frequently extends in a straight line. The cytoplasm is clear. It is very fatal to domestic pigs, killing them off in 5'3 days. It kills monkeys in io*8 days, goats and sheep in 46*6 days. 3'4 per 1,000 flies were infective after experiments. Its development in the tsetse is as that of T. pecorum. Group (C). The size only separates the species of this group. T. vivax. It causes the most important cattle disease in Uganda. It is widely distributed in Central Africa. It has been reported from the Soudan, Senegal and Northern Rhodesia. Its marked activity during life distinguishes it. It only affects horses, cattle, goats and sheep. Other animals are refractory. It has been found in the bush buck. Tsetse flies were found infected by it. T. uniforme. As above, but smaller. ESSENTIALS OF TROPICAL MEDICINE. PLATES A TO E FROM REPORTS OF SLEEPING SICKNESS COMMISSION. Plate A. Mott. o '^9 "*• ^. € i\v ^ Fig. 4. Section of spinal gan- glion, showing lympho- cyte interstitial infiltra- tion (/). Magnification A.Kelley del Bale gLDamelsson.L'^^ hih. Platk B. Mott. Fig. I. Three large glia cells (,!?), their branches ending in a network around and upon a small vessel: lymphocytes (/), and plasma cells (/>) are seen scattered about. Magnification 500. Fig. 2. Small vessel, showing endothelial nuclei proliferated, and three plasma cells. Magnification 500. o m <^^- tK9 ^% ^ 2. >S.K.f QCL ^«o 9 J'ft" .0 % i© t^ & ^ t) ..?* Fig. 3. A transection of a vessel in a very chronic case of sleeping sickness, show- ing marked perivascular infiltration. Magnifica- tion 250, '«& v.. (^ I ^ o <9 ^ 'H'. l_ % <^k Fig. 4. (^ J Active prolifer- ^-^ / ating young glia f cells found in great numbers in sleeping sickness tissues. The pale nucleus, with distinct nuclear membrane, contains chromatin granules, with an arrangement in- dicating mitosis. Surrounding the nucleus is the pink-stained cyto- plasm, with a tendency to form star- like processes. Magnification 500. ^sartfiP^^^^"*-" r\ ^:) -^^ »f 5. Fig. 5. Two large morular cells from a very chronic case of sleeping sickness. Magnification 500. Fig. 6. Rod cells (Stabchen Zellen) are rarely met with, although occasionally appearances like fig. 6 are seen. Magnification 500. A KeDey del Bde 3tDanieissoD,L'^''-lLth Plate C. Fig. I. TraiLsection of cervical nerve close to the spinal ganglion, showing an infection of the sheath of the nerve by diplo-streptococci. The adjacent lymphatic glands showed points of suppuration. Magnifi- cation 200. (a) The micro-organisms, magnified 500. Case 69, L. L. 1 • tf •*>?*?<>* .(■•"rK-i-fJi. »^ . <'' it-. • la. •'•vv*--'-.^.; Fig. V^essel of the internal capsule of a case of acute sleeping sickness, with a large plug of cocci. Magnification .Stained by Gram's method. 50a li 5)a..C«1 ^' % '^^ N Fig. 3. Various degenerated cells seen in section of sterile lymphatic gland. Magnifi- cation 1,000. Leishman stain. O/ ,fr». 1*? '-m^ ® si) 6 4i. f Fig. 4. Lymphocytes and their transition to plisma cells a, c ; d, degenerated plasma ceil seen in section of lymphatic gland. Magnification 1,000. Leishman stain. A Kelley del. Bale &.DainelsEOu..1-,*-^llth Mott. Plate D. Fig. I. Thread - like bodies and gran- u 1 e s deeply stained, seen in section of lym- phatic gland, probably altered and degenerated trypanosomes. Magnification 1 ,000. Fig. 2. Trypanosome in a lymphatic gland section amidst disintegrated cell products. Figs. 3 and 4 (Plate IV.), and figs, i and 2 (Plate v.), are drawings made from the same sections, 5 M in thickness, stained with Leishman's stain and prepared from an enlarged cervical gland removed during life from a case (Bara Risgallah) of trypano- some fever, before sym- ptoms of sleeping sickness had occurred. Magnifi- cation 1,000. Fig. 3. 'Trypanosoma Gainbiense i n , smear of fresh gland juice, several 1 y m- phocytes, micro- nuclei. Magnifi- cation 1,000. Fig. 4. Section of lymphatic gland from a recently fatal case of sleeping sickness in a European. The glands in tliis case were not much en- larged. There is a very marked proliferation of the endothelial nuclei. Magnifi- cation 500. Fig. s. Proliferation of the connective tissue cells of the reticulum of a lymph sinus; marked proliferation of the nuclei of the endothelial cells seen. This chronic change closely accords with the change observed in the perivascular lymph spaces of the central nervous system. Magnification 500. Fig. 6. Various granules and products of cell (and try- panosome ?) degeneration seen in the perivascular infiltration of the central nervous system in sleeping sickness. Magnification 1,000. A.Kelley- del. Baie &.Daai«l»soa, J>^ lith Plate E, Molt. Fig. I. Longitudinal section of vess?' rf brain of ox that died of Jinga infection. Trypanosonies in various modified shapes are seen. Some of these may be amcjeboid forms of trypanosomes ; probably some are trypanosomes which have been attaclced by leucocytes. Magnification 500. Stained in bulk — methylene blue and eosine. Fig. 2. Small vessel of the medulla oblongata of rabbit inoculated with Surra. The animal died three months after infection. Shows a plasmodial mass in the centre and trypanosomes in a whorl near by. Magnification i,oo- t. Fig. 4. Somewhat similar appearances as in fig. 2, seen in longitudinal section of vessel. Numbers of chromatin rings, probably macro-nuclei (A) ; (B) capillary blocked by trypanosomes; (C) trypanosomes in the tissue; (D) ganglion cell, showing marked chromolytic changes, probably due to capillary obstruction. The nucleus is swollen and clear, the body of the cell shrivelled, and there is an absence of Nissl granules. Magnification i ,000. Romanowsky. A Kf'Uey del Bale 8;I)faiiels60ii,L'^ litV AFRICAN TRYPANOSOMIASIS iZ7 It is only found in I'^anda. It is carried by Glossina palpalis. Its reservoir is in wild oj-ame near the lake shore. T. caprce. It has onlv been reported from Lake Tanganyika and Xyasaland. It only affects cattle, sheep and goats. It is very active during life, and measures 18-32 fx long. It is more heavily built than the vivax ; its posterior half is swollen and the end blunt. The anterior end is narrow and pointed. The cytoplasm is clear. The nucleus is centrally placed. The kinetonucleus is large, round, and close to the posterior extremity. The undulating membrane is better developed than in the T. vivax, and has bolder folds and a well-marked free flagellum. It kills goats in 56-5 days, sheep in 115 days, and rats in 2 days. The carrier is Glossina morsitans. 3'5 per cent, per 1,000 flies examined were infected. Its development is limited to the proboscis of the tsetse fly. Its reservoir is the water buck, reed buck, in per cent, of which M^ere infected. PATHOLOGY. The outstanding feature is a chronic inflammation of the lymph system, probably caused by toxins of trypanosomes. Trypanosomes enter the lymph-stream, blood-stream, and the cerebrospinal fluid. There is polyadenitis. The heart and other organs show lymphatic infiltration. There is fever in the early stage, followed by meningo-encephalitis and meningo-myelitis, proliferation of neuroglia, and lymphocytic accumulations around the vessels. These two processes compress the vessels and lessen the blood supplv to the brain and cord, which is followed by malnutrition, cerebral changes, and the sleeping sickness manifestations. The trypanosomes cannot pass through the placenta. An ultimate secondary infection by streptococci and pneumococci is common. MACROSCOPIC. There is usually emaciation, but the writer has lost many who have been particularly fat. There may be dry desquamation of the skin to exfoliation. One of my cases was called ''the serpent" because she shed her skin from time to time. There is polyadenitis in the neck, groins and all lymphatic glands. 138 DISEASES DUE TO PROTOZOA The cerebrospinal fluid is increased. The base of the brain is pale, the dura mater sometimes adherent to the bone, the gyri of the brain may be flattened. The pia arachnoid is thickened in places, some- times adherent to the brain. The brain substance is sometimes firmer than usual, but may be soft and edematous. There is usually congestion of the brain. The ventricular fluid is increased. The findings of the cord are similar. Sometimes there are haemor- rhages also. The Cauda equina may be surrounded by gelatinous tissue. Sometimes there is ascites and pericardial fluid in excess. The lungs may show pneumonic changes. MICROSCOPIC. Mott did not find it easy tc differentiate true trypanosome findings from those due to terminal affections caused by diplococci, streptococci and colon bacilli, but the following were generally agreed upon : — Cerebrospinal system. A round-celled infiltration surrounding the vessels of the pia arachnoid of the brain and cord, best seen in the membranes where there is excess of cerebrospinal fluid, and in the brain around the vessels of the medulla, pons, cerebellum, and those entering the base. There is a growth in size, and then a proliferation of the neuroglia elements. Round cells are found later in the meshes of this proliferated glia, which are : — (i) Lymphocytes. (2) Plasma cells of JMarschalko, having a nucleus at one end of the cell, probably derived from lymphocytes. (3) Morula cells of Mott, large, round or oval cells with an eccentric blue nucleus, probably degenerate cells of IMarschalko. (4) Some mononuclear leucocytes. (5) A few polymorphonuclear leucocytes. The lymphocytes are probably produced by proliferation of endo- thelial cells about the perivascular lymphatic space. The ependyma of the lateral ventricles may show proliferation and dense fibrous formation. There is atrophy of the dendrons and diminution of the Nissl bodies, and alteration of the nucleus, which becomes large, clear and eccentric. The changes are more marked in the cerebral cortex and medulla than in the cord. The cells of the posterior spinal ganglion show chromatolysis. AFRICAN TRYPANOSOMIASIS 139 The central canal of the cord may be dilated, but more often il is occluded by cell proliferation. Sometimes there is haemorrhage of the cord vessels. These changes were not noted in a cured Tr\^pan()somiasis case which died later from another disease. The lymphatic fj^latuls. Trypanosomes are often found in them. The lymphatic cells often change into cells of Marschalko. These then change into morula cells. Endothelial cells of a lymphatic sinus proliferate, become phago- cytic, containing lymphocytes, red cells and chromatin particles. The gland is congested. The fibrous tissue of the capsule and septa proliferate and become thickened. When the inflammation subsides, the gland tissue becomes less vascular, firm, hard and full of dense fibrous tissue. Secondary infection may occur and abscesses result. The lungs. These are hyperaemic often. They may show pneumonic compiicalions. The heart. There is small-celled infiltration in all its la\ers. Sometimes it shows haemorrhages. The liver and spleen. There is a thickening of the capsule. The spleen is congested and the trabecular thickened. The bone marrow. It is very cellular, vessels congested, hcTmorrhages. SYMPTOMATOLOGY. There are three stages : — - (i) Incubation. (2) Febrile or glandular. (3) Cerebral. In all three the clinical manifestations are irregular in degree and duration. INCUBATION. The time in man is not known. Probably two to three weeks, or it may be less than ten days. Some individuals have not shown any symptoms after being infected for five years. I had several patients who had carried trvpanosomes for two vears and shn\\'ed no other manifestations of the disease at <-ill. 140 DISEASES DUE TO PROTOZOA The local irritation of the tsetse bite may be so slight as not to be observed, but in some there is a raised itching patch which may last for several days. SUMMARY OF SYMPTOMS. To aid the memory these may be summarized as follows : Poly- adenitis, fever, erytiiema, paresis, tachycardia, somnolence, cedema, enlarged spleen, anaemia, headache, epileptiform fits, tremors, change of character, itching, hypera^sthesia, incontinence of f^ces and urine, enlarged liver, eye symptoms, delusions, insomnia, vomiting, melancholia, epistaxis, feet pains, paresis of lower ex- tremities, dermatographia, painful swelling of ankle, sexual impotence, hemiplegia, giddiness, deafness, loss of hair, phlebitis, facial paralysis and orchitis. FEBRILE OR GLANDULAR STAGE. This stage is known to some as the Trypanosome Fever Stage. The manifestations in Europeans are much more frequent than in natives, and may be considered as follows : — Fever. — There are attacks of fever unaffected by quinine, lasting for about one week and recurring at intervals, or the fever may not recur, or may be so slight as not to be noticed, or it may be taken as a " touch of malaria." Chart I, 1909, Onset of disease and marked temporary effect of soamin in the second week. The pulse-rate and respirations are increased. The pulse-rate may be very rapid during the febrile attacks and during the apyrexial period also. The spleen and liver enlarge, but it is difficult to exclude malaria. Neuralgic pains and headaches are common. Erythematous Eruptions. — Pinkish patches, irregular in position and outline clear in the centre, mav be horseshoe shape or circular; AFRICAN TRYPANOSOMIASIS 141 DATE f/orS 1 /O // \ 12 \ /3 \ /* /5 y*&/?3 2-? zs Z6 27 28 M E ■seJ M E 1 TIME M ; e 1 M : E M E M E : M , E M E M . E M E M E M : e M E M E 106° 5 105° -t i • — r- - •■ ■ ■ 9^ w qrW in fjrW L_A!2E ■ i.'--. ■ At oxt/f grYI '. - i ^ 103° ^ •08° ij 101° 5 '°°° A ■z:.X:::::: ^ m. ■/^ ^ • — X V /^ :::: * : - i - i- \7\ ■•■-■•T--~-- 99° NORMAL 98° 97° - t- — ^ ±_\ \r .•^^ L i EEEE .rtr;- :::r — - • r ■■-t--- 1 ! Chart II, 1909. Third and fifth weeks. Imperfect control of temperature by soamin and atoxyl in large doses. DATE Feb 9 10 // /2 /3 I'f /5 FeJiZj 2S /far/ 2 3 ■f 5 TIME M : E Mi e M ■ E M ■ e M ; E M E M ^ E M : E M E M E M; E M , E M E M . E [•41* 106° 1 L- .- -; 1 i ; — -i ! i _.,.. 1 '05° — , — Etjd aaun. ~^^ :, ; ,. ir4n:: :—-^^ jsa^Z. U. - zni- ^^^^4^ 1 10*° j nfrf- ^-1;;:;;;: grVIII ^ gddlh Ct 7^,7/" ^M- .."_Z."..Lr.T,.- Crr(// i/r/// - j__- 40* ^ 103° 1 101° H ' ZI A --;:-::- — ;— =F ^ "'\--~ E-i- '% i- — — i ). SS* I 100° 99° NORMAL -izn ^ W^^ fe v/i V.-:-;:- ^ ^^ W # ^ b/rr ^^ #^ 36* 37* ;- -.. — -i :'i:nr:z .-,_4....r; 1 ■■ --%--:: —^- .- ■: i — T— 97° r '■ r '"^ """ _ _ —-J — - '_ I Chart III, 1910. Two other periods some three months later, showing absence of any marked beneficial effect from these drugs. Trypanosomes were usually to be found. DATE /ftirg /ater there is a more extensive oedema. Asthenia and Ancemia. — The anaemia may be marked and ]3ro- gressive. Weakness is considerable, although no wasting may be present. Eye Lesions. — Dr. Daniels has called attention to these, and describes them as toxic irido-cyclitis, conjunctivitis, iritis, keratitis, retinal changes, photophobia and deep oedema of the lower eyelids, with deep ]5ain of the eyeball. Thev were lareh' j^resenl in my cases. Orchitis is present in some cases. This febrile stage may go on for Aears or it may be cured, either spontaneously or by treatment or both, except in Rhodesian cases. The appetite is usual! \- good. Wasting is absent until the sleeping sickness stage. The symptoms vary mucli in different individuals, no one showmg all of them except in very few instances. A few of m\' European cases chosen at random will indicate this point. Case (i). — In tr^panosome area for eight vears without leave AFRICAN TRYPANOSOMIASIS 143 (Central Africa). Fever almost constantly for months past, did not take quinine, marked anaemia, weakness marked, pallor, spleen nearly reached iliac crest, liver slightly enlarged, malaria also present, pains in legs and calves excruciating, worse at night, exhausted because no sleep, aspirin, bromides, trional, opiates useless. Sent to me as beri- beri. No trypanosomes in blood, no auto-agglutination, no eruptions, no eye lesions, pains in legs, with polyadenitis chief symptoms. Sent home and diagnosis confirmed. Case (2). — In trypanosome area, Central Africa, three years; some fever, probably malarial, trypanosomes found in blood, some auto- agglutination, polyadenitis, no other disease present, strong man at work and refused treatment, as no symptoms when first diagnosed. Given soamin intramuscularly and sent home. Case (3). — History exactly as above. A very stout, strong man. Given tartar emetic intravenously and Fowler's solution by the mouth, and sent to Europe. Dr. Daniels writes some months later that he does not find any symptoms of the disease in him. Case (4). — In trypanosome area six months. Central Africa ; an ideal man, physically and mentally, prior to attack; marked weakness, stubborn fever would not yield to quinine, frequent micturition for six months, sleeplessness, nervous prostration marked, admitted to hospital unconscious the day after the fever commenced. Temperature remained up for five days, in spite of quinine 30 grains daily, no malarial parasites in blood, no trypanosomes found after forty-two examinations, no auto-agglutination, polyadenitis marked. Long convalescence, prolonged weakness, memory poor, headaches, marked mottling of chest, back and thighs, purple colour, disappeared on pressure, deep pains of legs and muscles excruciating, then over body, face, head, agonizing pain on the slightest touch. Erythematous patches, fleet- ing, red, not raised, massage impossible, worse at night, as if " some- one was twisting his legs off at the ankle," opiates of little use. All the typical symptoms were present, except trvpanosomes, auto- agglutination and eye lesions. Was given Tartar emetic intravenously; ditto Galyl ; Soamin bv the mouth and intramuscularly. Temperature normal for ensuing eight months; when discharged all symptoms disappeared except slight leg pains. Natives may show some of these symptoms, but in my cases (over 4,000) there were no eye lesions, except oedema and one persistent double conjunctivitis not otherwise accounted for. Deep pain is very rare, fever also, but a dry, scalv eruption is fairly common. Headaches, delusions, hysteria and mania are common. Qidema of all parts common. Trypanosomes rare and aulo-aggutina- 144 DISEASES DUE TO PROTOZOA tion very common in fresh blood films. There is often tremor of the tongue and fingers. They decline treatment as a rule in this stage because treatment is more painful than the disease. 'fe^ Child with trypanosomiasis showing cedematous swellings of the eyelids. THE CEREBRAL STAGE. In the Sleeping Sickness stage death is inevitable, but when the former stage ends and this one begins is not accurately known. This stage lasts from a few weeks in acute cases to a few months in chronic cases. Some have lived for jears, and have then died from some intercurrent disease. One notices a change in the habits of the jjatients, the disposition is modified more often for the worse, they become apathetic, dull, there is disinclination for exertion, they become careless, dirty, find it difficult to walk, become indifferent to most things, and forget to masticate the food that lies in their mouths. Sleep is often excessive, but it is more frequently a lethargic con- dition thai is manifested. There are fine tremors of the tongue, hands, arms, legs, and even of the abdomen. There is a peculiar gait, a difficultv in raising the feet from the ground, he shuffles along or throws his feel outwards in walking. There is no jDaralysis as a rule; the superficial reflexes are normal, the deep reflexes are increased and then lost. Delusions and mania are fairly coiumon. Romberg's sign is sometimes present. Later AFRICAN TRYPANOSOMIASIS 145 there may be rigidity of the neck and legs, a tendency to permanent flexure of the legs, on the thighs, and abdomen. One case of mine could not bend his legs at all, and danced with them quite stiff all day and night, except when he was put down prostrate by attendants. He could not rise again himself, but he continued to dance when he was put in the upright position. Hypercesthesia is not common. They often wound themselves against sticks, &c. ; ulcers form which are difficult to heal owing to their reduced condition and their dirty habits. Daily fever is common when there are pneumonic symptoms, at night up to ioo°-i04° F., falling to subnormal in the morning. There may not be any fever at all, or the temperature may be sub- normal. There are no rigors or sweating in fever cases, but the pulse is unusually quick, 90-140, and is out of all proportion to the tem- perature. It is, as a rule, regular, readily compressible, and small. Respirations are increased. There may be Cheyne-Stokes breathing before death. Congestion and oedema of the lungs with pneumonic patches are common before death. Digestion is good. Sometimes there is constipation, but more often diarrhoea. Unclean feeding may account for it, e.g., fungi, baked clay, &c. The usual intestinal flora can be found. The blood shows trypanosomes, auto-agglutination, mononucleosis, and sometimes polyleucocytosis before death. The acidity of the blood is said to be increased, or probably better, the alkalinity is diminished, which is probably due to amino acids secreted by trypanosomes, and produced by the action of the amino acids upon serum proteids. Sexual desire does not necessarily cease, neither does menstruation, but they may disappear in some cases. The lymphatic glands become fibrosed, smaller and harder. The skin is usually dry and rough, but may be normal. Emaciation is common, but not the rule. Muscular weakness is very marked, tremors are pronounced, saliva dribbles from the mouth, urine and faeces are passed involuntarily, bedsores form, the pulse cannot be felt at the wrist, the temperature is subnormal, coma, and death . Perverted appetite is common ; they will sometimes eat earth when good food is at their side. One case died from intestinal obstruction, and 2I pounds of clay lumps were found in the intestines. Many of the people, however, are earth eaters when in normal health. Theft is a common propensity, but it is certainly more marked when this disease is present. Mania is common. One case was of a boy who attempted to drown 10 146 DISEASES DUE TO PROTOZOA himself. He was very fat, but he slept twenty-two hours out of twenty- four. He recov'ered under treatment, so that he slept but ten hours daily and went to work again. Some cases are very violent, and it is impossible to inject them intravenously. GEdema of the eyelids, face, legs, arms, penis, scrotum and abdominal w-all is fairly common in the final stages. Ascites may also supervene, also an increase of the pericardial fluid. Irido-cyclitis and other eye troubles were so rare in my cases as to be ignorable. My district was 4,800 sq. miles in extent, wdth a population of from 100,000 — 200,000, of whom 75 per cent, were infected with the disease. Some cases die from the disease without any enlargement of the lymphatic glands, and others survive w'hen they have become markedly enlarged. COMPLICATIONS. Pneumonia is common, and is one of the common terminal phases. Laryngitis, oedema of the glottis, and iritis have been recorded. Amoebic dysentery is fairly common, and usually causes death when present. Cerebrospinal meningitis due to streptococci, pneumococci, or meningitis is not uncommon. Epileptiform symptoms are frequent. Helminthiasis is common, but it may not give rise to any trouble- some symptoms. Filaria may be present. Malaria is common in some districts and rare in others. Jiggers and resulting " tattered toes " are almost universal. A considerable amount of septic absorption may result from ulcers caused by them. DIAGNOSIS. The finding of the trypanosome is conclusive. Always suspect Trypanosomiasis when fevers are not controlled by large doses of quinine in a trypanosome district. Look for erythema in Europeans. There will be a rapid pulse during the apyretic periods. Asthenia without wasting should arouse suspicions. Deep hyper^esthesia ; Kerandal's symptom is common in Europeans. Tremor of the tongue; Low and Castellani's symptom should be looked for. Cervical adenitis, Winterbottom's sign, is common and important. Search the blood for trypanosomes, auto-agglutination, mono- nucleosis, but remember that auto-agglutination is also present in Filariasis, Malaria, Syphilis and Yaws. AFRICAN TRYPANOSOMIASIS 147 In searching for trypanosomes, the following methods are avail- able : — (i) The peripheral blood, fresh blood films. Stained blood better for details of parasite, but less frequently successful. (2) Scarification of the epidermis. Examine resulting lymph for the trypanosomes. Not very successful. (3) Citrated blood, centrifuged repeatedly. Examine the third sedi- ment. The results are better. (4) Centrifuge citrated blood in small tubes and examine the leuco- cytic layer. Button and Todd's method. (5) Puncture the glands and examine the juice. The glands are often small and natives object to the puncture. A valuable method. (6) Centrifuge cerebro-spinal fluid for 15 minutes, examine sediment fresh and stained. It is negative in febrile but positive in sleeping sickness stage. A valuable method, introduced by Castellani. (7) Inoculate susceptible animals. Use 20 c.c. of blood or cerebro- spinal fluid and inject it into monkeys or guinea-pigs, dogs or white rats. Monkeys and white rats are soonest killed in positive cases. See p. 132. PROGNOSIS. It is always serious. It is curable in the febrile stage but not in the sleeping sickness stage. All Rhodesian cases, febrile and later stages have remained uncured hitherto. There is one queried case of recovery diagnosed in May, 1913. Of 500 trypanosome cases invalided to England, 300 are already dead. Improvement is always possible except near the end. With treatment, life is prolonged; without it death is almost certain. The Congo gambiense strain of trypanosome is the least virulent. The Uganda gambiense strain of trypanosome is the more virulent. The Rhodesian gambiense strain of trypanosome is the most viru- lent. Death is inevitable in the sleeping sickness stage. Whole villages have been depopulated by it in Senegambia, Angola, Uganda and the Congo. The populations of the islands of Lake Victoria Nyanza have been annihilated by it. TREATMENT. Nothing need be said here concerning good hygienic conditions, the exclusion of accompanying diseases, &c. There is no specific for the disease. vSoamin has not realized the hopes of its inventor. 148 DISEASES DUE TO PROTOZOA The chief drugs now reUed upon are antimony oxide, tartar emetic and arsenic. Arsenical preparations. Liquor arsenicalis has cleared up some cases. It was used before Soamin was known. It should be given well diluted in increasing doses, from 5-15 minims and omitted every fifth week. Salvarsan and Xeosalvarsan. These are not more useful than Soamin and much more costly. Atoxyl. This is as Soamin, but more toxic, causing optic atrophy, gastro-intestinal inflammation, and peripheral neuritus. It has now been replaced by Soamin. Atoxylate of Mercury. Less satisfactory than atoxyl. Soamin. The best arsenical preparation to use. The methods of giving it are various. By the mouth, by the vein and intramuscular. Examples : — 3 grains daily per os, omit every tifth week. 2-3 grains intramuscular every third day for at least two \ears. (Manson.) 71 grains intramuscularly every fifth day (Broden). 72 grains intramuscularly two successive days every ten days for ten months (Koch). The writer has giv^en 7^ grains (0.50 grm.) of soamin every fifth day for two years without clearing trypanosomes from the lymphatic glands in the majority. The drug was always suspended on mani- festations of arsenical poisoning. Thousands of injections were given following this method, but were abandoned for combined treatment as being unsatisfactory. Soamin will cause the disappearance in some cases of the trypanosomes, but we cannot rest contented with it. Orpiment. An organic salt of arsenic used for the lower animals. Not any use in human trypanosomiasis. Galyl. This has proved useful in some cases with tartar emetic given between doses of galyl. Useful in European cases. Antimony preparations. The following are new preparations which have not A'et been suffi- ciently tried. They are : Antileutin, antimony and ammonio-potassio- tartras, antimony aniline tartrate, and antimony-sodium tartrate. Tartar emetic is the best known and most widelv used. All tartar emetic preparations should be preceded by an injection of caffeine; as tartar emetic lowers the blood pressure. I have given thousands of doses of tartar emetic intravenouslv without anv heart symptoms of importance. Tartar emetic is too painful for intramuscular use. It was thus first used and abandoned bv Sir Patrick Manson in the earlv davs. AFRICAN TRYPANOSOMIASIS i49 It can be given bv the month or rectum, 1-2 grains in large quantities of water, say 1J-2 pints, every third day. 'J'artar emetic is perhaps best given by the vein, |-i^ grains every third day. Method of administration. I'se a 20-c.c. Record sAringe. Prepare a sohition of tartar emetic so that 10 c.c. contain ^ or more grains of the drug. Apply a tournicjuet to the arm so as to distend the veins, paint the spot with iodine, draw into the syringe 10 c.c. of the drug, fill syringe with boiling water, attach rubber connecting tube, expel the air, give syringe to assistant to hold, take needle and plunge it into the dis- tended vein, allow a few drops of blood to run through to ensure that it is well in the \-ein, attach syringe holding piston end upwards so that any air bubble will be at :he upper end, unfasten tournicjuet, inject the fluid leaving- one c.c. in the svringe, withdraw needle and empty syringe through the needle so as to expel any drop of coagulated blood that may be in the lumen, put the whole in a solution of antiseptic and it is ready again for use. A little iodine and bandage on the site of the injection is sufificient. It is not necessary to dissect out the veins except in ver\' few cases. With plenty of assistants one can give 40 injections in an hour in this wa}'. The reactions \\hich follow tartar emetic are alwavs marked. Young infected natives cannot take more than h-i grain at a time no matter for how long the drug has been taken. Soamin was given whh tartar emetic intravenously but toxic symptoms were marked and it was abandoned. After giving more than 6,000 injections of arsenic and tartar emetic the method and drugs found by me to be most useful up to the present were : — A combined treatment of : — One grain (o'o6 grm.) of tartar emetic intravenously every third day, every second day in selected cases. 1-2 grains (o"o6-o"i2 grm.) tartar emetic by the mouth in a mixture containing glycerin, sodium bicarbonate, and chloroform water. 11^ grains (o"jy grm.) soamin intramuscularly once weekly. Omit treatment every fifth week or on the appearance of toxic svmptoms. Arsenic alone tends to produce arsenic-fast trypanosomes. One must give heroic doses of whatever drugs one uses. Ascertain the idiosyncrasy of the patient towards the drugs and administer them just short of toxic symptoms, omi'.ting them ever\' fifth week. Solutions of merctirv, formalin and collargol have been tried separately and together, intravenouslv, but without success. Many natives would rather die than have intramuscular injections of any kind. They prefer intravenous injections in spite of the after reaction. 150 DISEASES DUE TO PROTOZOA Attempts have been made to procure a curative and immunizing serum, but without success for man. It is interesting to note that the physician, Kerandal, claims as his cure intravenous injections of tartar emetic given in four series of daily injections of lo cm. each, the number of doses in each series being 17, 15, 15 and 18 respectively, or 55 in all, equal to 5-50 grm. of tartar emetic. His weakness disappeared as " if by enchantment " after the first course of injections. Atoxyl, of which he took 70 grm. in all, did not appear to affect the course of the disease. PROPHYLAXIS. What has been said about sanitary measures for the prevention of mosquito breeding need not be repeated here. In whatever work is undertaken the Government must co-operate. There should be medical inspection of all the villages on the boundarv of the fly area. Natives must co-operate also, and this is the most difficult task. If they do not volunteer to do so they must be forced. Some suggest that the infected should be isolated and treated, but this is neither practicable nor possible in the District du Kwango of the Belgian Congo, where about 70 per cent, of the total population is infected. To adopt such regulations would mean the closing down of all important works in that district, and the natives would be far worse off than before. Flv-free areas should be chosen or prepared, new villages built and maintained, plantations prepared and maintained, all infected villages to be destroyed and the inhabitants removed to the new ones, the infected peoples treated drastically, and those in the last stage removed to lazarets. This is a gigantic task, and is beyond the purse of the Government or any private enterprise in Central Africa. It should be worked as far as possible. The bush should be cleared and planted for 300 metres around every village, and from the water's edge for 100 metres. Then a new generation of individuals would arise, free from the disease, capable of increasing their kind and developing their country under guidance and control. Fly catching is impracticable in most districts to be of any real good . The extermination of big game is, in my opinion, unadvisable. Wherever man may go some animals will accompany him, and these will become carriers as well as man. The legs of Europeans should always be protected with puttees or leggings when passing through fly districts. European residences should be well away from native quarters. Quinine does not seem to be a prophylactic in any way. NOTES ON THE GLOSSING 151 NOTES ON THE GLOSSIN/E. The glossing are limited to Africa and the shores of the Arabian Guh". Formerly they existed in North America. The Genus contains ten species, which may be distinguished as follows : — (After Manson.) GENUS GLOSSING. Large species, length of body at least 11 mm. G. longipennis. Thorax with four sharply defined dark-brown oval spots. G. pusca. Thorax without spots. Small species, length of body rarely reaching 11 mm. Hind tarsi black. Antennae black. Two last joints of front tarsi black. G. palpalis. Abdomen not very marked. G. tachinoides. Abdomen con- spicuously marked. All joints of front tarsi yellow. G. bocayci. Antennae yellow. G. paUicera, Two last joints of hind tarsi black. Front and middle tarsi yellow. G. paUidipes. Front and middle tarsi black. Abdominal stripe one-third of seg- ment. G. morsitans. Abdominal stripe one-sixth of segment. G. longipalpis. They are ordinary looking flies about half an inch long. A strong proboscis stands out horizontally. Both sexes suck blood. The wings are long and close over each other when at rest like blades of a pair of scissors. The dorsal aspect of the abdomen is marked by five or more distinct bands. The mouth parts consist of the labrum, labium, hypopharynx or terminal duct of the salivary gland. The labrum and labium together form a suctorial tube for blood and is called the labial cavity. The salivary glands are long convoluted organs lying chiefly in the abdominal segment. Head of Ghssina longipalpis, Wied. (After Griinberg.) 152 DISEASES DUE TO PROTOZOA Probably all the species are capable of carrying trypanosomes. We will give a few features of the two most important. GLOSSINA MORSITANS. This species was known first as a result of the writings of Livingstone and Cummings. Habits. It inhabits dry thorny scrub, which covers large areas of Central Africa. It is not found along the river banks or other water courses ; it dislikes water. It requires shade and is never found on the open plains exposed to the tropical sun. It begins to bite soon after sunrise on a fine day, usually disappears at mid-day, comes out again towards sun- set and is then very active. In rain and wind they will remain hidden. They are most numerous towards the end of the rains. Food. Of 500 flies examined in Nyasaland the intestines contained mam- malian blood, chieflv antelope's, in 57 per cent, of cases. They never suck fruit juices like the mosquitoes. They feed once during 30-70 hours. When feeding, the fly fully distends itself in I to i minute after it has punctured the skin. A male can absorb it, times its body weight of blood and a female r6 times its weight. In two or three minutes after the feed, minute d'rops of digestive fluids are exudated from the anus, a process which continues at the rate of 2 per minute for 20 minutes. Some hours later a thick brown excrement follows and the abdomen becomes markedly reduced in size. Reproduction. All Glossinre are pupiparous and in this differ from most of the Diptera. The female produces one white-yellowish larva once in ten days. This is retained in the oviduct until fully grown. When born it creeps into the soil or amongst the leaves and debris and within a few hours has changed to a hard, black puparium. The adult fly emerges in about 23-60 days according to temperature. The female generally chooses the under surface of a tree for this purpose, generally near a native path or a game track so as to facilitate the mother's obtaining food for her young and herself. GLOSSING PALPALIS. These are widely distributed. They are lovers of water and are to be found frequenting the edges of rivers, lakes, ponds, water holes in banks where there is clear water and plenty of shade, thick under- growth with high trees and dense jungle. They are never found on open beaches backed by grassy plains even NOTES ON THE GLOSSIN.^ 153 with scrub near to the water. They are not found amongst the reed beds or papyrus swamps such as exist in the Uganda river valleys. They are never found away from water except where tiiey have followed man or beast a mile or so for his blood. Habits. Their bites are as those of the G. morsitans. They flv rapidly, settle quickly on the skin and soon ingest enough blood to fill them out perhaps without a prick liaving been felt. Antenna of Glossina pallidipes, male. (After Austen.) Glossina palpalis and puparium. (After Brumpt.) Feeding. When a G. palpalis has fed on an infected animal it becomes infective on an average of 34 days from the feed. It remains infective for about 75 days. Food. In populated districts man supplies sufficient blood but in captivity or at any time they will feed on hot or cold blooded animals, birds or reptiles. Reproduction. vSimilar to G. morsitans. Sandy banks banked by a belt of vegetation are often chosen. The pup^e are found one to two inches below the surface of the ground amongst or near to vegetation. There is no hereditary transmission of trypanosomes in the tissue, all trypanosomes are obtained from the animals they feed upon. 154 DISEASES DUE TO PROTOZOA SOUTH AMERICAN TRYPANOSOMIASIS. HISTORY, &c. This disease is caused by Trypanosoma cruzi discovered by Chagas in 1909. It is spread by the bug Lamus megistus and alHed forms. Its reservoir is probably in the Armadillo, Dasypus novemcinctus. The bugs live in the burrows of the armadillo. The disease is only known amongst the poorer inhabitants of the State of Minas in Brazil where it appears to attack the whole population. iETIOLOGY. The Trypanosoma cruzi has a large kineto nucleus. It is found in domestic animals and man. Trypanosoma cruzi. Schizogony. /, merozoite in rei blood corpuscle ; 2, parasite totally enclosed in red cell, no flagellum or undulating membrane ; j-j", parasites partially enclosed in red cell ; 6, 7, parasites in human blood ; Sir, parasites in lungs of the monkey, Callithrix ; 12, ij, initial forms of schizogony ; 14, /j, schizogony in the lungs of Callithrix. (After Chagas.) Three forms of the trypanosome are seen in man : — (i) With a large nucleus, loose chromatin and a terminal kineto nucleus. (2) A narrower form with an oval nucleus and dense chromatin. (3) A form with an elongated nucleus. The trypanosome undergoes multiplication in one of three ways : — (i) Schizogony . — This takes place in the capillaries of the lungs of the callithrix where it loses its flagellum and undulating membrane, it curves itself and forms a disc which divides into eight merozoites. These enter the red cells and become adult trypanosomes. Later they leave the red cells and live free in the blood-stream. Schizogony probably differentiates sexual forms and lays the basis for infection of invertebrate hosts. SOUTH AMERICAN TRYPANOSOMIASIS 155 (2) Sporogony. — This takes place in the bug Lamus magistus. Sexual and asexual forms develop, the final stage of development being found in the salivary glands when they are ready to infect a new vertebrate host. The development in the gut requires about eight days . (3) Agaviony. — This is an asexual form of reproduction and takes place in the cells of the various organs of the callithrix, i.e., in the hypertrophied endothelial cells of the lungs, in the cardiac muscle, in striped muscle and in the neuroglia of the central nervous system. In these situations it appears as a rounded body but without flagellum or undulating membrane. The trypanosome is not known to undergo any longitudinal division in the peripheral blood or the internal organs of the host. The trypanosome is easily cultivated on blood agar. The Lamus is infective to vertebrates, 8-10 days after an infective feed and remains infective for a long time. PATHOLOGY. The trypanosome enters the body cells, especially of the muscle, more frequently about the back and extremities. In these cells it assumes a Leishmania-like form without flagellum but with a tropho-kineto nucleus. Division is by binary fission, the two daughter cells dilat- ing the mother cell, or more correctly, the cyst membrane which ruptures, liberating the two enclosed forms. The parasites now become flagellates and move about. Local inflammation now sets in with the presence of trypanosomes in the blood. There may also be a production and liberation of toxins because the liver undergoes fatty degeneration. Different organs may be attacked in this way, the local symptoms and pathological changes being in accordance with the organ or organs selected. P. M. : MACROSCOPIC. There is serous effusion into the abdomen. The liver is enlarged with fatty degeneration. The spleen is enlarged, hyper^mic and soft. The mesenteric glands are enlarged, hypera^mic and soft. There is serious effusion into the pleural cavities. The same condition affects the pericardial sac, there may also be hjemorrhagic pericarditis. The heart may be much enlarged, there may be intense myo- carditis. The lymphatic glands are swollen and h_yper£emic. The thyroid gland is enlarged. The dura mater is congested. There may be signs of leptomenin- 156 DISEASES DUE TO PROTOZOA Trypanosoma criizi. Trans- verse section of a striated muscle containing rounded forms of the parasite in the central portion. x 1,000 approx. (After Vianna.) gitis, encephalomeningitis, adhesions between the leptomeninges and the cerebral cortex. The cerebro-spinal fluid is increased. A general myxocdematous condition is usually present under the skin. MICROSCOPICALLY. Trypanosomes are foimd in the heart muscle destroA'ing the sarcoplasm and con- verting the muscle cells into cysts, ^\hich rupture and discharge their contents into the intermuscular tissues and causing patches of interstitial myocarditis. There are often signs of peri- and endo- carditis present. The central nervous svstem is affected in a similar manner, but it is a neuroglial cell that is invaded. The suprarenal capsule, kidneys or thy- roid gland may be similarly affected. SYMPTOMATOLOGY. Acute. — There is a violent attack of fever in a child or a new- comer. The fever shows a morning remission and an e\'ening rise. The thyroid gland enlarges. The face becomes o^dematous whh characteristic crepitations. The lymphatic glands enlarge, especially in the neck. There may be fugitive cx^demas of any part. The spleen enlarges and becomes painful. The same takes place \\ ith the liver. Sometimes there are signs of meningitis. Sometimes there is albumin in the urine. The fever passes off to recur at intervals. During the attack trypanosomes are found in the blood. The child eventually dies, recovers or the condition becomes : — Chronic. — There is marked thyroiditis accompanied by loss of hair. Mypertrophy of tiie lymphatic glands continues. There is a dull expression, a bluish-bronze tinge to the skin, tach}-cardia, intestinal and nervous disorders, convulsions. Chagus says that the chronic stage may show group s\'mptoms ;is : — (i) Psciido-myxoedcmatous. There is hypertrophy of the lateral lobes of the thyroid gland in PATHOLOGICAL MAMMALIAN TRYPANOSOMIASIS i57 quite young but not in older children. A peculiar bronze colour of the skin probably due to the invasion of the suprarenal capsule. The lymphatic glands enlarge in the neck, axilhe, groin and the parotid also. (2) Myxoedematous . The thyroid gland atrophies with the usual classical symptoms of myxoedema, e.g., rough skin, loss of hair, firm oedema, arrest of mental development in younger children, mental degeneration of older ones. There may be inflammatory eye troubles. (3) Cardiac. There is arrhythmia, alarrhythmia, extra systole, sinus irregularities. (4) Nervous. Spastic paralysis in the legs. Athetosis in the arms. Aphasia, pseudo-bulbar paralysis, suprabulbar paralysis. (5) Chronic with acute and sub-acute exacerbations. Preponderance of fever. This variety causes a heavy mortality. The parasites are rarely found in the blood. It has a long history. It usually occurs in patients showing marked enlargement of the thyroid gland. Infantilisms may be sequelae of the disease. TREATMENT. As for African Trypanosomiasis. Also treat for hyperthryoid^e and symptomatically. PROPHYLAXIS. Aim at the prevention of the bites of Lamus magistus. NOTES OX PATHOLOGICAL MAMMALIAN TRYPANOSOMIASIS. TRYPANOSOME EYANSI. It causes surra in horses, mules, camels and cattle. It occurs in India, Burmah, Indo-China, Java, Philippines, Mauritius and North Africa. The symptoms are : fever, emaciation, oedema of the extremities and of the ventral surface, eye lesions, great muscular weakness, paralysis and death. The treatment is by arsenic in big doses. It is transmitted by the bites of flies and fleas. Some suggest by the ingestion of infected meat also. TRYPANOSOME BRUCEI. It causes nagana (weakness). It occurs in Zuzuland, North Transvaal, Pretoria to Nyasaland, 158 DISEASES DUE TO PROTOZOA the basin of the Limpopo, German East Africa, British East Africa and Uganda. The carrier is Glossina morsitans and the Tabanidas. The trypanosome gives rise to : — An acute disease in mice, rats, dogs, monkeys and cats. A subacute disease in rabbits, guinea-pigs, equines and pigs. A chronic disease in cattle, goats, geese and fowls. It is fatal to horses, asses and dogs. The symptoms are : fever, infiltration of coagulable lymph in the subcutaneous tissues of the neck, abdomen and extremities, rapid destruction of the red cells, extreme emaciation, and often blindness. The treatment is by arsenic. TRYPANOSOME EQUINUM. It causes mal de caderas, a disease of the hind quarters in horses and dogs in South America. It is spread by the ingestion of the infected meat of dogs, also by fleas. Some blame the Tabanid^e and Stomoxys. It is very fatal to horses. The symptoms are : rapid weakness, fever, paralysed hind quarters, staggering gait, stumbles and falls. Albuminuria, h^ematuria, eruption on the neck, shoulders and hind quarters not uncommon. Conjunctivitis and chemosis. There are serous exudations into the serous cavities and the spinal canal. A mare will die in two months after the paralysis begins. TRYPANOSOME EQUIPERDUM. It causes dourine or mal du coit in horses. It occurs in Europe, India, North Africa, and North America. It is spread by coitus between stallion and mare, not by flies, hence the trypanosome is capable of penetrating a healthy mucous membrane. The incubation is eleven to twenty days. The symptoms are : oedema of the genitals, which is painless; it is not inflammatory; there is some fever; this lasts one month, when weakness and emaciation begin. An eruption comes in about forty to forty-five days, in circular areas, with oedema about the flanks, hind quarters, neck, shoulders and thighs. It is often transient, and lasts about one week in all. There is synovial engorgement of the joints and tendon sheaths. There is enlargement of the lymphatic glands, particularh^ of the inguinal glands. Anaemia and paralysis then set in. The mucosae are pale, and marked emaciation is rapid. There are superficial abscesses, non- healing in character, conjunctivitis, ulcerative keratitis. ESSENTIALS OF TROPICAL MEDICINE. (a) T. lewisii. The antiflagellar end is sharply pointed, the centrosome usually at some little distance from the end of the body, and the nucleus is always in the flagellar half of the body. Size 25 to 30 ;U. (b) T. gamlnense. The antiflagellar end is usually bluntly rounded, the centrosome close to that end, and the nucleus at the middle of the body. Size 20 to 25 yU. (:) T. nanum. Characterized by its small size, being only about 14 jx in length. The centrosome is small and the nucleus is round and in the centre of the body. (d) T. theileri. Characterized by its large size, being some 65 fx in length. >> I (e) T. dimortikon. The important characteristics of this type are the broad body, the short free portion of the flagellum, the closeapplicationof the undulating membrane to the body and the presence of a vacuole between the centrosome and nucleus. bfcilu & D-.,r.ulr,soi. .L^'*- del.et htli Face page 158- PATHOLOGICAL MAMMALIAN TRYPANOSOMIASIS 159 Micturition is difficult ; the urine is thick. SensibiUty is diminished, paralysis comes on due to softening of the cord. The animal dies in two to eighteen months from the onset. The disease is always fatal. The condition may be more acute than as described, with death after a few days from the eruption from acute paralysis. TRYPANOSOME CAZALBOUI (T. vivax of Bruce). It causes disease in horses and cattle in West Africa. It is carried by Glossinae. TRYPANOSOME SOUDANESE (T. evansi of Bruce). It causes tahaga in dromedaries and zausfana in horses. The former disease occurs in the Upper Niger, and the latter in Southern Algeria. It is carried by the Tabanidas. TRYPANOSOME HIPPICUM. It causes murrina amongst mules in North America. It is spread by flies which suck wounds and by coitus. Trypanosoma leivisi. Multiplication rosettes, x i,ooo. (After Laveran and Mesnil.) TRYPANOSOME CONGOLENSE. It causes trypanosomiasis amongst horses, cattle, goats, sheep and dromedaries in French and Belgian Congo, N.E. Rhodesia. It is carried by the Glossinas. i6o DISEASES DUE TO PROTOZOA TRYPANOSOME DIMORPHON. This attacks cattle, dogs, sheep, pigs and goats in several parts of Africa. It is carried by the Glossina palpalis. In the horse there is loss of vigour, in two or three weeks there is fever, the next month there is marked weakness, abdominal swelling,, the testicles hang down and are oedematous, the coat is staring, the whole appearance is apathetic. There is fluid in the serous cavities- Death takes place in about one year. There is hypertrophy of the glands, fatty liver and congested lungs. Probably the T. pecorum of Bruce includes the T. dimorphon, congolense and confusum of the above descriptions. The point is still suh judice. SECTION II. DISEASES DUE TO BACTERIA. GENERAL FEATURES OF BACTERIA PLAGUE. Notes on Fleas. LEPROSY. PSITTACOSIS. UXDULAXT FEVER. BACILLARY DYSENTERY. CHOLERA. ENTERIC FEVER OF THE TROPICS. Flies and Disease. II i62 DISEASES DUE TO BACTERIA DISEASES DUE TO BACTERIA. GENERAL FEATURES OF BACTERIA. (After E. W. Hey Groves.) GENERAL CHARACTERS. Fission fungi. Devoid of chlorophyl. Unicellular vegetable organisms. Consist of protoplasm surrounded by a cell wall. REPRODUCTION. (a) By simple fission. — The common method. (b) By Spore formation. — Only found in a few bacilli. Never found in common pyogenic bacteria. Occurs, e.g., in B. anthracis, B. tetani, B. cx^dematis maligni. Spores are formed when conditions for bacterial life are un- favourable. They have a thick capsule, and are very strongly resistant to desiccation, heat, or antiseptics. (c) By budding, e.g., yeast. LOCOMOTION. Passive. — By Brownian movement, physical or chemical currents. Active. — By flagelUe, i.e., actively contractile protoplasmic processes. Found in B. typhosus and B. coli. SHAPE. Cocci. Round; never produce spores. Gram + Staphylococci ; arranged irregularly. Diplococci ; arranged in pairs. Streptococci ; arranged in chains. Tetracocci ; arranged at four corners of a square. Sarcin^e ; B. arranged at eight corners of a cube. Bacilli. Rod shaped, often spore-bearing. Gram + and — . Streptobacilli ; chains of bacilli. Leptothrix; long threads. Spirilla; spirally curved. PHYSIOLOGY. They require organic proteids for food because they have no chlorophyl. Parasites obtain it from living animals or plants. Saprophytes obtain it from dead tissues. Facultative parasites ordinarily live on dead tissues, but can also grow in living, e.g., B. proteus. GENERAL FEATURES OF BACTERIA 163 Facultative saprophytes ordinarily live in living tissues, but can with difficulty be cultivated outside, e.g., gonococci. Conditions necessary for bacterial existence or activity. Proteid food in an assimilable form. Water. Temperature at or about blood heat. Darkness. Oxygen or its absence. Aerobes, e.g., pyogenic cocci, require oxygen. Anaerobes, e.g., B. tetani, cannot live in oxygen. But they can often live in company with other bacteria which absorb oxygen even in the presence of air; e.g., B. tetani can grow in a surface wound if it is contaminated by cocci. Conditions causing a suspension of bacterial activity or groivth. Absence of pabulum. Dryness. Cold. Sunlight. Conditions causing bacterial death. Heat at or below boiling pomt quickly kills all except spores. Spores require temperature of 25o°F. or long boiling to kill. Chemical reagents, e.g., carbolic acid, mercury salts, etc., must be of a certain strength ; act for a certain time and come into intimate contact. In all conditions in which the living tissues are more potent than the bacteria. Products of bacterial activity ivhe7i growing in living tissues. Acids or alkalies, e.g., B. coli produces an acid. Gases (rare), e.g., B. coli and B. oedematis maligni. Pigments (rare), e.g., B. pyocyaneus. Aromatics. Indol, phenol. Alcohols. Ferments. Diastase, curdling ferment, proteolytic ferment. Ptomaines. Crystallizable alkaloids. Toxins. The specific poisons, probably albumoses. (a) Intracellular toxins, e.g., tuberculosis. The toxin remains closely associated with the bacillus, and only acts in its neighbourhood. (b) Extracellular toxins, e.g., diphtheria, tetanus. The toxin is found in the bodv fluids, and acts at a distance from the bacteria. THEORIES OF IMMUNITY. The tissues acquire two methods of defence. (i) They kill the bacteria; antibacterial action. (2) They neutralize the toxins; antitoxic action. Antitoxic action is an actual chemical antithesis to the toxin produced in the blood bv infection. lliis is a proteid, and is called antitoxin : it can be made to neutralize the toxin outside the body. Best exemplified in diphtheria and tetanus. 104 DISEASES DUE TO BACTERIA Anli-bacterial action is brought about by two agencies : — (i) Phagocytosis. The leucocytes digest the bacteria. (2) Action of anti-bacterial substances in the blood serum which kill and dissolve the bacteria outside the leucocytes. Bacteriolysins. Exemplified in anti-streptococcus, anti-cholera, anti-plague, anti-pneumococcus, and anti-typhoid sera. Phagocytes. Is increased by the action of a substance called an opsonin produced by the action of the bacteria and the toxins in the blood. Opsonic Index is the proportion of bacteria devoured by leucocytes m an infected blood to those devoured by leucocytes in normal blood. Directly after an injection of a vaccine (bacteria of toxins) the opsonic index falls = negative opsonic phase. During this time a further dose of vaccine does harm. After a few days the opsonic index rises -- positive opsonic phase. During this time a further dose of vaccine increases the phagocytosis. DISTRIBUTION. In air and water. Plentiful in proportion to warmth and proximity to organic life. In earth. Always abundant near the surface. In animals (apart from disease). On and in the skin, hair follicles, and sweat glands. Mouth, especially round the teeth. Whole alimentary canal. Most numerous at the end of the small and beginning of the large intestine. Lower parts of the urethra, vagina and nose. INFECTION. The invasion of the living tissues by bacteria in such a manner as to produce local or general disease. CONDITIONS NECESSARY FOR INFECTION, (i) Dose of bacteria. Bacteria must be introduced in a certain number, or they will be destroyed before they produce any effect. (2) Virulence. — This varies enormously naturally. May be increased artificially : By passage through successive animals. May be decreased artificially : By cultivation outside the body, especiall}^ if done under unfavourable conditions. f,3) Pathogenicity. — Only certain kinds of bacteria are capable of producing disease in certain kinds of animals. PLAGUE 165 (4) Susceplibiliiy of llie host — i.e., :\ vulnerability of the living- tissues by the bacteria. Increased by : Any constitutional depression, cold or wet, starvation, youth of the patient, alcoholism, narccjtics and con- stitutional diseases, e.g., Bright's disease or diabetes. (5) Entrance of the bacteria into the tissues, provided by : — (a) A wound or abrasion or ulcer, (b) An inflamed or injured part, e.g., an inflamed tonsil or a sprained joint, (c) Pro- found constitutional depression, allowing the normally present bacteria to enter and multiply in tiie tissues. IMMUNITY. Is a condition of absolute or relative insusceptibility of the indivi- dual to infection after invasion by virulent pathogenic bacteria. There are two varieties : — • Natural Immunity. — Racial or individual. Acquired Immunity. — Active immunity; passive immunity. Natural Imiuuuily. — Nature of the condition is not known. No antitoxic or antibacterial substance can be separated from the blood. Is lessened by cold or wet, starvation, youth, hcTmorrhage, alcohol and poisons. Active Immunity. — ^Caused by a previous infection, either as the natural or modified disease. Involves an actual illness. Takes time for its development. Lasts many }'ears. Is brought about by : — (a) Previous attack. (b) Giving the disease, e.g., old-fashioned inoculation of small-pox. (c) Injection of attenuated virus, e.g., vaccination for small-pox, anthrax (in cattle), hydrophobia. (d) Injection of dead bacteria, e.g., plague, typhoid, tuberculosis. (e) Injection of toxins, e.g., in the animals which provide the anti- toxins of diphtheria and tetanus. Passive Iniinunity. — Caused bv injecting the blood of an actively- immunized animal. Involves no illness. Follows immediately on injection. Onlv lasts a few months. Is most successful against extracellular loxins, e.g-., diphtheria and tetanus. PLAGUE. DEFINITION. A septicaemia caused b\' the Bacillus pestis, spread amongst men and other animals by fleas, characterized 1)\' fever, rapid course, and high mortality. i66 DISEASES DUE TO BACTERIA HISTORICAL FEATURES. There is a coin of Lucius Severus showing ^sculapius, God of Medicine, witli the feel on a dead rat and a nude human figure in terror by his side. The Greeks worshippeci a rat-kiUing Apollo who was reputed to bring and remove plague epidemics. 1 140 B.C. the Bible records an epidemic in the country of the Philistines which produced buboes in man and killed rats (mice of the field), when 50,070 men died (i Sam. v. 4). 7/0 B.C. perhaps Sennacherib's army was attacked by a similar pest (2 Kings xix. 35). :;42 A.D. there was an outbreak in Pelusium, a great Egyptian market, whence it spread to Byzantium, the City of the World, into Asia, North Africa, Western Europe, Ireland, lasting in epidemic form about 200 years. iitli to 14th century it was pandemic, declining and leaving Western Europe in the 17th centur}'. 740J A.D. the Venetians erected the first lazaretto for the isolation of the sick by a quarantine of forty davs, also disinfecting clothing and merchandise. A yellow flag was to be hoisted by ships coming from a foreign port, and both crcAv and passengers inspected. The sacred Hindoo book, the " Bhagavat Purana," believed to be 800 \-ears old, speaks of plague in India. It advises the vacation of the house wherein dead rats were found. It is now endemic in India. There were epidemics : — 182^, in Delhi. i8j6 in Rajputana and in Rohilcund, the Pali Plague, at the same time. ifj6-i8og it was introduced into China by Mohammedans returning from Mecca. Since endemic in Junnan, it has spread southwards, reaching, i86y, Pakhoi. iSqz}., in June, Kitasato found the Bacillus pestis in Hong-Kong. i8g6 it spread from China to Bombay, hence over India. i8g8 the pandemic spread from India to Madagascar and Mauritius. i8gg, Malay States, Philippines, Australia, United States, South America. I goo, Capetown, Glasgow. igo'/, almost world-wide. Tripoli and Uganda are endemic areas in Africa. igog, in ]\Ianchuria, the pneumonic form was prevalent. The hot season of the tropics and the winter of the Temperate Zone are dele- terious to its spread. The bacilli rapidly disappear from the stomach PLAGUE 167 of the flea above 85° F.; at 10° F. they are virulent. High tempera- ture causes adult fleas to refrain from laying eggs and prevents larva; from developing. Below 50° F. fleas do not become infected when sucking blood. 1896-1905. During these ten years in Bombay, 1,154,613 people died of plague. Hygienic conditions have forced plague back from Europe, where it was once more prevalent than in the tropics. From 1896 to 191 2 plague in India killed 7,000,000, or about 7 per minute. 1664-1679, the last time plague was in England, 70,000 people died in London. The effect made upon English national life by this attack was most marked. Everv English hedgerow is a reminder of plague; they mark the change in land tenure which followed the Black Death. The loss of labour by the plague drove out villeinage and serfdom, after which it became necessary to define the fields. From that period dates the emancipation of the English labouring classes. Plague helped to kill the textile industries of the Eastern Counties, and laid the foundations of the modern prosperity of Lancashire and Yorkshire. It facilitated the growth of English literature. L'^p to the time of the plague French was the principal language of the schools and the wealth V, but so manv teachers died in the epidemic that a new race of English teachers arose. 1802, Whyte communicated it to himself, and died while conduct- ing an experiment. iSj-;, at Cairo, two condemned criminals were inoculated, but recovered. i8g8, in a Vienna laboratory, the pneumonic type was contracted from cultures. There was no epidemic present. Plague does not spread v.ell in sanitary districts. It is not nearlv as contagious as small-pox and scarlet fever. 1910-1911. The Plague in China was of the pneumonic type, the most severe. The great majority of the natives and Europeans attacked died, about 46,000 in all. The epidemic was brought by the hunters of the marmot, which is an animal susceptible to epizootic plague. The disease was spread bv the hunters when they returned home. No instance of plague was found amongst the rats examined. Rats are undoubtedly to blame in India and elsewhere. Their extermination is a problem. At Tokio, during five years, there were 4,800,000 rats killed at a considerable financial outlay, but even then there was not any reduction noticed in the rat population. i68 DISEASES DUE TO BACTERIA The isolated cases of pneumonic plague which occur in Siam do not appear to have any tendency to cause extension of the disease, and persons coming into intimate contact with such patients do not become infected. The Manchurian experience was very different (Manuad). 1914. During the plague in New Orleans, there was" one quarter where, although the people were living over a hotbed of infection, no human case ever occurred. It is suggested that the rat population was so large that human blood did not present any temptation to the rat fleas, as their natural hosts, the rats, provided ample food (Akin). 1916. There was plague in Bristol during July in humans and rats. Active measures eradicated it. Eight out of seventy-four rats caught in the rag factory were infected. The 200 tons of rags were then destroyed by fire, an excellent means of disinfection. This is the twelfth British seaport in which plague has occurred within the past fifteen years, apart from a sharp pneumonic attack in Essex about ten years ago, when a few people died and several varieties of animals were found infected. History shows that plague is wont to visit a country once in 300 years; the last epidemic occurred in Britain some 300 years ago; another is due now (Cantlie). THE CAUSATIVE BACILLUS. The B. pestis of Kitasato and Jerson is found in the initial cutaneous vesicle, buboes, spleen, blood and sputum in pneumonic cases. Monkeys, rats, guinea-pigs have been successfully inoculated with typical symptoms. Bovines and equines give local reaction only. Canines, birds and reptiles are apparently immune. Human plague is an offshoot of rat plague. In glucose the bacillus forms acid, but not gas. In lactose it gives no reaction. In broth with cocoa-nut oil it forms flocculent tapering masses. Haffkine's stalactite growth, verv delicate and verv readilv broken off. The pseudo-tuberculosis bacillus is much the same; inoculating guinea-pigs is required to differentiate them ; this kills in three weeks, the plague bacillus in three days. B. pestis is a short, oval rod with rounded ends, capsulated singly, but in cultures they grow in chains. It does not form spores. No true motility. Stains readily with basic aniline stains. Gram- negative; grows on ordinary media at body heat; flourishes best in ESSENTIALS OF TROPICAL MEDICINE. Plague bacilli. Streak preparation from spleen. Zeiss' homog. apochrom. immersion 2 mm., apertnre t.30, compensation oc. 4. (Prepara- tion kindly given to Dr. Mott by Prof. Sticker, Giessen). Bacilli lepriE in the nasal secretion. Zeiss' homog. apochromat. immersion 2 mm., aperture 1.30. (Preparation kindly given to Dr. Mott by Prof. Sticker, Giessen.) Sputum in pneumonic plague. Plague Ijacilli in pure culture. Zeiss' homog. apochrom. im- mersion 2 mm., aperture 1.30, compensation oc. 4. (Preparation kindly given to Dr. Molt by Prof. Sticker.) Fau Page 16S PLAGUE 169 oxygen; readily killed by heat; strong resistance against cold. Gains entrance through skin abrasions, more often flea bites. Bacillus pestis. Smear from gland juice, 1/12 oil immersion. Bacillus pestis. Blood film, 1/12 oil immersion. PLAGUE IN RATS. Acute and chronic. In the acute type bubo is found in the neck or axilku in 85 per cent, of infected rats. There is subsequent congestion, purplish-red 170 DISEASES DUE TO BACTERIA '/ muscles, waxy, mottled, or finely granular liver, haemorrhages, and pleural effusion. Bacilli in bubo, spleen and blood. In the chronic Ivpe. — Encapsulated caseous foci, abscesses with bacilli in viscera, but it does not spread the disease. Temperature largelv affects the prevalence of the disease. In Bombay, fr(;m December to May, 1,766 infected rats were found in one week during which a search was made. In the cooler season, from June to November, they are not so prevalent, there being onh- twentv to thirtv found during the week's search. All rats are not equally infected. Epimys norvegicus and E. rattus are the principal species. The former carries twice the number of fleas, and infection is more rapidly spread by it. E. rattus is more common in Bombay, lives in houses, less seldom in stables and outhouses. Breeds all the }'ear, and averages a family of five. E. norvegicus li\'es outside houses as a rule, in sewers, drains and stables. It is ne\er found above the third floor of a house. It breeds all the year, with an average family of eight. One species infect the other solely by the flea. Infected urine, faeces, air, soil and food will not give plague to a healthy rat. The flea cannot jump more than 4 inches. If rats are suspended above this height from infected fleas the\' do not become infected, hence the disease is not air-borne. Infected fleas b}- biting healilu' rals produced the disease in 55 per cent. The blood of the plague rat contains 100,000,000 bacteria per c.c. The stomach of a flea holds o'5 cm. of blood. Hence a gorged flea can receive 5,000 bacilli. They escape soleh- in the f^ces of the flea. Multiplication of bacilli takes place in the stomach and intestines of the flea. Infected fleas transmit disease in from seven to fifteen days. Take spleen smears and examine for B. pestis. Do a Gram stain ; if positive, the organism is not plague. Then grow cultures and inoculate guinea-pigs. In spleen smears there may be clumps of bacteria from h'mphatics and vessels. Xo other bipolar staining organisms give this. Plague in domestic animals in Bombay either does not occur or h£is little significance. Some Indian rats harbour B. pestis without svmptoms, but if injected into other animals i'. I;ills iliem. Young rats suckled by infected mothers are not infected if fleas are absent. PLAGUE 171 Cold dead rats are harmless, as the flea has forsaken them for another warm host. The Indian Musk Rat, Crocidura coerulea, is highly resistant to plague. Only one rat was found to be naturally infected witTi plague by the Indian Plague Commission (Kerandel). THE CARRIER. The flea most common in rats is Zenopsylla cheopis, but others, as Ceratophyllus fasciatus and Pulex irritans, are capable. Infection by the flea is due to faecal infection of the proboscis or of the wound made by it, which transmits the bacilli to the skin. Humans are infected by the Z. cheopis from the Epimys rattus. It is found on humans after cases of plague in man. Plague infection may persist in fleas for one or two months in the cool weather, and subsequently give rise to an epizootic (Bacot). P. vestimenti is capable of transmitting plague infection also (Swellengrebel). Air, however, does carry the bacillus in the pneumonic type from the sputum. The bubonic or septicaemia is not spread from man to man, but from rats to man. Bugs can also act as carriers, C. rotundatus. In California the ground squirrel, Citellus beecheyi, is subject to plague, and its common flea, C. acutus, spreads it from one to another and will bite man. In ^Manchuria plague started among those who handled the Tarahagan (Arctomys bol^e) ; no infected rats were found. The epidemic was pneumonic. PATHOLOGY. The site of the flea bite is sometimes marked by a vesicle, the con- tents containing B. pestis in large numbers; the bacilli travel by the lymphatics to the nearest glands ; some pass to the thoracic duct, thence to the blood-stream, and so cause a septicaemia. More often they remain and multiply in the lymph glands and the peripheral lymph sinuses. Their toxins cause cell degeneration, periglandular serous infiltration, and later, degeneration of the walls of blood-vessels and haemorrhage. The l^^mphatics are matted by the exudation, femoral, inguinal, axillary, iliac and cervical. The groin glands are infected most, as they drain the largest skin area. The bacilli may get direct to the blood-stream by injuring the veins in the primary bubo. Lymphatic glands also become affected after the infection has become a septicemia. Also the lung causing bronchitis and secondary pneumonia, spleen, liver, kidneys, skin and other organs. The sputum and saliva can be infected forty-eight days after the 172 DISEASES DUE TO /BACTERIA temperature is normal, and abscesses may contain bacilli ten weeks after. The chemical pathology is unknown. In epidemic pneumonic plague the primary infection is in the bronchi from inhalation, setting up peribronchial inflammation. Lobular and lobar pneumonia develop quickly, and then a septi- caemia. There is no evidence that it has ever started in the great intestinal tract, though many bacilli must have been swallowed. P.M. Post-mortem rise of temperature is not uncommon. Decomposition early. (i) The skin about buboes shows haemorrhage resulting from toxins acting on endothelial cells of vessels. The ha^mor- rhages are petechial or diffuse and contain bacilli. \'esicles, pustules, so-called carbuncles may be seen. (2) Glands. — The primary bubo shows periglandular infiltration. Glands matted, greyish, soft centre, numerous ha^morrhagic spots or large haemorrhages. The secondary buboes (those infected by drawing from the primary gland) are degenerate glands, no oedema, endo- and peri-glandular haemorrhages. The tertiary buboes (those infected after it has become a septicaemia) are hard, hyper^mic and h^emorrhagic. (3) Muscles, especiallv those of abdominal walls, are ha?morrhagic. (4) Viscera. — Spleen enlarged two to three times the normal size, congested, hjemorrhagic, bacilli very numerous, necrotic areas, dotted with pin points. Liver enlarged, somewhat mottled, haemorrhagic. cloudy swelling, fatty degeneration. Lungs, some bronchitis, and often patches of secondary broncho-pneumonia. Efi^usion into pleural sacs common with hccmorrliage. R. heart dilated, fatty degeneration, cloudy swelling, haemorrhage. Stomach hypera^mic, haemorrhage, solitary glands and Fever's patches swollen, mesenteric glands markedly so. For sections stain \\ith strong carbol thionin, stop its action with oil of cloves and remove the stain therewith. SYMPTOMATOLOGY. Incubation. — Two to ten days, average three days. Frodromal symptoms. — General malaise, headache, gastro- intestinal disturbance, glandular pain, chilliness, giddiness, mental dulness. PLAGUE 173 Onset.— Sudden, temperature on third day rises to i03°-i04° F., and falls on the sixth or seventh day (remember pneumonia). Pulse 130, respirations 30-45. Marked prostration, vomiting, diarrhoea, general bodv pains, rigor and staggering gait. In a few hours after the onset eyes become bloodshot, nostrils dilated, and temperature very irregular; if recovery it may fall by lysis, or if no recovery it falls rapidly to sub- normal, and rises rapidly to 107° F., and death supervenes. Thirst is marked. Tongue furred at first, later sordes on tongue, teeth, and lips. Abdomen not tender imless there are enlarged abdominal glands. Spleen always enlarged. Liver often. Cardiac dilatation important. Pulse may rise to 180 and become thready. Coagulation of blood diminished. Bacilli can be grown from the blood in manv of the cases. Red cells and lib. increased, leuco- Inguinal plague bubo. (From Prolessor Simpson's collection.) cytosis is marked 90,000 — 100,000, but leucopa^nia mav ensue in septicemic foi'ms. Breathing rapid, B.S. harsh with moist rales, signs of lobar pneumonia may occur, sputum is then ha?morrhagic and full of bacilli. Buboes, seen in groin, axillae and neck, are painful. The legs mav be drawn up, or the head bent over because of them, when seen in the first twenty-four hours. These glands may resolve or suppurate. Skin hot and dry, with vesicles, pustules, necrotic areas, petechia,, ecchymosis, epistaxis, hc-ematemesis, mal^ena, haematuria. Urine diminished. Specific gravity high; bacilli may be found. Anuria usually before death. Pregnant women alM^ays abort. Weakness, wild delirium, coma, death third to fifth dav. If recovery, temperature resolves by lysis, pulse rate is diminished and convalescence begins. Death may still ensue from cardiac failure, suppuration, septic infection, or secondary haemorrhage. 174 DISEASES DUE TO BACTERIA VARIETIES. (i) Ambulatory Type, the mildest form. — The symptoms can be looked upon as the prodromal symptoms, aggravated some- what. (2) Bubonic Type. — The bubo is usually in the groin. The fever maximum is reached on the fourth or fifth day, and lasts till the seventh or tenth day, falling by lysis, and rising again if suppuration sets in. (3) Septica?mic Tvpe. Onset sudden, temperature high, very rapid pulse, marked prostration, severe vomiting, diarrhoea, hc-emorrhage, death in one to three days. Children may be playing in the street in the morning, haemorrhage in the afternoon, and dead next morning. (4) Pneumonic Type. (i) Primary pneumonia. No prodromata ; incubation two to five days. Cough and dyspnoea within twenty-four hours; bloody expectoration with bacteria second to third day. Conjunctiva injected, respiration rapid, dyspnoea, cyanosis. Spleen not usually palpable. Very fatal. (2) Secondary pneumonia (after buboes). As general symptoms. MORTALITY varies. Apart from mild attacks it is 60-95 P^^' cent. Chinese 93*4 per cent. Japanese 60 per cent. European i8"2 per cent. Of known and controllable cases in hospitals, jails, &c., 35-45 per cent. TREATMENT. Bed, good nursing, fresh air. Fever with sponging and cold applications. Heart by digitalis, struphanthus and strychnine. Restlessness; opiates, chloral, potassium bromide. Haemorrhage; calcium chloride or lactate. Constipation ; calomel and saline. Pneumonia; the ordinary treatment. Kidneys, much fluid to keep them flushed. Diet; broths, milk, stimulants usually. Diarrhoea; ice pills and morphia, hyclroc}'anic acid, salol. Buboes. Glycerine and belladonna, when suppurating incise and drain. PLAGUE 17s PUBLIC PROPHYLAXIS. Institute a sanitary service in an infected country with collectors, bacteriologists, &c. Port sanitary authority to investigate and disinfect ships. Isolate as far as possible. Quarantine five davs. Medical inspection of passengers by rail, road and river. Disinfection of clothing, and merchandise by Clayton's method. Rats to be caught and examined. Recognition of early cases, investigations oi sudden deaths. House to house visitation by M. O. \'illage houses burned. Kill rats by SO., SO^, Danyz's virus on bread; encourage cats. Work from the outside of a circle. Cover hands with oil of aniseed as rats know if humans have touched food set to catch them. Phosphorus paste, with glucose to prevent com- bustion, with lard as a basis. Traps; two to 100 of the population (in proportion). Prophylaxis as suggested by Haffkine. (i) Discovery and notification of persons attacked with disease. (2) Isolation of those attacked. (3) Certain precautions with regard to the disposal of the dead. (4) Segregation of those who have come in contact with the sick or dead. (5) Institution of cordons round infected areas, or (6) Placing in quarantine arrivals from infected places. Detaining the sick and suspected, liberating the remainder. (7) Or examine travellers, isolate sick and suspected and let others free under surveillance. These are always difficult, often impracticable, and achieve little. Second method. Within the affected area. Destroy or disinfect houses, furniture, clothing, bedding, carriages, goods, warehouses, grains and other stores, garbage, drains and streets. Outside the infected area. Refusal to admit carts, trains and ships with goods from infected places; or refuse to admit only certain goods; or inspec- tion of trains, carts, ships with measures by which these and the goods they convey, as well as the belongings of travellers, are rendered harmless. The expense and difficulty of such is enormous. Third method. (i) Destruction and keeping away of rats by poisoning, trapping, tar and sulphuric acid mixture, or by the domestic cat. i;6 DISEASES DUE TO BACTERIA (2) Structural alteralions of dwellings and stores, demolition of in- sanitary buildings, prompt disposal of garbage, periodical inspec- tion of stores having drainage witii view of keeping down rats. (3) Destruction and dispersion of fleas by petroleum, &c. (4) Fumigation of houses against rats and fleas. (5) Obligation of ships from infected regions to anchor away from the shore. (6) Provide mechanical means for preventing rats from landing along mooring cables and gangways. (7) Fumigation of ships arriving with plague patients, plague rats or suspected bedding. Such would cause a dislocation of trafific and an outcry, formidable to face; the result is that plague is still spread. If men are honest, rals are not and regulations are broken down. PRIVATE PROPHYLAXIS. Yersin's serum, from a horse inoculated with fresh agar cultures; give 20-200 c.c. intravenously and subcutaneously near the buboes. There may be urticaria and pleurodynia for three days. For Yersin's serum to have anv appreciable effect on the course of. the disease, the first injection must be given wuthin forty-eight hours from the appearance of symptoms. Lustig and Galeottis' serum, from a horse injected with vaccine. Both these are supposed to stimulate phagocytosis and are not bacteri- cidal. Lustig and Galeottis' vaccine ; shake agar cultures with i per cent. of caustic potash, and after two hours add o'5 per cent, acetic acid, and thus obtain a precipitate of nucleo-proteids. Subcutaneous or intramuscular 2-3 milligrammes. Haffkinc's Prophylactic Vaccine. — Grow bacteria on broth and butter fat 4 to 6 weeks; stalactite growths form. Sterilize at 65°-70° C. for one hour. Decant into bottles with a little carbolic acid. Dose. — 3 c.c. for an adult man. Subcutaneously about deltoid. There is a local and general reaction arising in a few hours and disappearing in i to 3 days. Reaction may be severe or mild. This protects from 2 to 12 months and is used much in India. Good results. It requires 10 to 14 days to produce suflRcient immunity; during that time resistance is diminished. In a Punjab experiment in 1903 the mortality was 60 per cent.; in the inoculated it was 2^^ per cent. ATTENUATED CULTURES. Strong. — Intramuscular injection of one whole twenty-four hours agar slant of living virulent culture. The reaction is not excessive. PLAGUE— NOTES ON FLEAS \77 Opsonic index rises markedly ten days later. Guinea-pigs, mortality 66-6 per cent.; inoculated iG'G per cent. Klein's protective inoculoiion prepared from the organs of dead imimals of plague; he says : — (i) It requires ten to twelve days to prepare it; Haffkine's requires four to six weeks. (2) A large amount can be prepared of uniform strength. (3) Its efficacy is easily standardized by injection into the rat. (4) Being dry and sterile it can be preserved without antiseptic and kept unaltered. (5) That its injection into the rat protects certainly many weeks. (6) Cost of its preparation is much less than Haffkine's. This has not yet been tried on man. Masks of flannel cloth to cover the head tied about neck with window of sheet celloidin are advisable. NOTES ON FLEAS. (Order Siphonaptera.) Fleas are active parasites of mammals and birds. They usually have a preference for one host, and attack others with some reluctance. They act as carriers or necessary intermediaries, e.g. — (i) The common dog flea and the common European rat flea harbour the cysticercus of certain tapeworms of their respective hosts. (2) The trypanosome of the rat passes through certain stages of its developmental cycle in the European rat flea. (3) They are carriers of the plague bacillus among rats and other rodents, and from these to man. Pulex (Xenopsylla) cheopis most commonly infests house rats in the tropics. The Pulex irritans (the human ilea) and others are capable of carrying the plague bacillus. EXTERNAL APPEARANCE. Fleas are laterally compressed, wingless insects, with two piercing, sucking mouth parts. The head is broadly articulated to the thorax; all three segments of the thorax are distinctly independent. Eyes may or may not be present ; when present they are simple and not com- pound as in the house fly. A comb of teeth is found on the edge of the cheek or on the lower edge of the head in most species. The antennas, two basal segments and a club with nine rings, lie behind and above the eyes. Bristles are seen irregularly placed about the head and thorax. They have a pair of longitudinally grooved, serrated, needle-like mandibles, which form an efferent tube for saliva, 12 178 DISEASES DUE TO BACTERIA and an unpaired bristle which, opposing- iisdf lo these, forms am afferent tube for sucking blood. The three pairs of legs with their paired claws are long and strong. The abdomen has ten segments; the last three arc modified for sexual purposes. The male has on the ninth segment large claspers and a large complex penis. Pttlex itf-ilans. 14/1. Larva of flea. Enlarged. (After Railliet.) Pulex serraticeps. 22/1. ALIMENTARY TRACT. In the head is an elastic pharynx acting like a suction pump ; its cavity, when expanded by the contraction of certain muscles, forms a vacuum. The stomach is very distensible, the rectum is large. They carry- two pairs of salivary glands. REPRODUCTION. The eggs are large, dropped casually in places where domestic animals sleep, hatching in two to fourteen days according to tempera- LEPROSY 179 lure. The larvcB are active, white, hairy maggots with a head and thirteen segments, the last carrying a pair of hooks. They eat organic matter from dust, and spin a cocoon in two weeks or longer, in which they pupate. The cocoon coated with dust contains a hump-backed pupa which can develop in two weeks. There are two main families : — Pulicidce, which contains Pulex irritans, the common human flea, and Xenopsylla cheopis, the tropical rat flea. SarcopsyllidcB, which contain the Dermatophilus penetrans or jigger. Indigenous to South America, but carried to the Gold Coast, East Africa, and Bombay. It flourishes best in sandy places. It attacks man and other animals, including the pig. Both sexes suck blood, but the pregnant female embeds herself in the skin, often under the bed of a toe-nail, and in this inflamed pocket lays her eggs. Pain and inflammation result, leading to indolent ulceration and even gangrene. TO DESTROY FLEAS. Close the room, spray completely with 5 per cent, solution of formalin, or sprinkle copiously with powdered naphthalin, and leave closed for two days. Then burn all sweepings. Wash floor with formalin or lysol. Ants eat the larva5 and pup^e. For personal use, use quinine, quassia, sulphur, petroleum, which are repellent to fleas. LEPROSY. DEFINITION. A chronic infective disease caused by Hansen's bacillus, with characteristic lesions of the skin, mucosae and nerves. HISTORY. Perhaps brought from Egypt to Italy by Pompey's troops, dis- seminated throughout Europe by the Roman legions. The returning Crusaders (1098) increased it. Lepers were isolated in Europe in the 13th century. Thev were compelled to wear a special dress, to use clappers when on the roads, and to point with a stick to articles in the market which they wished to buy. They were forbidden to drink from the public fountains, or eat with healthy people. They were officially dead, and the burial service was read over them as soon as they were diagnosed as lepers. Lepers gradually diminished from this time onwards. i8o DISEASES DUE TO BACTERIA The Spaniards perhaps took the disease to America. In the i6th century the imported West African slaves carried it to the West Indies, the Chinese to the Sandwich Islands, Colombia, Ntnv Zealand, &c. It was carried to South Africa by the Dutch from Java in 1756, and by the East Indian troops in the 19th century, Hansen discovered a bacillus in 187 1, and associated it with the causation of the lepra lesion in 1877. The method of infection is unknown. DISTRIBUTION. Present in Ireland in 432 a.d., and in England in 950 a.d. The last British leper died in the Shetland Isles in 1798. Present in Iceland, Spain, Italy, Balkans, Crete, Cyprus, Norway, Sweden and Greece. Common throughout Asia, Ceylon, India, Australia (Queensland and New South Wales). The Sandwich Islands in 1891 had one in thirty infected, 1,500 in all. It is present in the United States, Mexico, Central America, Colombia, West Indies, Venezuela, Guiana, Brazil, Africa and Egypt, which was probably its original home. In India, in 1891, there was one leper in every 2,000 people, 105,000 in all. In New Caledonia there w^ere no lepers in 1865. A Chinese known leper w^ent there, and later in 1888 there were 4,000 lepers. In the 13th century there were 19,000 leper houses in Christendom, according to the Benedictine monk, Mathew Paris. In France there were 2,000 and in England 95, besides smaller pest houses in Ireland and Scotland (Sir James Simpson). 1890, there were 1,100 lepers in Norway. 1906, there were only 500 there. 1915, there were 40 lepers in the United Kingdom (Dr. George Pernet). THE BACILLUS. Hansen's Bacillus laprse resembles T.B. in size, shape, and stain- ing reaction. Stain as for T.B., but use a weaker solution of H2SO4, 5 per cent., in decolorizing. For films and thin sections use the H2SO4 solution for fifteen seconds. It has been found in nasal secretion, tears, saliva, sputum, milk, semen, urethral and vaginal secretions, faeces, skin scales, extra- and intra-cellular in liver, spleen, glands, and breaking-down tubercles. It has not been found in earth, dust, air, water or food. It is doubtful if it has ever been cultivated. It is acid-fast, but stains more readily than T.B. with cold, weak LEPROSY i8i carbol fuchsin, and is more readily decolorized, is motile, and easily obtained. It is numerous in nodular and scarce in anaesthetic forms. Not found in muscle, bone or cartilage. Apes have been inoculated (Nicolli). HOW SPREAD. It cannot arise de novo, hence it must be carried by one or more of the following: air, soil, water, plants, insects, beasts, food, or man. It has only been found in human tissue. Perhaps contagious. Benson, an Irishman, acquired leprosy in the West Indies, and returned to Ireland. He died from it in eleven months. His brother had lived and slept with him, and later wore his clothes; in four years he, too, was a typical leper. He had never been out of the British Isles. Note its spread throughout Europe, its rapid spread in the Sand- wich Islands. In twenty years 800 lepers were isolated, and one-tenth of the population was affected. Father Damien went as a missionary from Belgium to the Sandwich Isles in 1873, and died of leprosy in 1889. Ten per cent, of the children of lepers become lepers. The success after isolation supports the contagion theory. Against contagion. — The attendants of Hendela Leper Asylum of Ceylon have not contracted it. There is no proof that sexual intercourse spreads it. A child has never been born a leper. It is present among people who do not eat fish. All possible means of spread have their supporters. It may in all possibility be spread by insects, ? bed bug. As lepers are sterile early, if it is hereditary, leprosy would soon die out. The fish theory is not now held by many. If it is a good medium it should be good for cultivating the bacilli, but it is not. In Abyssinia there are 8,000 lepers who rarely, if ever, eat fish. PATHOLOGY. How and where it enters the body is unknown. Perhaps by the nasal mucous membrane (McLeod). They form colonies in the lymph spaces, and later are disseminated by blood and lymph vessels. Few diseases show so many bacilli. Plasma cells surround capillary vessels and lymph capillaries, which are much dilated. The Leproma. — Large lepra cells containing masses of bacilli. i82 DISEASES DUE TO BACTERIA A smooth white and brown ghstening nodule, hard from fibrosis or soft from degeneration, well supplied with vessels. No true giant cells. The bacilli do not invade the surface epithelium, nor the cutis beneath this, nor sweat glands, nor hair sheaths superficial to the open- ing of the sebaceous glands. In section one sees the epithelium normal, but with no inter- papillary processes. Then larger cells of connective tissue free from bacilli. Then lepra cells, plasma cells, connective tissue cells, vessels with little connective tissue, vessels much thickened, sometimes with the lumen obliterated, and then lymph spaces dilated and filled with bacilli surrounded by mucus forming the "globi." Beneath this is normal connective tissue. The leproma may break down the skin and ulcerate, disseminating the bacilli in the discharge. Bacilli may enter the nerves, causing hyperplasia of the coats, forming thickened leproma about the vasa nervorum, and later, in the perineurium and endoneurium. These press on the nerve fibres, causing degeneration of the neurilemma, and destruction of the nerve fibres, which become con- verted into connective tissue. The bacilli may attack the anterior cornua of spinal cord. Any organ may be the site of leprotic lesions. P.M. Skin tubercles may or may not be ulcerated. Pigmented patches may be seen. Liver enlarged, bacilli infiltrate portal systems, seen as yellow dots. Spleen also. Bacilli are never found in the liver cells themselves. Ovaries and testes may show infiltration and fibrosis of interstitial tissue, which destroys sexual elements and causes the sterility so marked in lepers. The lymphatic glands are infiltrated and enlarged. The ulnar, median, peroneal, post-tibial and great auricular nerves are affected most. Posterior sclerosis of the cord and meningitis are not uncommon. Trophic changes in joints and perforating ulcers. Lungs may be affected, more solid than in T.B., caseate less frequently, less prone to be destroyed. SYMPTOMATOLOGY. Incubation not known ; perhaps two or three years at least. Begins usually in subjects from lo to 13 years of age, rarely after 40. Sometimes children are lepers first and parents later. LF.PROSy 183 Blotches and patches for years may have been disregarded. Epistaxis, frontal headache, intermittent fever, numbness, abnor- mal, local or general sweating without sufficient cause. (l and 3) Hindoo girls : (2) Hindoo woman with nodular leprosy. These may be seen at intervals for several years. The point of "entry is perhaps the nose. 128 out of 153 lepers had the bacilli in the nose first. After general dissemination the bacilli settle in the skiu and nerves, giving us the tubercular, anaesthetic or mixed leprosv. 1 84 DISEASES DUE TO BACTERIA (i) Tubercular Variety. A severe fever accompanied by an erythematous, diffuse or macular eruption on the face and Hmbs. This may subside or macules may develop into tubercles. This is repeated, glands enlarge, fever may sometimes be absents Tubercles and nodules come first, usually on the face and forehead, cheeks, aU'E of nose, lobules or ears, lips and chin. They soon alter the appearance of the patient. The tubercles are the size of split peas, dirty pink or dark brown, resembling sebaceous follicles. Beard, moustache, and eyebrows drop out early. Complete madarosis is not uncommon. Paralysis of the frontalis muscles is sometimes seen. Deformities in anresthetic leprosy. Tubercular leprosy. Marked case. Abotit the eye. Eyelids show diffuse or nodular lepromata, these mav ulcerate and destroy the eyelids. Conjunctiva; may become infiltrated, ectropion, zerophthalmia. Episclera infiltrated external to corneo-sclerotic junction. Small spots on cornea — " keratitis punctata leprosa." Uveal tract is infiltrated, anterior and posterior iritis may occur; nodules may form in the ciliary body or near the canal of Fontana, causing irido-cyclitis, or irido-choroiditis. About the nose. Nasal mucosa shows nodules, occlusion may ensue with ulceration and destruction of the nose, disfiguration from cicatrization. Sense of smell is lost. LEPROSY i8= -a W (fi o oi to ^ tM «) •" Tl -^ IM o .^ K 1 rt S -a W ^1 >, w* -Q .v» TS H) ■."^ JZ Q. ^ rt --^ %■ t^ Wl CI "is* o ^ J5 Pi t; ^ • •'^^ :» ^ a> u- *«v tN U) •* ^ ^ -^ Vi U~t "^ o K ^ •vt 1> ■^ u •*>4 3 ^ &J3 C li. ol « )-i •« c •V* H) V a, S ^ o <-i c *^4 O \ < 3 ■>1 a, ;? S :^ m ,^ o ^ c '% o i86 DISEASES DUE TO BACTERIA About the mouth. Tongue, mouth and pharynx may be affected, mastication and deglutition difficult; when in larynx the voice becomes raucous, respiration impeded. Lips become paralysed, saliva dribbles, gums retract, teeth fall out, taste is lost. About the skin. A goat-like odour. Tubercles on hands, arms and legs which may ulcerate. Submaxillary, cervical and femoral glands may be enlarged and may suppurate. Testes fibrous, menstruation irregular and may cease. Fingers and toes atrophy, ulcerate, drop off, then phalanges and metacarpals likewise. Blood. Nil diagnostic. No marked or consistent changes. Nerves may be attacked and add their corresponding signs and symptoms. Ulcerations may cicatrize and produce deformities or suppurate and produce amyloidosis or become phaged^enic causing septic poisoning, gangrene of fingers or toes. Nephritis is common. (2) ANAESTHETIC VARIETY. Infiltration is chiefly in the nerves; fibres irritated at first, then destroyed. Shooting pains of ulnar and peroneal. There are sensory disturbances as burning, numbness, formication; vasomotor disturb- ances as flushings, glossy skin; and motor disturbances as facial twitchings of muscles. A macular eruption, flat red spots appear without any general disturbances, some being pigmented. Spots increase in size, centres become pale, the peripheries usually are raised, marked with papules t)r vesicles, or dry whitish scales. Such areas may coalesce forming patches half an inch to six inches in diameter. Within these, the skin is anaesthetic, hairs fall out, does not sweat. Wrinkles and scales appear. Hypersesthetic outer border may look like a big ringworm. The disease may become quiescent and fade at any time. Nerves. — Ulnar nerve thickened, felt behind internal condyle, great auricular felt over sternomastoid. Peroneal below head and fibula, &c. With destruction of nerve, hyperaesthesia ends and anaesthesia begins. Noticed first usually along ulnar side of hand and f<:)rearm. It may be patchy or in distribution of nerve. LEPROSY 187 Paralyses of interossei of hands (main-en-griffe), thenar and liypo- thenar eminences, also of forearm causing " drop wrist." Plantar muscles of toes, peronei, extensors — "drop foot " with an internal twist. Reflexes increased, later diminished, muscles waste, R.D. distinct. Trophic lesions, whitlows on fingers occur, necrosis of phalanges, or simple absorption of bone, the nail persisting. Maculae in anaesthetic leprosy. Also on lower extremities there are bullae varying in size from a pea to that of an Ggg. Perforating ulcers. Fissures in digits of hands, toes, dry gangrene, or bones of fingers may soften and become osteomalacic. Eye is more often damaged by secondary infection, the result of the absence of lachrymal secretion and lagophthalmus. Secretion of tears is diminished, xerophthalmia with posterior or total symblepharon, while desiccation and destruction of cornea may i88 DISEASES DUE TO BACTERIA result. Secondary infection leads to keratitis, onyx, hypopyon, iritis, irido-cyclitis and total destruction. Sterility is not so frequent. (3) MIXED VARIETY. Some tubercular cases develop nerve leprosy. Some nerve cases develop tubercular leprosy. Some advance equally. Diagnosis. Bacilli always present in the nodular variety. In early cases look in the nasal secretions. in the anaesthetic form the bacilli are more difficult to find. PROGNOSIS. Cure is exceptional. Periods of apparent cessation not uncommon. Tubei'cular or mixed, 2 to 12 years' duration. • Anaesthetic form, 6 to 20 years' duration. Intercurrent disease often kills. Death is seldom from the disease itself. TREATMENT. None specific. Fresh air, good food, isolation, removal of child- ren, light work, amusement, rural colonies. It is a wise procedure to emigrate the children of lepers; 160 of such emigrated to Canada and not one has become a leper (Hansen). Surgical treatment as required for ulcers, whitlows, &c. Chaulmoogra oil, obtained by cold expression from the seeds of gynocardia, some species. It is easily adulterated and often substituted. Rub into patches, also to be given internallv 111 5-10 to v\ 30-40 t.d.s. in capsules or in pill with tragacanth and soap or in emulsion. Limes remove the taste of the oil. Rogers prescribes gynocardic acid, also known as chaulmoogric acid, and believed by some to be the active principle of the oil. This latter contains almost certainly useless palmitic acid. Dr. Sandwith recommends the use of this oil by hypodermic injection. Hot baths may be tried. Strychnine for nerve cases gr. -r^r> t.d.s. Omit treatment every seventh week and use ichthyol ointment 5 per cent. X rays have been tried, Finsen and radium. Hg. perchloride subcutaneously early everv other dav is useful. " Nastin," a neutral fat from Streptothrix leproides, combined with benzoyl chlorine and made into ampoules Avith sterile olive oil, 0*0005 to o'ooo2 gramme of nastin, once weekly can be tried. PSITTACOSIS 189 Leproline (McLeod), good results, but too early to say as to ulti- mate utility. Rhizophora Mangle used much in Cuba. (Nicholson and Padilla.) Lepromata disappear definitely fifth to seventh month of treatment, they suppurate and scar or are absorbed, encysted and calcified. Ulcers heal by eighth month and anesthetic patches disappear. In the ninth month the eyelashes and eyebrows grow again. Patient is cured in a year. Subcutaneous injection of iodoform. 30 per cent, emulsion in olive oil. Inject 2-8 c.c. daily, first near the lesions. Paint with the tincture externally. The iodine may disinfect the body, or some bacilli liaving been killed, these set free anti-bodies which destroy the rest. Intravenous injection of iodoform. Place ^ grain tablet of iodo- form powdered, in hypodermic syringe. Draw therein iii iii of liquid paraffin and 111 vii of ether. • Seal needle with lanolin to prevent evaporation of ether. Shake till iodoform dissolves. Inject it aseptically into the medio- basilic or other superficial vein, given twice weekly at first, gradually increased to gr. i five times weekly. The nodules four to six at a time can also be injected )ii x to 111 xxx, PSITTACOSIS. DEFINITION. A fatal specific epizootic among parrots, capable of spreading a severe febrile condition to man. AETIOLOGY. In 1892, 500 parrots were shipped from South America for Paris. 300 parrots died en route from enteritis. 200 parrots were sold in two lots after arrival in Paris. In 26 days an epidemic of psittacosis broke out, affecting 49 persons of which 16 died. Several persons in the same house were attacked. There have been other small outbreaks since. The organism is a bacillus of the paracoli group, closely related to, but distinct from, the B. typhosis of Ebert and is pathogenic for parrots and other birds. The feathers become infected w ith faecal matter. These are cleaned by the bird's tongue and thus infection is spread among them. Humans caressing the birds are infected by the bill or through some slight wound or contamination of food. It rarely spreads from man to man. iQO DISEASES DUE TO BACTERIA PATHOLOGY. In parrots an enteritis is caused, in man a septicaemia often com- plicated by lobular pneumonia. There is congestion and degeneration of the liver, kidneys, lungs and heart. SYMPTOMATOLOGY. Incubation 7 to 12 days. Onset sudden, or insidious, may be much like typhoid. Temperature io2°-i04°F. Pulse 1 10-120, quick respirations, cough. Signs and symptoms of lobular pneumonia. Tongue dry and furred. Spleen enlarged. Diarrhoea or constipation. Rose coloured spots on skin, patient dull and apathetic. If no pneumonia, patient recovers in 15 to 20 days. If there is pneumonia the mortality is 35-40 per cent. TREATMENT. Adapt treatment as for typhoid fever and pneumonia. Quarantine of two weeks should be enforced for imported parrots. The dead (infected) burnt with their cages. Parrots should not be fed by hand or caressed. UNDULANT FEVER. (MALTA FEVER.) DEFINITION. A chronic infectious disease of low mortality caused by the Micro- coccus melitensis of Bruce and closely allied germs, characterized by a prolonged irregular remittent fever and enlargement of the spleen. DISTRIBUTION. The endemic areas are the coasts and islands of the Mediterranean, Italy, France, Greece, and also India, especially the Punjab. It also exists in S. Africa, Uganda and the Sudan, China, the Philippine and Fiji Islands. N. and S. America and the West Indies. Common between ten to thirty years of age in both sexes, mostly in the warmer periods of the year. AETIOLOGY. The cause is M. melitensis (M. paramelitensis ; M. pseudo- melitensis. The two latter differ from the former in agglutination and absorption tests, causing para-undulant fever). The organism is a small, flagellated micrococcus, grows on agar and bouillon, feebly on gelatine without liquefaction. Stains with basic aniline dves. Gram negative. Mav often be cultivated from the UN DU LA NT FEVER 191 blood, sometimes from the urine, occasionally from the faeces. It can be found in the spleen, kidneys, liver, lymphatic and salivary glands, blood, bile, faeces, urine, milk, ? alimentary tract. It can live in dust for two months and in water for one month. It has been found in mosquitoes, but they are not proven infective agents. Monkeys have been infected and the germ recovered. The organism has been found by agglutination in 50 per cent, of Maltese goats examined and has been obtained from the milk of 10 per cent. Milk is the chief medium bv which it is carried to man even though but a little in tea is taken. Hence the rich suffer most and hospital patients about the Mediterranean in particular. Captain Joshua Nicholson took sixty-live Maltese goats on board in 1905. An epidemic of undulant fever followed. Nearly all who drank of the milk suffered. Perhaps goats become infected bv drinking human urine when lacking salt : mules, asses, horses, cows, rabbits and foAvls can carry it without being obviously diseased. Modes of Injection : — (i) By the alimentary canal (common). (2) By the respiratory system (rare). (3) By the cutaneous (very rare. Flies not proved). (4) By sexual intercourse (possible). PATHOLOGY. A general septicaemia is caused by the germ entering the blood- stream by the alimentary mucosae. The spleen is enlarged and congested. Perhaps an attack produces immunity. The organisms produce liaMiioIysins, the body reacting bv produc- ing agglutinins lasting four to ten years, also a specific serum which can be used for immunization. P. M. Spleen enlarged, 10 to 44 ounces, congested, sometimes soft and friable. Liver enlarged, congested, cloudy swelling or glomerular nephritis.. The whole intestine congested, colon sometimes" ulcerated. Lungs congested especially at the bases. SYMPTOMATOLOGY. Incubation six to fourteen davs. Onset insidious, headache, sleeplessness, anorexia, general mus~ cular pains, perhaps vomiting and constipation for about a week. 192 DISEASES DUE TO BACTERIA in o ec bl M r. 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CM •< ^ CM u •>= > 0) I xc: Srt ao *^ > r> c ^ 1 ;g S ( «: > - 2 .*< . i*" - 2 9 !^^i?==® 2 UJ •c >o n I b=« = __^^^ Ul •c -^ ■>** 01 UJ --- _ >J 1 UJ < rr* 3« ul •c s p» to UJ E — •e >v^ 3a 10 UJ E :> 1 * UJ S <^ Ui in N m Ul E I > CM Ul E < <■■> ,> a to ul E ej V B u E I <. > 0) CM UJ E ( [ 1~ CM UJ E .._...«> U> CM Ul E < 10 CM \ "y UJ E y .1 UJ E ■— - ^ " ^ « U < Q OOOOOOOO ■^(OCM-OOOrv U.OOOOOOOO o 00 UJ CM S > o u 13 194 DISEASES DUE TO BACTERIA The temperature goes up somewhat ladder-like to about 103° F., pulse 80-90. Tongue coated, edges red, sliglitly congested fauces. Some bronchial catarrh, tender epigastrium and enlarged spleen. This continues for about two weeks, the temperature remaining between io3°-io5° F. and then declines with general improvement. In about two davs a relapse occurs. This subsides and another follows and these relapses and remissions may last months, during which the temperature is undulating, a marked rise in the morning and a fall in the evening. The patient becomes more anaemic and wasted. Dyspepsia sets in, constipation or diarrhoea reveals irritation of the intestines. Throat sore, gums spongy, spleen painful, lung- bronchitic, heart excitable with h^emic murmurs, drenching sweats, disagreeable odour, crops of sudamina after the bird week, big joints painful and swollen, orchitis, parotitis, a general nervous disorder shown by insomnia, hysterical emotion, jDhotophobia, delirium, hallucinations are trouble- some. A rapid ansemia is common. The red cells show 20-40 per cent, loss with some poikilocytosis, Hb. low. Decrease of polxmorphonuclears, increase of mononuclears up to 80 per cent. Leucocyte count normal. Phagocytosis and bactericidal power of blood diminished. Agglutination test; diluted i in 50 to i in 150, it lasts two to seven years. Course of disease 20 to 300 days, average 90. Convalescence long and slow, perhaps six months. Many soldiers and sailors are permanently invalided. Mortality low, about 2 per cent. Symptoms arising in connection with the genital organs are not unknown, such as ovarian pains, dysmenorrhoea, amenorrhoea, menorrhagia, &c. The M. melitensis has been frequently known to remain for long- periods in the vaginal mucous membrane and con- tagion during intercourse is quite possible. Mammitis, like orchitis, is a not rare complication. The influence of the fever upon a pregnant woman may vary very much according to the period of gestation, and when the woman is infected. Abortion and premature labour are favoured during the fever when it is high. In some Mell authenticated cases it has been shown that M. meli- tensis can pass through the placenta and infants born at term generally show signs of infection and are weakly. Whether or not the infant acquires the disease by drinking the 'nfected milk of a nursing mother is a debatable point. Generally the UNDULANT FEVER 195 child appears to have a congenital immunity as early infection is rare, according to the experience of some. Still it would be advisable to interdict the woman, whose mammary secretion was infected, from suckling her infant. It is worth knowing too, that horses, mules, cows, and sheep may all become naturally infected, that milk products may harbour the germ, and that the latter is fairly resistant outside the body. The malignant types cause death from hyperpyrexia or the typhoid state during- the second or third weeks. The intermittent types last from six weeks to six months without serious symptoms. The ambulatory types are dangerous as carriers of disease. COMPLICATIONS. Intestinal ulcers, haemorrhage, persistent vomiting, diarrhoea, hyperpyrexia, pneumonia, pleural effusion, cardiac failure, orchitis, parotitis, arthritis, neuralgia. DIAGNOSTIC FEATURES. The prolonged undulant fever. The profuse sweatings. The arthritic symptoms. The agglutination test. Exclude typhoid by a Widal reaction (see p. 611). Exclude malaria by blood parasites. Exclude kala-azar by spleen puncture. TREATMENT. Entirely symptomatic. General principles hold good. The utmost nursing care is needed. Be careful to change the clothes after sweating. The heart and lungs must be carefully watched. Vaccine and yeast therapy can be tried. Give 100-500 millions of autogenous germs as a vaccine. Give yeast, dr. ii, twice dailv. Avoid goat's milk in endemic areas or sterilize it before using, Leave the district as soon as possible. PROPHYLAXIS. This is all important. In Gibraltar this fever disappeared after the goats were removed. In Malta the case incidence amongst the British troops was reduced from 643 in 1905, to 7 in 1907 and i in 1910. (i) General measures. Notification, isolation, disinfection, steril- ization of water and milk, good hygiene. 196 DISEASES DUE TO BACTERIA (2) Personal measures. Cleanliness, vaccine, care in nursing mothers. (3) Veterinary measures. Examinations of blood and milk of all goats and other suspected animals. Slaughter of infected animals. Prophylactic vaccines to all goats. Prevention of the importation of infected animals. BACILLARY DYSENTERY. DEFINITION. Acute or chronic, sporadic, endemic or epidemic, specific infective intestinal disorders caused by several varieties of bacteria, associated with tenesmus, abdominal pain, frequent mucous and blood stools. DISTRIBUTION. Universal, but especially in warm climates and where sanitation is defective as in jails and asylums, during famines and war-time. In temperate climates the dysentery bacillus causes the infantile diarrhoeas. There seems more prevalence at the end of a dry season, perhaps because of the infection of water by flies. AETIOLOGY. There are numerous types of true dysentery bacilli and of pseudo- dysenteric bacilli. There are three main types : — (i) Bacillus dysenteriie of Shiga-Kruse, which does not ferment mannite. (2) Bacillus dysenterise of Flexner, which ferments mannite, form- ing an acid in it. These bacilli are found in the dejecta, and can be scraped from the bowel post mortem. Agglutination A\ill help in their differentiation. (3) The Bacillus of Hiss. They belong to the Coli group, and the members thereof have the following characteristics : — They are Gram-negative, non-sporing, non-resistant, none liquefy gelatine, all attack glucose, all change the reaction of milk, all form creamy growths on agar. For specific characteristics, see p. 619. The infection is b}' faeces, flies, dust, soiled clothes, contaminated water or soil. Convalescents act as carriers. 11 per cent, of persons in an epidemic were found to be carriers. The bacilli may live in the bowel, producing no symptoms until the patient's resistance is lowered, when the typical disease mav show itself. After the first few days other bacteria may overcrowd the dysentery bacillus so as to make its isolation difficult. BACILLARY DYSENTERY 197 PATHOLOGY. The bacilli are ingested with food or water and proceed to the intestine, where they grow and muUiply. There they form toxins, one acting upon the lower bowel and the other on the nervous system. These are absorbed by the blood. The first is excreted into the lower bowel and causes : — (i) In acute cases. An exudation of lymph into the submucosa and mucosa. This coagulates and is invaded by cells. The capillaries are pressed upon and the blood supply cut off for small areas. Coagulative necrosis and thrombosis of vessels ensues ; the mucosa and the muscularis mucosae are destroyed. This forms a fibrous or diphtheroid membrane on the ridges first. This membrane contains micro-organisms and leucocytes. The membrane separates oft" in flakes, leaving ulcers. These, at first superficial, become deeper and larger. The peritoneum becomes oedematous and mixed infection is common. The condition can be summed up thus : — (i) Intense hyper^emia, the mucosa is swollen, corrugated and h^emorrhagic. (2) Necrosis and fibrinous exudation with pseudo-membrane formation. (3) Ulceration, at summit of folds, extending deeply and laterally. The ulcers heal by scar formation, and become pigmented as a result of the HoS of the bowel acting upon the iron of the blood. The other toxin causes peripheral neuritis. Septicaemia is very seldom caused, (2) In chronic cases. The mucosa and the whole gut is thickened and granular. The ulcers have thickened edges. Scarring causes strictures of the bowel with dilatation above. A typical ulcer : — (i) Site, on the ridges of the large intestines. (2) Edges, irregular and thickened. (3) Base, may be formed of any of the coats. (4) Result, tendency to contract on healing. , These descriptions will also indicate the post-mortem findings. There would be adhesions and signs of peritonitis, and parts of thf gut may present a black friable mass. 198 DISEASES DUE TO BACTERIA SYMPTOMATOLOGY. There is an endless variety in character, urgency and significance. The nearer the lesion to the rectum the more urgent is the tenesmus. The nearer the caecum the more griping. There is never liver abscess. We will group them thus : — Acute, Chronic, and Infantile. (i) Acute bacterial dysentery . Incubation twenty-four hours to six days. Onset. — Sudden, abdominal pain about the umbilical region first. Incessant call to stool, griping, tenesmus, very small stools of slimy mucus, and later blood-stained. 50-200 in twenty-four hours. Passage of a stool gives no relief. Slight or moderate fever, 99°-io3° F. Great thirst, foul tongue, dry skin. Anus becomes painful, prolapse not uncommon. Blood in stools, rapid exhaustion, sleeplessness, restlessness. Vomiting is not common. There may be constipation of the upper bowel with diarrhoea of the lower, recognized bv distension. The typical dysenteric motions have no faecal odour. The pulse is quickened, especially if much blood is passed per rectum, and may become irregular. Bad signs are : — Irregular and rapid pulse, subnormal temperature, hiccough, diminished number of stools in midst of attack during the second or third week. Good signs are : — Motions more faeculent, less numerous, disappearance of blood and mucus, less pain and tenesmus. Cases have been known to improve much, and then with a slight faeculent diarrhoea the patient has died wiiliin a few hours from gangrenous dysentery, or with the latter type there mav be thin, watery, dirty, foul stools, with sloughs of every shape and colour. Profuse hc-emorrhage is always possible. Others may commence with rigors, and the temperature may keep high, 1030-105° F., with mental symptoms as stupidity, sleeplessness, delirium, abscesses, carbuncles and bed-sores, simulating somewhat enteric fever. Death may ensue in a few days from exhaustion, toxaemia or hyperpyrexia. The stools. In an average case they consist of odourless gelatinous blood and extremely tenacious mucus Avhich adheres to the pan. In three to four days they become of a more purulent nature, vellow in colour, and contain less blood. Later bile is seen, which indicates BACILLARY DYSENTERY 199 that the contraction of the lower part of the large gut has passed off. Faecal matter may then be passed. A stool of glairy mucus, like sputum, is usually a catarrhal inflammation due to the Y bacillus. In the most acute fulminating varieties the stools contain much blood, and have been compared to "meat washings." When necrosis of the mucous membrane has taken place the stools may be choleraic, but may contain dark green sloughs of mucosa (Bahr). (2) Chronic bacterial dysentery. Insidious onset or may ensue after an acute attack. The bowel is not healthy, and any dietetic error, chill, fatigue, or indulgence will cause the symptoms to appear. The stools are loose, five to ten per diem, partly faecal, much mucus, rarely blood, like " frog's spawn " or "boiled sago." The tongue is glazed red, anaemia and emaciation are progressive, cachexia is apparent. The digestion is impaired, all functions are beloAv par resulting from anemia and toxaemia. Fermentation produces much intestinal gas. These symptoms may subside and recur at intervals. The disease may continue until death from exhaustion or some intercurrent disease, or it may clear up spontaneously. If no blood is passed it is commonly dysenteric diarrhoea. (3) Dysenteric infantile diarrhoea. This is an extremely common disease in the tropics. Flexner's bacillus commonly, and Shiga's bacillus rarely, are believed to be the exciting agents. The symptoms resemble those of the enteric type of chronic dysentery. It begins by vomiting and a temperature of io3°-io5° F. The abdomen is distended and tender. The stools are facal, but often green w-ith blood and mucus. The fever is remittent. There may be repeated attacks. Death may be from exhaustion or convulsions. Recovery may take place, but the convalescence is always slow. COMPLICATIONS. Peritonitis with or without perforation (rare). Pleurisy, pericarditis, endocarditis. Arthritis, tenosinovitis, j^erhaps the result of secondary infection. Ana?mia and dropsy. Peripheral neuritis, frequent in mild forms; one nerve only may be involved. Iritis, toxaemia, yields to atropine. 200 DISEASES DUE TO BACTERIA Parotitis, abscesses, rarely pyaemia. Hemorrhage in gangrenous cases. Appendicitis may set in. T^'phoid is a most serious complication and has occurred. SEQUELiE. Stenosis of the large bowel due to cicatricial contraction of the healing ulcers. Constipation and diarrhoea intermitting result of above condition. Colic and vomiting, meteorism. DIAGNOSIS. Inflamed haemorrhoids can be seen and felt. Syphilis of the rectum can be diagnosed by the Wassermann reaction and excluded by "606" injections. Rectal carcinoma can be excluded by the history, examination with finger and microscope. Intussusception is very sudden in onset, the abdomen is not tense, a sausage-shaped tumour is felt. Operation will discover and correct it. Malarial dysentery parasites will be seen in the spleen by puncture and smear. Kala-azar dysentery parasites will be seen in the spleen jjuncture and smear. Amoebic and balantidic dysentery by microscopic examination of fasces. A bacteriological examination of the fasces should be carried out. The agglutination reaction should be tried with the cultures pre- pared from the fasces and other known organisms. PROGNOSIS. Mild acute attacks; good recovery the rule. Severe acute attacks; poor, mortality high. Gangrenous acute attacks; bad, nearly all die. 12-25 ppi' cent, in all classes together die. The lower down the bowel the better the prognosis. The higher up the bowel the worse the prognosis. Early prophylactic serum improves the prognosis. New arrivals in the tropics suffer more than native residents. In Japan, the mortality was reduced from 35 per cent, to 9 per cent, by serotherapy. TREATMENT. (i) Acute attacks. Rest in bed. Bland diet. Use of urine bottle and bed pan. Constipation must be overcome, no matter how long the patient has been passing mucus. Damp BACILLARY DYSENTERY 201 cotton-woo! instead of sanitary paper should be used. Stools to be saved for physician's inspection. Protection of stools from flies. Disinfection of stools with carbolic acid. Give castor oil 5ss with opium tincture, 10 minims; much opium causes constipation and distension of gut and flatus. In a few hours give astringents : — ^ Bismuth salicylate gi- v Salol gr. V In cachets two-hourly at first. High rectal enema, boric acid i in 500; normal saline gr. v to 51 are well borne in mild cases. In severer cases give a polyvalent or other serum (Shiga) as soon as possible. (i) In mild cases 10 c.c. only. (2) In medium cases 10 c.c. twice, six hours between. (3) In severe cases 10 c.c. twice daily for three days, or 40-80 c.c. intravenously first day, 60 c.c. second day, 60 c.c. third day. This hastens the cure, ameliorates the symptoms, and reduces the mortality. In connection with the rapid preparation of serum. Professor Flexner has hastened the process considerably. In summarizing his work, he says : — Antidvsenteric serum can be safely prepared in the horse by the method of three successive intravenous injections of living cultures with intervening rest periods of seven days. When this method of immunization is employed, the specific anti- bodies responsible for agglutination and protection appear early and rise rapidly. By inoculating alternately living dysentery bacilli belonging to the Shiq-a and Flexner groups a polyvalent serum of high titre may be prepared. A polyvalent serum so produced should be suitable for the thera- peutic treatment of acute bacillary dysentery, irrespective of the particular strain or strains of the dysentery bacillus causing the infection. An effective antidvsenteric serum suitable for therapeutic employ- ment in man can be prepared in the horse in about ten weeks. Calcium chloride or lactate gr. 15 to gr. 30 is good. Salines are useful, especiallv when sera are not available or are not very successful. Stop on the third da^- if no impriivement, other- wise continue : — 5; Mag. sulph oil Sod. sulph. ... ... ... 5ii Aqua. ad. ... ... ... ,5! 5i two hourly until two days after motions are feculent. 202 DISEASES DUE TO BACTERIA Laudanum fomentations to abdomen for pain. Suppositories of morphia or cocaine for tenesmus. Or hypodermic injection of morphia gr. i. Reduce prolapse and apply hazeline or gall and opium ointment. Rectal tubes will permit gas to escape and allow of lavage, but pain often contra-indicates this. After acute stage bismuth subnitrate gr. 10-20, two-hourly. Rectal enemata of boric or tannic acid. Milk and fruit good. Calomel, ^ gr., hourly, has been tried. Yellow santonin in olive oil and sour milk have their advocates. Appendioostomy will permit the washing out of the bowel from above in gangrenous cases. (2) Chronic attacks. Treatment as for mild cases sometimes suffices. Diet. — The bowel must have rest. Albumin water and whey only at first. Then diluted milk and barley water with sodium bicarbonate. Thin arrowroot, malted milk. Chicken broth and milk puddings later. Lightly boiled eggs and chicken. In severe cases give small quantities two-hourly. Food must be well masticated later. Avoid much brandy, strong meat essences, and fruit. High bowel irrigation of silver nitrate with buttocks raised. Solution, l^-i gr. to the ounce. This gives the best results of all astringents. Precede with two pints of i per cent, sodium bicarbonate to remove mucus. Sera should be tried. Tannigen, gr. v, three to six times daily, or Tannalbin, gr. xv, three to six times daily have given good results. Liquid paraffin is always good, soothing- the bowel, breaking up the scybalous masses, and is mildly antiseptic. Pilula plumbi cum opii, gr. iv, four-hourlv. Autogenous vaccines can be tried. Appendicostomy is preferred bv some. (3) lufaniilc diarrhoea. Castor oil 5i-5ii, followed by calomel gr. 1, or grey powder gr. ^ each hour until six doses have been given in a child of two vears. Later tannigen gr. iii oi- tannabin gr. v, ihree-hourh'. Sera are good when bacilli are diagnosed, 5-10 c.c. twice daily. Treat convulsions by bromides, gr. xv in enemata. General prin- ciples hold good. 4» CHOLERA 203 CHOLERA. DEFINITION. An acute, specific, endemic or epidemic disease, caused by Koch's V^ibrio cholerai, 1883, and characterized by violent purging, rice-water stools, vomiting, muscular cramps, suppression of urine, collapse and high mortality. DISTRIBUTION. The name is of Greek origin, and was perhaps applied because the violent watery stools resembled water rushing from a spout. It has been known in India since the most ancient times. Ahmed Shah's army was decimated by it in 1438. There were several outbreaks after this in India, Burmah and Ceylon. The first great epidemic outside India was from 181 7 to 1827, when China was infected. Although cholera is not an endemic disease in Europe, its mani- festations in the 19th and 20th centuries killed millions of its people. There have been nine invasions of Europe in a little over 80 years. The chief centre of attack was about the Caspian Sea in Russia. All the invasions probably came from India by indirect routes. The endemic centres of Java, Indo-China and the Philippines were probably not implicated. An excellent summary of these attacks is given by Professor W. J. Simpson as follows : — Epidemics in Europe Interval Principal entrance ; '^J^IH gate into Europe ^^^^ invasion Number of years continued in Europe General characters 1823 1830-37 1847-52 Astrakhan '! 7 10 Less than a year 7 6 Did not travel farther west than Astrakhan. The Persian and Turkish armies, which were at war with one another, sufifered severely. Severe and widespread. Very virulent among the Russian and Polish troops. The war was believed to be the great cause of the rapid propagation of cholera in Europe. Great epidemic among the pilgrims at Mecca. Severe and widespread. In- vaded a larger area of the world's surface than that of 1830-37 and more deadly. Epidemic at Mecca. 204 DISEASES DUE TO BACTERIA Epidemics in Principal entrance Interval in years between Number of years continued in Europe Genera! characters Europe gate into Europe each invasion 1852-59 Astrakhan nil 8 More severe and widespread than previous epidemics. On its way through Persia it attacked violently troops of the Shah. Cholera aft'ected the troops in the Crimean War. In 1859 it attacked the French troops in Algeria, and the Spanish troops in Morocco. 1865-74 Constantinople 6 JO Severe, but more Imiited in diffusive power. 1884-87 Marseilles and Toulon 10 4 Less severe and limited. Spain lost 180,000 people, and Italy 50,000. 1892-96 Baku 5 5 Less severe and limited. Hamburg lost 9,000 people out of 17,000 attacked. It owed its origin to the great bathing festival at Karagola, on the Ganges. This only occurs once in thirty years, and the officials were not prepared for it. CIh lera broke out among the pilgrims, and spread rapidly. 1905-12 Baku and Astrakhan 9 8 Comparatively mild and limited. It killed 100,000 in Russia during 1910. 1912 Constantinople Mild and liinited. Prevailed among the Turkish, Bulgarian, Greek, and Serbian troops. The relation of cholera epidemics to wars is all-important. It is of interest to know that during the Napoleonic wars the disease was not known to Europe, so that these were free from this devastating malady. (i) In the Egyptian War of 1882-3 the civil population lost 50,000 from cholera, but the troops were little afYected by it. (2) Cholera was virulent during the Russo-Polish War of 1831. (3) After the Crimean War came the infection of all Europe. (4) After the Balkan War its distribution was widespread. Both the French and British armies and fleets sufTered. There were prob- ably about 18,000 cases behind the Chataldja lines, whence it was conveyed to the Bulgarian army, and later to the Greek and Serbian armies. (5) The Great European War of 1914 : — At the commencement of the War cholera prevailed in — Russia, the Province of Podalia. Hungary, 53 different centres. CHOLERA 205 Austria, 39 different centres. Germany, 10 different centres. Turkey, 2 different centres. Persia and Arabia are seldom free from the scourge. In 1915 the Russians tool^ cholera to their Austrian guards and to the civil population. There were then 30,000 cases with 16,000 deaths in Austria, and 5,000 cases with 3,000 deaths in Hungary. During the same year there were 147,000 deaths in India, of which 68,000 were in Bengal. Tropical and South Africa, the Azores, the Pacific Islands have not yet been infected. The principal endemic centre is lower Bengal. It always adopts channels of human inter-communication ; ships, rivers, roads, railways, producing a widespread epidemic in places of bad sanitation. iETIOLOGY. The existing cause is Koch's comma bacillus. ),hi Cholera spirilla. (From Pitfield's " Bacteriology.") Predisposing causes are low-lying areas, contaminated soils, unripe fruit, lowered vitality from any cause, as seen in gaols. Infection is by — (i) Direct contact. A medical man examined a patient suffering from cholera, then had his lunch. Patient and doctor were both dead in twenty-four hours. Care is required in performing autopsies. (2) Fomites form a common means of infection. (3) Water is the medium. The comma bacillus passes out with the faeces, and as it lives and multiplies in water for 163 days or more, a place having a poor sanitary system would have all the conditions favourable for an epidemic. Hampstead, a cholera-free place in 1854, was infected by a lady and 2o6 DISEASES DUE TO BACTERIA her servant ^^■ho drank water taken to them from the I3roa(l Street well, for Avhich they had a special Hking. The Hamburg and Akona instance is well known. Both towns used water from the river Elbe for drinking purposes. The former townspeople did not filter their water; an epidemic of cholera broke out, and there were 8,000 deaths, or i3"4 per cent, of the population. The latter people filtered their water, and during the epidemic they only had 328 deaths, 2*1 per cent, of the population. (4) Milk is especially dangerous, as it affords a good growing medium. (5) Carriers are extremely dangerous; though not obviously ill themselves, they carry and give out virulent comma bacilli in their faecal excretions. (6) The bacillus vibrio has been found upon and within the bodies of flies, hence these should be considered an important means of trans- mission. Ants, too, should be looked upon with suspicion. (7) Green vegetables eaten raw, such as lettuces, watercress and tomatoes are liable to become infected. In the East vegetable gardens are often contaminated with human faecal matter. For details of the organism, see p. 621. PATHOLOGY. The vibrio has a local habitat, living and growing in the small intestinal mucosa, epithelial cells, glands and lumen giving off in all probability an endocellular toxin w^hich, when set free and absorbed, causes the general symptoms. This toxin causes the blood elements to enter the blood thus : First water, then inorganic salts, especiallv sodium chloride, later phosphates and potassium salts, and still later organic substances. This produces a great concentration of blood (T073-1078) and an increase of hb. and red cells to 8,000,000 per c.mm., also of white cells up to 60,000 c.mm. The alkalinity of the blood is decreased and the coagulative power altered. This concentration of the blood causes a fall in the blood pressure, shown by the feeble compressible pulse (50-80 mm. of Hg). The result of this low blood pressure is that the urine is scanty, high sp. gr., albumin, casts and much indican. Perhaps the blood pours out bactericidal substances. POST MORTEM. Rigor mortis marked and early. Rise of temperature and muscular movements after death not uncommon. Tissues dry. Blood thick^ may be tarry. Stomach empty, vessels injected. CHOLERA 207 Small intestine contains greyish grumous material, consisting of food particles, epithelial cells, red and white corpuscles, and micro- organisms. Mucosa hyper^emic and swollen, sometimes ecchymosis. Salivary and mesenteric glands enlarged. Liver congested, loaded with blood, ducts full of bile. Spleen shrivelled and small. Kidneys enlarged, tubules blocked with granular debris, cloudy swelling. R. heart dilated. \"enous system congested with dark, thick, tarry blood. L. heart empty. Arterial system empty. Lungs dry, anaemic and collapsed. Urinary bladder empty and contracted. The vibrios are usually confined to the intestines, but they have been found in the liver, kidney and heart. SYMPTOMATOLOGY. Incubation three hours to six days. Typical form. Onset sudden as a rule; sometimes malaise precedes it. There are three stages. (i) Evacuation stage. Diarrhoea with or without colicky pains. Loose f^eculent motions, followed quickly by the typical rice-water stools containing numerous white flakes of mucus, epithelial cells and vibrios. Vomiting early, food first, then watery fluid with bile and some- times blood, then rice-water material. (2) Algide stage. Always much thirst, sometimes hiccough, urine diminishes and may cease. Subcutaneous tissues give up their fluid and the facies alter, e.g., nose sharp, cheek-bones prominent, eves sunken, skin of fingers wrinkled. B.P. falls, pulse weak and rapid, cyanosis, dyspncea, huskv voice. Painful muscular cramps, in calf, arm and abdomen especially. Reflexes diminish. Mind clear, patient apathetic between cramps. Skin cold, axillary temperature lowered, rectal raised. Pulse runs, heart weak and irregular, urine suppressed, tempera- ture subnormal. Comatose and death in twelve to thirty-six hours. (3) Reaction stage. Improvement may commence at any stage. The symptoms gradually disappear and indications of normal health return. 2o8 DISEASES DUE TO BACTERIA Convalescence may be rapid, or a secondary febrile condition sets in and lasts two days to tAvo weeks. The status typhosus is not uncommon, especially just before death. Raised temperature, dry brown tongue, low muttering delirium, tremblings, toxic rashes, erythematous, papular or ha^mcrrhagic in nature. Other forms may show predominance of purgation symptoms. Other forms may show predominance of cramps. Others may show signs of collapse and die before diarrhoea and vomiting sets in. Other forms ma}^ show nothing but vibrios in fasces. Cases are usually worst at the commencement of an epidemic. The case mortality averages about 50 per cent. A coagulum in the R. heart or spasm of the pulmonary vessel refusing to transmit the thickened blood may cause sudden death. COMPLICATIONS. Hyperpyrexia is rare. Abortion the result of contraction (cramp) of uterus possible. Secondary infections account for most complications as pneumonia, enteritis, nephritis, parotitis, corneal ulceration. There may be errors of refraction. DIAGNOSIS. Easy in epidemic, difficult in sporadic cases. An extremely careful bacteriological examination is necessary to detect the true \^ibrio choleras of Koch. In dispatching material for diagnosis, collect and sample a piece of bowel ligatured into a boiled glass bottle well stoppered. No antiseptic to be used. Methods of diagnosis: — (i) Make ordinary films of the white flakes. Stain with diluted carbol fuchsin (i in 50) 10 minutes, or with Lofifler's blue 5 minutes. If a fish-in-stream arrangement of curved rods be seen cholera can be strongh^ suspected. (2) Smear the surface of a lactose-agar plate (MacConke^-'s media) w4th a rice-like flake, using a bent sterile glass rod. Inoculate whh ihe same rod not recharged two more plates and inoculate at 35°C. If small, delicate, yellowish, roundish dots appear within twelve to eighteen hours, cholera vibrio can be suspected. Examine the germs of a colony, if very active, comma-like or straight, if it agglutinates with anticholera serum in a dilution down to I in 4,000, it is in all probability cholera vibrio. CHOLERA J09 (3) Mix directly a drop of the stools with immune serum. If agglutination suspect cholera vibrios (Dunbar). This is useful only when the vibrios are very numerous. (4) Inoculate four tubes of peptone water with sample of stool \ CO., h c.c, I c.c, 2 c.c, respectively. A scum on the surface of the medium in 8-10 hours is suspicious of cholera. Examine scum for comma vibrio, inoculate plates with the germs to confirm. Add to peptone water medium a few drops of pure H2SO4. In true cholera the indol reaction is present in 8-10 hours. (5) Inoculate the surface of three serum tubes with the sample and incubate at 35°C. If no liquefaction in 16 hours, it excludes cholera. If liquefaction in 16 hours, exclude cholera by plating out, &c. If liquefaction then, the vibrio may be present, plate out and further examine. (6) Inoculate a sedimentative tube of peptone water and immune serum with the faecal sample. Incubate at 37° C. for three to seven hours. If true cholera, numerous small flocculi of agglutinating vibrios, at first suspended, sink to the bottom (Bandi). (7) Inoculate with fa?cal sample media of pure bile mixed with 3 per cent, of a 10 per cent, solution of XaoCOj. Incubate at 37°C. Plate and further examine. In epidemics due to cholera nostras, mushroom poisoning, bacterial food poisoning, trichinosis, pernicious malarial fever, all have a low mortality as compared with cholera. If an epidemic has over 50 per cent, mortality it is cholera. TREATMENT. The indications are : — To destroy and remove the vibrios. To neutralize the toxins. To prevent secondary infections. To relieve the symptoms. B^d at once under the best hygienic conditions. Warmth essential. Water to drink in sips. Turpentine stupes to abdomen. \o food during acute attack. Hot, strong cofifee, good. Rogers' method. Calcium permanganate water (gr. i to vi to a pint) ad lib. Permanganate pills : — Potassium permanganate gr. ii. Kaolin and vaseline as recjuired. To be taken every ^ hour for two hours, then one pill half-hourly. 210 DISEASES DUE TO BACTERIA Those vomited being replaced. Continue until the stools are green and less copious, which can be expected in twelve to twenty-four hours. In mild cases give one four-hourly, in severe continue as above. Pills old and hard are useless. In collapse, hot bottles and when pulse fails open median basilic vein with Rogers' special silver cannula inserted and hypertonic saline solution given until B.P. returns. Sodium chloride gr. cxx. Calcium chloride gr. iv. Potassium chloride gr. vi. Water to a pint. Boil for 15 minutes to sterilize. Inject at a temperature varied according to rectal temperature. Rectal temperature Saline injection 99° F. over 98 '4° F. 98° F. 100^-102° F. 100° F. 97' 5° F. 102° F. and over Warm If blood pressure falls below 70 mm. of Hg give intravenous saline at once. Give it in cases of restlessness, cyanosis, cramps, black blood as shown by pin prick. Stop the injection in cases of respirators or other distress. Leave the cannula in situ as it may be needed to repeat the injections. Warm rectal injections can be given. If no severe cramps, strychnine hypodermicallv. If suppression, dry-cup over each loin. In the stage of reaction give : — Bland foods and avoid meat extracts also. I^ Bismuth salicylate ... ... ... j^r. xv. Soda bicarbonate ... ... ... gr. v. Liq. opii sedatives ... ... ... ni v. Mucilage q.s. Chloroform water to 5 i. 5 i t.d.s. For persistent vomiting give : — (i) Cocaine gr. ^ dissolved in 5i of water. (2) INIist. pepsini co. et bismuth 10 minims, half-hourly for four doses. (3) Two drops of tinct. iodine in water. For cramps : massage, morphia, inhalations of mixture of chloro- form and oxygen. For delirium : bromides, with tincture of hyoscyamus. For prostration ; strychnine or camphor in ether. Watch for uraemia. Opium eaters all die. CHOLERA 211 Rogers gives some very interesting figures comparing the results of the old methods with the new as follows : — Old System, 1895-1905 Age Cases Deaths Percent. 52-8 51-3 5&-5 637 69-4 737 To 5> 5 to 10 'ears \ 36 . • 19 ,, 20 ■)1 ' " 150 . . 80 ., 30 11 . -. 468 . . 274 „ 40 ,, . .. 273 •• • 174 „ 50 ,, III .. • 77 )ver 50 )1 . . . 38 .. . 28 Cases 24 121 197 134 43 23 New System, 1913-1915 Deaths 17 44 28 16 1 1 Reduction er cii t. of mortality per cent. 36-3 } ( 6ro ^33^ 140 .. 730 22-3 64'c 20-9 670 365 .. 47'o 47-8 •• 35-0 The remaining mortality was due to collapse, uraemia, pneumonia, heart failure and exhaustion, hyperpyrexia, septic complications. The total mortality is reduced by his treatment to 20 per cent, or one-third of the former rate. Cox claims better results still as a result of using isotonic saline instead of hypertonic saline. Cox, who has treated over 2,000 cases, gives his figures as follows: — India China Collapse cases only Rogers, 1909-10 Number of cases, 103 Average amount transfused, 4^ pints Mortality, 32 per cent. Cox, 1910 Number of cases, 666 Average amount transfused, 13 pints Mortality, i8"8 per cent. In certain cases Cox gives hypertonic saline for the first eight pints and then continues with the isotonic salines. Rogers denounces opium in any case. Cox has found it very useful in cases of collapse. Cox continues : An adequate reaction proportionate to the degree of collapse must be looked for and assisted. This condition is never attained until the infusion reaction rigor (which occurs approximately when five pints have been infused) is w^ell passed. The continuance of the saline infusion after the occurrence of the reaction rigor up to 8-10 pints will procure the following benefits : — (i) Dilution of the blood. (2) Elevation of the blood pressure, with re-establishment of sup- pressed renal flow^ (3) Elimination of the endotoxins from the blood and later from the stools, thus obviating the onset of the febrile reaction stage of cholera, the remainder of the illness being usually apyrexial. No apprehension need be felt at a rise of temperature to 103° F. during the infusion, in fact, this degree of temperature oscillation I consider the most favourable for cessation of infusion of less than six 212 DISEASES DUE TO BACTERIA pints; the temperature of the saHne in the cistern should be loAvered and the infusion continued. That the reaction induced by the saline infusion may, to some extent, be due to a toxaemia induced by the endotoxins of water-borne bacilli used in the infusion is possible; that it entirely accounts for the reaction rigor I do not believe. In any case, it will be interesting to see to what extent the phenomena of the infusion reaction will be modified by filtration previous to boiling. PROPHYLAXIS (Castellani). (7) Public. (i) Protection of the frontiers, regular inspection, quarantine stations. (2) A central Cholera Board, with a full staff and apparatus for bacteriological work, disinfection, &c. (3) Instruction of the populace by pamphlets. (4) House-to-house search for cases. (5) Search for carriers and sources of infection. (6) Distribution of medicines and disinfectants. (7) Provision of medical aid to be readily obtained by all. (8) Crusade against house-flies. (77) Private. (i) Personal cleanliness. (2) Avoidance of foods liable to be contaminated. (3) Avoidance of foods liable to cause diarrhoea. (4) Filtration and boiling of all water for drinking and cooking. The regular cleansing of all filters and water receptacles. (5) Boiling of milk and protection against flies. (6) Clean sanitary dwellings. (7) Anti-cholera vaccination. Hafifkine's protects for six to four- teen months. (8) Immediate application for medical aid in the event of any diarrhoeal illness. Professor Simpson, working at Calcutta, was inoculating some civilians with Hafifkine's vaccine of living cultures, when an epidemic broke out four days afterwards with the following interesting results : — The 654 uninoculated had 71 deaths, or io"86 per cent. The 412 inoculated had 12 deaths, or 2*99 per cent. Not only so, but for the ensuing twelve months the inoculated were almost free from the disease, while cases were cropping up all the time among the uninoculated, the ratio of the mortality being as 3 is to 1 1 . Kitasato in Japan, and Castellani in Ceylon, used devitalized vaccines, but Simpson used living cultures. ENTERIC FEVER IN THE TROPICS 213 During the Balkan War, 1913, Greece used devitalized vaccines with interesting results : — Those with two vaccinations, 91,224 soldiers had 644 cases, or 1-1,000. Those with one vaccination, 14,613 soldiers had 618 cases, or 42-1,000. The non-inoculated, 8,968 soldiers had 834 cases, or 93-1,000. Those not vaccinated had fourteen times more cholera cases than those vaccinated twice. When the vaccinations were completed cholera disappeared as if by enchantment, sporadic cases only arising from newly arrived, non- inoculated soldiers. Equally good results were obtained from the civil population. One has to remember that the type of the disease was not a very virulent one. Epidemics of cholera vary much in their mortality from 90 to 20 per cent. Carriers are always troublesome. A convalescent may carry the vibrios for three weeks, some up to one year. The stools should be free on two examinations before the patient is discharged. At present there is no satisfactory way of clearing them out of the gall-bladder. ENTERIC FEVER IX THE TROPICS. DEFINITION. A specific infectious fever, three varieties caused by : — (i) Bacillus typhosus (Ebert) causes typical typhoid fever. (2) Bacillus paratyphosus A causes paratyphoid fever A. (3) Bacillus paratyphosus B causes paratyphoid fever B accom- panied by diarrhoea, pea-soup stools, rose coloured rash and running a prolonged course of about 21 davs. Typhoid fever has long existed in the tropics but was previously concealed under the term of " remittent fever," &c. It is now well- known to exist in many if not most tropical countries, occurring in Europeans and natives. It is alarminglv prevalent among young soldiers and civilians in the East, especiallv during their first three years' residence. AETIOLOGY. Caused by the above organisms. It attacks both sexes usually between 15 and 25 years, but no age is exempt. Infection is conveved bv : — (i) Contaminated water, ice or milk. (2) Foods contaminated by flies. 214 DISEASES DUE TO BACTERIA (3) Uncooked vegetables grown on infected soils. (4) Shell-fish groAvn on polluted beds. (5) Direct contact with the soiled linen, stools and urine, typhoid abscesses of the patient. (6) Contaminated soil resulting from defective drains and cess- pools. The soil may be dry and be blown on to food or swallowed in the dust. (7) Typhoid carriers. (1) F^CAL CARRIERS. The proportion of female carriers to the male is as five to one. As women have gall-stones more frequently than men, and as the gall bladder is a habitat of the typhoid bacillus it is not tO' be wondered at that symptoms of gall-stones occur in 14 per cent, of cases after enteric fever. The bacilli may be passed down the gall bladder to the intestines and expelled in the faeces without the patient being obviously ill, yet such bacilli may be very virulent and cause death to persons infected by them. The discharge of the bacilli appears to be intermittent. It is stated that women are more commonly carriers than men because their resisting powers are reduced by the decrease in the alexins of the blood during the menstrual and puerperal periods. (2) FLY CARRIERS. Infection by the house-fly (Musca domestica) and the fruit-fly (Drosophila ampelaphila) is most important because the fly takes up the bacilli into the alimentary canal in which the bacilli increase in number and virulence. (See habitats of house-fly, &c., p. 224.) The fly is a known foul feeder. After settling on fcecal material it goes on to human food, regurgitates a little fluid from its crop to dissolve the food substances and thus infects them. It also defc-ecates frequently. The term "autumnal fever" has been given to epidemics which are in the time of the greatest prevalence of the flies. (3) URINARY CARRIERS. In such cases the habitat is the renal pelvis which is usually chronically inflamed. It may also live in the urinary bladder and other processes of the urinary tract. The bacilli pass directly into the urinary stream and are thus excreted. F^cal and urinary carriers may infect directly the air, food, food utensils, drinking water and fomites, which in turn infect the victim. B. paratyphosus B, commonly met with in luirope, lives often in the gall bladder and infects the faeces. It has not been found in the urine. It has been found in the common house-fly. ENTERIC FEVER IN THE TROPICS 215 B. paratyphosus A is prevalent in India and China. Several out- breaks have been traced to fecal contamination. Epidemics may be due to the seasonal prevalence of flies, distribu- tion of milk, an infected well or stream, the seasonal use of shell-fish, eating of fried lish so common in the East End of London. For a description of the typhosus bacillus, see p. 619. Europeans newly entering the tropics should be particularly careful. In Bengal 50 per cent, of the cases in Europeans occurred within one year of their arrival from Europe. Rogers noticed that in India 41 "67 per cent, of the cases were in children under 15 years of age. Natives are asserted to be somewhat immune to the disease. Roberts in explaining this gives some interesting comparisons. The gut of the native is longer, more muscular and thicker than that of the European, also Fever's patches are less in evidence. Habitat and diet also are important predisposing factors. The Native The European Food cold and dry. Bulky, coarse, much waste. Vegetable grains, cereals, pulses ; large cellulose content ; low protein and fat content. Food partially cooked, plain and monotonous. Meals infrequent, twice daily, long fasts. Mastication generally good. Life and work in the open air. Fascal evacuations twice daily, large, 10-12 ounces. Strain on stomach and large bowel. The majority eat to live. Hot and fluid. Concentrated and soluble. Animal food, with high protein and fat content. Thoroughly cooked, well mixed, and varied. Meals frequent, 4-5 daily. Faulty in the extreme. Sedentary and indoors. Small, 5-6 ounces, constipation com mon, purgatives. Strain on stomach and small intestine More live to eat. PATHOLOGY. The disease is a septicemia produced by the invasion of the intestinal lymphoid tissue by bacilli which have entered by the mouth. In this tissue the}' multiply, many passing bv the lymphatics to the abdominal l}-mphatic glands and the spleen increasing rapidlv in each. In the blood they are destroyed if few in number and their toxins neutralized. If it does not proceed beyond this an ambulatory or abortive attack is produced. When the bacilli are more numerous but destroyed bv bacteriolysis there may not be sufficient antitoxin to neutralize their toxins, then the fever begins. Ferhaps the antitoxin is formed irregularly and so accounts for the intermittent nature of the disease and the relapse in the tropics. The endotoxin causes the endothelial cells to swell so that the small lymph channels in the liver are blocked and patches of focal necrosis formed. 2i6 DISEASES DUE TO BACTERIA While the bacilli may be found in any part of the body they prefer the lymphatic tissue. When a clump blocks a cutaneous lymphatic a rose-coloured macular papule appears which explains the characteristic rash. Autoinfection may possibly explain some cases of second and third attacks, the bacilli of the gall-bladder or other habitat injecting anew the general system of the patient. The gradual onset is the result possibly of the struggle between the antitoxins and the bacterial toxins. The rare sudden onset may be due to lowered resistance of the patient. Immunity is partial, sometimes complete for the particular bacilli causing the attack, but not against other varieties. P.M. Bowels distended with gas. Marked congestion of the mucous membrane about ileo-ca?cal junction. Mesenteric glands enlarged and congested. Spleen and at times the liver also enlarged and congested. The former is friable and dark red in colour. Perforation may be found. The heart soft, flabby and friable. The voluntary muscles undergo granular degeneration. Peyer's patches are affected according to the stage reached. First Week : — Swelling, the result of leucocytic infiltration. The submucous coat is also involved, and sometimes the muscular coat. Second Week : — Sloughing, the surfaces are abraded, the sloughs are bile-stained. Third Week ; — . Separation, the sloughs come away, leaving an ulcerated surface, with undermined edges in the long axis of the bowel having its base of muscularis mucosae, infiltrated mucosa or peritoneum. Fourth Week : — Scarring, the ulcers granulate up, the scar forming and contracting. The solitary glands may pass through the same process. The ileum and jejunum are usually affected. The bile is usually light coloured, watery, but may be inspissated. Kidneys enlarged, both cortex and medulla congested, fatty degeneration, rarely small abscesses. There may be an inflammatory condition of part or whole of the respiratory tract. H^emorrhagic infarcts, py^emic abscesses and puru- lent infarcts may be seen. Venous thrombosis is not uncommon. The bone marrow is generally congested. ENTERIC FEJ'ER IN THE TROPICS 217 Arthritis of joints and abscesses in various parts; sequelae may be found. SYMPTOMATOLOGY. Incubation three to twenty-three days, average ten days. Onset insidious, headache, sometimes epistaxis, increasing weak- ness. As the condition is a septiccemia any part may be affected, causing pleurisy, vomiting, or other symptoms tending to obscure the diagnosis. The disease is usually ushered in by some other fever, as malaria. First Week : — The tciuperatiire rises " staircase " manner, going up two degrees in the evening and falling one degree in the morning (not always) up to about 104° F. The pulse is slow and often dicrotic. The skin. — Cheeks flushed. Skin hot and dry, sometimes inter- mittent sweating. A bluish mottling on abdominal wall. Often yellow coloration of palms and soles. The tongue. — White moist fur on dorsinn, tip and edges are red. Mouth dr}', thirst marked. The abdomen is distended, tenderness in the right iliac fossa, and spleen is enlarged. Abdominal reflex is diminished or lost. Vague general pains. Exhaustion increases, patient becomes apathetic, drowsy, eyes bright; sleeplessness and vomiting are not uncommon. The stools. — Diarrluva in 20 per cent, of cases, becomes ochre- yellow (pea-soup) in appearance, but the bowels mav be confined throughout. Bacilli may be cultivated from the blood, but specific agglutination is not available. Second Week : — The symptoms above are aggravated, but headache ma}^ disappear. The temperature remains high. Mild delirium is not uncommon. Rash appears from seventh to twelfth dav in 70 per cent, of cases on abdomen or chest in crops; arms and legs may also be affected. The isolated maculopapules which disappear on pressure are slightly elevated, rose-red, 4 mm. in diameter, last three to five days, leave a yellow stain. They may continue to end of third week. Tendency to hagmorrhage (10 per cent, of cases) is marked, and danger of bowel perforation possible. The specific agglutination reaction may now be obtained. The diazo-reaction of the urine is now also possible. 2i8 DISEASES DUE TO BACTERIA The bacilli are not so numerous in the peripheral circulation, but more plentiful in the spleen, fasces, urine {33 per cent, of cases), and rose spots. Liver and gall-bladder symptoms may set in. B.P. diminished, dicrotism perhaps has disappeared. Cold extremities. Vomiting rare. The typhoid state may set in, lips and teeth being covered ^ith dark brown scales (sordes), tongue dry, furred, fissured, pharynx inflamed or ulcerated. More or less meteorism always present, and may be very troublesome. Reduction in red cells, Hb. and leucocytes shown, but the mononuclear leucocytes are increased. Coagulability of blood reduced. Third Week : — Temperature falls by lysis to normal about the twenty-first day, and with this symptoms may subside and convalescence begin. In some cases profound symptoms may appear. The heart is weak and rapid. The lungs congested, fatal. Epistaxis possible. Perforation not uncommon (3 per cent, of cases). Subsiltus tendinum often present. Emaciation increases. Liver dulness encroached upon by the tym- panites and breathing becomes thoracic. LTrine may be suppressed. Peritonitis or collapse may cause death. Fourth Week : — Temperature becomes normal; convalescence begins. Watch for relapses. In severe cases the status typhosus may continue; the heart may fail, for the myocarditis is considerable. The varieties are according to^ the severity of the symptoms, am- bulatory, abortive, mild, typical, severe and masked. H^emorrhagic cases have been known, when there has been bleeding from the mucous membrane, tongue, gums, bladder and intestines, also purpuric eruptions. In Ceylon the disease caused by B. paratyphosus, viz.. Paratyphoid fever, is indistinguishable from Typhoid fever, though it generally runs a milder course. The intestinal ulcers are identical with those of typhoid. Cases of mixed infection are not rare. COMPLICATIONS. Malaria very important. Haemorrhage from bowel, nose and mucous surfaces. Perforation mav occur in mild cases. Peritonitis, with or without perforation. ENTERIC FEVER IN THE TROPICS 219 ]\Ieteorism or tympanitis. Thrombosis, usual of femoral vein, embolism possible. Xeuritis, bronchitis and pneumonia, Earlv tvphoid state or cardiac failure. Bed sores and boils. Alopecia. Tvphoidal arthritis, typhoidal spondylitis, ascending myelitis. Periostitis. Inflammation of thyroid. Iritis, orbital cellulitis. Relapses during the third and fourth week after the temperature has been normal are not uncommon. Signs of perforation. — Sudden and severe pain, rapid and extreme distension of the abdomen, absence of abdominal respiration, tympanic percussion note, absence of hepatic and splenic dulness. Shock, rapid pulse and respiration, fluid in abdomen. Collapse. DIAGNOSIS. In typical cases easy. The insidious onset, dicrotic pulse, medium enlargement of spleen, rose rash, leucopenia; if all are present it scarcely permits of mistake. In the tropics the course is more often atypical. Malarial fever \\ill modify the temperature chart, alter the appear- ance of the rash, and easily throw one off his guard. Bacteriological diagnosis is therefore all-important, as seen in : — (i) The agglutination test (Widal). Important. See p. 611. (2) Hfemocultures. Important. See p. 623. (3) The bacilli in the stools and urine. (4) Spleen puncture gives good results, but should not be a routine procedure. {5) Ophthalmo-reaction and cuti-reaction, similar as for tuber- culosis. (6) Subcutaneous inoculation of dead cultures and \^incent's splenic diagnosis. (7) Complement fixation. With regard to the ]]^idal reaction (see p. 611), the three strains of bacilli should each be tried failing agglutination of one of them. It is absent during the first week in any case, and may be in excep- tional cases during the whole period. On the contrary, if a positive result is obtained, one must remember that a former attack would give it for months or years after it was over. It may be possible in vac- cinated persons. It has been found present in jaundice, Weil's disease, and puerperal fever. The rapid differentiation of the bacilli of the typhoid group by means of test papers has been devised by Hollande and Beuverie. 220 DISEASES DUE TO BACTERIA For the differentiation of the Bacillus typhosus, B. paratjphosus A and B and B. coli four test papers are used as follows : — (i) A piece of filter paper is dipped into a i per cent, solution of silver nitrate, and is then quickly dried; it is then dipped intO' a lo per cent, solution of collodion in equal parts of alcohol and ether, drained and dried in the dark. (2) A filter paper is dipped into a i per cent, solution of neutral red containing 10 per cent, glucose, and then dried and impreg- nated with collodion as before. (3) A filter paper is dipped into a 10 per cent, solution of lead sub- acetic and dried, as before, with collodion. (4) A paper is dipped into the following solution : o'z grm. litmus,. 4'o grm. neutral sodium phosphate, 5'o grm. lactose, I'o grm. sodium bicarbonate, 50 c.c. distilled water; it is then dried and' again treated Avith collodion. Portions of these prepared papers are then dropped into peptone' broth tubes, which are then autoclaved at 118° C. for twenty minutes. Results. (i) With the silver nitrate paper a growth of B. coli is obtained' in about twelve hours, of the three other bacteria in about two- to three days. (2) With the neutral red paper, the red colour of the paper and' broth are unchanged by B. typhosus, the paper remains at the bottom of the tube, and there is no gas formation. With the three other organisms the colour changes to canary-yellow, and gas is formed between the collodion and' the paper, and the latter then flloats to the surface. (3) Lead acetate paper is blackened after about twentv hours, except in the case of B. paratyphosus A, in which no change occurs. (4) With the litmus lactose paper the lilac colour of the paper and broth is discharged after about twenty hours, but in three days the colour returns in the case of B. paratyphosus B. In using hcprnocultures there are two methods : — (i) Dilution method. Take 2*5 c.c. of blood from the median basilic asepticallv, drop it into a large sterile flask at once containing 200 to 300 c.c. of faintlv alkaline broth. Incubate at 37° C. In twelve to twenty-four hours, in positive cases, the broth becomes- cloudy and shows a germ growth. Then test this in various media. The agglutination test should also be done. (2) Bile enrichment method. Take blood as above or from the finger tip. ENTERIC EEVER IN THE TROPICS 221 Drop il into a mixture of oxbile 90 c.c, glycerine 10 c.c, and pep- tone 2 grm., distributed into small flasks each containing 20 c.c. of the medium. Incubate and test as above. Ehrlich and Diazo Reaction. Generally present in typhoid during the second and third week. It may be absent in very mild cases. V^ery active tuberculosis gives it fairly constantly. jMeasles gives it more frequently than German measles. If it is present it is not diagnostic of typhoid, but may be used for confirmation, especially if the other diseases can be excluded. Prepare two fresh solutions: — (i) A saturated solution of sulphanilic acid in 5 per cent. HCl. (2) A 2|- per cent, solution of sodium nitrite. To 5 c.c. of urine, add an ecjual cjuantity of solution. (i) Then add a few drops of solution (2) and shake till frothy. Add ammonia till alkaline. If the liquid is port-wine colour and the froth is red, the reaction is positive. In examining the f^ces use Conradi-Drigalski medium. The malachite green solution inhibits the coli growth and permits that of the typhoid bacillus. In examining water, pass it through a filter; the organisms remain on the filter candle; brush these off into the above medium. Alum will bring down a precipitate entangling the organisms, which can then be treated as above. The typhoid bacillus is seldom found in the water that has caused the disease, because fourteen days have elapsed since the patient par- took of it and the organisms would have gone. DIFFERENTIAL DIAGNOSIS. In malaria, examine the blood for the parasites. In relapsing fever, the onset is sudden and the blood will show the parasite. In undulant fever, do an agglutination test; cumulative evidence is important. In yellow fever by sudden onset, albuminuria and black vomit. In typhus fever by sudden onset, mental symptoms appear early. In acute miliary tuberculosis, irregular fever, pulse and respiration rapid, and is not dicrotic. In psittacosis, the specific bacilli can be isolated from the blood and sick parrots will be about. In ulcerative endocarditis, by the murmurs and bacteriological examination. 222 DISEASES DUE TO BACTERIA In paratyphoid fever A and B the aggkitination test and cultural characteristics have to be relied on. One must not forget that typhoid and another disease may co-exist. The mortality in the tropics is about 20-25 per cent. TREATMENT. (i) General management. Patient to be put on a wire-woven mattress with a soft horsehair mattress placed upon it, two blankets, then the sheet with a draw sheet, and its waterproof covering in the centre. A mosquito net must be provided. The room must be large, as empty as possible, and well ventilated. All motions and urine and fomites sterilized at once in carbolic. A day and a night nurse well skilled and vaccinated are essential. The patient to be sponged all over twice daily with tepid water. Gently rub irritated parts with rectified spirits, and then dust with boric or starch powder. Mouthwash necessary. Bed pan and urine bottle to be used all the time. (2) Diet. No solid food is the safest rule. Milk, beef-tea, chicken broth, albumin water from white of eggs. Plasmon, barley water, malted milk, whey, junket and weak tea. Water ad lib., neither hot nor cold. (3) Drugs. The less the better as a rule. Simple enema for constipation. Urotropine gr. x t.d.s. in second week to disinfect urinary tract. (4) Serotherapy. Chantemesse's anti-typhoid serum has good results. The Wright-Leishman's vaccine from forty-eight hours culture, irr three doses 500 millions of bacilli, ten days later 1,000 million, ten days later another 1,000 million. This is used as a prophylactic. Leishman had 19,000 cases under observation in India with the following results : — 9,000 were inoculated. Case incidence, 5*3 per cent. Case mortality, 9 per cent. 10,000 were not inoculated. Case incidence, 30*4 per cent. Case mortality, 17 per cent. The immunity lasts about one year. If the whole Indian army was inoculated, 1,000 cases of enteric fever and 200 deaths would be avoided each year. Mixed vaccines can be obtained for the three stains. FLIES ASL) DISEASE 22^ SPECIAL SYMPTOMS. (i) Tympanitis. Fomentations, turpentine stupes, turpentine 15 minims every three hours. Hypodermic injection of eserine gr. sV . (2) Hcemorrhage. Stop aU food, drink sips of water only, rice- bag to abdomen, raise bedclothes on a cradle. Give simple enema. Morphia useful if one is sure that perforation has not occurred. Calcium lactate gr. xv t.d.s. Lead acetate. (3) Perforation. Laparotomy as soon as possible. Salines per rectum, 2-6 litres per diem for a week. (4) Diarrhoea. Tannalbin gr. x-xii t.d.s. An enema with gr. v of Dover's powder also. Avoid bismuth, as it obscures traces of blood. (5) Cholecystitis. Urotropine gr. x t.d.s., anti-typhoidal vaccina- tion or surgical treatment. (6) Hyperpyrexia. Sponging, bath immersion 75°-85° F. No- antipyretics. (7) Delirium. Bromides, lumbar puncture. (8) Cardiac failure. Digitalis and its preparations, or camphor and ether, strychnine and salines, (g) Phlebitis. Wrap leg in cotton-wool after applying ichthyol in lanoline (2 per cent.). (10) Bedsores. Harden skin with spirit lotion and disinfect H2O2 twice daily; dust with zinc oxide powder. (11) Abscesses. Incise and drain. (12) Bone lesions. Supports as necessary; operative treatment. FLIES AND DISEASE. FLIES ARE DANGEROUS TO HEALTH. (i) By carrying pathogenic organisms directly from infected matter upon which they have settled to a wound abrasion, or absorbent mucous membrane surface. Hence perhaps spreading disease as anthrax, ophthalmia, yaws and tropical sore. (2) By feeding on infected matter and then carrying that infection by means of regurgitation or defiecation upon a receptive surface as above. The germs passing through the flies' intestines with undiminished virulence or possibly multiplying therein. Staphylococcus pyogenes and the tubercle bacillus has thus been found. (3) By carrying the germs as above and infecting the food and drink of man. Hence diseases can be disseminated as typhoid fever and cholera, perhaps of infantile diarrhoea and dysentery - They also carry the eggs of parasitic worms. 22^ DISEASES DUE TO BACTERIA (4) By blood-sucking flies biting infected vertebrates sucking up the pathogenic organisms and injecting them later into the body of a healthy individual as the h^emamoeba^ of malaria, the trypansome of sleeping sickness, the filarice of filariasis and the unknown organism of yellow fever. (5) By biting flies causing local irritations and thus predisposing tO' septic infection. (6) Bv^ the adult flies laying their eggs in wounds and the natural orifices of the body like the green-bo'tle and the notorious screw- worm fly, the larvae later burrowing their way into the tissues and causing even mortal damage. (7) By the flies laying eggs on the food and the larv^ damaging the victims' health resulting from their presence in the intestine. The ignorant and apathetic slum population suffer most, especially in crowded bazaars and markets where offal is plentiful and sanitation bad. HABITS, &c., OF THE MUSCA DOMESTICA (House-fly). Order. — Diptera (= with two wings). Suborder. — Cyclorrapha (= a circle; = suture). The imago escapes from the puparium through a circular slit at the anterior end. Section (2). — G. schizophora (= a cleft; = I wear). In these adults the frontal suture is always well defined. Subsection (i). — Muscoidea. Family. — Muscid^e, including house-flies and tsetse-flies. Genus. — Musca domestica. Important in carrying typhoid fever; •98 per cent, of flies infecting houses are Musca domestica. These common flies are world-wide. Small, dull-coloured, blackish-grey thorax, yellowish abdomen, with a median dark stripe. Arista feathered dorsally and ventrally, proboscis soft, retractile and ends in :a large fleshy labella. The fourth longitudinal vein bends forward at an abrupt angle so as to nearly close the first posterior cell. In the female the eyes are wide apart, in the male they are set close together. In hot countries they breed all the year round. In cooler countries they breed summer and autumn and then die ■out except for a few sheltered ones. These survivors and new ones which have hibernated, emerging from pup^e soon increase their kind in warm weather. The female lays 120-150 eggs in a batch in any moist rubbish heap, stable sweepings, vegetable debris, house refuse, &c. The white, shiny, sticky eggs hatch in twenty-four hours in warm weather. The larva or maggot is whitish, cylindrical, tapers anteriorly, has Iwelve segments and a very minute head. It has a pair of large, black FLIES AND DISEASE 225 mandibles for tearing and burrowing into food material. At the oppo- site end the main tracheal trunks open by three slits. It feeds on decomposing refuse. It is full-grown in five days in the tropics, in England one to eight weeks . The larvct then becomes barrel shaped, skin hard, becomes dark in colour, forms the pupa, this stage lasting about five days. Period of development in the tropics about five days. Period of development in Itngland about two to ten weeks. An adult flv lives from three to sixteen weeks. TO SUPPRESS THEM. House refuse, street sweepings and all rubbish to be burnt or deposited several miles away from human dwellings and leeward of prevalent winds. Latrine refuse should be buried beyond reach of the flies. Horse dung required for agricultural or other purposes should be dumped at a distance, treated with c{uicklime, moved about with a fork frequently so that the birds may get at the larvae. Carts conveying refuse mtist not drip their contents on the highwa}'. Some enemies of the fly should be encouraged, as : fungi, e.g., Empusa muscat, spiders, centipedes, larvae of beetles, ants, wasps, toads, lizards and rats. The use of gauze and fly-papers adds to one's comfort but are use- less for suppressing flies. HOW THEY INFECT MAN. The mouth parts of this fly are so made that the}^ cannot get solid particles into their mouths. They taste all foods by pressing their oral lobes upon them. If such food is satisfactory a little fluid is regurgi- tated on to it from its crop in the attempt to dissolve some of the food substance so that it can jjass along the minute pseudo-tracheae. They pour upon the substance, later eaten by man, numerous typhoid bacilli from infected faeces and thus infect a new victim by the food, sugar, bread, milk, meat or edge of the cup, &c. Not only so, but they defascate about fifty times in twenty-four hours and the typhoid bacilli pass out perhaps in an enhanced condition of virulence and infect the food materials, water and utensils of the human host. These were very instrumental in spreading typhoid fever during the Boer War, igoo- 1902. The blue-bottle or blow-flv is of the same family (Genus Calliphora) and has similar morphology and life history. The fruit-fly Drosophila ampelophila is also a musca with a similar history. 15 SECTION. III. DISEASES DUE TO HELMINTHS. GENERAL REMARKS. DISTRIBUTION. THEIR PATHOGENIC ACTION. NOMENCLATURE. THE GROUPING OF HELMINTHS. I. — Trematodes Pathogenic to Man. General Morphology^ Life-History, &c. Classification. The More Pathogenic Varieties. Paragonimiasis (Endemic H^emoptosis). Schistosomiasis. II. — Cestodes Pathogenic to Man. General Morphology^ Life-History^ &c. Classification. The Pathogenic Species Seriatim. The Treatment of Tapeworms. III. — Nematodes Pathogenic to Man. General Morphology, &c. The Less Important Species. Strongyloides stercoralis. Gnathostoma spinigerum. The Filarid^. Historical Notes. FiLARIA BANCROFTI,' MORPHOLOGY^ LiFE-HlSTORY, &C The Diagnosis of Microfilaria. The Filariases. Distribution. Pathology. Clinical Varieties. Filarial Lymphangitis. ,, Orchitis and Hydrocele. ,, Lymphangiectasis. ,, Abscesses. ,, Phlebectasis. ,, Varicose Lymph Glands. Filarial Chylous Extravasations. Chyluria and Lymphuria. Chylous and Lymph.atic Diarrhoea. Chylocele or Lymphocele. Chylous Ascites. DISEASES DUE TO HELMINTHS 227 Elephantiasis. Clinical Varieties. Elephantiasis of the Leg. Scrotum. Vulva. Breast. Arm. Scalp. Localized Areas. Notes on Filarial Carriers. CULEX FATIGANS. Stegomyia calopus. LOASIS. Chrysops dimidiata and silacea. Calabar Swellings. Volvulosis. Dracontiasis. Trichocephaliasis. Trichiniasis. Ascariasis. Oxyuriasis. Ankylostomiasis. THE MODE OF INFECTION BY HELMINTHS. THE PRESERVATION AND EXAMINATION OF HELMINTHS. HIRUDINIASIS. POROCEPHALOSIS. 228 DISEASES DUE TO HELMINTHS DISEASES DUE TO HELMINTHS. GENERAL REMARKS. The animals causing disease in man are from three king-doms, viz. : Animal, Protista or Intermediate, and Vegetable. We are concerned here with the former or Animal kingdom, which for convenience is divided into the : — Sub-kingdom i, Protozoa, and the Sub-kingdom 2, Metazoa. The Protozoa are dealt with in another section. All Metazoa are multicellular, free-living, or parasitic animals, having groups of cells to perform definite functions and are sometimes referred to as the Animal kingdom in a restricted sense. The parasitic metazoa may be ectoparasites as insects, mosquitoes, &c., or endoparasites as helminths. The Metazoa parasitic for man are classified thus : — Phylum (i) Platyhelmia. ,, (2) Nemathchnia. ,, (3) Annulata. ,, (4) Arthropoda. In this section we shall deal with those Platyhelmia and Nemat- helmia pathogenic to man. These are principally to be found among- the Trematodes (Flukes), Cestodes (Tapeworms), and Nematodes (Threadworms) . DISTRIBUTION. Some helminths are found everywhere, such as the Ascaris lumbricoides, Oxyuris vermicularis, Trichocephalus dispar and others. Others are prevalent where dogs and sheep abound, as the Taenia echinococcus in Australia; Flukes are found ^hiefl^' in Asia, Filaria volvulus in West .Africa, and the Gastrodiscus in Assam. The ankylostomes are restricted to warm climates where the}' can obtain plenty of moisture, or to warm temperatures in other countries in the presence of moisture as in the Cornwall mines. Factors controlling the Distribution (Leiper). (i) General sanitary measures and personal hygiene. The latter measure thoroughly carried out would stamp out Oxyuris in six weeks. The eggs are laid about the buttocks, re-infection taking place by the eggs getting in the finger nails. (2) The preparation of food. Trichinosis is common where fresh-water lish and insufticientlv cooked food are eaten. GENERAL REMARKS 229 (3) The disposal of excreta. Failure in this measure causes apparent epidemics of ankylo- stomiasis. (4) Religion. Taenia solium is carried in pork and is practically unknown in Mohammedan countries. (5) Temperature. If the temperature is not sufficiently high, ankylostomes cannot develop. Meteorological conditions must be favourable for the growth and development of the parasite and its host. (6) The control of the water supply. The Guinea-worm is commom where the water in the village pond is used for washing purposes at one side and drinking purposes at the other. In China, men defjecate into ponds, the fishes consume the excreta, while at the other side are men fish- ing and devouring the results of their sport, becoming infected consequentlv with Clonorchis. (7) Carriers. Soldiers from the Boer War came home with bilharzial haemal- uria and infected others in England in this way. Some pigmies from Central Africa came to London bringing with them Necator americanus. ((S) Domesticated animals. Where sheep-rearing is common, the Echinococcus prevails as in Australia. (9) The distribution of the intermediate host. Snails and slugs are necessary for Flukes. The Bothriocephalus cannot spread without special species of fish. Trematodes require an intermediate host for their development. Theh' pathogenic action varies according to : — (i) The size of the worm which may cause mechanical injury as the Ascaris when blocking ducts, &c., causing thereby append- icitis, retention of pancreatic fluid, &c. (2) The position of the worm which will alter the symptoms and the seriousness of the infection. A paragonimus in the lung, a fluke in the liver, or a hcematobia in the bladder give a more \'aried set of symptoms than a Gui'nea-A\()rm in the subcutaneous tissue of the leg. (3) The number present, as when several lunibricoides form a coil and cause intestinal obstruction. (4) The condition of the host. Ascarides mav be harmless in a 230 DISEASES DUE TO HELMINTHS healthy individual, but when in a dysenteric or typhoid intestine their presence is more serious. (5) The bacterial infection induced by them. The Trichuris trichiura is harmless in itself but can introduce bacteria into the mucous membrane of the appendix, &c., and set up an inflammatory condition. Helminths are usually covered ex- ternally by bacteria, and their intestines may contain a most extensive microbic flora. (6) Their selective action. Ankylostomes are always found in the small intestine. They will pass through the skin, veins, heart, lungs, bronchi, trachea, oesophagus and stomach but will not rest anywhere until they have reached the small intestine. Perhaps there is a special secretion there which thev prefer. Again, trematodes select out their own special mollusc. If trematode embryos are placed in a tank with various molluscs the embryos will be attracted by one particular variety only. They will even prefer the fluid in which their special mollusc has been placed and removed, ignoring all other fluids that are the same in every other respect. The condition produced may be the result of : — A mechanical erosion of tissue. The absorption of food materials ingested. Toxagmic poisoning. Fibrosis, eosinophilia, and secondary amemia. The retention of essential glandular secretion. NOMENCLATURE. There has been and is still much confusion in the naming of parasites. A close study must be made of the literature of any sup- posed new species before names are applied. As a guide to those who may require them, a set of rules has been drawn up to regulate the giving of names, and are known as : — The International Rules of Xonicncldturc. (i) The Language Rule. The scientific names of animals must be Latin or latinized, or treated as such. The generic name has a capital, the specific name a small letter. The generic name must be one word and used in the singular. The sub-genus, when one is present, can be inserted in brackets, with a capital letter between the genus and the specific name. The family name ends in " Idx," the sub-family in " in^e." The author of a scientific name is the one who first publishes GENERAL REMARKS 231 that name. One man may describe the creature found but another may name it ; this latter person is the author. (2) The Rule of Priority. The first name given must be adopted by all unless rendered invalid. Hence Trichina was found to have been applied to an insect some 50 years before it was applied to the new worm and consequently was changed to *' Trichinela." Different spelling can be a different name. (3) The Rule of Homonyms. When two distinct genera and species of animals receive the same name that name applied first must stand. (4) The Rule of Appropriateness . No name is allowed to be changed simply because it is inappro- priate. An author cannot reject the name he has once given. THE GROUPING OF HELMINTHS. Helminths occurring in the human intestine belong to two distinct groups of the animal kingdom, viz. : — (i) Platyhelmia, (2) Namathelmia. Platyhelmia. These are flat and leaf-like. There is no body cavity. The mouth is at the anterior end, or near to it, and is on the ventral surface. It is simple, forked or branched, but always blind. There is no hind gut or anus. The muscular fibres are angular, longitudinal, and circular. • The excretory system is highly complicated and consists of a branched set of tubules discharging at or near the postero-central surface. The sexes are not separate with two exceptions, the important one being the Bilharzia haematobium. There are two classes of Platvhelminths, Trematoda and Cestoda. Cestodes are really proliferating trematodes. The latter consist of a single segment, the former of many. The latter have an alimen- tary canal, the former none. For classification see next page. The species will be described according to their pathogenicity in man under their respective headings. Nemathelmia. These are bilaterally symmetrically thread-like with a distinct cavity between the body wall and the gut in which the genital organs freely float. The alimentary canal, when present, is a straight tube from mouth to anus, or it may be absent. 232 DISEASES DUE TO HELMINTHS V - B 3 >. Q. K b ''3 ID H c — '3 > C/] 3 °.2 O w a. Q. 13 o — O o "o lass Cesi 1 H a. O "a. 5 c 6 U 1) u .2 Q 'S 'hm « a) 3 H O J3 "« J= Q Bothriocep! « S TS s O i o o ■i-j (A V3 3 ■•i en J= D- u u o JS - +J - c CI) O < c! o OS E - 1) . -o ■g o "IS a. E c4 en S u - o O s S o 4-1 - to IS S <1 - o c o D E 3 10 o _J3 C CS O - o 3 U B u O C IS u IH ">» - bu- c o £ 3 E o c IS .2 - 3 O Cl! ■ K t: X! o - rt . "o .s u - o J3 0.2 ' e4 IH *o c . o cl Es, _3 ■ o O o -"o » c/l bfl O B &£ O ha 6 4^ < CO GENERAL REMARKS 233 Testes branched. =Fasciolinrr. Testes simple. T.=Dicrocochinx. o7 T.=Opistlioichina.'. T. Tape sliaped. . Heart shaped. Hepnina. Gut branctied.^ ^ t'asciola. . Gut simple. =Fasciolo psis biiski. Special armature about liead. =Echinostomincr. No special armature. = Paya j< omiiiiniT. T. & T. (Testes horizontal). a F.Hiclrcma ... ,. 'T. (Testes oblique). OpUlhorchis felintis . =Testes lobed. • Opiithcirchh. Cloiwrcliis sinensis. . Ot >islhoichis novcrca. =Testcs simple. Helcrophymr. = Branched testes. - Heterophycs heierophycs, genital pore at side of ventral sucker, " Yeokagawa, genital pore and ventral sucker are fused. N.B. The dots in the diagram show the position of the eggs. T. O. T.=testis. O.— Ovary. T.^itestes over ovary. T.=ovary over testes. O. T. FASCiOLiDiB. Points of Differentiation. Name Size Ca;ca Testes Yolk Glands Cirrus Habitat Fasciola ... Large, leaf like Blanched Branched posterior Full length Present Liver Echinostoma Very small, narrow Not branched, long Bilobed posterior Posterior, half Well developed Small intestines Fasciolopsis Large Not branched, long and wavy Branched posterior Full length Very long Small intestines Opisthorchis Long and flat Not branched, long Lobed posterior Middle, third Nil Liver Clonorchis... Long and narrow, pigmented Not branched, long Branched posterior Middle, third Nil Liver Paragonimus Broad, thick Not branched, long Simple posterior Whole length Nil Lungs, &c» Ileterophyes Small Not branched, long Simple Posterior, half Nil Small intestines Dicrocoelium Medium Not branched, short Simple Middle, third Present Liver 234 DISEASES DUE TO HELMINTHS The muscular fibres are longitudinal. There are no cilia. The excretory system consists of a simple bilateral symmetrical system of tubules opening into a single excretory pore on the ventral surface of the body in the middle line. The sexes are separate. The Nematoda always have an alimentary canal. Nearly all those found in man are from this class. The Nematomorpha have an alimentary canal which atrophies in the adult. The Acanthocephala have no alimentary canal. Nemathelmia pathogenic to man will be dealt with later. THE PLATYHELMIA HAVE THREE CLASSES. Glass (i) The Turbellaria. Flat worms, ciliated^ free-living. They are not important for man. Class (2) The Trematoda. Flat worms with an alimentary canal. They are parasitic to man. Class (3) The Castoida. Flat worms without an alimentary canal. They are parasitic to man. I TREMATODA PATHOGENIC TO MAN. THE MORPHOLOGY. Their average length is ^ in., but their extremes are i'2^ to 3 in. They are leaf-like or tongue-shaped, rarely cylindrical. There are two suckers, one ventral and one oral, which fix the parasites to the lining of the intestine or other organ. The mouth lies in the oral sucker. The oesophagus may be long or short, and often has unicellular salivary glands. The intestine is branched or simple and ends blindly. There is no anus. The testes may be branched, or simple, or lobed. The ovary may be branched, simple, or lobed, and is usually in front of the testes. These characteristics are used to differentiate the species as shown in the preceding table of the Fasciolidas. The genital pore is usually near the ventral sucker. The cirrus pouch lies behind the genital pore and is present in some as a muscular collar which, when it contracts, inverts by its spines the canal they surround and thus gives an erectile organ which comes out of the genital pore. The yolk glands, also used to dififerentiate the species, are arranged in one of three ways, viz. : — In the middle third of the body placed laterally. In the posterior third of the body placed laterally. GENERAL REMARKS 235 In the whole length of the body placed laterally. They are always small and numerous. Laurer's canal is on the dorsum and is for the escape of yolk food when it is in excess, thus preventing the uterus being blocked with volk (Leiper). THE LIFE-HISTORY. This is taken from a known typical example, viz. : Fasciola he pa tic a. The ovum passes along the ovarian duct from the ovary and in this tube is fertilized and surrounded by yolk cells. The shell gland then secretes a shell around the mass w'hich then passes to the uterus and escapes in the faeces of the parent worm. The egg thus passed has a lid. (Except the Schistomidse.) The ovum segments and grows, using up the yolk and forms a Miracidhim. This escapes in a few weeks from the lid of the egg into the water. It has two eye spots, anterior papillae and cilia by which means it swims about. It now grows and develops an alimentary canal. By means of its anterior papillae it enters the cavity of some snail, otherwise it dies in about eight hours. The special organs are now lost. The organism grows and a sporocyst is formed. Cellular differentiation again takes place. The organism now has a cuticular lining, under which is a muscular layer lined with epithelium internally, forming thus a cavity which answers as an alimentary canal. This form is the redia. It now- forces its way out of the cyst and wanders about the snail. It has a ridge or collar about its anterior end, and two stumpy protuberances posteriorly to aid locomotion. Cells now bud off from the inner side of the body wall forming the cercaria. This is something like a young Fasciola with a tail. These cell groups pass out from the redia by the genital pore, then leave the snail, swim about in the water, become encysted on grass and water weeds, and are then devoured by sheep, &c. In the process of ingestion they lose their cyst, travel to the bile ducts, and there develop into mature flukes in about six weeks. It will be noticed that many flukes develop from one egg. HABITAT. They occur in the liver, intestines, lungs and urinary tract of man. Dogs, pigs, cats and cattle are also infected. In sheep they cause what is commonly known as " sheep-rot." They may not cause obvious symptoms in man, but there may be irritation of any of the above organs by the eggs or the parasites themselves. Sometimes thev cause serious diseases in man. 236 DISEASES DUE TO HELMINTHS TREATMENT. In cases of diarrhoea of obscure causation examine the fcTces, urine and sputum microscopically. Be careful about domesticated animals ; they are often a source of infection. All green vegetables should be cooked. Avoid the so-called edible snail. For the specific treatment see the following paragraphs. THE CLASSIFICATION OF TREMATODES. There are three important families : — (i) Fasciolidce, having two testes. (2) Schistosomid^e, having one testis. (3) Paraphistomidie, having two testes. For other details see previous tables. THE PATHOGENIC VARIETIES. These will now be dealt with serintim. Watsonius watsoni causes diarrho'a and anaemia. It lives in the small intestine and inflames the mucosa. It has two pharyngeal pouches. The oesophagus divides into tAvo long intestinal caeca arranged laterally. The testes are lobulated and lie the one behind the other in the mid-line. The ovary lies behind the testes. Treat Avith eucalyptus and chloroform as in Ankylostomiasis. Fasciola hepatica has usually been found in the liver of man, but it has been .found also in the blood-vessels, in the cranial cavit>-, and about the feet, forming there superficial abscesses. It is the common liver fluke of herbivorous animals. It is very common in Africa, Burmah, Egypt and other parts. It is very widelv spread. It is the cause of the dreaded " sheep rot." The intestine divides into two principal lateral c^eca, which in turn give olT man}' branched c^eca. The two testes are much branched and lie behind each other in the mid-line. In front of the ventral sucker is a cirrus pouch. The ovary is tubular and branched. It lies above and in front of the testes. These worms are situated in the bile ducts and cannot be dislodged. GENERA L REM A RKS 237 238 DISEASES DUE TO HELMINTHS Fasciolopsis huski, a large trematode, 24 to 70 mm. long, is not uncommon in men and pigs. It is prevalent in the south of China and other places. The intestinal c^eca which extend tO' the posterior are not branched. The cirrus is very long, being one quarter the length of the worm. The testes are branched and are situated below the ovary. The worms cause dysentery and diarrhoea. ^/s. ,va>;^-;. , ('/. 1^ / ! A: :, g — — -n*?^: 'C.f. ■Mr'r*r V '- , -* m i->^'- S.z. fitV^./'3. : ■ 7. ''iw' ^ 7'. 1 ■■'•■ii:' Fasciolopsis buski. Lank. V.s. , ventral sucker; C.p., cirrus pouch; /., intestinil fork; S.V., viiellaria : T., testes; O., ovary; Ms., sucker; Skg., shell ^land ; Ut., uterus. Magnified. (After Odhner.) Opisthorchis felineus has been found in the bile ducts of man,, causing inflammation thereof, with atrophy of the liver, jaundice and ascites. The eggs containing a ciliated miracidium are expelled in the faeces. These parasites are more commonly found in the gall-bladder and bile-ducts of dogs and cats. The intestinal c^ca are imbranched. The testes are lobulated and are situated the one behind the other. GENERAL REMARKS 239 Clonorchis endcmicus has been found in the liver of man, It causes an enlargement of the liver with diarrhoea. The intestinal CcKca are unbranched. The yolk cells are arranged laterally in the middle tiiird. Ms V.s _. I'.sr. Dicroccelium lanceatiim, Stil. and liass. 15/1. V.S., ventral sucker; Cp., cirrhus pouch; /., intestinal bifurcations; V.sc., vitelline sacs; T., testicles; C, ovarium; His., oral sucker ; Ut., uterus. Clonorchis sinensis. C.L., Laurer's canal ; Dst., viiellaria; Ej(., excretory bladder; ^., > testes; K., ovary; R.s., recep- tacuhim seminis ; Vd., terminal sectinn of vas deferen-;. Magni- fied 4^ limes. (After Looss.) Ova of Clonorchis sinensis. The knobs on the ends of the eggs are not shown, gco/i. (After Lcoss,) 240 DISEASES DUE TO HELMINTHS The testes are much branched and are situated behind the uterus. The ovary is trilobate. Paragonimus zvcstcrmauii mid the schislosonui are important patho- logical trematodes, causing diseases in man known as Paragonimiasis and Schistosomiasis. These will now^ be dealt with in more detail. PARAGOXLMIASIS (Endemic Ilccmoplysis). DEFINITION. The chronic, local or general infection of man b}' P. \\estermanii producing characteristic cystic lesions. Schistosoma\Iuxmatobium^ Bil. : male carry- ing the female in the canalis gyncecophorus. 12/1. (After Looss.) DISTRIBUTION. In China, Korea, Japan, Formosa, Philippines, Sumatra. THE PARASITE. This is the P. westermanii. PARAGONIMIASIS 241 MORPHOLOGY. A greyish leaf-like parasite quarter of an inch long. The oesophagus is short, the two lateral caeca are wavy but not branched. The testes are simple, one at either side of the mid-line arranged diagonally. The yolk glands are situated in the full length laterally. There is no cirrus or cirrus pouch. Their life history is not known. They infect man, cats, dogs and pigs. The true host is the tiger cat. Man may be infected through food or drink, and hence the worms are distributed to other parts through the lymphatics. This is, how- ever, not yet proved. The eggs are yellowish with a thick shell. PATHOLOGY. The lesions have been classified thus (Musgrave) : — (i) The suppurating lesion. (2) The tubercle-like lesion. (3) The ulcerating lesion. These may occur in the skin, bronchial or intestinal musosa, or in the bile duct. At first the connective tissue seems to be infiltrated with eggs, forming a cirrhosis or a round-celled infiltration with eosinophiles. An abscess may form containing caseous matter, or an ulcer develops. If this occurs in the liver cirrhotic changes take place. If it occurs in the serous membrane there is an adhesive inflam- mation with brown patches of eggs. If it occurs in a solid organ, a small focal cyst forms surrounded by fibrous tissue. The abscess, cyst or ulcer contains degenerated cells, blood, eggs and parasites. The fibrous lesion spreads in a star-shaped manner with small cysts in their centre. These reach the cutaneous or muscular layer and so open intO' the skin, bronchus, intestine, or the bile duct, causing there an ulcer. These ulcers may become secondarily infected. The ulcers sometimes heal by scarring. Post mortem, these typical lesions may be found in muscle, lungs, serous membrane, spleen, pancreas, intestine, bladder, epididymis, prostate, and the choroid plexus of the brain. The body is often emaciated and anaemic. 16 242 DISEASES DUE TO HELMINTHS Ulcers sometimes form in the axilke or groin, from which can be found an infected mass to the glands. The lungs may show diffuse cirrhosis, bronchiectatic cavities, pneumonia and caseous abscesses. SYMPTOMATOLOGY. In a general infection there are fever, enlarged lymphatic glands, muscular pains and cutaneous ulcers. In a thoracic infection one has cough, purulent or bloody sputum with eggs, characteristic Leyden crystals. There may be the physical signs of broncho-pneumonia, a pleural effusion, serous or purulent. The sputum may be of a red viscid gummy consistency. The cough is more troublesome in the morning than at night. In an abdominal infection there is a dull general pain with tenderness. There may be the signs and symptoms of diarrhoea, appendicitis, hepatic cirrhosis, &c. In a cerebral infection there are the signs and symptoms of epilepsy which may be Jacksonian. DIAGNOSIS. This rests mainly upon finding the eggs in an endemic area. TREATMENT. This is symptomatic. * Remove the patient from the endemic area. Pot. iodides may be tried. Give creosote for the cough and to reduce the number of eggs. SCHISTOSOMIASIS. DEFINITION. A chronic endemic disease of the urinary tract and rectum, causing hematuria, cystitis and dysenteric symptoms. The causative parasites are : — (i) Schistosoma haematobium. (2) ,, japonicum. (3) ,, mansoni. In all these trematodes the sexes are separate. (i) INFECTION WITH S. HAEMATOBIUM. DISTRIBUTION. Egypt, South Africa, Asia, India, Syria, Mesopotamia, and the West Indies, Madagascar, Mauritius and vSouth America. In Egypt the infection occurs in the early winter months after the floods. 50 per cent, of the people are infected. SCHISTOSOMIASIS 243 Calcified eggs liave been found in mummies of the 20th dynasty 1 250-1000 B.C. THE PARASITE. S. haematobium, it is a bisexual trematode. MORPHOLOGY. The Male. — This is from 12 to 14 mm. long by i mm. broad. It is thin and flat, the lateral margins may be turned inwards forming the gyn^cophoric canal in which the female lies, thus giving to the male a filiform appearance. The cuticle is bossed with short spines to enable it to cling to the walls of the vessels and travel against the blood-stream. There is no Ovum of Schistosoma hamalobium, Bilh.,with miracidium, which has turned its anterior end towards the posterior end of the egg. 275/1. {After Looss. ) Ovum of Schisiosomum kcematobium, with terminal spine. (Not found in China.) The patient was in the African mounted police. (By William Pepper, Philadelphia.) pharynx, but the oesophagus is long with two c^eca which unite behind the testes into a median trunk. The excretory pore is postero-dorsally situated. There are four to five testes. The Female. — This is 20 mm. long by 0-25 mm. thick. It is a long, thin trematode with a smooth cuticle except about the sucker and tail-end, where there are large spines. The alimentary canal is as in the male. The uterus ends in a genital pore just behind the ventral sucker. The eggs are large, o"i8 by o'o6 mm., oval, yellowish, with a thin shell, slightly transparent, no lid, and a terminal spine at the posterior end. 244 DISEASES DUE TO HELMINTHS THE LIFE HISTORY. The young immature male and female are only found in the portal system from whence they go to the portal vein. Here they pair and then pass to the liver. The male carries the female down along the portal and the inferior mesenteric veins to the bladder. Here oviposition takes place and the eggs are deposited in the superficial capillaries. From this position they gradually work their way to the surface and enter the bladder itself. Some of the eggs, however, become calcified in the process. If the eggs are taken from the urine and examined they will be seen Micrograms of sections of skin of a newly-born mouse which had been immersed for half an hour in water containing large numbers of Bilharzia cercarise. to contain a living miracidium which can be liberated if the egg is broken while imder the microscope. The eggs must pass to water at once or the miracidium dies. It does not live more than thirtv to forty hours even when it is deposited in water, but must be again taken up by man. No other host except man has been found to carry on the infection. How he becomes infected has not yet been proved. The infection is by ingestion, also probably they enter the skin while people are Avorking in the mud fields or bathing in the muddy pools infected by the urine of diseased persons. The eggs may work their way to the rectal veins and mucous membrane, and then be passed out in the fseces. SCHISTOSOMIASIS 245 Others believe that the life-cycle, like that given of a typical trema- tode (p. 235), is necessary. The African natives believe that it gets along the urethra while they are bathing, and tie twine around the penis to prevent the infection. Bathing does seem to account for many infections and drinking impure water for others. There is no evidence for direct contagion. PATHOLOGY. The irritation set up by the eggs causes a round-celled infiltration. The epithelium proliferates, and flattened projections are formed which Ovum of Schistosoinum luemaiobhim. For comparison witli Schistosoinu»i japotnciiin and Schistosomum tnansoni. This parasite has not yet been reported in China, and is probably not found there. (By William Pepper, Philadelphia.) feel sandy to the touch ; these may go on to form vesicles and ulcers in which eggs can be found. The eggs can escape without ulceration. The bladder wall is much thickened. The pelvis of the kidneys and the meatus urinarius may also be affected. Turner has found the eggs in the lungs. P.M. The bladder mucosa is much thickened with bilharzial tissue, covered with adherent mucus containing many eggs. Vesicles are most frequently found around the trigone, containing a whitish fluid and eggs. Papillomata may be formed. 246 DISEASES DUE TO HELMINTHS These bleed readily and cause hcematuria. Many eggs become surrounded by connective tissue and calcify^ forming sandy patches, and cause atrophv of the mucosa. Ova of Schistosoinuiii japonicuin in biliary ducts, \ objective. (By Bell and Sutton, Hongkong.) Section of intestine, showing ova of Schistosotnum japoniciim, x 250. (By J. Bell, Hongkong.) The urine collects in the bladder depressions, decomposes, phos- phates form, and a further phosphatic incrustation lines the bladder wall more or less in patches. SCHISTOSOMIASIS 247 The ureteric orifices may be occluded, causing retention of urine and hypertrophy of the ureters with dilatation, thus making ascending Case of Schistosoniuin japonicum. Severe infection of three years' duration. Ova very abundant in stools. After tapping, a large mass of glands forming a tumour as big as the two fists together could be felt in the caecal region. Liver dulness was diminished. After tapping, by pushing the hand well up under the ribs, the liver surface could be felt to be bossed. Spleen not enlarged. Age twenty-one. The patient left the hospital a few days after the photo was taken, and looked as if death was imminent. In hospital he was tapped four times, but the abdomen filled up to as great a degree within ten days of each tapping. This illustrates what one might call the final stage of schistosomum disease, when the previously enlarged liver shrinks with cirrhosis. The only other photos I have seen published were those of Dr. Peak's cases, but I think they illustrated an earlier stage of the infection (earlier, or perhaps less severe). (Notes, case and photos by J. A. Thomson, Hankow.) septic infection easy. Calculi may form in the bladder be interstitial nephritis. There may 248 DISEASES DUE TO HELMINTHS Bilharzial tissue may form in any part of the urinary tract. It may spread to the rectum and abdominal wall with sinuses, and may affect the prostate. SYMPTOMATOLOGY. After the Transvaal War, many of the soldiers took it with them to England, India, and to other places. Incubation (?) from three to six months (Sandwith). The symptoms may be absent or considerable, according to the amount of the infection. There are : frequency of micturition, burning pain about the urethra and perin^eum, straining after micturition. Haematuria at the end of micturition at first (endemic hcematuria). The urine centrifuged shows the ova. There may be pain in the back, gluteal region, and down the legs. The urine is foul-smelling, decomposes, is alkaline, turbid, and contains pus, phosphates, blood and ova. Cystitis sets in and the other symptoms increase. There is no rest dav or night. A calculus may form to add to the misery. The prostate enlarges. A urinary fistula may form above the pubis. Pyonephrosis may develop, the kidneys enlarge, and septicaemia set in. Prostatic inflammation predisposes to new growths. Stricture is not uncommon. In females there is vaginitis with papillomatous masses about the vulva. The uterus and ovaries have been found infected. Severe haemorrhage may ensue from the large vessels. There may be cirrhosis of the kidneys with high blood-pressure. When the spinal cord is attacked the symptoms may imitate tabes dorsalis or disserninated sclerosis. TREATMENT. Most cases cease to discharge eggs within five years of leaving the endemic area. There is no specific drug for the parent worm. Give male fern, u^ v, t.d.s. for a long time. Give bladder washes of silver nitrate i in 10,000 at first, or quinine 4 per cent., or adrenalin in saline. Helminthol, grm. i, t.d.s. may be tried. Urotropin, salol, benzoic acid, buchu, and hvoscyamus all have their advocates. Good results are claimed for emetine. Christopherson claims that antimony tartrate intravenously will cure. In vesicle infections inject along the dorsal vein of the penis. Much water and fluids should be given to act mechanically. SCHISTOSOMIASIS 249 Surgical treatment for calculus and fistula as rec(uired. All stimulants and excesses must be avoided. Prohibit micturition and defiecation inlo Mnler; boil and filter all drinking water. The mortality is low. Amongst affected Europeans removed from the endemic area less than i per cent. die. The recent Bilharzia Mission to Egypt, 1915, consisting of Drs. Leiper, R. P. Cochin, J. G. Thompson, has thrown much valuable light upon this subject. A few points are as follows : — The incubation of the disease is probably one to two months, and is not as long as previously thought. The absence of a pharynx in the cercaria is the one reliable character by which Bilharzia cercarise can be distinguished from other distomas. Storage of water for thirty-six hours will destrov all cercariae. If this was carried out with regard to the Cairo water supply alone, prob- ably the 10,000 children now infected annually would be spared. The extension of perennial irrigation in Egvpt appears to have encouraged the spread of the disease. Of 625 men who became infected in South Africa, 359 were still on the list in 191 1, exclusive of those permanently pensioned. The total cost to the State was about ;^'io,ooo per annum (Leiper). The conclusions arrived at by the Mission are of interest as con- trasted with those of I^oos. They are shown thus : — Conclusions based on the Loos Hypothesis. i,i) All transient collections of water, such as those resulting from occa- sional showers of rain, road water- ings and domestic waste, are dangerous if freshly contaminated. (2) Large bodies of water, such as the Nile canals, marshes and birkets, are little liable to be infective. (3) All water in a given area would automatically become safe in 30 hours if the native infected popula- tion were removed. (4) Infected troops would be liable to reinfect themselves, to spread the disease among other troops, and to convey the disease to any part of the world. Conclusions based on the Results of THE Present Inquiry. (i) Transient collections of water are quite safe after recent contamination. (2) All permanent collections of water, .such as the Nile, canals, marshes and birkets, are potentially dan- gerous, depending on the presence of the essential intermediary host. (3) The removal of infected persons from a given area would have no effect, at least for some months, in reducing the liability to infection, as the intermediate hosts discharge in- fective agents for a prolonged period. (4) Infected troops cannot reinfect themselves or spread the disease directly to others. They could only convey the disease to others in those parts of the world where a local mol- lusc could efficiently act as carrier. 250 DISEASES DUE TO HELMINTHS (5) Infection only takes place through (5) Infection actually takes place both the skin. by the mouth and through the skin. Recently contaminated moist earth or water is not infective. (6) Infection in towns is due to con- (6) Infection in towns is acquired from tact with recently contaminated moist unfiltered water which is still sup- earth or water. plied, even in Cairo, in addition to filtered water, and is delivered by a separate system of pipes. {7) Eradication depends upon educa- (7) Eradication can be effected without tion and complete sanitary control the co-operation of infected in- throughout the country. The sus- dividuals by destroying the mollusc tained co-operation of the affected and intermediaries, individual is essential. The practical conclusions are as follows: — That unfiltered water taken from canals, ditches, or birkets would be rendered safe : — (i) If kept beyond the survival period of the cercaria, i.e., forty- eight hours. (2) If heated to 50° C, a temperature at which the cercaria is imme- diately killed. (3) If previously treated with those chemicals that are lethal to the cercaria. The use of tabloids of sodium bisulphate, 16 grains to a pint of water, giving a dilution of 1-567, is recommended. The following points should be attended to : — (i) Personal contact of any kind with unfiltered water is dangerous. The surface of the water is the most likely to be infective as the cercariae congregate there. An intake pipe should always be led, therefore, to the centre of the stream, and should draw the water from near the bottom and at a place where there is little or no vegetation. (2) It is essential in drawing water for storage, in order to destroy the bilharzia cercaria, that no infective mollusc be admitted. This can be ensured by screening the intake pipe with gauze having about sixteen meshes to the inch. The common mosquito gauze or prosphor- bronze wire gauze is very serviceable. (3) The water in the wells and " sakias " may be regarded as much safer than that from other sources. Hitherto molluscs have not been found in these wells. (4) Shallow barrel sand filters are open to suspicion. It has been found experimentally that after fifteen minutes cercaria succeed in passing in large and increasing numbers through four inches of desert sand. (5) Although the reproductive activity of bilharzia in molluscs is probably most intense during the summer months, the occurrence of mature cercariae in infected molluscs in February shows that there is a certain liability to the infection throughout the year. SCHISTOSOMIASIS 251 (2) IXFECTION WITH S. JAPONICUM. DISTRIBUTION. This is known in Japan as Katayama disease from a Japanese town in which it was common. The parasite is similar to S. haematobium. Schistosoma japonicutn : from dog. Uterine egg. X c. 800. (After Katsurada.) Schistosoma japonic urn : from dog. X c. 800. (After Katsurada). Schistosoma japonicum : from dog. Egg from faeces. X c. 800. (After Katsurada.) It is found in Japan, China, and in the Philippines. In China the cases are only found in the low-lying districts. THE PARASITE. The S. japonicum is introduced by the skin or mouth from polluted water. 252 DISEASES DUE TO HELMINTHS Males only have been found to be infected, and these were usually farmers and boatmen from the ages of youth to 54. The parasite differs from S. haematobium in but one or two small features, viz. : it is smaller, the male has no tubercles, the eggs are oval, yellowish, without an operculum, and no definite spine, but Leiper has found a small protuberance in 75 per cent, of those examined. Some suppose that the parasites feed on blood, and others that they produce a toxin that causes a progressive anaemia in man. The life-history is unknown. Perhaps some fresh-water mollusc or crustacean is necessary. PATHOLOGY. The blood-stream distributes the eggs, which are carried onwards until they lodge as emboli in various organs, especially in the alimen- tary canal and liver, ^\ liere bilharzial tissue is formed, causing hsemorrhagic enteritis. P.M. On opening the abdomen there are signs of chronic peritonitis. Schistosoma japoniciim : liver showing eggs in the intra- and inter-lobular connective tissue. X (T. 80. (After Katsurada.) The liver is small, cirrhotic, with nodular surface. Glisson's capsule is thickened, and is found to contain numerous ova. The intestine is thickened, mucous membrane swollen, hyperasmic, friable, with patches of ulceration and necrosis, sometimes papillomata. SCHISTOSOMIASIS 253 The recto-vesical pouch is almost obHteraled. The outer coats of the intestine are very tough, almost cartilaginous. The rectum may be three-quarters of an inch thick and adherent to the ■■A -.vi ■■■\i ■■■ rf^i •»«■* €•0 "<®- k ^ ^ I- ■ 1 '^-^' # «Ni ® ■M> f^. o ^; t. ^•«- &. m <~L.a^.,-.it^i.*^J^- .^l^S.' - .»^ iL.L..'i.:^ffiu . JiiSi^iiJS y Schistosoma japonicum : section through the gut of a Chinaman showing eggs, x 58. (After Calto.) bladder. The mucous membrane of this organ is not usually affected as in the case of S. haematobium. There may be haemorrhagic infiltration of the dura mater, with wedge-shaped sclerosed areas of brain matter (Katayama). The eggs may be found in the mesentery, mesenteric glands, mucous membrane of the gall-bladder, pancreas, pylorus, lungs and brain. 254 DISEASES DUE TO HELMINTHS The adult worms are found in the portal system, especially at the bifurcation of the smaller mesenteric vessels. SYMPTOMATOLOGY. These are very irregular. They may be nil or slight with urticarial rashes and eosinophilia. There may be cough with scanty expectoration, diminished breath sounds, and crepitant rales. During the ensuing months these may increase and be accompanied by diarrhoea, with ova in the fasces, enlargement and tenderness of the liver, with general abdominal pains. The hvpogastrium shrinks and the epigastrium enlarges. There is dyspepsia and the passage of undigested food materials. The liver may then shrink and the spleen enlarge, followed by ascites, anaemia, emaciation, eosinophilia, which latter may reach 50 per cent. If the lungs are affected there are signs of bronchitis or of broncho- pneumonia. If the brain is affected there are signs of Jacksonian epilepsy. The knee-jerks in these cases are increased. The urinary tract is usually normal. There may be a muddv complexion. DIAGNOSIS. Look for a chronic enlargement of the liver and spleen with ascites, chronic diarrhoea, and marked eosinophilia from 10 pev cent, to 50 per cent. Look for ova in the stools containing a miracidium. PROGNOSIS. Death nearly always ensues. Intercurrent disease is usually the immediate cause. TREATMENT. This is as for S. haematobium. (3) INFECTION WITH S. INIANSONI. This parasite is held to resemble that of S. hcTmatobium, but some helminthologists \\ill not accept that it is a distinct species at all. THE THEORY OF SAMBON. In 1903 Manson found eggs with a lateral spine which had attacked the rectum. He suggested that it came from a new species of worm. INTESTINAL SCHISTOSOMIASIS 255 In 1907 Sambon formed a new species of it and called it S. mansoni. His reasons were that : — (i) Lateral-spined eggs are never found in the urine or bladder, but only in the faeces, rectum and liver. (2) The egg is oval with a lateral spine; that of S. haematobium is more oblong with a terminal spine; and S. japonicum is more rounded with a very small lateral spine in 75 per cent, of those examined (or, as some declare, with no spine at all). The average size of the S. mansoni egg is 150 by 65 fi with a straight terminal spine. The average size of the S. haematobium egg is 115 by 58 /^ with a thick lateral spine. The average size of the S. japonicum egg is 82 by 68 /^ without a spine. (3) The females differ in the genital tract, and the uterus contains lateral-spined ova. (4) The geographical distribution is different. S. haematobium only is found at the Cape. S. mansoni only is found in the West Indies and S. America. THE THEORY OF LOOS. Loos disagrees with the above saying that the lateral-spined eggs are the products of unfertilized females. The females not being embraced by the male cannot withstand the blood-stream and become carried into side channels, finding their way into the bowel. These unfertilized females only shed laterally-spined ova which are passed in the fasces. Again he says that lateral-spined ova are frequently found in the fceces. He declares that there are no differences between the female generative organs. The straight-spined ova have been found in the urine in the West Indies. As man is probably the intermediate host, there can be no limit to the S. haematobium. In 191 1 Looss modified his view, and stated that the eggs develop pathogenically. There are many supporters of Sambon's theory. It is agreed that lateral-spined ova cause : — INTESTINAL SCHISTOSOMIASIS. DISTRIBUTION. It is found in Egypt, Central Africa, Uganda, South Africa, Belgian Congo, America, and the West Indies. 256 DISEASES DUE TO HELMINTHS PATHOLOGY. The worms live in the puilal vein and capillaries of the bowel^ where Uiey lay their eggs. The eggs burst the capillary, enter the mucosa, cause cellular infiltration, thickening, mucus-covered papillo- mata and ulcers. A dense fibrous infiltration of the peritoneum results. Large polypoid masses may protrude through the anus. A fistula may be caused in the subcutaneous tissue about the sacrum and coccyx. The ova reach the liver by the blood-stream, and there form a patch of fibrosis or an abscess. Gallstones may form around the ova of the bladder. The pancreas, spleen, urethra and vagina may be infected. A chronic interstitial pneumonia may be caused by ova reaching the lungs, and from thence may enter the heart and the general circulation. SYMPTOMATOLOGY. Sometimes nil in slight infections. There may be symptoms of chronic dysentery, abdominal pain, blood, mucus, and ova in the stools. Prolapse of the rectum or of papillomatous growth is not un- common, which is sometimes mistaken for hcemorrhoids. There is great agony from tenesmus when at stool. The prolapse, inflamed and painful, is the source of great discomfort. In cases where there is more fibrosis there is diarrhoea and consti- pation. Tumours are sometimes found about the Ccecum or colon, which are hard, movable, and are elongated in the long axis of the bowel. These may increase during the following months or years. Emaciation and attacks of colic are common. The liver may be enlarged and cirrhotic, also the spleen. The urine may be normal. PROGNOSIS. This is always unfavourable when the symptoms are marked. The patient must be moved from the endemic area, if improvement is to be expected. TREATMENT. Give male fern. Treat on general lines as for S. hjcmalobium. Whitehead's operation may be done for the treatment of many rectal polypia. Irrigation of the intestine can be tried with sodium hypochlorite, lo in 1,000, or of tannic acid, 3 in 1,000. / I XT EST IN A L SCHISTOSOMIASIS 257 II CESTODA PATHOGENIC TO MAN (Human Tapeworms). (Kestos -= a girdle.) GENERAL REMARKS. Cestoda are Plalyhelmia which differ from Trematodes in that : — (i) There is no alimentary system, the food being absorbed through the cuticle. (2) There is a simple fixative apparatus at the anterior extremity of the body. (3) The parasites are divided into segments, each segment being a distinct hermaphrodite animal. (4) Thev are longer and flatter, varying from ^ to 24 inches long. The adult inhabits the intestine, and the larval form usually in- habits some other host. Every vital function is subordinate to the development of ova. They have been known for centuries. Moses forbade the Israelites to eat pigs and similar animals because parasites were then known to exist in them. Aristotle recognized the proglottides of tapeworms. MORPHOLOGY. Cestodaria with only one segment and not important. Cestoda having a scolex and segments. We are concerned with these latter. The true cestodes have a tape-like whitish segmented body. The anterior end has a scolex attached to the intestinal wall, the segments or proglottides follow and increase in size from the head downwards. The head attaches itself to the mucous membrane of the intestinal tract by means of muscular suckers. There may also be one or more circular rows of hooks situated upon the most anterior part of the head or rostrum. Each segment contains male and female sexual organs. The thick cuticle contains lime salts in abundance. Among the cellular elements are calcareous corpuscles, 3-30 /x in diameter, which are characteristic of the cestodes, having perhaps a protective or skeletal function. There is an outer layer of longitudinal and an inner of transverse muscle fibre which encloses the parenchyma. There is an excretory svstem of anastomizing capillaries passing into collecting tubules w^hich open to the exterior on the last proglottis. The nervous system consists of one ganglion and two nerve cords. The male generative organs reach maturity first. The vas deferens from the follicular testes enters the cirrus pouch and terminates near the vaginal orifice at the genital atrium. 17 258 DISEASES DUE TO HELMINTHS Two ovaries develop, connected by a common oviduct which joins the spermatic duct. This latter is then joined in turn by the common duct of the yolk gland and the ducts of the shell gland, then it passes on to the uterus. This latter is usually a blind tube but it may be open by a special aperture. ^^^hen the uterus is full of eggs it fills up the proglottis, and the male organs atrophy and disappear. Hence : — In the first segments no sexual organs are seen. In the slightly mature segments the male organs are made out first. In the more mature segments the female organs develop as the male organs diminsh. In the fully mature segments the male organs have disappeared. THE LIFE HISTORY. The mature proglottis can fertilize itself or another segment. The spermatozoa pass along the spermatic duct, meet the ovum and fertilize it. The ovum then receives its yolk and shell, and passing to the uterus escapes by the uterine orifice, when there is one, or when the proglottis is destroyed. The egg is oval, yellowish with or without an operculum. Two membranes are formed, one near the shell, the other near the embryo. The shell and the outer envelope are lost and in the faeces is seen the embryophore in its inner envelope with three pairs of hooks. This is the Onchosphere. Some species are ciliated. This onchosphere is then taken up by a new host of a difTerent class, the envelope is then cast oflf, the hooks burrow their way to suitable tissues, after which its hooks are lost and a bladder-like cyst is formed. In the walls of this cyst develops a scolex. This cyst is called the CYSTICERCUS. From Onchosphere to Cysticercus requires two tOi six months. This infected tissue is ingested by another animal, the cyst is dissolved and the scolex develops in a few weeks to an adult tape- worm, which can live for about a year. They obtain food by osmosis from the intestine. CLASSIFICATION OF CESTODA. Order (i) Pseudophyllidea. The scolex may or may not be armed with two groove-like suckers. It has three genital orifices. Order (2) Tetraphyllidea. These parasites are not found in man. IXTHSTINAL SCHISTOSOMIASIS 259 Order (3) Cyclophyllidea. The scolex has four suckers and tlie anterior end in a rosteUum with or without hooks. The segmentation is distinct. There is no uterine orifice. The eggs are without lids. Order (4) Diphyllidea. These are very rarely parasitic in man. Order (5) Trvpanorhyncea. Not parasitic in man. The sub-families, genera and species of Orders (i) and (3) found in man are given in the following table. Order and family S:2 >> n. a. " 0.2 u) o '-a o K Stib-family Dibothriocephalinx Ligulinae ... Dipylidiinee IlymenoIepiniriEe Davaineince Genus and sub-geniis Dibothriocephalus Diplogonoporus Sparganutn Treniinae Braunia ... Dipylidium Hymenolepis Davainea / Tajnia' .. Echinococcus j Hymenolepis Drepanido- l£enia(?) ... { Ta-nia Tasniorhynchus Species li: D. latus D. cordatus D. parvus ( 4- U. grandis I 5. D. braundi 6. 7. S. mansoni S. prolifer 8. S. batteri 9- B. jassyensis 10. D. caninum fii. H. nana "I12. H. diminuta 13- H. lanceolata |I4. D. madagascariensis D. asiatica 16. T. solium /I7. T. saginata 18. T. atricana 19. T. hominis 20. T. philippina 21. T. confusa ^22. T. bremneri . 23- (24. E. granulosus E. multilocularis MAN IS THE HOST FOR :— T. solium, saginata, africana, hominis, philippina, confusca and also T. bremneri. Dibothriocephalus parvus and Hymenolepis nana. Davainea madagascariensis and asiatica. Rarely Dibothriocephalus latus which is usually in the dog. Rarely Dibothriocephalus cordatus which is usually in the seal and walrus. Rarelv Hymenolepis diminuta which is usually in the rat and mouse. Rarelv Drepanidot^enia lanceolata which is usually in ducks and geese. CYSTS MAY DEVELOP IN MAN FROM :— T. solium. Echinococcus granulosus and multilocularis. Larval forms of Sparganum. ? Cysticercus of T. saginata. 26o DISEASES DUE TO HELMINTHS THE FOLLOWING LIST OF TAPEWORMS FOUND IN MAN will be useful for reference. Table of Tapeworms found in Man. (After Daniels). Platyhelminths Turbellaiia Tremaloda I Cestoda Pseud ophyllidise Dibothriocephaloidea Cyclophyllidiae Dipylidium Hymenolepis Davainea D. caninum H. nana D. mada- Dibothrio- Diplo- Sparga- H. diminuta gascariensis cephalus gonoporus num (?) I I.I. D. latus D. grandis S. mansoni Tcenia T. solium T. saginata T. africana T. confusa T. echino- cocius Only the important species found in man will be dealt with. DIBOTHRIOCEPHALUS LATUS. This is the only important helminth of the first Order. It occurs in man, dogs, cats and foxes. It is nine metres long and has 3,000 to 4,000 segments. It has two deep laterally placed suckers. The proglottides are very broad, 10 to 20 mm., and are broader than long. ""iri Various chain of segments of Dibothriocephalus latns, show- ing the central uterine rosette. (Natural size.) »«■ .* »T & • • o «•. ^ -^n) and (;l»ii"j/?- AS man\ as ^OO immature parasites ^^.^^^^^ caninum. (After Grassi and have been found in one pound of the Rovelli.) Both oncospheres show six • - pines. psoas muscle of an intected beast. ECHINOCOCCUS GRANULOSUS. This causes the cystic form of hydatid disease. Hydatid disease has been known since the days of Hippocrates. The cysticercoivi form only occurs in man. DISTRIBUTION. In Iceland, Australia, Europe, and Xew Zealand; rarely in India and South Africa. Egypt and the Philippines. The adult lives in the intestine of dogs, jackals, and wolves. The cvsticercus lives in man, sheep, ox, and pig. MORPHOLOGY. It is about 2 '5 to 6 mm. long. It has a scolex and three segments. The last proglottis, when mature, equals all the others in size. The scolex has four suckers. The rostel- lum has a double row of twenty-eight to tift}- hooks. The genital pore is alternate. The mature uterus has only lateral pro- tuberances, the eggs ma\' form in heaps. THE LIFE CYCLE. Man is infected with the onchospheres when petting a .dog, or by ingesting con- taminated food. From the stomach the para- 7\cnia echinococciis : the cirrus sac, the vagina, uterus, ovary, shell gland and vitellariuni, and the testicles at the sides are recognizihle in the second proglottis; the posterior prog- lottis shows the uterus partly filled with eggs, as well as the cirrus sac and the vagina. 50 i. 268 DISEASES DUE TO HELMINTHS site bores its way to the liver or other organs, g•ro^\ s and forms a cyst of three layers : — (i) A thin layer or endocyst with granular, nulceated cells. (2) A thick outer layer or ectocyst which is laminated and opaque. (3) A connective tissue layer about the whole. The inner layer of cells in cattle forms numerous hollow brood capsules called the E. cysticus sterilis, which have the endocyst external and the ectocyst internal. Of these brood capsules, heads develop called E. cysticus fertilis, but these more commonly occur in domesti- cated animals. In man daughter-cysts appear between the strata of the cuticle into which endocystic cells have found their way and formed cysts. These latter may grow and escape internally or externally. If externally they lie between the capsule and the mother-cyst and form E. hydatidosus exogenus, or if internally they fall into the mother- cyst and are then known as E. hydatidosus endogenus. These •daughter-cysts may remain sterile or produce brood capsules and heads which are then called grand-daughter-cysts. The wall of the mother-cyst may disappear and leave the daughter-cysts free. PATHOGENICITY. The cysts grow slowly so that the organs have time to accommodate themselves somewhat to the changes. If the organ cannot expand the symptoms are early and marked. If the cyst ruptures the fluid will cause urticarial symptoms, rigors, local pain, and tenderness. The cystic fluid is toxic and a sudden discharge of a large cyst into the abdominal cavity may be so toxic as to kill, acting upon the heart like prussic acid. It may rupture into the lung and drown the patient. The cysts may become fatty, cheesy, and calcified. They may become secondarily infected. ECHINOCOCCUS MULTILOCULARIS. This causes the rnuUilocuJar form of hydatid disease. DISTRIBUTION. South Germany, Switzerland, Austria, Russia, and Serbia. It is absent in Iceland, Australia, and the European districts where the cystic form is met with. It occurs in animals and man. MORPHOLOGY. The cysts are composed of parenchymatous tissue internally and ■externally. There is no third outer fibrous coat. These produce not only scolices but immature amoeboid embryos INTESTINAL SCHISTOSOMIASIS 269 which enlarge the cvst and may enter the blood-slream and cause metastases. The amoeboid embryo is a muUiple, folded, chitinous vesicle which forms a toxin detrimental to the host. It is stated that ripe proglottides develop directly from the cyst because it is capable of producing living embryos with or without a capsule. The scolices are often destroyed by phagocytes from direct contact with the host's tissue. Feeding experiments have failed. PATHOGENICITY. A primary tumour is formed in the liver, brain, spleen, kidney^ adrenals with metastases in different organs. The symptoms varv according to the organ afifected. There may be anaemia, emaciation and weakness leading to prema ture death. THE TREATMENT OF TAPEWORMS. (1) PRELIMINARY. When the patient is not in hospital. Give a brisk saline purge. No food to be allowed for twelve hours. Then give one to one and a half drachms of freshh' prepared oil. of male fern in gelatin capsules or as an emulsion. Follow this with one ounce of castor oil in two hours. (2) THOROUGH. When the patient is treated in hospital. Absolute rest in bed. Light diet for two days. Remove the mucus from the intestine and about the worm by giving during this period : — Ammonium chloride, 10 grains thrice daily, &c. Small doses of podophyllin each morning. At the end of the second day omit all food after 4 p.m., and' give at that hour one ounce of Epsom salts in warm water. On the third morning at 7, 8, and 9 a.m. respectively, give half a drachm of the freshly prepared oil of male fern each time. At 10 a.m. give : — Eucalyptus oil ... ... ... ... ui. xv Chloroform ... ... ... ... "i. xx 01. ricini ... ... ... ... ... dr. v No movement by the patient is allowed during this treatment.. 270 DISEASES DUE TO HELMINTHS No food to be given until a motion lias been passed. Fluid foods are to "be given for the remainder of that day. Preserve and examine all stools for the scolex. The treatment for Echinococcus is largely symptomatic. (3) PROPHYLACTIC. Keep cattle from all faecal matter. Urge absolute cleanliness with regard to food and water. I'ork and beef meat should always be well cooked. Ill NEMATODES PATHOGENIC TO MAN. Nematodes belong to the Xemathelminlhs, Ph\lum (2) of !he Metazoa. Their study is most important as Filariasis and Ankylostomiasis are among the diseases caused by these helminths. MORPHOLOGY. They are white filiform worms covered with a cuticle, usually tapering at both ends and enclosing a large undivided body cavity. There is a mouth at the anterior end with two to six lips leading to a thick muscular oesophagus which may be armed with teeth. The intestine is a flattened tube leading to a short rectum or anus. The excretory pore is in the mid-ventral line behind the mouth, the pore being the outlet for two excretory tubes which unite to discharge there. The nervous system is a circum-oesophageal ring with six anterior and six posterior nerve trunks. The sexes are separate. The male genital organs, testes, vas deferens, vesicula seminales and ductus ejaculatorius are modifications of one tube which opens close to the anus. There are also spines and papilla. The female genital organs, ovary, oviduct and uterus are modifica- tions of two much-coiled tubes. These unite forming the vagina which opens in the ventral mid-line in front of the anus. The parasites appear to live upon intestinal juices. Some enter the villi. Their life histories differ and are dealt with separately. THE PRESERVATION AND EXAMINATION OF NEMATODES. See end of present section, p. 321. The most important of these Nematodes will now be dealt with seriatim. STRONGYLOIDES STERCORALIS (Family Angiostomida) . The adult is very small, 2' 2 mm. by 34 mm. long. There are four lips to the mouth. THE FILIARIASES 271 The oesophagus is one quarter the length of the whole body. The anus is just in front of the tail tip. The sex is doubtful. It is perhaps an hermaphrodite. It is found in the duodenum and jejunum, deep in ihe mucosa. The parasite is widely distributed. The ova are 54^^ by 32 ^^i and occur in the fccces during attacks of diarrhoea. The ova are normally deposited in the mucosa, here the embryos hatch, reach the lumen of the gut and pass out in the faeces. They grow into male and female adults on reaching the water. These conjugate and the females then lay eggs. Free living embryos develop from these which moult and become filariform embryos which will penetrate the horny layer of the skin and reach the corium (Mozocchi). They pass, via the lungs, trachea and oesophagus to the small intestine (Fiilleborn). They may also pass directly by the blood stream. In the small intestine they burrow into Lieberkiihn's follicles and lay their eggs. These parasites cause an intestinal catarrh. They are the only worms that pass embryos in fresh fa?ces. GNATHOSTOMA SPINIGERUM (Family Gnathostomidas) . The male, about 10 mm. long, has two fleshy lips guarding the mouth. The cuticle in front of the neck has eight transverse rows of hooks pointing backwards. There are two unequal spicules. These parasites are very rarely found in man. Only two specimens are known. They wander about the connective tissue and form subcutaneous tumours. THE FILARIDiE. Diseases caused by Filarice are called Filaruiscs, manifestations of which include F. lymphangitis, orchitis, lymphangiectasis, abscesses, phlebectasis, varicose lymphatic glands, chylous extravasations and elephantiasis, Loasis, Calabar Swellings, and Volvulosis. These will be dealt with seriatim. THE FILARIASES. HISTORICAL NOTES. Elephantiasis was noticed by the ancient Indian writers. Celsus first used the term to indicate leprosy, and all writers since have repeated the error. Arabian physicians described it in the ninth and tenth centuries. Hillary in 1750 clearly differentiated it from leprosy. 2/2 DISEASES DUE TO HELMINTHS Chapoton in 1812 described Hjematochyluria in Mauritius. Demarquay in 1863 found a Microfilaria in a hydrocele at Paris. \\'ucherer in 1866 found a Microfilaria in urine, in Egypt, but neither at the time recognized its importance. Lewis in 1868 found the Microfilaria in the blood and lymph of persons with elephantiasis of the leg and assumed it to be the cause. Bancroft in 1876 found adult females in a lymphatic abscess of the arm, and in a hydrocele of the cord. He afterwards called it F. bancrofti. Manson in 1878 found the disseminating mosquito of the F. bancrofti as well as the periodicity of the Microfilaria, and he also showed that the worms retired to the large vessels of the lungs during the day. Only about ten adult filaria have been collected. These parasites are non-bursate nematodes with a simple mouth and a limited number of genital papillae. The spicules are dissimilar in shape and size. These nematodes always live in the connective tissue, lymphatic vessels and in the blood-stream, but never in the intestine. When they leave the human body they pass at once into some inter- mediate host. They do not pass into water or any other media. The exception to this is the F. dracunculosis. Tlie skin of these nematodes mav be : — (i) Smooth, as in F. bancrofti, perstans and demarquavi. (2) Striated, as in Dirofilaria mag. (3) Bossed as in Loa loa. (4) Corrugated transversely as in F. volvulus. FILARIA BANCROFTI. MORPHOLOGY. It is a long, whitish, filiform worm, with a smooth cuticle and a globular head, with an unarmed lipless mouth. Only one complete specimen has ever been found of the adult. The tail of this worm incurves when dead. The male measures 36"6 mm. long by o"i2 mm. thick. The anus, close to the posterior end, is guarded by two projecting lips. There are six pairs of papillae, three pre-anal, and three post-anal. There are two curved retractile spicules, o"6 mm. and 0*2 mm. long. The female measures 76 mm. to 100 mm. long by otS thick. The vulva is close to the anterior end and opens into a single vagina, from which two uterine tubules run almost the whole length of the body. These contain eggs and embryos. THE FILIARIASES 273 THE LIFE-HISTORY. The Adult. — The males and females, from three to four inches long, may be found coiled together in the lymphatic glands, or in the lymph- atic vessels of the scrotum, arm, leg, epididymis, testicle and hydroceles c c 3 C 3 C 0) c 3 o o S := « -3 ^^ D G . ■3 o i X -a ■^^ O of the cord; rarely in the lymphatics of the pelvis and abdomen. The males are less numerous than the females. The Ovum. — The intra-uterine egg, 50 /^ by 40 /y, coniaining a coiled-up embryo, becomes elongated by the embrvonic movements. 18 274 DISEASES DUE TO HELMINTHS The embryo is set free and is discharged from the genital pore. It is then free in the lymph stream in which the adult female happens to be. The Embryo. — The embryo or Microfilaria nocturna passes from the lymph stream to the thoracic duct, the right heart and lungs to the peripheral circulation where it is to be found at night. These Microfilaria wriggle about in the blood-stream, moving the blood cells to and fro, but without making progress. They are about 300 bv 8 fj,, with rounded anterior and tapering posterior ends. They are enclosed in a sheath, longer than itself, inside of which it darts to and fro. Were it not for these sheaths the embryo might use its anterior spine to escape through the wall of the blood-vessel, and so avoid the mosquito that transmits it. A thick proboscis carries the spine, which can be covered by a retractile and protractile six-lobed prepuce. The dermo-muscular transversely striated body encloses many granules whicli are wanting in definite parts of the parasite thus — (i) In the anterior extremity of the body (not the sheath). (2) In a transverse spot, 21 "5 per cent, of the whole length from the anterior extremity. (3) In a \'^-shaped spot, 30 per cent, of the ^hole length from the anterior extremity. (4) In a median line, the centre, 63 per cent, of the whole lenglh from ithe anteritM" extremity. (5) In an oval spot (tail spot), 85 per cent, of the whole length from the anterior extremity. (6) In a central spot, 91 '5 per cent, of the whole length from the anterior extremity. The significance of these granules is not known. Its Habits in Man. — They are to be found in the peripheral blood ar night from 5 j).m., increasing to midnight, then until 8 a.m. diminishing. During the day they live in the lungs, large thoracic vessels, carotid artery, heart, muscle and kidney. If man sleeps during the day instead of at night the periodicity will be reversed, but not completely, hence sleep may have something to do with its periodicity. The common carrier, Culex fatigans, biles at night, but the carrier in Fiji, Stegomyia pseudo-scutellaris, bites in the daytime, and Bahr says that there the Microfilaria are found in the blood during the day- time also, so that the periodicity is controlled bv the habits of the more efficient insect host. How the Microfilaria maintain their position against the blood-stream has not been shown. One blood film may show as many as 500 embryos. It has been calculated that there may be 45,000,000 in a fully grown man. THE FILIARIASES 275 The number of adulls necessary to produce ihem is not known. One Filaria can live for several years in the human body, and a Microfilaria can live in the blood-stream for several months (Bancroft). Its Habits in the Mosquito. — The UKxsquito sucks infected blood; the Microfilaria passes to the stomach, where the sheath is fixed by the surrounding haemoglobin and also altered by the gastric juice. Mf. loa: in thick film, dried and stained with hseniatxylin. x 1,000. (After Fiilleborn.) Mf. Persians in thicl< film, dried and stained with haematoxylin ; 4, unshrunken ; 5, shrunken, x 1,000. (After Fiilleborn.) As a result of these changes the embryo is able to rupture the sheath with its spine and to escape. The stomach wall is then pierced and the embryo passes to the thoracic muscles, where it grows con- siderably during sixteen to twenty days. In this position they develop four lips, an alimentary canal and a three-lobed tail. The position is now changed, and the embryo finds its way to the prothorax, head and 2/6 DISEASES DUE TO HELMINTHS labium. Here the parasites wait, and when an animal, usually man, is bitten, the Microfilaria passes through Dutton's membrane, and enters the wound made by the proboscis of the insect. When a fly is fed upon vegetable matter, however, the MicrofilariiE will not pass through. From the wound the embryo passes into the lymphatics, where it becomes sexually mature, fecundation is affected, and new generations of larv^ are poured into the lymphatic stream. These then pass to the thoracic duct as described above. The embryos are often harmless; it is the injured parent worm and the immature products of conception that are dangerous. A man's blood may Mf. demarqiiayi in thick film, dried and stained with hsematoxylin. 6, unshrunken ; 7, shrunken. X i,ooo. (After Fiilleborn.) swarm with the embryos, and yet he may show neither signs nor symptoms. To demonstrate the Microfilaria. — Take an ordinary blood slide at night, place it at once in weak fuchsin, four minims to one ounce of water, leave it for one hour, and examine it wet without a cover-glass. To partly decolorize use weak acetic acid. To fix, stain Avith methylene blue for thirty seconds and examine it wet. The haemoglobin is washed out, and the only coloured objects are the leucocytes and the embryos. To keep them alive for six or seven d£iys, ring a cover-glass with vaseline and place it upon the fresh specimen in the ordinary way. THE FILIARIASES 277 The Diagnosis of M ICROFILARIA. Mf. BANCROFTi (noctuma) Mf. Loa (diurna) Mf. perstans Mf. demarquay Length 0317 x o*oo84mm. 0-245 >r chyle. This effusion mav become coagulated and persist, or it may form a filarial h3^drocele which may be absorbed or require tapping. TREATMENT. Rest in bed, saline purges, lead and opium lotion. (3) FILARIAL LYMPHANGIECTASIS. DEFINITION. A dilatation of the lymphatic vessels from obstruction due to Filaria bancrofti. SYMPTOMATOLOGY. It can occur anywhere but it is commonly found in the scrotum, spermatic cord and extremities. When it occurs in the scrotum there is fever, redness, swelling, pain. After the fever is over the scrotum may remain swollen and elastic. It may be smooth or rugose, or it may show vesicles which on rupturing show lymph or clnle with filarial embryos or very rarely eggs. The discharge of l^mph ma}' be so much in twenty-four hours as to cause marked exhaustion, the condition requiring operation. An attack usually ends in diaphoresis. When it occurs in the spermatic cord there is pain, swelling in the testes, cord and lower abdomen. Fever is less frequent than in the above cases. Later a swelling may appear along the cord which dis- 282 DISEASES DUE TO HELMINTHS appears when the patient lies down, and reappears when he is standing. The vessels are softer, less tortuous and more pouch-like than in true varicocele. When it occurs in the leg there is fever, enlargement of glands, a soft swelling in the groin which disappears on the patient lying down and reapjDears on standing. It does not give any impulse on coughing. TREATMENT. Antiseptic dusting powder. Use a suspensory bandage. If the patient is exhausted from discharged lymph remove some of the distended tissue and tie the dilated vessels. Elephantiasis or chyluria may result. (4) FILARIAL ABSCESSES. These may occur in the thorax and the retroperitoneal ilj'jue. In the latter case the symptoms may be those of peritonitis. The dead body of the parent worm is usually absorbed but if it acts as an irritant an abscess may arise. (6) FILARIAL PHLEBECTASIS (F. varix). This consists of masses of enlarged superficial veins which may occur in the axillae, groin or other regions. (6) VARICOSE LYMPHATIC GLANDS. These occur chiefly in the groin, the inguinal and femoral glands, less often in the axillary and the lumbar (P.M.) regions. The glands enlarge after each fever. They form soft elastic swell- ings, easily movable, at first covered with ncirmal skin, but later they become fixed to the deep fascia. The fluid from an exploratory puncture shows at times microfilariae, and always lymph or chyle. The glands are usually small, but they may become very large. They are seldom painful. TREATMENT. Remove if necessary. The condition is difficult to eradicate completely. Radium may be tried. (7) CHYLOUS EXTRAVASATIONS. Lymph or chyle may be extravasated by dilated lymph or lacteal vessels into the — (i) Urinary passage causing chyluria and lymphuria. (2) Bowel passages causing chylous and lymphatic diarrhoea. (3) Tunica vaginalis causing chylocele. CLINICAL VARIETIES 283 (4) Peritoneum causing chylous ascites. These four conditions will now be dealt with scrialini. (i) Chyluria and Lyviphuria. The dilated lymphatic vessels of the urinary tract rupture owing to obstruction in or below the thoracic ducts and may discharge : — Chyle, when the condition is called chyluria. Chyle plus blood, hence ha^mato-chyluria. Lymph, hence lymphuria. Lymph plus blood, hence luenialu-l\ inphuria. The only difference between lymph and chyle is that the latter, which is derived from the lacteals, contains 65 per cent, of fat, while lymph contains about 35 per cent, of fat. SYMPTOMATOLOGY. The onset is usually abrupt, with \'ague jjains in the perineum, thighs and back, rarely fever; more often the passage of milky or bloody urine is the first sign. (A) The urine 7nay pass out without effort. The urine generally clears, then milky or bloody urine occurs intermittently for years, less frecjuently it is continuous, and may last days, months, or even years. Exertion or emotion may increase the symptoms or precipitate another attack. (B) The urine may clot into a semi-transparent, gelatinous, pinky mass in the bladder, causing severe pain and strangury. There may be considerable pain in passing small clots, efforts lasting some hours. On standing the urine separates into three layers : — (i) A creamy upper layer of fat. (2) A whitish fluid with a floating coagulum. (3) A reddish sediment. This sediment contains fat and oil globules, fatty granular matter, a coagulum of fibrin entangling microfilaria, free microfilaria, white corpuscles, especially Ivmph cells, red cells, and calcium oxalate crystals. The specific gravity is 1015 to 1020. The reaction is acid. To estimate the fat, shake with ether, separate, evaporate the etheF, and weigh the fat. This latter is from o*6 to 2>'3 P^r cent. Albumin is present, o'6 to o'9 per cent, in the resultant urine. If the fat is not in excess, it is lymphuria or hsemato-lymphuria if blood is present. The amount of fat and blood may vary in the same patient. 284 DISEASES DUE TO HELMINTHS TREATMENT. This is symptomatic. Rest in bed. Salol and urotropine. A non-irritating diet. A'ery little fat. Gentle purgation. Astringent injections and bladder washes are of little use. Ouinine should be given. The X-rays can be tried. If clots persist in the bladder, ana?sthetize the patient, wash out the bladder with an aspirator or open and drain. (2) Chylous and Lyuiph Diarrhoea. This condition is rare. The treatment is symptomatic. (3) Chylocclc or Lymphocclc. This condition is often preceded by fever and orchitis. It may develop gradually, the tunica vaginalis filling up with an opaque fluid which may contain microfilaria. The tumours never become very large, but they may require tapping. (4) Chylous Ascites. This is common in animals, but rare in man. Two cases only have been recorded. There has been traumatic rupture of the receptaculm chyli when it has been necessary to cut down and repair the wound. In such cases the intestines are matted together from the exuded lymph, but there are no indications for removing the adhesions, as they are sterile and will resolve. (8) ELEPHANTIASIS. DEFINITION. A chronic inflammatory hypertrophy induced by lymph stasis in fibrous connective tissue, occurring usually in the skin and sub- cutaneous tissues of the leg, scrotum, vulva, arm and breast. CLINICAL VARIETIES. (1) Elephantiasis of the Leg. The lower extremities are affected in 97 per cent, of all cases. SYMPTOMATOLOGY. There are attacks of filarial lymphangitis, dermatitis and cellulitis. The leg swells and partially resolves after each attack. The limb permanently enlarges, the natural folds of parts, such as the ankle- joint, are exaggerated, the dorsum of the foot becomes swollen, while CLINICAL VARIETIES 285 in tlic* deep sulci of the folds epithelial debris, sebum and sweat accumulate, resulting in a foul discharge, followed sometimes by ulceration. The skin becomes dark, hard and thickened. Roughened bosses or warty elevations are common (verrucose variety). Elephantiasis of the legs. Before operation. There is malnutrition of the part, followed by the shedding of hairs and nails, the latter being rough and thick. Perspiration is diminished. The cutaneous sensibility is reduced. Ulcers may occur anywhere. The thigh may become implicated. The febrile attacks may cease at any time, leaving the leg enlarged even to immense proportions. This condition may also result without any fever. 286 DISEASES DUE TO HELMINTHS TREATMENT. Rest in bed. Methodical massage and bandaging, the latter with flannel or rubber. The pressure must be evenly distributed. Avoid minor injuries. Highly laced boots are contraindicated. Give fibrolysin or thiosinamin injections, 2 to 4 c.c. daily, into the gluteal region for three to six months, omitting every seventh day. Elephantiasis of the legs. After operation. Elevate the limb. Never expose it to the sun. To remove horny masses, employ a spirit lotion of resorcin and salicylic acid. After six months remove long strips of redundant skin and sub- cutaneous tissue. CLINICAL VARIETIES 287 Poor results are obtained in acute, but better in chronic cases. Some have tapped the affected parts with Southey's tubes, others have cut out long square masses and have sutured up the cavity, while others have inserted fine threads to form the bases of new lymph channels (Lymphangioplasty), All improvements in consec^uence of these measures are more or Elephantoid tumour of the buttock. less slight and transitory. Final and permanent results of all surgical measures are disappointing. A QUERIED POINT. Some still ask : " Is elephantiasis arabum caused by the filaria, as these are not usually present in the blood or elsewhere?" Sir Patrick Manson answers : " Yes," for the following reasons : — 288 DISEASES DUE TO HELMINTHS (i) The distribution of Filaria bancrufti and elephantiasis arabum correspond. (2) Warix and elephantiasis arabum occur in the same districts and individuals. (3) As varix is proved, elephantiasis arabum is inferred to be filarial. Elephantiasis of the prepuce (and legs). (4) Lymph scrotum often terminates in elephantiasis scrotum. (5) When the latter is removed there may follow elephantiasis of the leg". (6) Elephantiasis and varix are both diseases of the lymphatics. (7) Both are accompanied by recurring lymphangitis. The worm is not found because it may have died after aborting the ova, causing embolism of the lymphatics. There then follow : lymph stasis, reduced resistance of tissue, repeated mild sepsis and imperfect CLINICAL VARIETIES 289 absorption of inflammatory products, the natural result being the hypertrophy of the Hmb. Elephantiasis scrotum. Twenty-eight years duration. Elephantiasis may occur four to ten years after microfilariae have been seen in the blood. 19 290 DISEASES DUE TO HELMINTHS There may be sexually mature living filari^ in the glands when none of the embryos have passed into the blood (Bahr). (2) Elephantiasis of the Scrotum. SYMPTOMATOLOGY. A gradual enlargement with or without recurring erysipelatous attacks, erythema and fever. A large triangular mass is formed, base Elephantiasis. Scrotum. downwards. On its anterior and superior aspect a canal is formed by an inverted prepuce leading to the penis. This organ is buried in the tumour. The testicles are above and behind, and are usually surrounded by hydroceles. The base of the tumour may be ulcerated. A tumour has weighed 224 pounds; 10 to 20 pounds is common. Tumours weighing 40 to 50 pounds are not infrequent. A localized groin tumour may weigh 10 to 20 pounds. Elephantiasis of the penis alone also occurs. CLINICAL VARIETIES 291 TREATMENT. Rest, especially during- the acute phases. Cleanliness. Avoid minor injuries. Massage. Exercise the enlarged glands. The removal of the mass has a mortality of 5 per cent. The opera- tion is carried out as follows : — Put the patient to bed for at least two days, clean the skin carefully, suspend the mass in order to drain it. Place a figure of eight elastic Elephantiasis. Breast. West Coast of Africa. bandage around the pelvis and the neck of the tumour. Select good skin for the flaps if possible. Turn the tumour upwards and incise for flaps in front of the anus. Then cut out the anterior flaps from the pubes downwards in the mid-line, ligaturing the vessels as required. Cut down the penile canal with scissors and dissect out the testicles and penis. Pass a catheter as soon as possible; it will serve as a guide to the urethra and penis. Dissect out and separate the mass, loosen the tourniquet, and ligature any vessels. Puncture or otherwise open all hydroceles, invert the sac, remove the redundant tissue, and stitch 292 DISEASES DUE TO HELMINTHS the inverted sac around the testicles. Suture skin flaps over testicles and penis like the letter T or Y with the penis at the junction. Drain the lower portion of the wound. Make skin flaps for the penis if possible ; if not possible, then cover the raw area with oil protective and allow it to granulate. Dress aseptically. Skin grafting should be done early where it is necessary. The functions of the organs are retained and restored. It will facilitate repair to loosen the skin from the thighs with the Elephantiasis. Penis. European some years after leaving Egypt, from photo, by Dr. Hunt. fingers and draw it inwards if there is insuf^cient skin. Turn prepuce back to cover the anterior part of the penis. The skin around the penis, though inverted, is usually healthy and should be retained. Complications are haemorrhage and septicaemia, also sometimes difficulty in copulation, as the scar tissue may bind the penis down. (3) Elephantiasis of the Yulva. The labia majora and clitoris are sometimes affected, but it is a rare condition. CLINICAL VARIETIES 293 These tumours may weigh from eight to twelve pounds. Remove the mass aseptically. (4) Elephantiasis of the Breast. The condition is rare, but when present the tumour may grow to a large size. One or both breasts may be affected. Remove the tumour. (5) Elephantiasis of the Arm. This is a rare condition, but may develop as in the leg, affecting one or both upper extremities. The muscles are not affected. Treat as for the leg. Elephantiasis. Leg. India. (6) Elephantiasis of the Scalp. The whole scalp becomes very much thickened, and numerous folds and deep furrows are formed. Treatment is symptomatic. (7) Elephantiasis of Localized Areas. Pendulous masses of filarial origin are said to have been found. They may be single or multiple and should be removed. 294 DISEASES DUE TO HELMINTHS Double conjunctivitis discharging chyle has been recorded, filaria also being present (Lewis). Acute synovitis of the knee associated with filaria is possible (Maitland). NOTES ON FILARIAL CARRIERS. CULEX FATIGANS (Culex = gnat). This fly of the sub-family Culicin^e is one of the carriers of filaria, and possibly also of the dengue parasite. Larvse and pupte of C. fatigatis, Wied., photographed from life, about twice natural size. MORPHOLOGY. The palpi are longer than the proboscis in the male, and one-sixth the length of the proboscis in the female. The larva has a breathing tube. The lateral thoracic and abdominal hairs are not feathered. The head is covered with narrow curved and upright forked scales on the dorsum. The scutellum is covered with LOASIS 295 narrow curved scales, and the wings with long, lateral, slender scales on the veins. It is of a brownish colour, with a broad white and pale yellow band across each abdominal segment; the ventral surface is pale. The legs are brown except for a small pale " knee " spot at the tip of the femora. The larvcB may be found in any water near to iiuman dwellings or in sewage. They have a long, slender breathing tube two and a half times the length and twice the breadth of the slender pointed tracheal gills. The antennae carry a fan-like tuft of twenty long hairs. Habits. — They breed in water-butts, drains, and any temporary Larva of Anopheles iiiaciilipeniiis, Fabr. Enlarged. (After Grassi.) Larva of Culex. Enlarged. (After Grassi.) collection of water. Thev are the commonest mosquitoes in the Tropics. LOASIS. DEFINITION. An inflammatory condition of the superficial connective tissue or conjunctiva caused by the Loa loa. DISTRIBUTION. In Africa, chieflv in Angola, Congo, and on the West Coast, where it is endemic. It is very common in Old Calabar and the Cameroons. Perhaps it causes the Calabar swellings. It has been imported to the West Indies. 296 DISEASES DUE TO HELMINTHS It seems to have a restricted geographical range. Europeans are often infected. CAUSATIVE PARASITE. That a filaria has occurred in the eye has been known for four centuries. The Loa loa has been found in the ocular and palpebral conjunctivae, crossing the bridge of the nose, under the skin over the sterno-mastoid, scalp, fingers, penis, &c. Loa loa : the anterior end of the male, magnified. (After R. Blanchard.) Loa loa : anterior portion of the female as far as vulva. (After Looss). '''^:4'i^-'' '' Loa loam ^\\.\x. Natural size. (Afler Fiilleborn and Rodenwaldt.) Loa loa : male on the left, female on the right. X 2. (After Looss.) It has rarely been found in the anterior chamber of the eye. MORPHOLOGY. The male is a thin, white, semi-transparent worm, 25 to 34 mm. long by o'4 mm. thick, tapering at each extremity with a head like a truncated cone, and the tail incurved with a rounded tip. It has transverse corrugations of the cuticle with a wavy outline, wide apart in the females and close in the males. LOASIS 297 / / Loa lea: on the left, the hind end of a male; on the right, of a female. Note the cuticular bosses shown in the figure of the female. x 285. (After Looss.) Loa loa : lateral view of tail of male showing papilkie. (After Lane and Leiper.) L Loa loa. a, ventrolateral aspect of tail showing papillce and one spicule ; b and c, terminations of the two spicules. (After Leiper.) 298 DISEASES DUE TO HELMINTHS The anus is 80 i-i from the tip of the tail. There are three pairs of pre-anal and two pairs of post-anal papillse. The worm carries two spicules of unequal length ; the larger is traversed by a fine canal (Penel). There are rounded bosses scattered over the cuticle averaging 30 yu, in height. The mouth is terminal, small, unarmed, with a powerful muscular cone. The oesophagus is short and is not bulbous. The excretory pore is 0*65 mm. from the anterior end. The worm has a tubular testis and vas deferens filled with spherical spermatozoa, which organ terminates in a vesicula seminalis near to the base of the spicules. The female is 44 to 63 mm. long by 0*4 mm. thick. The vulva is 2*5 mm. from the anterior end. LIFE-HISTORY. The unsegmented egg is 32 by 17 /x | The morula stage is 40 by 25 /x. In uterus. The rolled-up embryo is 50 by 25 /x.) The embryo approaches the vulva, unrolls and elongates itself inside the egg membrane before it is extruded ; the embryo then measures 250 by 6 /x The embryo now escapes into the lymph stream and blood current, where it is known as Microfilaria diurna. In the circulation it enlarges to 298 by 7*5 /x, perhaps by osmosis. The microfilarias do not completely fill their shealh. HABITS. They are seen in the peripheral blood during the day, but not at night. They have no relation to sleep as the Microfilaria bancrofti. The curves are irregular; in the Mf. bancrofti they are graceful. The microfilarias when found in the peripheral blood are never in such numbers as the Mf. bancrofti. The Mf. diurna requires from three to four years in the human body before it reaches maturity; they then live for fifteen years or more. The immature forms are usually found in children, but the mature forms in adults. The rate of progress in the human body is supposed to be one inch in two minutes. Warmth such as that from a fire or the direct sun will attract them to the surface. The worm becomes cretified when dead. CARRIER. This is the Chrysops dimidiata and silacea (Leiper). It is one of the Tabanidse with hind tibias armed with spurs. CALABAR SWELLINGS 299 It has a short proboscis, the antennfe are longer than the head, the wings have a black band running across them, the eyes are golden green during life, marked with purplish spots. The wings are half open when resting. The female bites very severely, causing pain and sometimes inflam- mation with oedema. The eggs are deposited upright on leaves and plant stems near water in a single layer. They are whitish or brown in colour. The larvce and pupce are not unlike those of the Tabanus. The complete life-history is unknown. SYMPTOMATOLOGY. These are often nil. When the worm is under the conjunciiva there are piercing pains, uncertain vision, and swelling of the eyelids. There may be some general itching. They may cause painful swellings in various parts, but these are exceptional. The swellings do not suppurate and subside in a few days. The blood may sho^\ a marked eosinophilia up to 70 per cent, of the total leucocytes. TREATMENT. This is symptomatic. CALABAR SWELLINGS. DEFINITION. Calabar swellings are smooth, temporary, slightly raised tumours about the head, ankles and feet, probably caused by Loa loa and other filarite. DISTRIBUTION. On the West Coast of Africa only, especially about Southern Nigeria and the Cameroons. SYMPTOMATOLOGY. It is not certain as to how the lumps originate, but the most likely theories are : — (i) That they are the result of the expulsion of microfilariae from the uterus of the parent worm. This would explain their evanescent nature (Manson). (2) That they are due to the expulsion of the waste products of the worms. The swellings are often painless, the size of half a goose's egg. Some of them disappear quickly, others gradually during two to three days. 300 DISEASES DUE TO HELMINTHS There may be nausea, headache, slight pruritus, with some eosino- philia up to 50 per cent, of the total leucocytes (Stephens). The swellings do not pit on pressure, neither do they suppurate.. They may develop singly, one coming as a former one declines. TREATMENT. Apply ichthyol ointment or 5 per cent. liq. plumbi to the swellings.. VOLVULOSIS. The parasite, Onchocera volvulus, (F'. volvulus) was first found in tumours of the scalp and chest of a negro on the Gold Coast by a medical missionary. DISTRIBUTION. Sierra Leone, Gold Coast, Dahomey, Nigeria, Cameroons, and the Congo. MORPHOLOGY. The male F. volvulus is a whitish, filiform, sheathless embryo as found in the microfilarial form, 30 mm. by 0*14 mm., with slightly attenuated ends and transversely striated cuticle. The tail is strongly incurved. There are nine pairs of papilla^ about the anus (Brumpt). It carries two unequal sj^icules 177 /x and 82 ft long. They are found in the axillae, popliteal space, elbow, sub-occipital region and intercostal spaces. They are common about the chest. They are not painful and are easily enucleated. They do not suppurate. Eggs and embryos may be found in the swellings when incised. The female is 65 mm. by 0*36 mm. The vulva is o'76 mm.. from the anterior end. LIFE-HISTORY. The worm lies in a lymphatic vessel which becomes inflamed and causes a condensation of the adjacent connective tissue, in which become embedded both males and females. In a central lymphatic space the posterior end of the male and the anterior end of the female project, and in this way copulation takes place. Later the embryos are passed into this space. These latter are from 250 ^ to 300 yit long t>y 5 /"■ fo 6 ^ thick, with pointed tails and no sheath. The micro- filaria have not been seen in the blood. The adults may live for years in the human body. Their complete history and carrier is not known. PATHOGENICITY. Lymphangitis and perilymphangitis v/ithout or with fever, leaving a small tumour. DRACONTIASIS 301 DRACONTIASIS. DISTRIBUTION. I'ropical Africa. In the Sudan it is to be found at Gallabat, Gedaref, Upper White Nile, Kordofan and the Bahr-el-Ghazal Province. India, Persia, Turkestan, Arabia and a few places in South .America where it has been carried from Africa, such as al British Guiana. It is also present in the Fiji Islands. It has been seen in Europe. In parts of the Deccan at certain seasons 50 per cent, are infected. In parts of the West Coast at certain seasons 95 per cent, are infected. The disease has been reported in horses, oxen, dogs, &'C. THE PARASITE. Dracunculus medinensis. (Guinea worm.) Perhaps this was the fiery serpent of Moses as he knew the method of twisting the creature about a stick. The host is man. The intermediate host is the Cyclops quadricornis. This worm is the largest of human lilaria, its average length being about 40 inches with extremes of 12 to 70 inches. The female, of which we know the most, is a long, white worm with a hooked tail and a large uterus which occupies nearly the whole of the body cavity. The embryos when ready are evacuated from it at the anterior end near to the mouth. The uterus protrudes througli the head parts, rupturing them (Leiper), and when about one inch of it has passed the sac fills with opaque fluid and ruptures. When a little water is added the motionless embrvonic forms uncoil themselves and swim about. LIFE-HISTORY. The young are discharged into fresh water soon after the parent has broken the overlaying skin and before sepsis has set in. These young forms are taken into the body cavity of a cyclops where in about five weeks they will develop into mature larvae. These are taken into the human stomach with drinking water or vegetables, where the o'2 per cent, of HCl kills the cyclops and at the same time stirs up the larvce to such activity that they break through the cyclops at the mouth, anus and genital opening. They then swim about in the gastric fluid after which they penetrate the gastric wall and so reach the mesenteric connective tissue. Here they copulate and the males die. The preg- 302 DISEASES DUE TO HELMINTHS Anterior extremity of Guinea worm, showing dorsal and ven- tral lips, one lateral and two tubmedian papillre and the lateial line. (After Leuckart.) Guinea worm, Dracun- cnhis medinensis. (After Leuckart.) Dracuncuhis medinensis. a, anterior ex- tremity seen end on ; O, mouth ; P, papillse ; b, female reduced more than half; c, larvae enlarged. (After Claus.) DRACONTIASIS 503 Transverse section of female Guinea worm ; it. uterus containing embryos; ?. intestinal canal!; 0. ovary. (After Leuckart.) Cyclops virescens, ? . 8, Female, ventral view, X 120; 9, anterior antennae, x 240; 10, urosome and last thoracic segment, x 240; il, foot of first pair, x 320; 12, 15, 16, foot of second, third and fourth pairs, x 240; 14, foot of fifth pair, x 440; 13, last thoracic segment and first segment of urosome of male, X 240. I 304 DISEASES DUE TO HELMINTHS nant female tlien settles down ultimately in a place where it can deposit its young in or close to water. The parts chosen are : — (i) The ankle or lower leg in 85 per cent, of cases. (2) The backs of water carriers in India (doubtful). (3) Rarely about the knee joints. The life span of a parent worm is abt)ut ten to twelve months. Therefore, the embryos are discharged into the water where they must be taken up bv an intermediate host, e.g., cyclops in which they develop into mature larvae in five weeks but in which they can survive for 41 days. The larvcC are then swallowed b\' man, or as some assert, they enter the skin of the subject while he is bathing or standing in the water or mud. The mature worms form in about one year and they can persist for ten to twelve months during A\hich time they dis- charge their embrvos. The life cycle is broken : — (i) Bv death of the embryos as a result of sepsis of the wound. (2) Bv death of the embryos when there is no water near at liand. (3) If nO' cyclops is present in the water or if the cyclops dies or is not ingested by man. (4) If the larvce are immature when ingested or fail to escape from the body cavity of the c\'clops. (5) If there are not the two sexes in the embryos and if the female is not impregnated while wandering through the connective tissue. PATHOLOGICAL LESION. A small bulla on the surface of the skin about the external malleo- lus marks the anterior end of the female worm. The bulla bursts, the uterus prolapses, the young are discharged and a jjortion of the worm is often extruded, A\hic]i the natives t\\isl around a stirk in an attempt to extract it. This area is very liable to become septic. SYMPTOMATOLOGY. An ulcer appears as above. Urticarial eruptions are not un- common. Rigors and fever may occur. Eosinophilia may go up to 13 per cent. Synovitis and arthritis are rare. The writer extracted one from over the internal tuberosity of the knee after synovitis. The svnovitis trouble cleared up when the worm had been removed. TREATMENT. The worm lies zig-zag and even though nuicli may be removed the posterior end may have remained in the same place, the worm has only been straightened in the majority of attempts to remove it by twisting it around a stick. TRICHOCEPHA LIASIS 305 Douche the pari, where the uterus presents, wiih cold water, when it will empty its uterus. The worm will then be absorbed, emerge or in any case it will be easier to extract. The douching may be required several times daily over two to three ^\eeks. If the worm is visible or palpable under the skin several incisions can be made and the worm removed in parts. Some inject perchloride solution, i in 1,000, but they are painful and not very successful. The native method is often one of straightening and not of extracting. Treat the ulcer on ordinary lines. PROPHYLAXIS. Carefully boil and filter all drinking water. A fine handkerchief is sufficient. Steam should be passed into wells to kill the cyclops present. Avoid drinking water used for bathing purposes. Improved sanitation will cause its disappearance. TRICHOCEPHALIASIS. This is an infection of the intestine by Trichocephalus trichiurus or whipworm. It is cosmopolitan in its distribution. THE PARASITE. It belongs to the famih' Tricho- trachelid^. The male is 40 to 45 mm. long with a spirally coiled posterior end. Its spicule, 2 to 5 mm. long, lies in a retractile pouch. The female is a little longer than the male. The ^gg, unsegmented as it appears in the faeces, is brown, oval, thick-shelled with a pale area at each pole. Several months are necessary before the embryo matures. No' intermediate host is necessary. The embryo is ingested inside its shell taken with either food or drink, human hands or flies acting as carriers. The gastric juice dissolves the shell and in about four weeks the embryo reaches maturity in the intestine. The worm can live for years in moist earth. 20 Trichurh trichiura: on the left, male ; on the right, female with the anterior extremity embedded in the mucous membrane of the intestine ; below, egg. 3o6 DISEASES DUE TO HELMINTHS PATHOGENICITY. The worm is usually harmless although some affirm that it causes appendicitis at limes; this, however, is very doubtful. Diarrhoea in children living in insanitary conditions is more common. Perhaps the head is buried in the mucous membrane which makes their ejection more difficult and thus disposing to bacterial infection at the site of the wound. No ecchymoses are seen at the point of fixation. The eggs can infest utensils from dust long dried and hence the infection is not ah\'avs due to fa?cal contamination. TREATMENT. When there are svmptoms present treat as for ankylostomiasis. TRICHINIASIS. This is an infection of the gastro-intestinal and muscular system by the nematode Trichinella spiralis of the family Trichinellida^. The condition caused bv the infection is of considerable importance as shown bv the fact that in Hamburg alone loo inspectors were employed to examine pork, the carcases numbering from 25,000 to 30,000 per month. This work cost /,'25,ooo annually. DISTRIBUTION. It is common in German v and in some parts of America, India and China. It is rare in England and France. THE PARASITE. LIFE-HISTORY, &c. Two mammalian hosts are necessary for its development which need not be of diiTerent species, but no intermediate host is required. The cysts are founci usual! \' in human or pig''s muscle and appear as minute white specks which are the encysted larvae. Their long axis lies in that of the muscle fibre. The\- measure 400 b\' 230 ^a. The cyst membrane is formed by inflamed connective tissue. The larvce may thus live for years but may become calcified and die. The\- are chiefly found in the muscles of the diaphragm, larynx, tongue, abdominal and intercostal regions. These cysts are ingested alive witli the muscle fibre unless severe cooking has destroyed them. The gastric juice dissolves the cyst wall and the parasites emerge and pass to the intestine where they become sexually mature, reaching i to 3 mm. in length. Copulation takes place about tMo days after the cvsts have been ingested, after which the males die. The females grow, penetrate the mucous membrane of the bowel and reach the lymph spaces and there deposit living larvae. One adult female may give rise to 1,500 larvae. TRICHINIASIS 307 The female lives from about five to seven weeks doing this. The larv^ are carried by the blood and lymph stream all over the s d. Trtchinella spiralis. ? , mature female : E. embryos ; V, vulva : Ov, ovar)-. 3 , mature male : T, testes, c newly born larva, d. larva in the muscles, c. encapsuled larva in the muscles. Magnified. (After Claus.) body. They then leave the capillaries, burrow their way into the tissues and in from nine to ten days become encapsuled in the muscles. The muscle fibre infected degenerates, becomes inflamed, and a cyst is formed from the inflammatory tissue. 3o8 DISEASES DUE TO HELMINTHS The cyst resists a temperature of 8o°C. or smoking, pickling and freezing. The adult worm has an anterior part thin and whip-like, the .V' r- M .^^^^ MKi^- ! \'i v.^S*' ^ Vaiious phases of the calcification of Tri- i chinella of the muscles, which starts at the poles /- 1 c J T- ■ u- 1 ■ V 1 "f i'^^ capsule. Calcified Trichintlia m ihe muscular ' system of a pig ; the capsu'es are not calcified. (After Osterlag.) posterior is thick and carries the genitalia, but there is not the abrupt transition as in the Trichocephalus. There are two cone-like appendages. The female vulva is placed far forwards. This worm is really a parasite of the black rat (Kpimys rattus) and the sewer rat (Epimys norvegicus). SYMPTOMATOLOGY. There are : irregular fever not unlike typhoid ai times, some general abdominal pain and tenderness with agonizing pains as the larva? burrow through the muscle, which pain lasts intermittently for from five to seven weeks. When the muscles of respiration, mastication or deglutition are invaded the essential functions are rendered difificult. When the female has finished depositing embryos and all have become encysted the symptoms clear up. The eosinophilia is verv high. The larvie are not found in the blood. There is often diarrhoea, raised temperature and oedematous swellings. Fatal peritonitis may occur in a heavy infection. TREATMENT. Anthelmintics are useless. The treatment is symptomatic. ASCARIASIS 309 PROPHYLAXIS. All rats near to pigsties must be destroyed. Pigs must be kept away from the offal of slaughter houses. Meat should be cooked at a temperature of 62° to 7o°C. in all parts. In some sausages the pork is uncooked. Such pork should be examined, passed and marked by an inspector qualified for the work. The parts affected chiefly are the tongue, laryngeal muscles, diaphragm and abdominal muscles. To search for the cysts press a small portion of the muscle fibre between two translucent glasses or plates when the larvas are more readily seen. The larvae are not killed by freezing, and hence frozen meat may be infected. ASCARIASIS. DEFINITION. This is an infection usually with the Ascaris lumbricoides or round worm, rarely with the Toxascaris canis or Belascaris. The two latter are smaller and are more commonly found in cats and dogs. DISTRIBUTION. In all tropical and sub-tropical climates. The A. lumbricoides is parasitic only in man. When the eggs are passed externally their development is limited until re-introduced into man . THE PARASITE. LIFE-HISTORY. The eggs are laid in the small intestine and measure from 50 /ti to JO ju, by 40 ya 10 50^- They have a thick yellow transparent shell coated /^"P^^^'i "%«x::^ Ascaris lumbricoides. a, posterior extremity of Ov\xn\oi Ascaiis lumbricoides, the male witii the spicules protruding from the with shell and albuminous en- orifice of the cloaca {Sp.) ; b, anterior extremity velope. 400/1. from the dorsal surface, the two lobes of the pulp of the lip separated by the " saddle " ; c, anterior extremity from the ventral surface ; P., excretory pore. (From Claus.) irregularly Avith albumin and stained a brownish yellow by fcecal material. This outer covering may be removed during the passage through the intestine. The shell affords high resistance to changes in temperature and moisture. The contents are granular but do not divide into nuclei as in the &gg of the ankylostome. 3ro DISEASES DUE TO HELMINTHS a, Ascaris Itimbyitoiaes; b, Trichocephalus dispar ; c, Oxyuris vertiiicttlaris ; c\ c~, Ankylosiomum duodetmk ; d, oncosphere of Cestode ; e,/,g, various Fasa'o/tdt? ; /i, Sc/iis- ioso»iu»i{?) haviatohiiiin (from foeces) ; /, Schis.tosomtim h^Tmatohittin (Irom urine). ASCARIASIS 311 In warm and muisl soil a spiril embryo is seen in one month, but requires to be ingested by man before hatching and developing into the adult form. The source of infection is by polluted vegetables, fruit, water, and soiled hands. The eggs ])ass unaltered tiirough the alimentary canal of the house-fl\', hence house-flies are carriers (Stiles). The eggs liatch out in the small bowel where the adults remain as spindle-shaped yellowish worms, the male 15 to 25 cm. long by 3 mm. thick. The female is from 20 to 40 cm. long. They look very like the ordinary ground worms. The male carries two spicules posteriorly, and there are aboul seventv papillcC around the cloaca. The vulva of the female is at the junction of the anterior and middle thirds of the body. The eggs are tisuallv in the small intestine but have been seen post mortem in the stomach, oesophagus, nose, larynx, trachea and bronchi, more rareh' in the li\-er, pancreatic duct and vermiform appendix. SYMPTOMATOLOGY. Symptoms are often nil. Skin eruptions and irritation ma}^ be present. If manv are present there ma)' be signs of toxemia or intestinal obstruction. Odd worms may wander in many places, when -the symptoms are according to the mechanical obstruction caused, as when one passes into the stomach, vomiting may set in. Passes into the appendix, inflammation of that organ arises, ,, ,, large gut, an ulcer may be perforated, ,, bile duct, an abscess may result, ,, duct of Wii"sung, pancreatic instifficiency and death, ,, ,, nose, itching and discharge. They have caused obstruction, perforation, peritonitis and death (Prasad). In searching the faeces for eggs one must remember that : — The eggs may have an albuminous coating, or They may be decorticated, or They may be unfertilized, or They may have become embr^'os, each stage presenting a different picture. TREATMENT. Give santonin, grains i to 3, each morning for three days. Accompany this by calomel in equal doses. For children give one-sixth of a grain of each for each year of life for three days. Repeat the treatment after one week if the eggs are still present. Santonin in excess may cause yellow blindnt-ss. 312 DISEASES DUE TO HELMINTHS OXYURIASIS. THE PARASITE. The Oxyuris vermicularis or thread-worm is world-wide in its distribution and occurs only in man. M A, male and B, female, of Oxyu- ris vermicularis. 5/1- 'Si^-fpiW On the left, female ; on the right, male. A, anus; M, mouth : V, vulva. Greatly enlarged. (After Ciaus.) Oxyitiis vermicu- laris : egg freshly de- posited, with tadpole- like embryo. X 640. Oxyuris vermicu- laris : egg twelve hours after deposition, with nematode- like embryo. x 640. The male is 3 to 5 mm. long and the female 9 to 11 mm. long. They live in the lower part of the small intestine but the gravid females migrate to the caecum, colon and anus. The males die after copulation. The eggs are given off in the gut and measure 30 by 20 ^l■ They have a thin shell and contain a well developed embryo when the egg is passed in the fasces. These eggs escape and are re-intro- ANKYLOSTOMIASIS 313 duced upon fruits and vegetables. The Qgg capsule is dissolved in the stomach, the embryo passes to the small intestine, grows and becomes mature in fourteen days and then copulation takes place. The adult worm is a fine, minute, thread-like, round worm with a long bulbous oesophagus and transversely striated cuticle. The male is coiled up at the posterior end and carries one spicule. The female is straight and the posterior end tapers to a point. SYMPTOMATOLOGY. Irritation about the anus is common. One often meets with nocturnal enuresis and insomnia. Entero-colitis and slight fever are rare. Nasal irritation is uncommon. The worms may cause vaginitis in girls and masturbation in both sexes. TREATMENT. To kill the young forms use santonin and calomel as for Ascaris. To kill the gravid females give rectal injections of quassia, alum, one drachm to one pint, or of salt, two drachms to one pint. For rectal irritation or vaginitis give diluted mercurial ointment, one in four. Iodoform or napthalin suppositories may be used. ANKYLOSTOMIASIS. DEFINITION. This is a toxaemia passing to a progressive anemia caused by the Ankylostome duodenale and the Necator americanus associated with fatty degeneration of the heart, liver, kidneys, and of the intestinal mucosa. DISTRIBUTION. The disease is found wherever there is moisture and a suitable temperature for the growth of the parasite. It is present in America, Africa, Asia, Australia, New Guinea, Fiji, and in the mines of Cornwall and Belgium. It was taken to the United States by African slaves. In Porto Rico 70 per cent, of the people are infected and 30 per cent, of the death rate is due to this cause. In the Army of the Southern States 6 per cent, were carriers. In the mills of the Southern States 12 '6 per cent, were carriers. In Java 97 per cent, of the population is infected. ' THE PARASITE. This is the Ankylostome duodenale. (Also the Necator americanus as it gives rise to similar svmptoms.) 314 DISEASES DUE TO HELMINTHS The disease was perhaps known and treated bv the ancient Egyptians 1,550 years B.C. U WHl VI »!,/, male and female Ankylostomes : a, head of Ankylostovium ducknale ; b, head of Necator americamis. It was rediscovered by Dubini in Milan, a.d. uS^cS. The parasite is a white cylindrical worm living in the upper intestine, the jejunum chiefly, retaining its position with its four hooks and two conical teeth, which are carried about the mouth. ANKYLOSTOMIASIS 315 The disease was perhaps Icnown ;incl treated b\' the ancient Egyptians 1,350 years B.C. B A B A, A, head and tail of male, Aiicylostoina duoJenale ; v., B, head and tail of male Necator americanus ; x, x, dorsal rays. Ancylostoiiia duodenale : eggs in different siages of development, a to c, in fiesh fiieces ; d, conlaining a larva, only in old faeces. X 336. (After Looss.) Two long and slender spicules can often be seen projecting through the opening of this bursa. 3i6 DISEASES DUE TO HELMINTHS The female, 12 to 13 mm. long, has the vulva at the junction of the middle and hinder parts of the body, so that when copulation takes place the worm looks like the Greek letter gamma 7. LIFE-HISTORY. The adults live in the jejunum, where the females lay their eggs. These eggs are colourless, with a thin, plain double shell, the cellular contents being separated from the shell b)- a clear space. During its passage through the intestine the cellular mass divides into two, then four parts, and is usually seen in this form in the faeces. With sufficient air, water and heat the embryo forms in twenty-four hours, escapes from the shell, and begins to feed on faecal material. Larvae measure from 200 to 250 fi by 15 to 17 /a. Ecdysis is completed in four to six days in the tropics; the larvae then ceases to grow. It can remain alive in this condition for months, living on the food in its own cells. The larva may be quite active, swimming or climbing to any other suitable place. It enters the hair follicles of man, causing " ground itch," and may even penetrate gloves, paper and boots in order to reach the skin. Thence it passes to the lymphatics and venous blood-vessels. Some of them reach the right heart and the lungs, whence they pass from the capillaries to the alveoli along the bronchioles, bronchi, trachea and larynx to the oesophagus, stomach and intestines, where they remain. This occupies from seven to ten days, during which time several ecdyses take place. In eight days these larvae, 3 to 5 mm. long, attain maturity. In fourteen to sixteen days copulation has taken place, and the eggs are seen in the fccces. The whole cycle takes eight to ten weeks. Sambon says that when the larv^ are in the lungs they pass from the pulmonary capillaries to the pulmonary veins into the general blood-stream, and hence into the mucosa of the jejunum, which they pierce, and so enter the lumen of the bowel. He believes that those seen by Loos in the respiratory tract are stray ones. Perhaps both are correct, but experience has shown that the great majority pass as Loos has described. Some may enter directly by the mouth, as when miners eat their food with soiled hands. In order to grow the larvse, place a thin layer of fseces in a Petri dish and a piece of moistend blotting-paper on the top. The worms will grow in two to three days and come upon the top of the blotting- paper, where they can be well examined. Keep the paper moist ; later breathe on the paper ; this will stimulate movement. For mounting them, embed in gh'cerin and egg-white smear, treat ANKYLOSTOMIASIS 317 with absolute alcohol, wasli dut glycerine, and stain with hsematin and eosin. SYMPTOMATOLOGY. Clinical Course. Papules or vesicles may form v/here the larv« enter, perhaps due to the pus cocci introduced. This is known as " ground itch " or "bunches." A leucocytosis and an eosinophilia can be seen under the microscope before other symptoms are manifest. The first symptoms generally observed are, however, pallor, weakness, breath- lessness, oedema, general or local, emaciation perhaps concealed by the oedema. Flatulence, dyspepsia, nausea, vomiting, epigastric pain, constipation or diarrhcjca ; later in tlie final stages there may be a general anasarca. One finds the ova in the stools with, sometimes, blood and mucus, also Charcot-Leyden crystals. In some cases there is a perverted appetite, perhaps due to mental disturbance (geophag\'). Impotence is common, 68 per cent, of Sandwith's cases. Puberty is delayed in both sexes. It arrests growth and develop- ment generally. Lemann noticed that infantilism was present in voung hookworm patients of the Southern United States. He finds that the disease produces : — (i) A general retardation of skeletal changes. (2) A general retardation of growth, symmetrical and harmonious. (3) A failure of development of the genitals as well as the absence of secondary sexual characteristics. (4) A general slowness and dullness. THE BLOOD EXAMINATION. The volume of blood is increased, causing dilatation of the heart and hjemic bruits at the apex. Coagulation is diminished, the blood readily spreading over the skin when punctured. The blood condition predisposes to palpitation, and a quick, thready, dicrotic and inter- mittent pulse. The red cells are markedly diminished ; one patient had but 930,000 and recovered. The haemoglobin may be as low as 15 per cent. There are many changes in the red cells, but they are more uniform than in pernicious anaemia. One finds poikilocytes, megalocytes, normoblasts and megaloblasts. Polychromasia is not infrequent. The eosinophilia is from 10 per cent, to 50 per cent., sometimes well- marked in children, but may be absent in adults (Low). The leucocytes, total count, vary from 20,000 to 50,000 per cm. 3i8 DISEASES DUE TO HELMINTHS The disease is often fatal during parturition and during operative treatment. Sometimes a low fever is present, but this is the exception. The aucemic condition is probably caused by a toxin excreted by the Axorms which passes into the circulation through the wound made in the mucosa of the jejunum, together with the actual blood lost at the site of the bites. The condition is aggravated undoubtedly by septic absorption from the same foci. Post mortem, }'ellow pigments and iron granules are found deposited in the liver and kidneA' cells in bad cases. COMPLICATIONS. Albuminuria, present in 80 per cent, of Sandwith's cases. General oedema may be present. Any inlercurrenl disease, as d\senlery, which is common. Pregnane}' or operatiA-e procedure are serious complications. The former cases die of heart failure just before the child is born. TJiere is a tendency to post-partum hccmorrhage. Cardiac failure is common. PROPHYLAXIS. The ankylostome embryos, wlien passed under good conditions for them, can survive and develop as free living larvae awaiting access to man in order to complete their development, hence prophylaxis is important and may be summarized thus : — (1) Educational. The instruction of rich and poor a\ ilh regard to methods of infection, symptoms, treatment and prophylaxis. (2) Public. Search for and treat carriers, aucemic people and those with skin eruptions. The provision of sanitar)- conveniences which should be kept in good condition. (3) Private. Protection of the feet bv boots, &c. The proper cleaning of hands before meals. Immediate treatment of eruption on hands and feet. TREATMENT. 1 he indications are to expel the worms and to aid blood formation. There are four main lines of treatment as follows : — (1) Thymol Treatment. Put the patient in bed on starvation diet for two days. Exclude all other possible ailments. ANKYLOSTOMIASIS 319 Alcohol is strictly forbidden as it dissolves the thymol and may produce a fatal result. Some ofive str\(^hnine, but this is verv soluble with th\mol and in anv case should not be given b}- mouth. Give a saline purge at the end of the second day. All food prohibited during the thymol treatment. Give thvmol, one to two grams next morning. ,, ,, ,, two hours later. ,, ,, ,, two hours later. Give a saline aperient four hours after the last dose of thymol. Castor oil must not be given as thvmol is soluble in it. Sandwiih recommends strychnine injections before the treatment. Do not give thymol to patients with fatty hearts, visceral disease or with an anaMiiia below 1,500,000 red cells per cm. (2) The Eucalyptus Treatment. The preliminary two days as above. Give a saline purge at 6 p.m. Xext morning at 7 a.m. and 7.30 a.m. give the following mixture : — ^ Olei eucalypti ... ... ... ... ... 15 minims Chloroformis .. ... ... ... ... 22 ,, Olei ricini ... ... ... ... ... half a drachm This amount to be gi\-en on each occasion. For children divide tlie whole dose into three parts and give each pan t\\eniy minutes later than the preceding. The total amount being one half ihat of the adult. (3) The Beta-naphthol Treatment. The preliminarA' treatment as before. The beta-naphthol must be fresh and kept cool. It is a popular remech' \\\i\\ the I'rench. ]^ Beta-naphthol, finely-powdered ... ... ... 30 grains Mucilaginis tragacanthae ... ... ... ... i drachm Aciiiifi menthfe piperita ... ... ... .... 5 drachms Give a purge overnight. At 6 a.m. give full dose as above. At 8 a.m. repeat. At 10 a.m. repeat. At 12 noon give a saline purge. (5') The Oleum Chenopodii Treatment (Dav and Ferguson). Preliminary treatment as above. Give the above oil in three doses of 16 drops on sugar at two hour intervals. Give castor oil purge 17 grm. with chloroform 3 grm. 320 DISEASES DUE TO HELMINTHS This oil has a disagreeable flavour and is expensive. In any of these methods three repeated treatments may be necessary, in which cases allow an interval of four to seven days. In some cases it is difficult to clear out all the worms even with the repeated courses. The ana?mia should be treated on general lines. Iron, grains 30 or more should be given daily. Reduced iron, ferric perchloride, ferrous sulphate, iron carbonate (Blaud), and the ammonia citrate are useful in the order named. Arsenic and digitalis can also be given. Points of Difference between the Ankylostome duodenale and THE Negator americanus. A. duodenale The worm is thicker and longer The bend of the neck is slow The mouth capsule is large and thick The oesophagus is long and tubular The teeth are small and shallow, with a large brownish pear-shaped hook There are two separate spicules in the male The dorsal ray of the bursa has three prongs N. americanus The worm is thinner and shorter The neck bend is sharp The mouth capsule is small and thin The oesophagus is bent and bulbed The teeth are large pointed, spheroidal and colourless There is one spicule in the male The dorsal ray of the bursa has two prongs Table indicating briefly the Mode of Infection by Helminths. (After Daniels.) Worm Leave Man Life ouiside Man Re-enter Man Ascaris lum- As eggs with un- Development of egg con- Eggs containing embryos b r i CO i des developed con- tents change into em- are swallowed, usually and Tricho- tents bryo in water or on with food c e p h a 1 u s earth dispar Oxyuris ver- Adults leave rec- Eggs undergo little or no Eggs containing embryos micularis tum and deposit further development, are swallowed — usually eggs on skin as embryo is already remtroduced into the formed same patient Strongyloides Embryos passed Develop, become sexually Enter man with food, or intestinalis with faeces mature, and multiply in any substance con- sexually taminated with infected earth, or through the skin Ankylostome Eggs ; division of Embryos hatch out and Embryos re-introduced by duodenale egg contents develop to a consider- the mouth, probably aiid Necator has commenced able extent in moist in food contaminated americanus earth with earth. Also enter through the unbroken skni Trichina spir- Embryos develop Only in animals eating Usually from eating pork alis to their limit in the infected flesh containing encysted the muscle of larvas the host F. bancrofti... Embryos ab- Embryos develop in mos- Larvae discharged by mos- stracted with quito, into larvae with quitoes on man and blood by mos- an alimentary canal enter through the un- cjuiloes broken skin PRESERJ\iTION AND EXAMINATION OF HELMINTHS 321 Worm F. loa F. medinensis T. saginata ... T. solium T. echinococ- ciis 'J'rematodes, both Fascio- lidge and Paramphis- tomidae Schistomidte Leave Man By Chrysops dim- idiata Embryos dischar- ged into water Oncospheres Oncospheres "Hydatid cysts." Does not leave man, who is an accidental host Eggs with unde- veloped ovum in feces, or in one instance in sputum Eggs with unde- veloped ciliated embryo, mira- cidium, with urine or feces Life outside Man Similar development in salivary glands of Chrysops Embryos swallowed ? by chrysops and there develop to a certain extent In muscle of cattle (Cys- ticercus bovis) In muscle of pig (Cys- ticercus celluloste) Adult worm in intestines of dogs, &c., who derive infection from food, offal from slaughter- houses, &c. Ovum develops in water, embryo enters molluscs or fish and there multi- plies asexually, produ- cing ultimately young flukes, cercariie, encys- ted on vegetables or free swimming in water Embryos escape from egg when urine or fasces are diluted. Further development, if any, outside man, is un- known Re-enter Man Cyclops containing devel- oped larvat swallowed by man Eating beef containing Cysticercus bovis Eating pork containing Cysticercus cellulosa" By swallowing oncosph- eres from fteces of infected dogs Swallowed by man on vegetables or in water or in undercooked fish Probably enters through the skin during bathing THE PRESERVATION AND EXAMINATION OF HELMINTHS. (After Daniels.) SMALL NEMATODES. Preservation. (i) Shake up the live worms in a i per cent, salt solution, to remove mucus. (2) Kill by dropping into boiling 70 per cent, spirit and allow to cool. (3) Transfer to fresh 70 per cent, spirit for storage. For Clearing and Mounting. (i) After treating with stages i and 2 as above, transfer to a mixture composed of 70 per cent, spirit, 95 parts with 5 parts of pure glycerine. (2) Evaporate in a water or paraffin batli until all the alcohol has gone. (3) Mount in glycerin jell v. (4) Ring with gold size. Examination without Mounting. (i) Take from the 70 per cent, spirit and place in methylated spirit. 21 322 DISEASES DUE TO HELMINTHS (2) Transfer to colourless cold tar creosote, allow to clear, and examine in that fluid. After the examination is concluded pass through methylated spirit back to 70 per cent, spirit as before to store. LARGE NEMATODES. These are treated in the same way as small ones except that they cannot be cleared and mounted by the glycerine method. SMALL TREMATODES. Preservation. (i) Place alive in a test tube one-third full if i per cent, saline, and shake vigorously. (2) Add to the test tube rapidly an equal quantity of saturated solution of sublimate. (3) Shake vigorously for three minutes. (4) Transfer to 70 per cent, spirit to store. Examination without Mounting. As for small nematodes. In order to make stained and mounted specimens : — (i) Transfer from 70 per cent, spirit to a i per cent, solution of alum to which is added a little ha^matoxylin, until the whole is a light claret colour. The ha^malum solution (ha?matin, 2*5 grm., absolute alcohol 50 c.c, alum 50 grm. or to saturation, water 1,000 c.c.) diluted with distilled water gives good results, and so does a weak solution of carmine, but in that case longer staining is required. Leave in this one to four days. (2) Decolorize slighllv with ^ per cent, acid water. (3) Wash well. (4) Dehydrate with spirit and oil of cloves. (5) Pass through zylol and mount in balsam. LARGE TREMATODES. Preservation. (i) Drop alive in a i per cent, saline and shake vigorously. (2) Add formalin (commercial) to this to make about a 10 per cent, solution, and shake vigorously until death occurs. The specimens can be kept in 10 per cent, formalin. Examination. This is best done by embedding and cutting sections. To mount Specimens whole. (i) Press between two slides wliilst alive, and drop into 70 per cent, spirit. (2) Stain and clear as in small specimens. HIRUDINIASIS 323 CESTODES. Preservation. (i) Shake gently in i per cent, saline. (2) Add formalin to this to make a 10 per cent, solution and shake pfentlv until thev die. The specimens can be stored in 10 per cent, formalin. To stain and mount Segments. (i) Place alive in weak glycerin, faintly coloured with carmine, and leave until stained, or dilute hiemalum may be used. (2) Press between two slides and drop into methylated spirit. They should remain in this for twenty-four hours. (3) Remove the pressure and place the segments in fresh methylated spirit for an hour or so. (4) Clear in oil of cloves. (5) Pass through zylol and mount in balsam. Creosote may be used to clear instead of oil of cloves. The Preservation of Helminth Ova in Faeces. Method (i). Alcohol, 70 per cent., with 5 per cent, glycerine added, is raised to boiling point. Fluid faeces, or faeces made fluid by dilution with saline, are poured into the boiling alcohol, stirred, and then set aside to inspissate in a warm place. When the fasces have become a sticky mass, sufficient pure glycerine is added to make a soft paste (Leiper). Method (2). To fluid faeces add equal parts of Langeron's lactophenol. This latter consists of carbolic acid one part, lactic acid one part, glycerin two parts, and water one part. Shake vigorously. This mixture will form a pasty jelly and will keep indefinitely. A permanent preparation can be made at any time by stirring a small portion into a loop of melted glycerin jelly on a slide, a cover glass is placed on the jelly, and when this is set the preparation is completed by sealing with gold size (Leiper). HIRUDINIASIS. DEFINITION. An invasion of the mouth, nose, pharynx and larynx, or an afi'ection of the skin by leeches, a group of unsegmented worms allied to Chastopoda. 324 DISEASES DUE TO HELMINTHS >ETIOLOGY. Leeches are troublesome chiefly in the Near East, Ceylon, Philippine Islands, Japan, Australia and the Asiatic and the American jungle. There are many species but few readily attack man. There are the : — (i) Land leeches or Hctmadipsa. These live in the damp jungle country, as the ILemadipsa ceylonica of Ceylon. They rest upon twigs and leaves await- ing the presence of some mammal to attack. '1' '^1\ They are very. active and are able to pass through very narrow orifices such as the lace-hole of a boot. Their bite is painless and the first indication of their presence may be that the boot is full of blood. In such cases there is often some local inflammation and sloughing. (2) Water leeches, or Limnatis. These live in springs like the Limnatis nilotica and are trouble- some to man when he drinks the spring water. The ..Ml thirsty traveller at dusk is usually the victim. The salivary glands of these parasites open into the mouth and secret a fluid which prevents the coagulation of the blood When it has gorged itself it drops off but the bleeding continues. The pharynx of the leech has a powerful mus- cular sac which bv contracting and dilating forms a sucking pump. The blood is stored up in the crop and its caecal diverticula and onlv a little is used daily for food. ^> The internal organs of the leech. The creature has been opened from the dorsal surface, and part of the intestine has been removed. The testicles, with vas deferens, may be seen between the blind ducts of the intestine ; beyond these on either side the segmental organs. The female genital organs are in front of the most anterior pair of testicles. (After Kennel.) SYMPTOMATOLOGY. This is according to the variety and position of the leech. There may be bleeding from the nasal or buccal cavities which may indicate that the leech or leeches are anvwhere in the respiratory tract to the trachea and the deglutition tract to the stomach. There may be irritating cough and dyspnoea. Bleedinp- from the skin with land leeches. O Anaemia. TREATMENT. Saline solution will loosen them when it is possible to apply it. Saline solution upon the clothing or boots of jungle travellers is POROCEPHALOSIS 325 protective. A " clip in the briny" witJi one's clothes on before com- mencing a march is sufficient in most cases. Cotton wool soaked in 30 per cent, cocaine applied to the parasite will paralyse it and cause it to drop off, but if the leech is in the larynx the patient must be held with the head downwards or the leech will drop into the trachea. Leeches should not be removed forcibl}-. The gastric juice is said to kill them. Leeches are not known to carrv disease. POROCEPHALOSIS. There are twenty known species of Porocephalus, two of which occur in man. They belong to the parasitic Arachnoidea and Lingua- tulida. They have elongated vermiform bodies and a continuous coelom. The female is 9 to 12 cm. long, the male 3 to 4*5 cm. long by 2 to 4 mm. broad, with twenty-six to thirt\' rings. They are commonly found in the nasal cavities and lungs of pythons and snakes. The eggs probably pass from these reptiles into water and thence into man. These eggs develop into larvae and nymphas which may then become encysted in the lungs or the liver of man, or thev may move freely in the small intestine and even, at times, enter the peritoneal cavity. The P. armillatus and the P. moniliformis affect man. The\' are a bright lemon yellow colour when fresh. DISTRIBUTION. The P. armillatus is found in Africa only. Chiefly in Egvpt, West Coast and the Congo. The P. moniliformis is found in Ja\a, Philippines and India. PATHOLOGY. The larvae are found coiled up in cysts of the liver and lungs. Here they become nymphfe, leave the cysts and wander about the body . They may pass into the lungs causing bronchitis or broncho- pneumonia. Or into the peritoneal cavity causing peritonitis. Or into the intestinal tract causing diarrhoea. SYMPTOMATOLOGY. The distinctive symptoms are not appreciated until they become terminal. Then one has emaciation and weakness associated with an 326 DISEASES DUE TO HELMINTHS attack of bronchitis or pleurisy. There may be cavities in the lungs and offensive sputum which may contain the parasites. One patient was known to expectorate from 75 to 100 of these parasites. The liver is usually enlarged. The condition has been mistaken for phthisis. There is no known effective treatment. SECTION IV. DISEASES OF UNCERTAIN ^ETIOLOGY. PELLAGRA. BERIBERL EPIDEMIC DROPSY. HILL DIARRHCEA. SPRUE. PHLEBOTOMUS FEVER. VERRUGA PERUVIANA. YELLOW FEVER. NOTES ON THE STEGOMYIA CALOPUS (FASCIATA). SPOTTED FEVER OF THE ROCKY MOUNTAINS. DENGUE FEVER. TYPHUS FE^VER, HEMOGLOBINURIA. FAVISM. HEATSTROKE. SOME UNCLASSIFIED FEVERS AS : — Japanese River Fever. Nasha Fever. Pigmentary Fever. Archibald's Fever. Hyperpyrexial Fever. Bacillus Asiaticus Fever. Double Continued Fever. The Macular Fever of Tunisia. Low Intermittent Non-malarial Fever. Rat-bite Fever. Five-day Fever. Trench Fever. THE EXANTHEMATA. TROPICAL HAY FEVER. TROPICAL NEURASTHENIA. ENDEMIC PERIPHERAL FEVER. ENDEMIC PARALYTIC VERTIGO. LATAH. AMOK. ENDEMIC FUNICULITIS. EPIDEMIC GANGRENOUS RECTITIS. 328 DISEASES OF UNCERTAIN ETIOLOGY INFANTILE BILIARY CIRRHOSIS, GOITRE. CLIMATIC BUBO. GOUNDOU. BIG HEEL. AINHUM. GANGOSA. CHAPPA. PONOS. TROPICAL LIVER. BOOMERANG LEG. WHITMORE'S DISEASE. ONYALIA. ^ AFEBRILE SPLENOMEGALY PELLAGRA 329 DISEASES OF UNCERTAIN ^ETIOLOGY. PELLAGRA. (Pellagra — rough skin; " pelle," the Italian word for skin, " agra " meaning rough.) DEFINITION. A chronic endemic disease of unknown causation with cutaneous, gastro-intestinal and nervous symptoms which usually recur in the spring and autumn. DISTRIBUTION. Perhaps Francis of Assisi suffered from it. It was well known by medical men to be widespread in Italy at the beginning of the eighteenth century. Casal discovered it in Spain in 1735. Also present in Portugal and France. Some of Napoleon's soldiers became infected in Italy. It is still very prevalent in Austria and Hungary. Roumania has 200,000 cases (Babes). Reported in the British Isles in i860. In Scotland and the Shet- lands in 1909. It is also found in Egypt, West Indies, Mexico, North American Indians, India, Straits Settlements, Philippine and Sandwich Islands; Africa, Europe, Asia, Oceania, America, and perhaps is world-wide. It is found chieflv in country places and along- certain streams, less seldom in towns. Attacks most frequently appear during the late springtime and the autumn. It tends to disappear in the winter. None are exempt. Females are attacked to males as two is to five. Jews are rarely affected. It is tO' be noted that those engaged in agriculture appear to be affected most. ETIOLOGY. The chief theories are : — (i) The Deficiency Theory. (2) The Maize Theory. (3) The Parasitic Theory. (4) The Mineral Acidosis Theory. (1) The Deficiency Theory. The lack of some nitrogenous complex in the food. When steam-milled mealie bread alone w^as supplied to prisoners 330 DISEASES OF UNCERTAIN ETIOLOGY in the \'ictoi"ia jail in Rhodesia the disease broke out; when hieat, vegetables and rice replaced the mealie the epidemic ceased, and when hand-milled maize was obtained the improvement was " immediate and almost magical " (Nightingale). But Pellagra ma}^ occur in people having the best of suitable food. (2) The Maize Theory. Pro. (i) The liistory of maize production and consumption. Maize is native to America, where it has been found in the graves of the Incas. Columbus or his followers introduced it to Europe, but it did not grow well in the British Isles, which therefore remained free from the disease until the nineteenth century, when maize was imported in larger quantities and used in the preparation of cakes, porridge, pop-corn and whiskey. It grew well in Spain, Ital}' and France, Avhere Pellagra appeared. (2) In the Nile delta there is plenty of maize and plenty of pellagra, but higher up the Nile millet is used instead of maize, and pellagra is found less frequently. (3) In Colombia it is said to be found only in people who take the drink made from fermented maize called "chicha." (4) Maize is found more or less all over the world, so is pellagra. Con. (i) There are entire districts in Italy and Brazil where the people have never lived on maize, but where pellagra is prevalent. Other districts where bad maize is used almost exclusively there is no pellagra. (2) Relapses occur in jails over long periods, five to fifteen years, where maize is rigidly excluded. (3) Pellagra was present in Europe before maize was intro- duced, e.g., the attack of Francis of Assisi, before the time of Columbus. (4) Prophylactic and curative measures based on the maize theory have yielded very little result. Progressive symptoms continue after absolute prohibition of the cereal (Alberto Cencelli). Various Maize Theories. The Photodynamic Theory (Raubitschek). Pro. An exclusive maize diet proves deleterious to white mice and guinea-pigs if such are exposed to the sun. PELLAGRA 331 Other cereals do the same. It is maintained that photo- dynamic substances are introduced by cereals into the blood. These with sunlight produce toxins and cause pellagra symptoms. In darkness mice have been cured. Cox. Hirschfelder searched the blood of severe cases for the photodynamic substance, but failed to find any. Pellagra occurs in jet-black negroes, whose pigment protects them consjderablv from the sun's rays. The Deficiency Theory. Pro. Insufficient protein in maize food. Con. Many live on rice and potatoes which contain less nitrogen ratio than maize. The Toxicity Theory. Some claim that there is an — Individual susceptibility to maize intoxication. Others that there are toxins produced in the spring bv the germina- tion of maize. Others that there are toxins generated in the bowel by aid of the B. coli. Others that there are alkaloidal and other poisons in fermenting maize. The Infectivity Theory. The most popular view. The maize is cultivated and harvested under unfa\ ourable conditions, and stored in damp places and be- comes mouldy. Ilirsch states that after a bad season cases increase. This infection may be : — (i) Func^i as Pernicious glaucum, Aspergillus, &c., the fungi or their toxins. (2) Bacteria as B. solanacearum, B. subtilis, B. pellagr^e. (3) The Parasitic Theory. This is supported by the Illinois Commission. A. Vegetable Parasite, e.g., Tizzoni's streptobacillus. He claims to have found it in the blood, cerebrospinal fluid, and viscera of pellagrins after death. Others refute this. B. Animal Parasites. (i) A slender nematode worm (Filaridae alessandrina) in drinking water. (2) A phase of ama?bic dysentery (Long). (3) A protozoan infection spread by a biting fly (Sambon). 332 DISEASES OF UNCERTAIN .ETIOLOGY Pro. Sambon supports his view c!T; tlie basis of its being protozoan because : — - (i) There is a mononucleosis present in the blood. (2) There are long intervals of quiescence followed by relapse. (3) There is a constant and characteristic topographical dis- tribution. (4) The symptoms, course, duration, and morbid anatomy are similar to those found in other parasitic diseases. (3) Sambon found a spirochcCte in a bulla on the hand of a severe pellagra case. Con. No parasite has yet been found. Fluids from pellagrins have not reproduced the disease when injected into other animals. A biting fly is bhivicd because: — It is a disease of rural districts essentiallv. It is in some way related to moving water. It has a definite seasonal influence, spring and autumn, which coincides with the appearance of certain flies. It affects labourers in the field. It is not contagious (Goldberger). Young children and whole families often are readilv affected in an endemic centre. Sambon suggests one of the simulidcv because: — Their larv^ live in running water. They have two seasons, spring and autumn, when they attack man and beast in swarms. But They are not found in the Xile, where pellagra is common. The Illinois Commission does not agree on this point. (4) The Mineral Acidosis Theory. The findings of Professor Alessandrini and Scala of the Pellagra Commission of Rome may be summarized thus : — Pellagra is strictly localized and limited to areas where the water drunk has almost exclusively been in contact with clav. Clay is silicate of alumina. The action of rain water upon tliis produces bv hvdrolvsis silicic acid and hydrate of alumina which pass into the water in a colloidal form . A colloidal silica-alumina is formed, some as a deposit and some remaining in suspension. PELLAGRA 333 The inp-estion of this latter causes a retenlion of salts in the tissues resulting- in their excessive fixation which, when liberated in excess, causes the pathological lesions of pellagra. They aftirm to have considerably improved, if not to have cured, cases bv muscular or subcutaneous injections of neutral citrate of sodium. Dailv injections of a lo per cent, solution of trisodic citrate were given. The acidosis is said to be neutralized by it. PATHOLOGY. There is an infiltration of the true skin and oedema of the con- nective tissue. The rete Malpighii is infiltrated with cells, the stratum corneum is thickened and shows hyperkeratosis. A blood examination shows a reduction of the red cells. Fattv degeneration and characteristic deep pigmentation of all viscera. Wasting of all muscles. Intestinal mucous membrane hyperfemic, sometimes ulcerated. Liver and spleen atrophied. Brain and cord show chronic leptomeningitis with much thicken- ing, a perivascular cellular infiltration with pigmentation and degenera- tion of nerve filaments. Ventricles distended. Brain shrunken. Lateral columns and crossed pyramidal tracts affected, mid-dorsal region most marked. The condition is not unlike G.P.L SYMPTOMATOLOGY. Incubation not known, but the disease has occurred in a child three months old. There is no support for heredity. The skin eruption has occurred in a healthy person two months after visiting a pellagrous area. Onset, insidious. A sunburn may appear on the back of hands or feet, face and neck. It burns and may blister. Perhaps sore mouth, giddiness, muscular weakness. In a few weeks the redness fades and pigmentation occurs; the skin may be thickened. In a few days there is desquamation of these areas, the underlying skin being- apparently normal. Autumn comes and the patient gets better. The next spring, or several seasons later, it recurs surely and more severely ; dermatitis and bulk-E may appear; inflammation of the whole mouth, tongue pro- truded with difficulty, edge may have a greyish membrane, there is enlargement of the parotid gland, dyspepsia, abdominal pains, diarrhoea, or even dysentery. Marked vertigo, the patient may fall, weak, trembling in head, arms and legs, melancholic, highly emotional^ patient may seek to drown himself. He has burning pains at night and may go to the river to relieve them. Someone pulls him out of the water and reports that he was 334 DISEASES OF UNCERTAIN ETIOLOGY seeking to drown himself. He lias abdominal pains, and thinking that the cook has been poisoning him, he seeks to kill the cook and finds himself in an asylum. There is reason in his madness. Winter comes and with it relief, but the skin does not become normal. With repeated attacks the skin changes are marked, the mind Pellagra in Egypt. Photograph by F. M. Sandwith, M.D., M. R.C.I'. becomes permanently affected, melancholic or maniacal symptoms set in. Pain about the back at either side of the dorsal spine, over spinal nerves in dorsal and lumbar regions. K. J.'s plus later. Patient ^alks with his legs apart, may fall backwards or forwards Facies of anxiety and mental worry, sleeplessness, discontent, and mental depression or excitement, and irritabilit}' or stupidity. PELLAGRA 335 There is often loss of memory. He may refuse food. Dementia may develop. There may be ptosis, hemianopsia, diplopia, amblyopia and mydriasis. In extreme cases the bladder is paralysed, there is profuse diarrhoea, dropsy and death. This latter in five to fifteen years from onset. Very rarely there are acute cases lasting only a few months. Skin eruption shows congestion, inflammation, thickening and pigmentation of a light sepia tint. Atrophic wasting. The tongue sheds its epithelium and is known as Sandwith's bald tongue (also present in sprue and scurvy). Blood pressure is low. Pulse-rate increased, extremities cold, skin often bluish. Sexual power is diminished. Saltish taste in mouth common. Temperature but little altered. Emaciation marked. Complications and terminal affections are naturally numerous. To sum up : — (i) Cutaneous signs are : a remitting erythema and dermatitis of the exposed parts. The skin loses its elasticity. (2) Gastro-intestinal signs are : salivation, stomatitis, oesophagitis, dyspepsia due to hyperchlorhvdria, nausea, vomiting, diarrhoea, dysentery symptoms and constipation. Proctitis with anal excori- ations. (3) INIental symptoms are : vertigo, melancholia, myasthenia, trem- blings, curious delusions, irritability. (4) Genital symptoms are : intense vaginitis, a sero-sanguineous discharge with excoriation of surrounding parts. Mucous membrane a scarlet red like that of the mouth. (5) Nephritic symptoms are : acute or chronic nephritis in many cases, albumin, and casts in varying proportions. DIAGNOSIS. From acute dermatitis as erythema solare, &c., by the gastro- intestinal and nervous symptoms. Fro'm chronic dermatitis as eczema by pigmentation, peculiar localization to the exposed parts chiefly. Ichthyosis is all over the body and congenital. Gastro-intestinal symptoms as sprue by their not having an eruption. PROGNOSIS. Be always guarded. Early mild cases may recover if removed and placed in good suitable surroundings. 336 DISEASES OF UNCERTAIN ETIOLOGY Cases have relapsed after two to fifteen years. It is not easy to say when a person is free from the disease, once they have been attacked b}' it. It is better to speak of recovery from an attack than a cure of the disease. Recovery is more frequent and more permanent in children than adults. The death-rate in the initial attack is i5;8 per cent. (i,i8o cases). The death-rate in the recurrent attack is i2'3 per cent. (i,i8o cases). It is higher in Black than White races (Siler, Garrison and MacNeal). Low blood pressure may cause death after exertion. Typhoid complications have a high mortality. Complications such as ankylostomiasis are always unfavourable. TREATMENT. There is none specific. Protect from the sunlight. Use soothing ointments. Diet important, fresh fruit and fruit juice, meat broths, miik. Avoid starchy foods. Dilute nitric acid 15 to 30 minims in four ounces of water, thrice daily, one hour before meals. A 10 per cent, solution of trisodic citrate, intramuscular or sub- cutaneously. Atoxyl 3 grains daily, intramuscularly, are good. Liq. arsenicalis in small doses can be tried. Radio-active serum injections are on trial. Later one can give eggs, meats, fish, green vegetables and fresh fruit with dilute nitric acid continuously. Remove the patient to a non-pellagrous area. The Italian Government prohibits the sale of bad maize. The line of treatment largely depends on the causative view held by the practitioner. BERIBERI. DEFINITION. An acute or chronic, endemic or sporadic disease of unknown causation ; characterized by a degeneration of peripheral nerves asso- ciated with gastric disturbances, oedema and cardiac failure. DISTRIBUTION. Eastern Asia, Japan, China, Philippines, Indo-China, Java, and Malaya, also in other parts frequently where Chinese and Indian BERIBERI 337 coolies are imported. It has been reported in the Congo (Van den Branden). It is the scourge of many mines and plantations in the Malay and Eastern Archipelago. HISTORY. Beriberi probabl}- attacked the Roman army in Arabia (24 B.C.). In the Straits Settlements and Malaya (population 1,250,000) there have occurred 150,000 cases with 30,000 deaths in the Government Hospital during the last twenty years (Bradden). In the Japanese navy, prior to 1884, 23 P^r cent, of the sailors were continuously disabled by it. In the Japanese army, during 1904 and 1905, 24 per cent, of the total sick and wounded were its victims. The Government of Malaya pays ^10,000 per annum for direct hospital cases. Labourers, sailors, soldiers and prisoners are most frequently attacked. It is common in large cities, and overcrowding favours its spread. It is very common amongst Mohammedans, who do not take alcohol. iETIOLOGY. It is a deficiency disease. It tends to be racial in young adults between fifteen and thirty, but no age is exempt. Disturbances of the soil and high atmospheric pressure are pre- disposing factors. The exciting cause is unknown, but theories are legion. The chief are : — (1) Arsenical Poisoning (Ross, 1900). It is based largely upon finding arsenic in the hair of recent beriberi patients. Herzog failed to find it in ten patients. (2) Oxalate Poisoning (Treutlein). When oxalates were given in the food of fowls beriberi symptoms set in. The acid was supposed to remove the calcium salts and so predispose to nerve degeneration. Excess of calcium salts was found in the urine of beriberi patients. (3) Carbon Dioxide Poisoning (Ashmead). The result of excessive inhalation of carbon dioxide. Overcrowding alone, however, does not cause it. 22 338 DISEASES OF UNCERTAIN ETIOLOGY (4) Food Poisoning. Ichthyotoxismus from eating bad fisli, but those not eating fish have developed it. Sitotoximus due to eating rice without the husks or when stale or badly kept. Some blame a parasite living in the husk which is ingested when the rice "is insufficiently cooked, biit it has appeared where the people never eat rice. c d a, a highly milled or polished rice stained by Grams iodine solution. The starch, being completely exposed, stains uniformly a dark blue. This rice will produce beriberi. b, an undermilled rice stained in the same way. The unstained areas show where the adherent pericarp has protected the starch from the action of the iodine. This rice will probably not produce beriberi. c, a sample of undermilled rice that contains still more pericarp. The use of this rice will surely prevent the development of beriberi. d, the unhusked grain or "palay." When the husks are removed by hand pounding, a rice like c or /^ is produced. (5) Food Deficiency. This is the view held most widely. Deficient nitrogen. The peripheral layers of the rice, lost in milling, contain a vitamine substance. This is necessary for BERIBERI 339 the metabolism of nerve tissue, and if not supplied in food, beriberi appears (Funk). Increase in the food of nitrogen for Japanese sailors was followed by less beriberi. Deficient fat. An epidemic at Chaudabum was supposed to be stopped by an increase of fat in the food. Deficient phosphorus. Normal rice contains 0*4 per cent, of ? pentoxide. If less it is a dangerous rice (Fraser). Deficient vegetables with an infection. The disease disap- Section of myocardium from case of beriberi, showing segmentation and fragmentation. peared when a sufficiency of vegetables, chiefly potatoes, was given (Fales). The deficiency causes the micro-organism to flourish (Fales). Fletcher concludes that uncured rice is either directly or indirectly a cause of beriberi, the actual cause being either: — A poison contained in the rice. Protein deficiency. Bad nutrition resulting from uncured rice rendering the patient liable to invasion by the specific organism. 22A 340 DISEASES OF UNCERTAIN ETIOLOGY (6) An Intoxication (Manson). Caused by some germ living out- side the bodv, in the soil, house or ship occupied by human beings under certain conditions of temperature and moisture; the toxin inhaled or swallowed causes the disease. Evidence. Wiien patients are removed from an endemic area they begin to recover. The germ ma\- be carried from place to place. The same ship redevelops the disease annually on reaching the Tropics. Section of myocardium from a case of acute wet beriberi, showing more advanced fragmentation. (From article by Herzog, and plate lent by the courtesy of TAe Philippine [onrnal of Science.) (7) An Autointoxication (Deurch). This condition is asserted to be produced by substances formed in the body. (8) Parasitic Causes (Sambon). The parasite in some way enters the body. Insects such as cockroaches may carry it. The infection is not by the fceces (Daniels), nor by air or water. BERIBERI 341 Perhaps an intermediale host, such as lice, is necessary (Daniels). It may he the P. capitis as such have a tendency to clins" to one race. Amongst the suspected parasites are : — Various protozoa, nemathehninths, bacilH, fungi, cocci, and a specific bacillus causing duodenitis, the symptoms of this latter arising from the absorption of the toxin as in diph- theria (Hamilton Wright). Daniels denies duodenitis and thinks that perhaps a protozoan may yet be found. Section of myocardium from a case of sub-acute wet beriberi, hsematoxylin-eosin strain, showing loss of striation, vacuolation and granular degeneration. (From article by Herzog, and plate lent by the courtesy of The Philippine /ournal of Science.) PATHOLOGY. Blood taken from a beriberi patient and injected into a cat produced a fall in B.P., with dilatation of the gastric vessels, also those of the intestines and liver. The right heart was dilated and there was general venous engorgement. P.M. There is always some oedema in acute cases. Often froth at the mouth. The body is either swollen with dropsy or emaciated. 34'2 DISEASES OF UNCERTAIN ETIOLOGY Longitudinal section of jiopliteal nevve from a case of acute beriberi. VVeigerl-l'al stain, showing different degrees of degeneration of the medullary sheath. (P'rom Ilcrzog, plate lent through the courtesy of 7/ie Philippine Journal of Science.) Fibre from sciatic nerve of fowl suffering from polyneuritis (Marchi method), showing advanced degeneration. (From Vedder and Clark, and plate lent through the courtesy of The Philippine potirnal of Science.) BERIBERI 343 The subcutaneous tissues are usually oedematous. The veins are filled with dark fluid blood. There is serous fluid in the abdomen, chest and pericardium. The mucous membrane of the trachea and larynx may be oedem- atous with the lumen full of fluid. The lungs are congested and oedematous. The right heart is dilated and fatty degeneration is present. The muscles show atrophied and normal fibres side by side. There is nerve degeneration of the bulbar nuclei, thoracic ganglia, vagal nerve endings and peripheral nerves. The congested liver sometimes shows h^emorrhagic patches. The kidneys show cloudy swelling and sometimes hjemorrhages. Tile meninges are hyper^emic with an increase of fluid in the ventricles. There is marked degeneration in the bulb. Thus summing up one finds : — Degeneration of nerves. Secondary degeneration of muscles including the heart. Excess of blood in the right heart and veins. Serous effusions into the cavities and cellular tissue. Oedema of the lungs. VARIETIES. Atrophic, Dry or Paralytic. Hypertrophic, Wet or Dropsical. Mixed. Infantile. The incubation is unknown. (1) The Atrophic, Dry or Paralytic Variety. Insidious onset, malaise, dull pain in epigastrium, tenderness on pressure, headache, palpitation, dyspnoea, subcutaneous oedema, K. J.'s slightly increased, sense of heaviness in the legs, difficulty in walking, K. J.'s disappear gradually. After the first week there is usually a peculiar high stepping gait, tender calves, "pins and needles," anaesthesia and paraes- thesia. The anterior tibial and peroneal muscles are chiefly affected. Sometimes the forearms are aft'ected with diminished grip and wrist drop. There is no tremor but the patient is often too weak to hold a bowl of rice. The sphincters are normal. There is wasting of muscles, the paralysis ascends from the calf to the thigh, gluteal region, arms, abdomen, diaphragm, intercostals and larynx. There is loss of sense of heat, pain and cold, but the areas do 344 DISEASES OF UNCERTAIN ETIOLOGY Beriberi : oedematous variety. Japanese immigrant in Fiji. Beriberi : atrophic variety, showing muscular atrophy and drop-wrist. Japanese immigrant in Fiji. Photographs by Henry Noble Joynt, Labosa, P'iji. BERIBERI 345 not correspond with tlie segmental or nerve areas. It is very patchy. Diffuse apex beat, dilated right heart, loud systolic murmur, reduplication of the pulmonary second sound, palpitation and epigastric pulsation. The pulse rate is increased and the tension diminished. With increasing oedema the urine is diminished, when the oedema is clearing up the urine is increased. Urea and chlorides are diminished, phosphates and indican increased. There is cutaneous oedema ,of the legs, scrotum, abdominal wall, face and arms, with exudation into the abdominal cavity, pleural sacs and pericardium. Digestion is fair but a good meal increases the epigastric dis- tress. The bowels are often constipated. The temperature is normal or sub-normal. The patient may remain like this for weeks or montiis, some- times better, sometimes worse; he mav recover with or without paralytic deformities or he may die suddenly. If fever occurs it is a complication, usually T. B., malaria or dysentery. One attack predisposes to another. The patient may die at any time during the attack. There is lymphocytosis 30 to 68 per cent. (2) The Hypertrophic, Wet or (Edematous Variety. This variety is usually somewhat acute. There is nausea, epigastric pain, clean tongue, throat con- gested, cardiac oppression, epigastric pulsation, palpitation, dyspnoea, pulse rate much increased by the slightest exertion, hcemic murmurs, right heart dilates, urine diminishes, there is effusion in'o the cavities of the pericardium, pleural and peri- toneum. The oedema is somewhat localized and fugitive. It is firmer than in Bright's disease. There are patches of anaesthesia and In-perassthesia in the course of the anterior tibial and musculo-cutaneous nerves. The paralysis may be slight or extensive. The heart becomes more embarrassed, the lungs engorged, the nostrils dilate, the mouth opens in the struggle for breath, the pupils dilate, the face becomes cyanosed, the extremities cold, the patient becomes unconscious and dies. This may take place in a few hours. Some account for ihe uxlema b\- suggesting that the patho- 346 DISEASES OF UNCERTAIN JF.TIOLOGY logical condition of the nerves will not permit of the regulation of transudation and absorption of fluid in the connective tissues. Acute wet beriberi. Great oedema of legs and feet. (From Herzog ; plate lent through the courtesy of The Philippine [oiimal of' Science.) (3) Mixed Variety. There is oedema over the shin, feet, flanks, sternum, and the root of the neck. Some hypera^sthesia, paresis and ataxia. BERIBERI 347 The K. J.'s are diminished. Heart as before. The general heaUh is unaffected. Some appear almost normal, others lie like logs. Some appear to be dying one day and seem well the next. Some are like skeletons while others are bloated with dropsy^ and again others have just enough dropsy to hide the muscular wasting. The laryngeal muscles are more often affected so that coughing is difficult. A profound diuresis converts a bloated victim into a skeleton in one day. (4) Infantile Variety. This is seen in the Philippines in the infants of beriberi mothers. They have a defective diet and suffer from oedema, dyspepsia and cyanosis. They often die suddenly. It causes 56 per cent, of the infantile mortality in the Philip- pines P.M. shows degeneration of peripheral nerves. Children seem to improve when weaned, suggesting that the cause may be due to cessation of absorption of milk. DIAGNOSIS. Look for : — Increase followed by loss of K. J.'s. Patches of anaesthesia or hypersesthesia on the legs. Pain on handling the calf muscles. Subcutaneous oedema, usually of the leg first. There is no albumin in the urine and no fever. In alcoholic neuritis, there is a history of habit and general trembling. In arsenical neuritis, there is abdominal pain and diarrhoea. In lead neuritis, there is colic and blue line on the gums. In dropsies due to heart there is history of rheumatism or other fevers. ,, ,, kidneys there is albumin in the urine and casts. ,, ankylostomiasis there are ova in the fasces. ,, epidemic dropsy there is fever and no anass- thesia or paralysis. ,, ,, mvelitis one finds relaxation of sphincters. ,, ,, pellagra there are skin eruptions and mental changes. Scurvy should be excluded by the spongy and bleeding gums. 348 DISEASES OF UNCERTAIN ETIOLOGY In diagnosing the condition from epidemic dropsy note : — (i) The Resemblances and (2) The Differences. (1) The Resemblances. There are epidemics in bolii diseases. The K. J.'s are altered. Wet beriberi. General .edema below ihe waist. Patient shows typical facial expression of air hunger. Taken on admission one week before death from heart failure. (By JefTerys.) There is a dropsical condition. There is some cardiac disturbance. Some disturbed cutaneous sensation. Some hyperc-esthesia in both. Death with dyspnoea or orlhopnc^a. BERIBERI 349 (2) The Diflferences. Beriberi (i) K. J.'s painful for 24 hours, then dis- appear in 95 per cent, of cases (2) Anaesthesia marked and not limited to dropsical areas (3) True paralyses even when no swel- ling is present (4) HyperjEsthesia is found in muscles on deep pressure (5) Death is more sudden and more dis- tressing, often in cases that have not been obviously bad (6) There is no antemia (7) Ihitial fever, dry skin, rashes, slight desquamation, not common 8) There is peripheral neuritis but the central nervous systen) is not affec- ted Epidemic Dropsy K. J.'s seldom if ever lost Anaesthesia is due to pressure on the nerve terminals about the dropsical patches Paralysis is due to the swelling and weight of the parts Hyperoesthesia is found when the skin is pinched up Death is the result of excessive pressure and the impediment of essential organs There is anaemia and ieucocytosis Initial fever, dry skin, rashes, and slight desquamation common All nerve tissues are affected somewhat equally PROGNOSIS. This varies considerably and is according to the country and the type of the disease. In Java the mortahty is 2 to 6 per cent. In Sumatra the mortahty is 60 to 70 per cent. Cardiac failure is always bad. To move much is fatal. Vomiting is a bad sign as it indicates that the vagus is involved. This latter feature is also manifested by the marked dilatation of the stomach and embarrassment of the heart. Death may be due to dilatation of the heart and syncope, hydro- thorax, pericardial effusion or paralysis of the diaphragm. The dropsical variety is more serious and uncertain than the paralytic. TREATMENT. This is purely symptomatic. Absolute rest in bed is essential. Digitalis or strophanthus is good. Amyl nitrite or trini trini should be handy. Venesection, eight ounces to relieve the right heart when necessary. Oxygen during dyspnoea. For paralyses, strychnine, massage and electricity to prevent atrophy and cramps. Removal from the supposed site of infection as soon as possible. Atropine, one 150th to one 50th grain, hvpodermicallv, or tincture of belladonna for dyspnoea (Braddon). Plenty of good nourishment, in small quantities. Full diet plus one drachm of yeast and 200 grm. of beans daily (Simpson). 350 DISEASES OF UNCERTAIN ETIOLOGY Yeast can be obtained as — Export yeast, of which give 2 ounces daily. Royal yeast cakes of 15 grm. each, give six daily. Fresh yeast from local bakeries, 250 c.c. daily. Pour into the yeast some boiling milk, stir it into a thin cream, add more hot milk and sugar to make it more palatable. It can be flavoured with essence of lemon. Foods should be given, as the patient improves, in the order men- tioned, viz. : Pea soup, eggs, fresh milk, brain, liver, sweetbread, kidneys, peas, beans, lentils, porridge, brown bread, meat, and fresh lemon-juice the whole time. An extract of the outer husk of rice after polishing daily, to infants (Vedder), in twenty-drop doses, two hourly. Eliminate rice from the diet as a rule. Good hygienic surroundings are essential. Little water is necessary. Disinfect the supposed infected house. EPIDEMIC DROPSY. DEFINITION. A specific endemic disease, lasting from three to six weeks with fever, profound anaemia and the sudden appearance of anasarca. DISTRIBUTION. In Calcutta, Assam, Daka, Mauritius. It disappears as the hot weather comes. In Mauritius, one tenth of the population was attacked with a mor- tality of 2 to 3 per cent. 729 died during the epidemic. In Calcutta the attack was more limited, but it had a mortality of 20 to 40 per cent. Europeans in these localities were not affected. ^ETIOLOGY. Both sexes of all ages are equally susceptible. The disease may remain latent, breaking out later. It is not very contagious if at all. How it is transmitted has not been ascertained. The causation is unknown. SYMPTOMS. In Mauritius the epidemic was introduced by diarrhoea and vomiting. There is itching and burning of the soles of the feet. Oedema was invariably present, the legs being involved first. HILL DIARRHCEA 351 It may affect the whole body. Fever to 102° F. is usually present at some time during the attack. Aching of muscles, bones and joints comes on early as a rule. Anaesthesia is not consistent and muscular paresis is rare. An eruption, erythema of the face and rubeola of the trunk and limbs was seen in Mauritius but less so in Calcutta. It comes seven days after the oedema appears and goes in ten to fourteen days. Cardiac dilatation with the concomitant symptoms was common in Calcutta. Pleural and pericardiac effusions, oedema of the lungs with their corresponding signs and symptoms were common in all but mild cases. Anaemia, wasting and prostration was marked. DIAGNOSIS. See " Differences " in Beriberi, p. 349. TREATMENT. This is symptomatic. Diuretics, diaphoretics and saline purges to remove the fluid. Tapping may be necessary to relieve the lungs or the heart. For cardiac weakness, digitahs or strophanthus. For attacks of orthopncea, nitrites and trini trini. Iron and arsenic during convalescence. HILL DIARRHCEA. DEFINITION. A gastro-intestinal catarrh occurring in high altitudes in the tropic s, with liquid, pale, frothy morning stools. It is somewhat epidemic in the Indian Hill Stations. AETIOLOGY. Causation unknown. Perhaps it is an infection, because good sanitation and good water diminishes its frequency. THEORIES. A diminished atmospheric pressure (Crombie). Irritation by mica in the water (Duncan). Fcccal contamination of water. Exposure to cold. Functional digestive disturbance in the low temper- atures of high altitudes (Bahr). PATHOLOGY. The mucous membrane of the stomach and bowels is congesttJ, there is also a proliferation of lymphoid and fibrous tissue. There is a thick layer of mucus but no ulceration. The tongue is seldom affected. 352 DISEASES OF UNCERTAIN ETIOLOGY SYMPTOMS. It begins soon after arrival on the hills from the plains. The onset is sudden with abdominal pain in the early morning and the passage of stools followed by relief. This is repeated next morning. The stomach feels to be much distended, there is gurgling. The patient is better on returning to the plains. In Ceylon, how- ever, there are similar symptoms with patients when on the plains (Castellani). The tongue and mouth are never involved. It has a very low mortality. TREATMENT. The patient must avoid hills over 6,000 feet high. Rest in bed. Warm clothing. Liquor hydrarg. perchlor. i to i^ drachms, fifteen minutes before each meal. Pepsin, 12 to 15 grains, two hours after meals. Milk diet diluted as necessary. SPRUE (PSILOSIS). DEFINITION. It is a chronic catarrhal inflammation of the alimentary canal ; characterized by large, pale, frothy motions; ulceration of the tongue and mouth with digestive disturbances. DISTRIBUTION. Asia, Burmah, India, China, Japan, Fiji; West Indies, South America, rarely in West Africa and Europe. Probably world-wide in tropical and sub-tropical countries. It is a regional as opposed to a climatic disease. ETIOLOGY. The causation is unknown. Some of the suggested causes are : climate, food, helminths, bacteria, fungi, protozoa and a symptom-complex. Fungi are often found in the mouth and the intestines of patients, the commonest being the genera Monilia and Saccharomyces. They are perhaps secondary infections causing the frothy diarrhoea, because sodi-bicarb. will clear out the fungi, when the frothy stools will cease, but the disease continues. Many fungi grow badly in alkaline media. SPRUE iPSlLOSlS) 353 Any depressing influence, intestinal irritation, or an exhausting malady will predispose to the disease. It is generally seen in old tropical residents during or after being in the tropics. It may be a specific infection falling upon over-stimulated glands owing to certain meteorological conditions (Manson). Intestinal fermentative changes, bacterial or parasitic in origin, may cause it in those long resident in hot climates (Cantlie). It is a disease of the European in the tropics. Natives are very rarely attacked. Both sexes of all ages and classes are subject to it. There is some evidence of its being a direct infection. Inoculation of sprue tongues, scrapings and stools injected into animals have failed (Bahr). Bahr, a recent worker, submits evidence of its being a blastomy- cotic infection which may be summed up as follows : — (i) Yeast cells and m}'celial elements are found intracellularly in tongue lesions earlv, but not later, when the inflammation has subsided. (2) Yeasts are the only organisms found in the deep layers of the tongue. (3) The desquamation of epithelial cells and subacute inflammation of the tongue and ciesophagus are changes one could expect from yeast infection. (4) Yeasts were found in intestinal mucus of sprue, but not in other cases of chronic diarrhoea. (5) The stools are such as one would expect in yeasts. (6) Its relapsing nature is compatible with the life-history of the Blastomyces. (7) The sprue yeast is apparently identical with the thrush fungus. (8) Wasting, anaemia, and degeneration of hepatic capillaries and endothelium, the symptoms of sprue, are reproduced by intra- venous injections of broth cultures of a pathological veast in animals. (9) Similar sprue symptoms are found in infants, the subjects of thrush infections. (10) The scattered portions of the digestive tract affected by this fungus would best explain the varying clinical manifestations of sprue. (11) The local tropical conditions favour a luxuriant growth of fungi. Dold in examining sprue stools for yeast found that — Normal stools yielded yeasts in 7*5 per cent, of cases. Diarrhoea stools (not sprue) in 16 per cent, of cases. 354 DISEASES OF UNCERTAIN ETIOLOGY Faeces from cases of sprue in 92" i per cent, of cases. Either Blastomycetes or Oidia or both were present in the latter. Sprue. "Small" ulcer of intestine. X 55. Dense infiltration of submucosa by embryonic cell growth. Invasion of villi and crypts of Lieberklihn with subsequent destruction of mucosa. Sprue. Edge of "small" ulcer. X 55. Destruction of mucosa by infiltration, and subsequent shedding of epithelial structures. They gave acid and gas reactions on all kinds of sugars, Avhich -explains the acid reaction and the gaseous character of the sprue stool. SPRUE (PS I LO SIS) 355 The liver is diminished in size due to carbohydrates being quickly decomposed in the digestive tract by tl;e specific orgrmisms of sprue, Sprue." Base of small ulcer of intestine. X 55. The mucosa has been shed, and the dense infiltration of the suhmucosa is causing it to break down and come away as a necrotic slough. The lymphatic vessels in the centre of the infiltrated portion are full of pus. Sprue. Base of small ulcer in intestine. X 350. Dense infiltration and formation of pus in superficial layers. leaving little or none to be absorbed and deposited in the liver as glycogen. 356 DISEASES OF UNCERTAIN ^ETIOLOGY But The thrush fungus, Alonilia albicans, is a terminal though un- common infection in other chronic wasting diseases as phthisis, cancer, diabetes, &c. Gastro-intestinal infections have been reported in the temperate zone. PATHOLOGY. One finds desquamation of the mucosas of the gastro-intestinal tract with atrophic changes of mucosa, glands, pancreas and liver. There is fatty degeneration of the tongue; inclusive elements in the epithelial cells is a well-known feature. There may be large structure- less cells, keratohyalin or other cells containing granular agglomera- tions, cell degenerations or inclusions. The gastro-intestinal tract shows submucous congestion, conges- tion, thrombosis, exudation of haemoglobin, round-celled infiltration and necrosis of the mucosa. Digestion and absorption of food is hindered, but the absorption of poisons facilitated. The toxins damage the liver and a toxaemia results. The liver is congested and enlarged, or more often atrophied and small, the result of hyper-activity and early exhaustion, which accounts for the early bilious stools and later the pale frothy motions. On opening the intestines — The upper third contains normal faeces of a yellow colour due to bilirubin. The middle third contains white or grey faeces due to alteration of bile pigments into chromogens. The lower third contains green faeces (Vaughan Harlev). The blood picture in the last stages of severe cases may resemble that of pernicious anaemia. Chromatin granules are commonly seen enclosed in red cells. P.M. Body emaciated, wasting of all organs, absence of fat. Skin hangs in loose folds, oedema of ankles. Tongue shows patches of infiltration in the connective tissue, vesicles, small ulcers, filiform papilh-e atrophied and fungiform papillae swollen. Pillars of fauces and tonsils show sub-epithelial inflammation, suppuration and ulceration. (Esophagus inflamed, mucous membrane attenuated in patches. Stomach : mucous membrane pale, atrophied, rough and cirrhotic. Small intestine : mucous membrane somewhat eroded. Large intestine tilcerated. Peritoneum thickened, chronically inflamed. SPRUE {P SILO SIS) y:,7 Bowel wall ver}' thin, sometimes like tissue paper. Mucous coat atrophied, submucous coat has fibrosed areas with dirty grey tenacious mucus. The ^'illi and glands destroyed. Erosions are most marked in the colon. In the swollen endothelial cells of the venules of the spleen are certain hvaline bodies, probably of a degenerative nature not found in other diseases, perhaps produced in response to the extensive yeast infection found in sprue. These yeasts are small. Gram-positive, and have no affinit)' for fuchsin. They are not Russell's bodies (Balir). SYMPTOMATOLOGY. Insidious onset. Sore mouth, dyspepsia, diarrhoea, tongue in- flamed but clean with small vesicles, ulcers and bare patches, ditto on palate, pillars of fauces, inside of cheeks, acid salivation. Warm and spiced foods, hot, acid, or alcoholic drinks cause pain. Mucus accumulates about the mouth. Though hungry the patient eats little. There is a burning pain behind the sternum on swallowing; the neck and thorax are emaciated, the abdomen is distended with gas, and the ankles with oedema. There is discomfort and distension after meals, acid eructations, and sometimes vomiting. In the earl\- morning there are several copious, painless, grey offensive, frothy stools. The fasces contain mucus, epithelial debris, many bacteria and fungi. The nitrogen and fat are increased (undigested food and fatty acids). Often the hydrochloric acid of the gastric juice is diminished or absent (Manson). The same applies to the intestinal digestive juice. The blood coagulates slowly. There is anaemia, 1,000,000- 2,000,000 reds. The colour index is low. Leucopenia to 3,000. Depression and irritability; tongue glazed, small and fissured, is more like cartilage. Pulse slow and feeble. Emaciation. An acute diarrhoea or cardiac failure may cause death. The symptoms are often intermittent, but steadilv growing from bad to worse. The disease may be mild or virulent, liable to sudden remissions and latent periods. A denuded tongue makes mastication difificult. ,, cesophagus makes swallowing painful. ,, stomach causes dyspepsia, ,, intestine causes diarrhoea. 23 358 DISEASES OF UNCERTAIN ETIOLOGY The stools are pale because of — (i) The farinaceous diet. (2) A colourless reduction-product of hydrobilirubin. (3) The abnormal percentage of cijnlained fat. The stools are large owing to (i) The lack of absorption of carbohydrates, &c. (2) The lack of digestion ,, ,, The acid reaction is due to lactic and butyric acids (not to HCl), and the absence of pancreatic ferments. Cammidge's urinary reaction is negative (Bahr). DIAGNOSIS. An irregularly, chronic, pale, frothy, morning diarrhoea with ulceration of the mouth and flatulent dyspepsia in a tropical resident is in all probability sprue. In Stomatitis the characteristic stools of sprue are not present. In Thrush, look for the fungi Monilia in the wliite patches of the tongue. This condition, however, may complicate sprue. In Hill Diarrhoea the mouth symptoms are i^ften absent. There is a history of living at an high altitude. In Chronic D3^sentery the mouth symptoms and pale stools are absent, while blood and mucus is passed. There is usually no griping with sprue. Look for amcebje and the dysentery bacillus. In Chronic Pancreatitis the mouth is normal, there is much fat in the stools, and there are Cammidge's crystals in the urine. Remember that the denuded epithelium of the tongue is only seen in Sprue, Pellagra and Scurvy. TREATMENT. The patient must assist the practitioner. His co-operation is essential. Absolute rest in bed. Avoid chills. Remove all sujDposed causes. Clear the bowel contents with castor oil. The diet is all-important. Milk Diet. The milk must be free from contamination and adulteration. If it contains much fat dilute it with whey made ^itli the juice of limes. Sterilize the milk. If the attack is severe begin with whey onl}-, ad libitum, 7 to 8 pints daily. Milk, sipped, three to four pints daily as soon as possible. .A.S the symptoms improve increase the milk gradually bv half a pint daily until seven pints are being taken. Let it be distributed over tw^elve meals dailv. SPRUE {P SI LOS IS) 359 For six weeks there should be no other food. The patient may then get up. If the svmptoms do not improve reduce the amount of milk and return to whey. Starvation diets are dangerous. Improvements are noted bv the stools becoming brown and the mouth troubles diminishing. Should the milk cause vomitina^ add sodi-bicarb. or sod. citrate or a little lime water. Relieve constipation by enemata. In addition to the milk some recommend fruit, such as strawberries, apples or bananas. Eggs in milk can then be given, chicken broth, Benger's food, fish, biscuits and potatoes. Relapses are common. Give a purge at once and begin with milk. Some give more fruit than milk. Fruit which is not acid should be given, such as peaches, pears and bananas. It is necessary to avoid : — Dark meats, most vegetables, spiced foods, cold or hot drinks, all indigestible substances, all alcoholic drinks and smoking. Meat Diet. Six ounces of raAv meat juice with a little dilute h^'drochloric acid and salt. Give one teaspoonful each fifteen minutes, rapidly increased when possible. Then meat, free from fat, cartilage or fibrous matter, take 2 lbs. with 2 ounces of fresh suet, mince and pound, cook, and give the w^hole in six separate meals daily. A little water or tea with lime juice instead of milk should be taken twuce daily for six weeks. '(The Salisbury cure.) In seven days introduce fruit, chicken, eggs and fish. Some add curdled milk. Cantlie's Treatment. Put the patient to bed. Apply hot wet packs from the nipples to the groin for two hours morning and evening. A binder around the body. Three meat meals daily of 5 ounces of meat with beef-tea, calves'-foot jelly or plain jelly and salt to taste, two-hourly. Castor oil, ivi ounces, each morning for three mornings. Santonin, 3 grains, morning and evening. Strawberries, 3 lbs. to 4 lbs. daily between meals. When the stools are fairly solid, about the fourth day, add poached c^g and minced chicken. "\^egetable marrow later, and 36o DISEASES OF UNCERTAIN .ETIOLOGY thin slices of bread baked in an oven for twenty minutes. Give milk every fourth day for twenty-four hours. Drugs. Astringents are dangerous, antiseptics useless. Yellow, santonin, 3 to 5 grains, twice daily in olive oil. If the santonin is white expose to the sun for a few days. Ipecacuanha, 20 grains daily, for three days in severe cases (Cant lie). To be discontinued when the stools are brown and free from odour. Paint the mouth with glycerine and borax; for pain, spray or paint on 2 to 5 per cent, cocaine or stovaine. Give morphia for painful oesophagus. Adrenalin, 5 to 10 minims (i in 1,000), gives immediate relief. For muscular pain, massage and pilocarpine, i/ioth gr. to i/5th gr. thrice daily. For acute diarrhoea^ opium or lead and opiimi pills. Send the patient to a temperate zone as soon as possible. Alkalies diminish, acids increase the symptoms. Cantlie savs that milk clots in the acid fermentation, the patient absorbing only the whey. Emetine and streptococcal vaccines can be tried, the latter prepared from the mouth lesions (Rogers). Good results have been obtained with the following medicinal remedies : — Large doses of pancreaiin, 2 grm. dail\-, dilute hydrochloric acid, calcium carbonate and a liille tannic acid. The pancreatin was con- tinued for months with good effects while being taken, and slight relapses A\hen it was omitted. Some claim good results from Monilia vaccines. Six injections of ihe emulsion, eight to fourteen days apart, the primary dose of 0*03 c.c. increasing to a final dose of r40 c.c Of 62 patients tluis treated, 49 were cured, 12 improved, and i died (Michel). PHLEBOTO:\IUS FEVER (THREE-DAY FEVER). DEFINITION. An acute specific three-day fever of unknown causation, spread by the Phlebotomus papatasii. DISTRIBUTION. Around the Mediterranean and Adriatic seas, India, Egvpt and South America. ' ■ It agrees with the distribution of the P. papatasii. PHLEBOrOMUS FEl'ER {THREE- DAY FEVER) 361 It is not found on the heights. It confines itself chiefly to inhabited places (Doerr). It is a disease of tlie summer. The fly dies out in winter, but perhaps the infection is continued by the Qgg. iETIOLOGY. An unknown virus is infective during tlie first and up to the end of the second day of the fever only. The Pasteur-Chamberland filter keeps back the virus. The carrier, P. papatasii, is not infective until one week after it has itself become infected, hence some organism develops in the fly. The infection nia\' be transmissible to the young broods. An antibody is probably produced. Serum from convalescent patients may neutralize infected serum. SYMPTOMS. Incubation one to seven davs. Sudden onset, as a rule, like most fevers with chilliness, severe frontal headache, pain about the eyeballs, general body pains, injected conjunctivce. Skin hot and dry, temperature rises rapidly to 104° F. in twenty- four hours, pulse 100 to 116, often slow. Ocular movements painful. Patient irritable, sleeplessness, appetite lost, taste impaired, epigastric pain. Diarrhoea sometimes, congested mouth and throat. Pain in joints, knee and elbow especially. Sensation of burning in the palms and soles. Leucopenia 4,000 to 5,000. Sometimes a general ervthema. Temperature falls in thirty-six to forty-eight hours, slowly with (often) epistaxis, sweating, vomiting, diarrhoea and weakness. Convalescence is long. No death has been recorded. Relapses are common. Perhaps there are no reinfections. DIAGNOSIS. The short duration, three days, is about the only diagnostic feature. From Influenza by there being no catarrhal symptoms with Three- day fever. From Dengue by the short duration only. From Malaria by there being no parasites. From Malta fever by the duration, sudden onset, absence of organisms in the blood and negative agglutination test. TREATMENT. Rest in bed. Saline purges. Aspirin. Tonics later. Prophylaxis as in Malaria. 362 DISEASES OF UNCERTAIN ETIOLOGY THE PARASITE. Family : Psxchcjdidas. Sub-famih' : Phlebotominae. An owl midge, P/ilebo/oiiius sp. Greatly enlarged. (From Giles's " Gnats or Mosquitoes." Genus : Phlebotomus. Species : P. papatasii. Characters. Small wings, hairy, second long vein twice forked. Legs long, slender, densely covered with scales. Abdomen of ten segments, the last carrying the genitalia. The oesophagus divides into two, one to the sucking tube, the other to the mid-gut. Life-History. The female after fertilization sucks blood, lays 30 to 80 eggs, singly, in damp places such as fissures in stones and bricks. They hatch in four to six days in warm, twelve to fourteen days in cold weather. The larvse have no eyes, well developed mouth parts, body of twelve segments, spiracles on the first and penultimate segments. Two very long bristles on two tubercles on the ultimate segment. This is characteristic. These are as long as the body. Larval stage lasts two to fourteen days. Pup^e motionless, wrinkled brown skin on the last three segments which fixes it to stones in dark crevices. The pupal stage lasts eight to twenty-eight days. The whole time required is from one tO' two months. Habits. Nocturnal, attracted by light. During the day it is found in shady places, latrines, under stones, &c. The female only bites. The fly passes through the ordif.ary mosquito net. Spider webs are useless as they do not catch them. The bite is shar^'5, it leaves a rose red papule set in a reddish macula. It itches for days. Sunlight drives the fly away. It is not a house-fly. J'ERRUGA PERU J 'I AN A 363 VERRUGA PERUVIANA. DEFINITION. It is a clironic, endemic, non-contagious disease of unk-no\vn origin, resembling raws. It is characterized by irregular fever, associated with rheumatoid pains, anaemia and granulomata of the skin, mucous membrane and viscera. HISTORY. It was in South America before the Spaniards. It was recorded there in 1543. In 1885, D. A. Carrion, a student of medicine at Lima, desiring to know if a fever then present was related to verruga, vaccinated botli arms with the blood from a verruga tumour. In twenty-one days symptoms set in and he died of the fever five weeks later. Conse- quenth- it is sometimes known as Carrion's fever. DISTRIBUTION. It is confined to certain provinces in South America. Peru is the most endemic area. It is prevalent on the western slopes of the Andes and Ecuador, Bolivia, and the northern parts of Chili. It is found in narrow valleys, along tributaries of rivers and small streams. The disease only occurs in summer when rivers are in flood and insects abound. Drinking-water is blamed by some of the people. AETIOLOGY. The causative organism is unknown. Perhaps it is some blood- sucking animal that carries it such as the arachnoid. As a rule one attack confers immunity. Strangers visiting an endemic centre are very prone to it. Xewly-born infants may acquire the disease. In some respects it resembles yaws, but unlike that disease, it attacks both domestic animals and man. PATHOLOGY. Some doubt the identification of Carrion's fever with nodular fever. The two diseases have not yet been proved tO' be identical. The disease is said to commonly occur among animals, &c., as horses, mules, asses, dogs, and also fow^ls. Post mortem, there is marked pallor of the bod\', oedema and dropsy, hypostasis of the lungs, enlargement of the liver and spleen, hyperasmia of the bone marrow. Then there are the verrugas of the skin and other parts of the body. HISTOPATHOLOGY. A kind of neoplasm begins about a capillary vessel, the areolar tissue reacting through some perivascular irritant. The connective tissue fibres swell, embracing embryonic connective 364 DISEASES OF UNCERTAIN ETIOLOGY tissue cells. The interareolar spaces contain polymorphs and macro- phages. A non-ulcerative skin lesion shows the cells of the surface epithelium swollen and distended with glycogen. The papillary layer disappears, the dermis is infiltrated with round cells, there are numerous small vessels which may become cavernous, hence the possibility of much hemorrhage. The subculaneous fatty tissue is ahva}"S inflamed. Ulcerations favour secondary infections. SYMPTOMATOLOGY. Incubation is unknown. Perhaps eight to forty days. Prodromata, malaise, lassitude and depression. Gradual ancemia, rheumatoid pains, local or general, sometimes morning fever which may rise to i04°F., insomnia, and sometimes delirium. Pulse soft and rapid. The fever terminates in about twelve hours with sweating and cessation of pains. The liver and Ivmphatic glands are enlarged. There is constipation as a rule but some have diarrhoea. There is a great destruction of red cells to 900,000 per cm. The HB is increased. There is always a marked leucocytosis, 20,000. The polymorphs being about 75 per cent. The bone marrcnv shows excess of normo- blasts and neutrophile myelocytes. SEVERE TYPE (Carrion's Fever). The fever is marked, and is accompanied by severe pains and diarrhoea. The urine is acid, dark, scanty, high specific gravity, never blood, rarely albumin, reduces Fehling's solution. The anaemia is profound to 500,000 in extreme cases (Monge). Death in from two to three weeks, MILD TYPE. The febrile stage is from one to eight months, the skin itches, the eruption is on the face, neck, arms, legs, conjunctiva, about and within the mouth. Small erythematous spots, sometimes with small vesicles, rarely with bulU-e. The erythema develops into a papular eruption about the size of split peas. These are discrete, red, firm, small warts, liable to bleed, which may also occur on the mucous membrane and viscera. vSome larger nodules may appear to be free under the skin, then adhere, ulcerate, bleed, then becf)me large, red, fungating masses, chiefly about the elbows and knees. There may not be any health v area of skin left. What there is becomes oedematous, ilie fever declines with the presence of the eruption, general symptoms abate, the patient feels better but the anjemia is marked and haemorrhage from the nodules may cause death. YELLOW FEVER 365 Wrrugas occurring in the larnyx cause dyspncea, bronchi cause bronchitis, lungs cause pneumonia, pleurae cause pleurisy, nose cause epistaxis and occlusion, oesophagus cause dysphagia, intestines cause blood and diarrhoea. ,, ,, meninges cause cerebral symptoms. ,, ,, uterus cause metrorrhagia. In four to six months there are several crops each preceded by attacks of fever. The eruption then disappears, nodules dry up without scarring, ulcers cicatrize. The patient is convalescent but anaemic and weak. The eosinophiles may disappear. ATYPICAL TYPE. Sometimes the eruption is less typical and somewhat localized or it ma\' develop and disappear, the general symptoms returning later and are then more serious. Some cases show but little fever. PROGNOSIS. An early general eruption is a good sign. A mild eruption with ana?mia is bad. Subcutaneous nodules with Carrion's fever, bad. JNIortalitv 10 to 40 per cent. The disappearance of a poor eruption with a return of the fever and the pains are bad. TREATMENT. There is nothing specific known. Remove the patient from the endemic area to warm country districts. Try arsenic, atoxyl, arsenobillon. Avoid chills and cold baths. Drugs are useless in the febrile stage. Give tonics during the convalescence. Treat Carrion's fever as typhoid. YELLOW FEVER. DEFINITION. It is an acute specific, endemic and epidemic fever, characterized by two paroxysms of fever separated by an intermission; albuminuria, jaundice, black vomit and haemorrhage. The Stegomyia calopus carries the virus. DISTRIBUTION. Yellow fever is supposed to have attacked the troops of Columbus 366 DISEASES OF UNCERTAIN ETIOLOGY in 1495, in ihe island of St. Domingo. These Spanish troops carried it to America. It is endemic un ihe east coast of Mexico, Central and South America as far as Rio de Janeiro, and the Antilles. Also in Guatemala, Spanish Honduras, Nicaragua, Costa Rica, Labrador, French Guiana, Dutch Guiana, Ecuador and along the rivers Magdalena, Orinoco and Amazon. The true home centre is Central America and the West Indies. It was formerly common but now is extinct on the Isthmus of Panama. Since 1905, eleven cases have been, d^ected and isolated by the Canal Zone authorities. These cases came from Cartagena, Guayacjuil and Buenaventura. The epidemic of 1635 to 1690 affected Guadeloupe, Cuba, Jamaica, San Domingo, Martinique and Vera Cruz. West Africa has probably been a second endemic centre since 1520, when the Cape \>rd Islands and the Gulf of Benin had an epidemic. From these endemic centres ships carr}- the disease to 46° 56' X., and 34° 54' S. Towards the North the disease becomes milder but towards the South it may become very severe. England, Swansea, was attacked in 1S65 but it died out. France was attacked in 1861. Madrid in Spain, in 1878. The distribution seems to coincide with that of the mosquito, S. calopus. This is supported by the fact that : — The disease is endemic in warm climates. It increases in the summer and disappears during the winter in temperate climates. It is carried by ships. It affects low-lving parts of the coast, especially (he insanitary districts. An atmospheric temperature of over 75° F. is required for its active propagation. Towns upon the sea coast, banks of rivers and near deltas are often infected. The disease follows lines of communication. In Rio de Janeiro visitors maintain the disease. Long residents in an infected district tend to become immune. AETIOLOGY. The causative organism is an ultra-microscopic, non-filtrable virus, because : — o'l c.c. of infected blood will reproduce the disease in a non- immune person. YELLOW FEFER 367 Diluted blood passed through a Fasteur-Chambeiiand filter will cause the disease when injected intravenously into a non-immune. Time is recjuired for the virus to develop in man and the mosquito before it is infective, three days in man and twelve days in the moscj[uito, hence it cannot be a chemical substance. If infected serum is diluted the virus becomes more and not less potent after time has been allo^ved for growth. The virulence of the blood is destroyed at 55° C. The S. calopus is absolutely necessary for its spread. Contact with the bedding, fomites and excretions of an infected person will not cause it. The virus may only live in man and the S. calopus. The higher apes, guinea-pigs and fowls are suspected. The fly must go twelve days after feeding upon an infected patient before its bite will reproduce the disease in man, but these flies are then infective for life. According to French physicians the virus can be transmitted by the mosquito to the first and second generations. These cannot infect man until they have been adult flies for thirteen days. The adult mosquito can live for about five months and la}s seven batches of eggs. The fly, before her first egg-laving, is immature and bites at any time but is harmless. Afterw^ards she is strictly nocturnal. PATHOLOGY. The Liver. — The liver cells swell, pressing upon the bile capil- laries obstructing the bile, causing hepatogenous jaundice, staining the skin and tissues yellow and passing out in the urine. The swollen liver cells also block the intralobular capillaries causing congestion of all viscera drained by the portal vein, especially the pyloric region and the duodenum. This impaired circulation predis- poses to secondary infection. Portions of liver are so degenerate that the urea function is impaired and a universal toxic condition due to the resulting ammonic-emia sets in. Haemorrhages are caused as a result of the damaged epithelial lining of the capillaries. The Blood. — A few normoblasts may be present, otherwise the number and shape of the red cells are normal. The loss of hb. is marked after the third or fourth dav. The specific gravity of the blood falls, its coagulation is diminished. Hasmoglobin^emia often occurs before death. Ammoniaemia is present in bad cases. The polymorphs are slightly increased, 3,200 to 20,000 per cm. The Urine. — Albumin on the second day which increases rapidly. 368 DISEASES OF UNCERTAIN ETIOLOGY Bile appears about tlie fifth or sixth day. Red cells may be present, leucocytes are rare. Casts, h\a!ine, i^ranular and epithelial appear in turn. I'rea is diminished in bad cases. The diazo reaction is usually absent. The Yomit. P^irst white, consisting of mucus; acid and colourless, or it may be blood-stained. Then red, consisting cliiefly of bright, red blood. Later black, consisting of red cells, debris, fat, epithelial cells, micro-organisms and hydrochloric acid in traces. The IICI converts the hb. into acid hcLMiiatin giving the black cohjur. The Immunity. Racial immunity, so-called, in endemic regions is really due to their having had mild attacks in childhood. Acquired immunity usually is lifelong, and is given by a typical attack. Relative immunity is acquired by receiving an inoculation of infected blood serum, heated for five minutes to 55°C. It has been shown conclusivelv that negroes of the West Coast are not immune to yellow fever but are as liable as whites, BUT the practitioners of Guayac|uil recognize the natural immunity of very young children and have presented evidence in support of their views (O'Brien). This appears to pass off with age, during which transient periodic mild attacks give an acquired immunity. P. M. The skin is yellow and stained with hccmorrhages. The buccal mucosas is fissured, the mouth may contain blood. The liver is yellowish brown, h^emorrhagic, cells swollen and fatty. The gall-bladder contains inspissated bile, perhaps mixed with blood. The spleen is congested and soft, normal in size. The gastro-intestinal tract is full of black tarry blood. The mesenteric glands are sometimes enlarged. The kidneys are congested, not enlarged. The urinary tubules show fatty degeneration with granular debris in the urine. The urinary bladder is usuallv empty. The pericardium may show effusions and the heart ecchymoses. The pleurae may show haemorrhages; the lungs are often congested. The uterine mucosa? are congested and the organ mav contain blood. The meninges are congested and may show hcemorrhagic spots VELLOJV FEJ^ER 369 SYMPTOMATOLOGY. Incuhiitiou . — Two to seven days. Prodrnniiitit usualU' absent. JMalaise may be present for several days. The First Fever. — This comes on the first or second day, severe frontal headache, sometimes rigors, pain in back and Hmbs, face and skin flushed, eyes injected and painful, temperature rises rapidly to 103° F. or higher, respirations quick and laboured, pulse increases from 100 to 120, full and bounding. \"omiting with epigastric pain, constipation, urine diminished with high specific gravit_y, acid re- action, albuminuria on second day, insomnia. TIME M E M E M E M E M E M E M E M E M E M E M 1 E M E M E M E r ° 105 1 04 1 03 ro2 1 1 1 00 S3 98 A / \ / \ / A A ^, / J ^ \ A / V ^ A \ A, V \^ '\ V , ^ A A V ' s J y v V \ \, A V \ r V V/ V Yellow fever. Severe attack. The Crisis. — This occurs about the end of the second day. The temperature falls suddenly to normal or subnormal with sweating, the pain and the flush both disappear, the patient feels better and sleeps well. The urine increases. A mild abortive case mav recover at this stage. The Second Fever. — This occurs on the second to the fourth dav. A few hours after the temperature has fallen to its lowest and the crisis has taken place the temperature begins to rise again steadily until it reaches 104° or 105° F. But the pulse decreases to sixty or fortv beats per minute (Faget's sign). The skin becomes jaundiced, and it deepens with the days. The vomiting and the epigastric pains return with thirst and prostration. Tongue dry, furred with red tip and edges. Haemorrhages everywhere, vomit black, mal^ena, epistaxis,. subcutaneously, from the mouth, &c. The urine diminishes, albumin increases. There may be anuria. Restlessness and delirium are often present. The Termination. — If recovery, then, after about four days, the temperature declines, sweating commences, more urine is passed, albumin diminishes, vomiting ceases, sleep is usual, and convalescence sets in. 370 DISEASES OF UNCERTAIN ETIOLOGY Recovery is rapid. If fatal, then jaundice deepens, bleeding becomes worse, urine is suppressed, subsultus tendinum is seen, coma and convulsions precede the fatal issue. Death may ensue in an acute attack, preceded by a rapid rise of temperature. Relapses may occur at any time within two or three weeks of the attack, and are predisposed to by dietetic errors. PROGNOSIS. As a rule convalescence, when it has set in, is not protracted or com- plicated. Pre-existing heart or kidney affections are bad. Congestion of the lungs, abscesses, gangrene and intussusception are dangerous complications. Dvsentery and hepatitis are common sequelae and add to the gravity of the case. In the United States the mortality is lo to 25 per cent. In West Africa and the endemic area the mortality is 45 to 80 per £ent. In children ihe mortality is low. Anuria, hvperpyrexia, black vomit, malsena are all bad omens. All cases are serious, especially for alcoholics. Abortion is the rule. DIAGNOSIS. Early cases are always difificult. Typical attacks are easy. Mild attacks in a non-endemic area are difficult. It is all-important to diagnose early. Look for albuminuria, Faget's sign, jaundice, and the black vomit. Dengue shows a preliminary rash, leukemia, no albuminuria, and "Faget's sign is absent. Subtertian malaria shows the blood plasmodium and absence of Faget's sign. Blackwater fever shows a mononuclear increase with destro^'ed hb. rin the urine. Relapsing fever shows blood parasites and a leucocvtosis. TREATMENT. The indications are : — (i) To prevent the spread of the infection. (2) To eliminate the toxins rapidly. (3) To alleviate the symptoms. We will deal with preventive measures last. YELLOW FErER 371 To eliminate the Toxins rapidly. By the BoivcL — Give small doses of calomel to disinfect the alimen- tary tract. Follow this with doses of sodium sulphate until the bowels are well opened. Afterwards give enemata, twice daily, of sodium sulphate, ij drachms to i pint. By the Skin. — Wrap the patient in warm blankets, but not so as to oppress the patient with them. Precede this by a hot mustard bath. By these measures the skin will be stimulated and the headache relieved. By the Kidneys. — To stimulate the kidneys and dilute the toxins use Sternberg's treatment : — I^ Sodii bicarbonatis ... ... ... ... grains 150 Hydrargyri perchlor. ... ... ... ,, J Aquas ... ... ad 60 ounces Give li ounces hourly or, a drink of sodium bircarbonate and fresh limejuice n-,ade neutral with sodium sulpliate if necessary. This may be administered per rectum. To alleviate the Symptoms. Relieve pain by aspirin or phenacetin, never opium. Apply hot fomentations for severe lumbar pain. Warm mustard bath for increasing the urine. Do not give food during the first few days. Prevent vomiting by sips of champagne, iced if possible. Put plasters to pit of stomach. Treat hyperpyrexia by cold sponging. Bleeding should be treated b}' calcium lactate or adrenalin injection or ergotin. Anuria by hot fomentations to the loins, cupping, hot-air baths. Cardiac insufficiency by strychnine, camphor, or ether. Weakness should be met, after three days, w^ith milk, lime water, toast water, cream, lemon jelly, olive oil bv mouth or skin. After three days of normal temperature, chicken broth, custards, &c. Avoid strong alcoholic stimulants and meat extracts. Be very careful during remissions not to give food. Always increase diet with great caution. PROPHYLACTIC MEASURES. To spread the disease three factors are necessary : — An infected person from the first to the third dav of the disease. The presence of non-immune persons. The presence of the Stegomyia calopus (fasciata). To spread the infection the fly must bite the patient infected during the first three days. Twelve days must elapse for the development of the virus in the mosquito; then it can bite and infect a non-immune 2,72 DISEASES OE UNCERTAIN .ETIOLOGY person for the rest of its days, and may also hand down the virus to the first and second generation, these latter spreading the disease fourteen days after becoming adults. An infected ship should be ancliored a quarter of a mile from the shore or other ships as the fly is not likely to cross this distance. The quarantine should be five to seven days because the incubation is up to seven days. Place the sick in mosquito-proof rooms, mesh twenty strands to. one inch, and tjuarantine the remainder of the crew or members of the household. Disinfect the ship by a Clayton's disinfector. A.S the flies are cjuiet between 9 a.m. and 3 p.m. visits can then be made without risk. Houses should be fumigated by sulphur dioxide or pyrethrum powder, burnt in the proportion of 2 lbs. to 1,000 cubic feet of space. The breeding places of the flies should be destroyed. BOYCE'S SUMMARY. (A) When the fever is endemic : — (i) Segregation of non-immunes. (2) Screening of bed, verandah, or, if possible, the house- completely. (3) Systematic mosquito destruction by : — Removal of breeding places. Screening of water cisterns. Oiling of waters not screened or drained. The infliction of fines for non-observance of sanitary rules. Drainage and bush cleaning. (4) Education. (5) Quarantine administration. (B) When vellow fever has already broken out : — (i) Removal of non-immunes from the infected area and deflection of the trafific from this area. (2) Isolation of all cases, sure and suspected. (3) Provision for isolation of contacts. (4) Early notification. (5) Fumigation. (6) Emergency mosquito measures : — Removal of receptacles, oiling, screening, and draining- (7) Education by lectures, meetings and pamphlets. (8) General organization of the medical forces. NOTES ON THE YELLOW FEVER MOSQUITO 373 NOTES ON THE YELLOW FEVER MOSQUITO, STEGOMYL^ CALOPUS (FASCL'VTA). (oreyo"? = a house; jjLvia a fly.) The S. calopus belongs to the CuHcales of the sub-family, CuHcinse. On account of its wide distribution, domestic habits, vital tenacity of its eggs, the different infections it is capable of carrying, yellow fever in particular, it is one of the most formidable insects in existence. They are small black mosquitoes, with bright whitish markings on head or thorax, and bright w^hitish transverse marks on abdomen and legs. They are common in all tropical and sub-tropical climates between 40° N. and 40° S. from sea-level to nearly 3,000 feet high. THE ADULT FEMALE. The head is black with white markings not unlike a crown in shape; the palpi are short, black, tipped with white. The scutum is brown, with a lyre-shaped set of marks thereon. The scutellum is white. The abdomen is blackish brown, with white transverse bands across the dorsum and on the sides of the segments. The femora are black with a white tip; the tibia black, the tarsus black with two to five white bands. It has the common mosc|uito wing, with the third and fifth long vein forked. The adult male is similar, but has long palpi, and does not bite man. HABITS. A house-haunting mosquito always. Perhaps the commonest mosquito on board ship. It bites in the daytime as well as at night. It breeds close to human habitations. Its eggs are laid in anything that holds water — a sardine tin or water-barrel. EGGS. Almost black, laid in seven batches, they stick closely together, but not in rafts. They are very resistant; if kept dry they will remain fertile for six months. The yellow-fever virus is transmitted to a second generation. LARY^E. Dark in colour, has a short, stout breathing tube and very large tracheal gills. Laterally, on the eighth abdominal segment is a single row of eight to nine scales like miniature arrow heads and a wisp of three small hairs. It can remain submerged for a long time, and can live in filthy water aided by its large tracheal gills. 24 374 DISEASES OF UNCERTAIN ETIOLOGY SPOTTED FEVER OF THE ROCKY MOUNTAINS. DEFINITION. An acute endemic, non-contagious, febrile disorder, with a petechial or papuric eruption following the bites of infected ticks. It is found in valleys, in siiarply defined areas, and occurs at definite times and seasons. DISTRIBUTION. The United States only. In Montana it is found along the Bitter Root valley, at Rock Creek, and Bridger. In Idaho throughout the entire valley of the Snake River and its tributaries. In Wyoming at Cody and Meeteeste. In Nevada, in the north only, along the valley of the Quinn River. In Oregon towards Idaho in the east only. The fever occurs in those seasons when the ticks (D. andersoni) are most prevalent. The elevation is in all cases between 3,000 and 4,000 feet above sea-level. AETIOLOGY. The causative parasite is stated to be localized in the endothelial cells and smooth muscle fibres (Wolback). Its exact nature is not known. The organism is said to be present in the blood-vessels of man, monkeys, rabbits, guinea-pigs and ticks. The virus cannot be separated from the blood cells by washing, neither will it pass through a Berkefeld filter. One attack produces immunity. The virus can be acquired and transmitted by the larvae, nymph, male and female adults of D. andersoni. Other ticks are also suspected. Men are more frequently attacked than women, commonly from fifteen to fifty years of age. Hence with out-door work there is greater risk of infection. Jack rabbits and deer mice are important hosts of the carrier ticks as well as domestic animals. PATHOLOGY. Post mortem, rigor mortis is well marked. PetechicC are found on the skin. Tick bites may be visible. Liver and spleen are congested, SPOTTED FEl'ER OF THE ROCKY MOUNTAINS 375 enlarged and soft. Kidneys are congested, sometimes with sub- capstilar haemorrhages. Microscopically one finds capillary congestion of the viscera with excess of leucocytes. Extravasation into and pigmentation of the skin. Acute parenchymatous degeneration of heart muscle, spleen, liver and kidneys. SYMPTOMATOLOGY. Incubation. — Two to seven days. Prodromata. — Pains radiating from irritating tick bites, malaise, nausea. Oiisc't. — Fairly sudden with chill, severe headache, pains in back, temperature 103° to 104° F., furred tongue, dried skin, congested con- junctiva?, dry cough, epistaxis, febrile urine. Course. — Temperature gradually rises to 105° to 107° F. from the sixth to the twelfth day. There is an eruption about the third day on the wrists and ankles, co\ering the bod}- in two days. The macules, i to 5 mm. in diameter are not raised, at first they disappear on pressure, then become permanent and later petechial, sixth day. There is also a dusky red mottling of the skin. In very mild cases the eruption may be absent. The pulse is no to 150, becomes weaker, often dicrotic and may be irregular. There is a slight reduction of the red cells and hb. with a slight increase of leucocytes. In severe cases oedema of the face and limbs may be present. Constipation is troublesome. There may be mild bronchitis with a slight increase in respiration. The urine may show a trace of albumin with a few granular casts or it may be suppressed in bad cases. From the fifth to the twelfth day the tvphoid state may lead to death. If not, then lysis about the eighteenth day and convalescence. COMPLICATIONS. Pneumonia is common. Gangrene of the fingers and toes and the skin of the penis and scrotum may occur. Nephritis, cardiac weakness and meningitis are not unknown. DIAGNOSIS. Typhoid fever may be troublesome. It has, however, a more in- sidious onset, the nature and commencement of the rash are difTerent, there are intestinal symptoms and a Widal reaction can be done. 376 DISEASES OF UNCERTAIN .ETIOLOGY Typhus fever ends by crisis, otherwise they are almost indistinguish- able. Two varieties of the same organism are possibly the causes of both diseases. Japanese river fever may be very similar, but one should look for one or more eschars near the genitals or the axilla in this disease. The eruption, which begins on the face, does not become petechial. PROGNOSIS. In Montana the mortality is about go per cent, and is always high. In Idaho the mortality is about 2*5 per cent., always low. The outlook is good when the eruption is not general and poorly defined, TREATMENT. Remove the tick by applying ammonia, turpentine, kerosene or carbolized vaseline. Cauterize the bite with pure carbolic acid. Cold applications, Dover's powders, &c., for the headache. Cold sponging for hyperpyrexia. Cardiac stimulants may be necessary. Avoid the districts where the disease is prevalent. Destroy the ticks and their breeding places as far as possible. In Montana they practise the following measures : — (i) The reclamation and cultivation of arable land. (2) The burning over of the foot-hills. (3) The killing of wild animals. (4) Hand picking and the dipping of domestic animals in arsenical dips. (5) Sheep grazing. (6) The destruction of ground squirrels by the use of carbon bisul- phide pumps. DENGUE. DEFINITION. An acute specific, infective, non-contagious fever of unknown causation, spread by the bite of the Culex fatigans and Stegomyia fasciata, characterized by two febrile paroxysms, the pulse varying directly with the temperature, and a marked leucopenia. DISTRIBUTION. In tropical and sub-tropical zones where the Culex fatigans abounds. In Egypt, Arabia, Persia, India, Burmah, Indo-China, China, North America, Spain, Peru, West Indies, West Africa, Fiji Islands, Western Australia, Ceylon. DENGUE 377 An epidemic or pandemic takes place about every twenty years (Manson). Often 75 per cent, of the population are attacked. It prefers the coast line, deltas and valleys of great rivers, but there are many exceptions to this. In 1870 to 1873 it spread all over India. iETIOLOGY. An unknown organism living in the blood is the cause. An intravenous injection of 20 c.c. of dengue-fever blood, filtered or unfiltered, produces, after an incubation of two to three days, the typical symptoms of the disease. This organism passes through a filter which will retain M. melit- ensis, the filtrate producing the fever. Some people appear to have natural immunity against the disease. An attack produces a temporary acquired immunity. Hot countries suffer most. Cold limits the disease. SYMPTOMATOLOGY. Incubation, two to six days. Prodromata are usually absent. Onset is sudden, introduced often by some severe cold, extreme fatigue, deep flushing of the face, a shivering in man, convulsions or delirium in children. Initial fever commences with a rapidly rising temperature, 103*-* to 106° F., pulse quickens, 90 to 140, buccal mucosa becomes congested, conjunctivae injected, while occasionallv vomiting and diarrhoea are present. Severe pains in the head, eyeballs, lumbar region and legs. Joints when moved actively cause agonizing pain, but when moved passively are almost painless, hence the pain is really caused by the adjoining muscles. Very rarely are the joints red and swollen. The patient may be unable to w^alk because of the pains. Gastric disturbance and vomiting may occur. The lymphatic glands are not enlarged. Insomnia and delirium are not infrequent. Leucopenia is almost constant, 3,800 per c.mm. The small lymphocytes are increased and the polvmorphonuclears decreased. OtherAvise the blood is normal. Intermission or remission then occurs from the second to the fourth day as a rule. The temperature falls by crisis, accompanied bv profuse perspiration, diuresis, diarrhoea, and sometimes epistaxis. The latter relieves the headache at once. The pains almost disappear and the patient may be able to resume his work. 378 DISEASES OF UNCERTAIN .ETIOLOGY In some cases ihe lemperature remits only to ioo° or 102° F., and the symptoms abate only. Terminal fever and eruption. This occurs about the fifth day, temperature rises tO' 102° or 103° F., the pains return and are severe, a rash appears on the palms and the backs of the hands, elbows and knees, rapidly spreading to the trunk and legs. This rash may be : — (i) A measly eruption, small circular dusky patches. (2) A scarlatiniform eruption, numerous bright red, small papules forming larger patchy areas. (3) A mixed type or abortive only. The eruption lasts two to eight days followed by a furfuraceous des- quamation lasting two or three weeks. The second temperature falls by crisis about the sixth day. The pains may come back again at intervals for weeks afterwards. Convalescence may be C]uick and permanent or protracted and com- plicated. The seven-day fever of Rogers is held by some to be a varietv of Dengue. The mortality is almost nil (o'l per cent). SEQUELS AND COMPLICATIONS. Relapses are not uncommon. Pains in the joints and muscles. Hcemorrhage from any of the mucous membranes. Hyperpyrexia is rare, so also are pleurisy, pericarditis, orchitis, endocarditis and meningitis. DIAGNOSIS. Look for sudden onset, severe muscular pain, intermission on the third day, and rash on the fifth or sixth day. Yellow fever has its low pulse with a high fever, jaundice and haematemesis. Influenza has catarrhal symptoms, and rash is absent. Scarlet fever has sore throat and enlarged cervical glands. Measles has catarrhal symptoms, but no severe muscular pains. Rheumatic fever has swollen joints. Small-pox will be difficult until the eruption is seen. Early enteric cases are not easy to distinguish; the cause of the fever will decide it. TREATMENT. It is useless to attempt to cut the fever short. Cool applications to the forehead for headache. Dover's powder or morphia for the pain. TYPHUS FEVER 379 Stimulants should be avoided. Purgatives and emetics tend to increase the muscular pain. Massage. Electricity and iodides can be applied. Change of air and place are necessary. TYPHUS FEVER. DEFINITION. An acute specific contagious fever of unknown causation, charac- terized by sudden onset, marked nervous symptoms, macular eruption terminating by crisis. DISTRIBUTION. It is a disease of temperate and cold climates, but in the tropics it may occur in high altitudes and during cool seasons. It is present in Xubia, Egypt, Tripoli and Morocco, Asia Minor and Persia, and from thence to India. It is also found in North China and Hiogo, Japan. It is endemic in Mexico and common in Peru and North Chili. It is prevalent among the Balkan States and Austria, who lost 30,000 of 150,000 cases. It has been present in Ireland for centuries. In Egypt, 1914-1915, there were 23,855 cases with 6,132 deaths. ^ETIOLOGY. The specific organism is unknown. It exists in the blood, which is virulent from the third to the tenth day of the attack (Nuttall). The disease has been transmitted to apes by typhus blood. Human body lice carry the causative organism. It is associated with dirt and filth. SYMPTOMATOLOGY. Incubation about twelve days. Onset sudden, frontal headache, pains in body, sometimes in chest, temperature rises rapidlv, 101° to 104° F., pulse Cjuick, 100 to 120, face flushed, appearance dull, heavy and pathetic. Tongue thickly furred, rapid exhaustion, a mousy odour from the skin. Delirium sometimes early. Rash on abdomen or chest about the fifth day. At first a transient erythema, then a macular, measly eruption, followed by the petechial form. The rash is mild or absent in 20 per cent, of cases. When present it covers the whole body quickly, except the face, palms and soles. The typhoid state comes on rapidly with low muttering delirium. The pupil, before contracted, is now dilated. 38o DISEASES OF UNCERTAIN ETIOLOGY The urine may be detained. Paralysis of the sphincters or grave complications terminate the attack. About the thirteenth or fourteenth day the fever terminates by crisis, profuse sweating, critical diarrhoea and diuresis, with excess of urates. Convalescence then begins. Second attacks are rare. COMPLICATIONS. Bronchitis, Broncho-pneumonia, Retention of urine. Hyperpyrexia, Parotid bubo, Pyasmic abscesses. Thrombosis of femoral vein, Bed sores. Gangrene of extremities. Relapsing fever and Acute miliary tuberculosis. TREATMENT. Good air and plenty of it is essential for this disease. Shield the eyes from excessive light. Liquid and bland foods should be given as they can be assimilated. All noise in the sick room should be avoided. Strychnine, digitalin, &c., are necessary for the heart. Hyoscine, bromides, or morphine may be required for nerve symptoms. 20 c.c. intravenously of the serum from patients who have been convalescent twelve days have been useful in some cases; repeated if necessary. All clothing must be thoroughly disinfected at once. All hair must be shaved ofif and the whole body thoroughly cleansed. No lice, no t3^phu9. H^MOGLOBINURIC FEVER (Blackwater Fever). DEFINITION. An acute fever of uncertain causation characterized bv excessive blood destruction, jaundice, h^emoglobinuria, diminution and sup- pression of urine. DISTRIBUTION. Most commonly in tropical Africa and parts of India. It is less commonly found in South Italy, Sicily, Greece, Asia Minor, Southern Russia, China, Siam, Malay Peninsula and the Southern regions of the United States. Central and South America and Brazil in particular, West and East Indies, and Polynesia. It is extremely rare in the Roman Campagna, the classic land of malaria. Its endemicity is said to be limited to low swampy grounds. HJEMOGLOBINURIC FEVER 381. It appears to have some dependence upon meterological conditions. It attacked the Chinese labourers when building the Congo railway. It attacked the labourers constructing the Corinth canal. It attacked the Chinese army at Kwangsi like a plague. It attacked the prisoners in Sardinia in 1885. AETIOLOGY. Theories. — These are numerous. The chief are as follows : — (i) A manifestation of an active malarial infection. (2) The result of quinine poisoning. (3) That it is due to a specific organism. (4) That it is a condition brought about by previous malarial infection. (1) That it is a Manifestation of an active Malarial Infection. Pro. It has been pointed out : — (i) That where the malarial mortality is high, blackwater fever is not uncommon, but it is scarce where the malarial mortality is low. (2) That people attacked with blackwater fever had pre- viously suffered from malaria and had usually been attacked several times. (3) That the day preceding the hsemoglobinuria the patient's blood contained parasites in 95'6 per cent, of cases, while the day after the attack they were seen in only 1 7" I per cent, of cases (Stephens). (4) That there is found a monoieucocytosis. Con : — (i) That it has occurred in people who have never had malaria. (2) That it is uninfluenced bv quinine. (3) That in Panama h^emoglobinuria is rare, but acute malarial infection very common. This view is not widely held. Most seem to agree that acute malaria may be the exciting factor, but that some other agent is necessary. (4) That blackwater is rare in some districts where malaria is most rife. (2) That it is the Result of Quinine Poisoning (Koch). This view is not widely held because — Quinine administered to patients without previous malaria has never caused hasmoglobinuric fever, no matter how great the dose. H^moglobinuric fever has occurred when no quinine has been administered. 382 DISEASES OF UNCERTAIN .ETIOLOGY The taking of quinine does sometimes determine blackwater, but much more often it does not. Blackwater fever was known to Europe by Hippocrates and others long before cinchona bark was imported. Some assert that quinine will improve and in some cases cure the condition. (3) That it is due to a Specific Organism. Sambon in 1898 proposed a Babesia. Many parasites have been described since. The idea perhaps arose because of a somewhat similar disease in animals caused by a piro- plasmosis. The similarity unfortunately is only superficial for : — With hcemoglohinuria in animals — It depends upon infection by a definite organism. That organism is present in numbers proportional to the severity of the disease. Its insect host is well known. No previous illness is necessary or usual before the disease is manifested. If the animal recovers, immunity for it is established. All non-immune animals sufifer in proportion to their exposure to the infection. The symptoms are progressive as a rule, little blood at first, but more later. There is no natural immunity. With hcemoglohinuria in man — No organism except the malarial parasite is constantly found. Where malarial fever is absent hcemoglohinuria is absent also. Those races relatively immune to malaria are relatively immune to blackwater. One attack of hcemoglohinuria does not produc«! immunity, but perhaps increasingly tends to predispose to another attack. The writer had a patient with three attacks within eighteen months, each one increasingly dangerous. Relapses are not uncommon. Most blood is usually passed early; the amount diminishes with the disease. That it is not in the least infective is against its being of parasitic origin. Hasmoglobinuria is so acute that the parasite, if one there is, must be numerous and possessing high powers of vitality. There may be long interv^als between two cases in the same district. If a parasite, how does it survive? H^MOGLOBINURIC FEVER 383 (5) That it is a Condition brought about by a previous Malarial Infection. A case of h^emoglobinuria usually gives a history of one or more attacks of malaria. Small doses of cjuinine in some such Central African patients is sufficient to precipitate the disease (Sandwith). The subtertian parasite seems to be usually the parasite of the malaria. This accounts for the statement that malaria (benign tertian or cjuartan) may be prevalent, but no h^emoglobinuria. The Ancon Hospital Records show that malaria complicates prac- tically every other disease, but neither clinically nor at autopsy has blackwater fever complicated any infectious disease other than malaria. In not one case of blackwater can evidence of malaria, either remote or immediately prior, be excluded (Decks and James). The hiemoglobinuria seems to be a h^emolytic toxic action. Subtertian malaria has a strong toxic action, as evidenced by the cytolytic action upon the kidney cells and the parenchymatous focal neurosis of other viscera. Haemolysis is closely allied to cytolysis, in the former case the cells of choice being the erythrocytes. 25 per cent, of the red cells may be destroyed as a result of one paroxysm of sub- tertian malaria. Although the life of a red cell is perhaps only four weeks and the whole is regenerated every twenty-eight days, the vascular system could not long stand the strain. The writer had a case that gave 850,000 red cells per cubic millimetre the second day of the fever. In studying 230 cases of hcemoglobinuric fever at Ancon Hospital, Decks and James write their views thus : — An haemolysis has two groups, a combining and a destructive group. The first must unite with the cell before the latter can destroy it. The exciting factors are : — (i) Renewed malarial paroxysms to produce sufficient toxin to overwhelm the cells. (2) Then a lowering of body resistance. (3) The adiliinistration of ciuinine which may act in either of two ways : — By depressing the vital processes of the bodv, or By acting as the toxophore radical of the h^emolvsis. No regularity of results following the administration of ciuinine can be predicted. H^emoglobinuria has followed the taking of i grain of quinine, in others it has not resulted after taking 30 grains over several days, but it does not occur except in tliose who have had a previous attack of malaria. Forty-two thousand cases admitted for diseases other than malaria did not develop one single case of blackwater. 94-6 per cent. (246) of 384 DISEASES OF UNCERTAIN ETIOLOGY blackwater patients showed one or more previous attacks of malaria. In 230 cases subtertian parasites were found in 76'4 per cent, of cases^ and benign tertian in 23*6 per cent, of cases. Most of the cases develop after twelve months' residence in the tropics. After three to four years' residence in an endemic region the ha^moglobinuric rate diminishes, hence length of residence appears to be a factor. Decks and James sum up their investigations thus : — (i) Hiemoglobinuric fever is a manifestation of malarial toxicity, for the most part brought about by repeated attacks of malaria. (2) It mav appear coincidentally with an acute malarial paroxysm. (3) It mav be determined by any depressing influence. (4) It mav be induced by the administrations of quinine. (5) Neither quinine alone, nor malarial infection alone, causes hccmoglobinuria, but one or both of these, plus the toxin eventuated during the course of one or more malarial attacks. (6) Syphilis is a predisposing factor, because of its influence in the production of malarial recrudescences. (7) The treatment varies with the condition present. (8) To ensure against the recurrent attacks of malaria, with the subsequent production of hasmoglobinuric fever, it is necessary to raise the patient's resistance to a maximum, and to eradicate the malaria by a thorough course of treatment with quinine. There is no proof that it has spread from one country to another ; on the contrary, the disease manifests itself when certain conditions relative to the epidemiology of malaria and to that of no other disease are present. The conditions are : — (i) The presence of a population non-immune against malaria. (2) The prevalence of malaria in such quantity as to produce an almost continuous infection in this population. (3) A large proportion of subtertian malaria, because the amount of blackwater fever is in direct proportion to the intensity of this variety. (4) The neglect of prompt and continued administration of quinine, especially in primary attacks, to persons non-immune against malaria. In every locality, without exception, where these conditions obtain, hcemoglobinuric fever is found (Deeks and James). PATHOLOGY. Christophers and Bentley, working on the malarial theory, put forward the following views : — (i) Laverania malari^e, the subtertian parasite, acts upon the endo- H^MOGLOBINURIC FEVER 385 thelial cells of the blood capillaries, stimulating them to excessive destruction of red blood cells by phagocytosis. (2) This phagocytosis results in the production of an auto- Diagrammatic representation of the condition of the kidney in health (A), during experimental hemoglobinuria of rabbit (B), and in suppression of urine following upon blackwater fever (C). In B small casts are present in some of the uriniferous and collecting tubules ; in C large casts are present in many of the uriniferous and collecting tubules. In the latter, considerable enlargement of the kidney is also observed. For the sake of comparison B is represented as tri-papillary instead of being uni-papillary, as in the rabbit. — (From the " Annals of Tropical Medicine and Hygiene," Liverpool University, by permission.) h^emolysin retained in the endothelial cells until set free by some exciting cause as chill, over-exertion, &c. (3) The hc'emolysin is then suddenly set free and destroys the red cells by solution in the plasma, principally in the blood of the liver, kidney and spleen. (4) This lysiemia produces h^emoglobinaemia, quickly appearing in the urine as oxyh^emoglobin, which may become meth- haemoglobin on standing. (5) Some of it, the liver probably converts into bile; the remainder passes out in the urine. (6) Large coarsely granular casts in the ducts of Bertini mechani- cally block the tubules and cause suppression of urine (Barrett). JOU Plahn believes it to be the result of nervous inhibitioi glomerular secretion. Others suppose it is the result of i Diagrammatic representation of a renal lulmle. (A) normal; (B) co:-nmencing d( h£emoglobinuria ; (C) sufficient deposit to be washed on and cause obstruction of t^ the pyramid. (After J. O. Wakelin Bariatt and Warrington Yorke.)— From the ' of Tropical Medicine and Hygiene;' Liverpool University, by permission. caused by the disease. The improvement of the conditi the B.P. is raised, as when after salines are given, supi mechanical theory. P.M. The cardinal features are : — Jaundice of the tissues. Liquid blood. Swollen and congested kidneys. The kidneys are enlarged, dark red, degenerated tubular epi the tubules block with granular material. The liver is enlarged, the gall-bladder full of inspissated bi of livf;r necrosis with thrombi in the sub-lobular veins, and h^em in the cells. The bone-marrow is yellowish, fluid, or gelatinous. ESSENTIALS OF TROriCAL MEDICINE. BLOOD-SPECTRA COMPARED WITH SPECTRUM OF ARGAND-LAMP. Spectrum of Spectrum of Spectrum of Spectrum of Spectrum of Spectrum of Spectrum of Spectrum of Spectrum of Spectrum of Most of the above Argand'lamp with Fraunhofer lines in position. Oxyhaemoglobin in diluted blood. reduced Haemoglobin. carbonic oxide Haemoglobin. acid Haematin in etherial solution. alkaline Haematin. Chloroform extract of acidulated Ox-bile. Methaemoglobin (alkaline. ) Haemochromogen. Haematoporphyrin. Spectra have been drawn from observations by Mr, NA/. LEPRAIK. F.C.S. Face page 386, HEMOGLOBIN URIC FEVER 387 The blood is thin, watery, diminished tonicity, red cells and hb, much reduced showing degenerative changes. Malarial parasites or pigment may be seen. There is leucocytosis during the fever, leucopenia with a mono- nuclear increase afterwards. The urine is yellow, dark red, blackish. Diluted, the spectroscope shows oxy- or meth-ha?moglobin, low specific gravity, a dark brown granular deposit from destroyed blood cells. When boiled and allowed to stand for some time a bright purple colour develops (Plhen's reaction). The urine does not decompose for some time. Albumin is plentiful. Phosphates are diminished. Urobilin can be seen with the spectroscope after acidulating the urine with acetic acid and extracting witli amyl alcohol. SYMPTOMATOLOGY. As a rule the patient has had recurrent malarial attacks, and has taken quinine spasmodically or not at all. White people are more prone to it than coloured. Prodromata are often absent. When present there mav be lassi- tude, general pains, loss of appetite, restlessness, yellow tinging of skin and conjunctivae. Course: shivering fits, headache, severe pains in back, hiccough, nausea, retching, vomiting food, then green bile. Excessive thirst,, constipation, urgent desire to micturate. Liver and spleen tender, skin hot and dry, yellow skin and conjunctiva. Temperature rises rapidly to io3°-i04° F., pulse 100-120, small, regular, readily com- pressible. Blackish urine with burning sensation of the urethra. After a few hours perspiration sets in, temperature falls to 100° F., the urine clears, convalescence begins, or in a severe case vomiting increases, temperature again rises, diarrhoea sets in with bilious motions and blood. Some recover, others die of exhaustion, hyper- pyrexia, coma, anuria, and ura?mia as a result of this or successive attacks. In any cases of recovery convalescence is much protracted. There is always grave anaemia. The mortality varies from 4 per cent, to 50 per cent. The figures on the West Coast are of interest, as compared with those of East Africa and Nyasaland : — Gold Coast . 21 cases ... r cent. mortality Sierra Leone 10 lO'O Southern Nigeria . 21 ... 23-8 Northern Nigeria ... 17 ••• 35'-9 East Africa Protectorate . i^ ... 26-6 Uganda 58 ... 20'0 ') Nyasaland 7 ... 14-2 1' 388 DISEASES OF UNCERTAIN .ETIOLOGY The urine is dark brown, acid, separates on standing into two layers, the upper clear or port-wine colour, the lower brownish grey with hyaline, and hb. tube casts and debris. Red cells are few or absent. Epithelial cells may be seen. TREATMENT. Rest in bed is absolutely necessary with the best nursing available. The patient must not move if the attack is severe. All kinds and plenty of bland fluids as the stomach will retain them. Calomel followed by mag. sulph. can be given with care. Hot, moist applications over the stomach and loins and hot-air baths are always good. If parasites are present cjuinine is indicated, but the results must be watched. If the condition is aggravated withdraw it for a few days, and then repeat it. The chief essential indications are : — (i) To flush the kidneys. (2) To raise the blood-pressure. (3) To strengthen the heart. Give digitalin, ergotin and morphia for the vomiting when present. Normal salines, and plenty oj them, must be given one way or other. These can be given per rectum with a rubber catheter well inserted ; Or, and also subcutaneously, 8 to 16 ounces every three hours; Or, and also intravenously (Rogers), four pints at a time. Some claim good results from salvarsan given in two pints of saline (Burkitt). Burkitt and MacGilchrist agree that the cause may be due to increased alkalinity of the blood, in consequence of which the former administered potassium and sodium bicarbonates with success, giving them in i drachm doses hourly in plenty of water. When the danger is past give some mild ferruginous preparation, followed by Fowler's solution. Syphilis when present must be treated as soon as possible. The patient should leave the district early and advised not to return. The saline treatment is all-important. Fluid must be passed into the circulation. It is useless to give pilocarpine when the blood has little fluid to give up and the kidneys already exhausted by the lack of it. All urine must be carefully measured and the time noted when passed. If the amount is decreasing put in more fluid by mouth, rectum, subcutaneouslv or intravenouslv, until the amount increases to the FA VISM 389 normal, hut an excess of fluid injected and none excreted may so over- tax the heart, already weak, as to cause sudden death. A red cell count should be done every other day, and the move- ments of the patient, such as sitting up and using the bed-pan, &c., must be controlled thereby. To attempt to Avalk too early may cause sudden death. Exercises should be graduated and permitted according to the red cell regeneration, this being a much safer guide than the feelings of the patient or the temperature chart. One patient mav regenerate in much less time than another. FAVISM. DEFINITION. An acute febrile anaemia with icterus and haemoglobinuria. DISTRIBUTION. It occurs in Sardinia, and perhaps other Mediterranean ports. ETIOLOGY. Sufferers blame fresh beans, raw or cooked, and even the smell of bean flowers when in blossom. It usually occurs in the season when the bean ripens. SYMPTOMATOLOGY. A few hours after ingestion of beans or exposure to the scent of the flowers an acute febrile anaemia develops, and the red cells may be rapidly reduced to 2,000,000 per c.mm. and the hb. to 20 per cent. There is icterus; the liver may be tender to pressure; the urine contains free hb., urobilin and indican. The blood-serum, however, is clear and does not contain any hb. Sometimes there is bilious vomiting and diarrhoea. Children usually die, adults recover. The blood quickly regenerates. Malaria and quinine can be excluded from the causative factors. Little is known about it at present. TREATMENT. As for hiemoglobinuria. HEAT SYNCOPE AND HEAT STROKE. Of this disease there are two groups, which may be classified thus : — (i) Heat syncope, an exhaustion with little or no fever, but with some cardiac failure as a rule. 25 390 DISEASES OF UNCERTAIN ETIOLOGY (2) Heat stroke : (a) Direct, with liigh body temperature after exposure to the sun ( =- sunstroke). {b) Indirect, with high bodv temperature but exposure to the sun is not necessary. The difference between heat s}'ncope and heat stroke can be tabulated thus (Bram) : — Heat Syncope (i) History of exposure to excessive heat, usually indoors (2) Onset gradual, no convulsions or paralysis, but prodiomata as head- ache, dizziness, nausea, &c. (3) Rarely, loss of consciousness (4) Skin cool, pale and clammy (5) Conjunctivas pale, pupils dilated or normal (6) Temperature normal, subnormal or slightly elevated 100"- 102° F. (7) Pulse weak and thready (8) Respiration shallow and sighing (9) Course greater in duration, pro- gnosis favourable, usually termi- nating in recovery in a few days (10) Recovery usually uninterrupted and complete (11) Usually debilitated by disease Heat Stroke History of direct exposure to the sun's rays Onset sudden, often with convulsions or paralysis Usually complete unconsciousness Skin hot, dry, flushed Injected conjunctivae, contracted pupils Temperature very high, io5'^-ii3'' F. Pulse high and bounding Respirations irregular, often Cheyne- Slokes in type Course brief, with guarded prognosis, terminating in death or recovery in from a few hours to a day or more Complications and sequelae not uncommon Previously in normal health (1) HEAT SYNCOPE. DEFINITION. Faintness or fainting as a result of exposure to a high atmospheric temperature associated with humidity and bad ventilation in persons whose bodies have been debilitated by disease. vETIOLOGY. The two necessary factors are ; — (i) High wet bulb temperatures. (2) Abnormal bodily health. This latter includes any organic disease, especially chronic alcoholism A\hich causes fatty degeneration of the heart's muscle, allowing dilatation under conditions of moist hot air in badly ventilated places. Unsuitable clothing and vigorous exercise also predispose. Alcoholism is the most potent factor. SYMPTOMATOLOGY. The patient may be in a badly ventilated building as a theatre or church, in a crowd, or wearing unsuitable clothing as soldiers on the march, or unduly fatty. The patient becomes giddv, staggers and falls. There is pallor, small pulse, dilated pupils, shallow breathing. HEAT SYNCOPE AND HEAT STROKE 391 cold skin, temperature normal or sub-normal, partial or complete unconsciousness. Headache is common. Death is the exception. There are usually no after symptoms. TREATMENT. Open air, apply cold water to the face, loosen the clothing about the chest. Ammonia salts to the nose. Brandy to drink. Injection of strychnine when necessary. Bed, hot bottles and stimulants if the temperature is sub-normal. (2) HEAT STROKE (Sunstroke). (A) Direct. DEFINITION. A febrile condition resulting from exposure to the direct rays of the sun accompanied by pulmonary congestion, convulsions, coma, recovery or death. iETIOLOGY. A dog shaved and exposed to the direct rays of the sun, dies. If it is covered with coloured glass, nothing happens. This variety is common in Persia and India, but may occur any- where if the temperature is high enough. The theories as to the causation are : — (i) Caloric, a hyperpyrexia! condition. (2) Actinic, due to the sun's chemical rays. (3) Microbic, due to some germ (Sambon). (4) Toxic, due to poisons generated by the excessive heat. Manson's classification is as follows : — (a) Superheating of the blood. (h) Paralysis of the thermic centres causing: — (i) Excessive production of heat. (2) Retention of body heat. (3) Expansion of cerebro-spinal fluid causing pressure on tb,e brain. (4) Vasomotor paralysis. ^ (5) Paresis of heart ganglia. (6) Excess of carbon dioxide in the blood. (7) Coagulation of the mvosin. (8) vSuppression of sweat. (9) Deficient serositv of the blood. The thick skull and black skin of negroes are protective. 392 DISEASES OF UNCERTAIN ETIOLOGY Punioni, who has done recent work on this subject, concludes thus : — The tissues which compose the cranium from the dura mater to the skin, are diathermal both to the yellow-red and to the violet-ultraviolet rays, but they absorb the red and green-blue rays. Sunstroke is brought about by the action of the violet-ultraviolet rays upon the meninges and the cerebral substance. At the same time, one must not completely forget the red-yellow rays, which facilitate the photo-chemical action of the violet-ultra- violet rays by means of the heat which they produce. With regard to prophylaxis against sunstroke, it is well to protect the susceptible parts (head, neck and spine) with green clothing, which absorbs the violet-ultraviolet rays as well as the red-yellow, letting pass the green rays only, which are harmless because they are arrested altogether by the tissues of the cranium. Since in practice it is necessary to combine the prophylaxis against sunstroke with that against heat stroke, it is advisable to cover the green, heat-absorbing clothing with white material, which is well known to possess the greatest reflecting properties. The eyes should be protected by means of coloured glasses; these again, for the above reasons, should be green. SYMPTOMATOLOGY. The patients may be affected in various ways under different con- ditions, thus : — (i) One may have been marching long in the sun, with tunic fastened up to the throat, when there are headache, convulsions, and not infrequently incontinence of urine. (2) Or the patient may perspire profusely, turn pallid with rapid respirations and fall partly unconscious. (3) Or excessive thirst may be experienced followed by coma. (4) Or a headache may become more and more severe, with intoler- ance to light; this may be followed by partial coma, with recovery or death. If recovery there is often headache for six or eight weeks. (5) Or after prolonged exposure to the sun, a hot dry skin, estab- lished intolerance to light, sound and movement. There may be vomiting. Recovery may be : — (i) Sudden and complete. (2) Or prolonged over several days or weeks, then clearing up. (3) Or persisting and leaving some permanent trouble as impaired memory, partial blindness or deafness, insanity, epilepsv. HEAT SYNCOPE AND HEAT STROKE 393 It appears to be a form of meningitis. The temperature rises suddenly as a rule, 104°, 107°, 110° F. There may be frequent desires to micturate. PATHOLOGY. Post mortem, there may be little found. There may be a post-mortem rise of temperature, or a raised tem- perature maintained for some time after death. When the temperature has been known to fall after death it has never been known to rise again after any disease. The lungs are congested. The vessels in the meninges are con- gested. There may be minute hemorrhages in the brain substance. There is a coagulative necrosis of the nerve cells. (B) Indirect. This is much the same as the direct but exposure to the sun is not necessary. It may come on at night. There may be prodromata. Sambon savs that it has a distinct geographical distribution, and is caused by some microbic agency. Newcomers are more liable to it. Long residence produces a relative immunity. The predisposing causes are as before mentioned. It is most prevalent in the hottest season. It may become epidemic at times. It has a definitive course, peculiar lesions, tends to terminate by crisis and thus behaves like a specific fever. Some authorities affirm that this is the same as the direct form. THE MORTALITY OF HEAT STROKE. Early judicious treatment is very effective. The mortality is 15 per cent, to 20 per cent. It is stated that among the English troops in India one in four die. During the Great War, 1,026 men were passing some hours in a train in India. There were 136 cases of heat stroke with 15 deaths. Overcrowding was blamed chiefly. Sir Victor Horsley died from heat stroke while on active service in Mesopotamia. DIAGNOSIS. Diagnose from A, E, I, O, U, and sometimes D and T. A Icoholic poisoning. E pileptic conditions. / ntracranial causes such as meningitis, cerebral haemorrhage, thrombosis, embolism, gummata, and all tumours. 394 DISEASES OF UNCERTAIN ETIOLOGY O pium poisoning. U raemic conditions. D iabetic conditions. T ropical diseases, malaria, sleeping sickness, &c. TREATMENT. Remove the patient to a cool place and loosen clothing. Application of cold water and cold sponging. Ice is essential for hyperpyrexia. Put the patient upon a rubber stretcher covered with a sheet and the head raised, a sheet also covering the patient. Place ice on sheet for two minutes and put the patient between blankets in bed. Give tincture of digitalis, 30 minims. If the patient is plethoric, bleed from the median basilic vein. Cease treatment when the temperature is down to 102*^, 103° F. in the rectum. Later apply hot bottles and stimulants. Avoid strychnine as convulsions are not uncommon. Artificial respiration may be necessary for an hour or longer. Antipyretics are dangerous. Relapses are common. Salines and bromides may be useful. Urge total abstinence. Blue glasses and helmets should always be worn afterwards. Spinal pads and neck shields are preventive measures. SOME UNCLASSIFIED FEVERS. (1) JAPANESE RIYER FEVER (Tsutsugamushi Disease). DEFINITION. An acute endemic febrile disorder caused by the bite of the larval form of the mite Leptus akamushi, associated with a small local necrotic area, enlarged proximal glands, and an exanthematous eruption. DISTRIBUTION. The Island of Nippon (Japan), in the Akita and Xugata districts. The causative mite appears in the areas flooded bv rivers a few weeks after the waters have subsided. Because of them the districts have been almost abandoned. iETIOLOGY. This is unknown. Bacterial, protozoal and chemical theories have been advanced. SOME UNCLASSIFIED FEJ'ERS 395 An attack does not confer immunity. Poor people of reduced resistance entering the infected lands from Julv to October may contract the disease. SYMPTOMATOLOGY. Incubation is four to ten days. Prodromata, nothing definite, sometimes malaise and giddiness. Course. It lasts about fourteen days. Rigors, frontal headache, temperature 101° to 103° F. Tender enlarged lymphatic glands nearest to the bite of the mite ; a vesicle or blackish necrotic patch indicates the latter. Temperature rises to 105° F. The necrotic area is thrown off leaving a circular red punched-out ulcer. The sixth to seventh day a large red papular (2 to 5 mm.) eruption occurs on the face and then spreads over the body with a somewhat macular appearance. The rash does not itch. The gums may become spongy and bleed. Respirations are increased, B. S. harsh, rhonchi all over chest. The conjunctivae are injected. There is lachrymation. Hyperaesthesia is common and is present all over the body. Lysis begins about the fourteenth day and lasts about one week. In bad cases, coma, hvperpvrexia, cardiac failure or pulmonary oedema ma}- carrv off the patient. MORTALITY. About 30 per cent. die. It increases with age. i2'5 per cent, during the first ten years of life and 57 per cent, in the seventh decade. TREATMENT. This is symptomatic. (2) PIGMENTARY FEVER (Cobb). Occurs in Bengal during the hottest months. Sudden onset; the temperature rises to io3°-i04° F. Headache, nausea, vomiting, and a peculiar pigmentation of the nose and cheek. The fever lasts eight to ten da^'S. Little is known about it. (3) HYPERPYREXIAL FEVER. Seen on the West Coast of Africa and Ceylon. Onset like malarial fever with sweating, but no parasites are seen. The second day the patient feels almost normal. The third day the temperature begins to rise and reaches from i04°-io7° F., at which it tends to remain. Drue's are useless. 396 DISEASES OF UNCERTAIN ETIOLOGY Cold baths reduce the temperature temporarily during the first six or seven days. The temperature then rises to iio° F. about the eighth day. Delirium sets in, coma and death in 50 per cent, of cases. Others recover. The temperature remains at about 105° F. for three weeks, and falls to normal about the sixth week. Little is known about the aetiology, &c. The viscera, blood and urine appear to be normal. (4) DOUBLE CONTINUED FEVER. This is seen in China. Onset insidious. Temperature gradually rises to 104° F., remitting three degrees daily; pulse slow, tongue moist and red, constipation. After ten to fifteen days the temperature falls to normal by lysis. After a lapse of two to seven days the fever is repeated and lasts about ten days. The anaemia is considerable. Convalescence is prolonged. The mortality is low. Quinine is useless. (5) LOW INTERMITTENT NON-MALARIAL FEVER. This is seen in India, China, Siam and Ceylon. The onset is insidious, or it may follow a mild form of influenza. The fever is remittent between 98*4° and 102° F. Chilliness is felt daily between 10 and 12 o'clock. The eosinophilic cells are increased even when worms are absent. The course of the fever is long, some over five months. Nothing else abnormal is found. The patient should be sent to another climate. (6) NASHA FEVER. It is seen in Bengal from April to August annually. It is rarely present in the cold weather. The onset is sudden M-ith chill, high fever, hyperemia, swelling of the nasal mucosas, pains in head, neck and shoulders. The face is flushed, the pupils contracted. There is a papular eruption, some bronchial symptoms. The fever is remittent and disappears in three to five days, when the nasal swelling subsides. Relapses may occur between the first and fourth week after the attack. Some may be severe, terminating in delirium, coma and death. Give saline purgatives, mild diaphoretics, spray nose with iced water. Apply tannin, 10 per cent., and cocaine solution to the nasal mucosae. SOME UNCLASSIFIED FEJ'ERS 397 (7) ARCHIBALD'S FEVER. DEFINITION. An Linclassilied septicaemia in the Anglo-Egyptian Sudan caused by a bacillus of the B. cloaca group. SYMPTOMATOLOGY. The temperature rises 101^-103° F., drowsiness, sometimes delirium, dry furred tongue, sometimes the spleen is slightly enlarged. The temperature falls to normal in about one week, after which a long remittent fever continues. Pneumonia, abscesses, femoral thrombosis may set in. Treatment is symptomatic. (8) BACILLUS ASIATICUS FEVER. This is seen in Ceylon. It is caused by B. asiaticus, two varieties. The disease is a septicaemia. There is a long low remittent fever, sometimes intermittent with marlvcd abdominal pains, but no diarrhoea. The specific bacillus can be recovered from the faeces. The agglutination test can be used. Autogenous vaccines may be injected. (9) THE MACULAR FEVER OF TUNISIA. DEFINITION. An acute febrile disorder characterized by a macular eruption on the abdomen, palms and soles, often persisting for several davs after the temperature has become normal. SYMPTOMATOLOGY. The onset is sudden, rigors, fever, joint pains, injected conjunctiva?, nausea, vomiting, constipation and insomnia. The rash comes from the second to the fourth day, red spots dis- tributed as above. There is lymphocytosis, 35 per cent. The fever lasts two weeks. The rash fades without desquamation. Perhaps this fever is related to typhus fever. (10) FIVE-DAY FEVER (VOLHYNIA FEVER). The findings and views of different observers are very conflicting The causative organism is unknown. Lice have been blamed as the carriers. The course is mild, the prognosis good, and complications are rare. The peculiar features are its periodicity and an increase of the leuco- 398 DISEASES OF UNCERTAIN ETIOLOGY cytes as the fever subsides. Bone cells are seen in the blood. A mild eruption is seen in some cases. Quinine and salvarsan are said to be useless. Collargol is said to act as a specific when given, lo c.c. of a i per cent, solution three doses intravenously. This is said to cure (Heyden). (11) RAT-BITE FEVER. DEFINITION. An acute infectious disease, probably caused by spirochaetes characterized by a local ulcer, followed by constitutional disturbances of pyrexia, eruption and body pains. DISTRIBUTION. It is found in Japan, England, the United States, and Italy. iETIOLOGY. Futaki discovered spirochaetes in the blood and tissues of patients in 1916. The organism was pathogenic to guinea-pigs. Spirochaetes have been found in the suprarenals and kidneys of people dead of the disease. At first the organism circulates in the blood ; then, when immune bodies are formed, they are found in the kidneys. The antibodies thus formed act upon the causative spirochaetes, producing degenerate forms. In this particular the disease simulates Spirochetosis ictero- hsemorrhagica. The etiology seems now to be established, so that upon con- firmation of the above findings it will be necessary to include this disease in another section of this work. SYMPTOMATOLOGY. The incubation is one to three weeks. The onset is sudden. An ulcer forms seven to fifteen davs later at the site of the bite which had previouslv healed. The proximal glands are swollen. There is a papular purple eruption on the body in some cases, pains about the joints and muscles, pyrexia to 104° F., and sometimes delirium. After a few days the fever abates and the patient feels better; then it recurs. These relapses are rather characteristic of the disease. Each attack leaves the patient somewhat better, but it may be months or years before the disease has run its course. The prognosis is good and complications rare. The mortality is about ip'5 per cent. TREATMENT. Arsenical treatment is the rule — as for Relapsing fever. 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The causative organism is present in the blood plasma, and is transmitted naturally by the louse. The blood is always infective in the earlv stages. The organism is not filterable. Spirochetes have been blamed. The virus has been recovered from the urine and from mixed sputum and saliva, but not from the faeces. SYMPTOMATOLOGY. The incubation period is fourteen to thirtv davs, or in some cases shorter. The onset is sudden, with headache, dizziness, pains in the legs (shin pains), back, and behind the eyeballs, pyrexia i03°-i04° F., THE EXANTHEMATA 401 which becomes relapsing in one-half of the cases, erythematous spots in 70 to 80 per cent, of cases, enlargement of the spleen, and slight albuminuria. The fever may be but one sharp rise, or it may oscillate for four to six days, or relapse over six to seven weeks, wdth intervals of five to seven days. Some patients have had some fever for periods of forty to sixty days with only slight remissions. There are three to five, or even seven relapses. RecoverA' is the rule. TREATMENT. This is symptomatic. Arsenical preparations as for Relapsing fever can be tried. All lice should be destroyed and clothing sterilized. Sputum cups and special urine bottles should be reserved for patients and their contents sterilized. THE EXANTHEMATA. As the majority of these are described in general text-books of medicine a few remarks only will be necessary. Scarlet fever may be introduced into the tropics, but does not spread there. Measles is endemic in most tropical countries and may give rise to severe epidemics. Chicken-pox is usually mild, but it may be severe. It more often attacks adults in the tropics. It is common in India from February to March. Variola has long been present in India and Africa. It was perhaps introduced into China from India about the third century B.C. An African mummy has been found with a cutaneous eruption belonging probably to the twenty-eighth dynasty (1200-1100 B.C.). How it came to Africa and India is not known. It is common all over the tropics to-day. " Alastrim." — Perhaps this is a mild variola that does not breed true. This acute specific fever resembles a mild form of variola. It is widely distributed in the tropics. Jenner's vaccination is generally held to be protective. It differs from chicken-pox because of — (i) Confluence of the vesicles in certain cases. (2) Its frequency amongst adults. (3) Partial protection by Jenner's vaccine. 402 DISEASES OF UNCERTAIN ETIOLOGY It differs from typical variola because of — (i) Its low mortality, i to 2 per cent. "Varioloid varicella," Trinidad. Froia a photo by Dr. Scheult. (2) It is less severe in children than in adults; it is often found amongst babies. (3) There is no secondary fever in children. (4) The disease can occur after recent successful vaccination. (5) Vaccination can be successful shortly after an attack of alastrim. THE EXANTHEMATA 403 (6) Some assert that small-pox does not render immunity from alastrim. The onset is sudden, with severe pains, high fever, vomiting, sometimes delirium. The rash appears on the third day, the tempera- ture is reduced and the symptoms disappear, and the patient feels well again. Secondary fever is very rare, about the eighth day when present. Papules become pustules and scales. These fall off with some pigmentation, but very little permanent scarring. Yesicuiar Fever begins like chicken-pox and ends like small-pox. The symptoms are in accordance with these two diseases. The diagnosis is not easy, but the important points to note are : — There is no true pustulation with scarring as in small-pox. And Jenner's vaccination is successful during convalescence. In chicken-pox the vesicles are larger and leave crusts. In alastrim the eruption is often confluent and pustular. The prognosis is good. Papular Fever — This resembles measles, but it has no catarrhal symptoms. The onset is insidious. The prodromata are malaise, depression, rheumatoid pains in back. Course. — The rash appears on the third or fourth day suddenly all over the bodv, morbiliform, bright red, pin-head papules and red macuUe. The face is not much affected. There are papules in the mouth. A slight fever lasts one to two days. There is no enlargement of glands. The eruption lasts two to five days. There is no desquamation, and there are no marks left. The rash itches. Aspirin relieves the pains and calamine lotion the itching. HsBmorrhagic Febrile Gastro-enteritis of Children. It is seen in Guadeloupe. It somewhat resembles yellow fever. The onset is sudden with vomiting, followed by febrile biliousness. There is a remittent fever, slight icterus, obstinate constipation, and later, black vomit. After two to five davs, improvement sets in or the child may die. Convalescence is prolonged. The prognosis is grave. The treatment is svmptomatic. 404 DISEASES OF UNCERTAIN ETIOLOGY DISEASES OF UNKNOWN ^.TIOLOGY AFFECTING THE RESPIRATORY SYSTEM. (1) TROPICAL HAY FEVER (Rhinitis spastica vasomotoria). Adults are attacked. There are violent fits of sneezing, lasting from two minutes to two hours. There is an excess of nasal secretion. Lachrymation, conjunctivae injected, eyelids swollen. These attacks may recur the same day or over several weeks. There may be accompanying asthmatical symptoms. The mucous membrane over the turbinate bones becomes swollen and may cause nasal obstruction. A spray of cocaine, i per cent., and adrenalin locallv is useful. Atropine and strychnine pills may be tried. A clTange of climate may clear up the malady. (2) GANGOSA (Rhino-pharyngitis mutilans). DEFINITION. An ulcerative condition affecting the palate, nose, pharynx, larynx and skin, destroying cartilage and bone, thus producing permanent deformity. DISTRIBUTION. It appears to be endemic in the Batanes Islands, where some hold it to be the early stage of leprosy. It is also found in the Ladrone Islands, Guam, Caroline Islands, Fiji, Murray Island, Panama, British Guiana, Ceylon, Nevis, Dominica and Italy. Dr. Anton claims that it is a blastomycosis due to a specific parasite, the Cryptococcus mutilans. This requires confirmation. SYMPTOMATOLOGY. A sore throat is complained of, caused by a nodule on the palate or at the back of the pharynx, or on the posterior pillar of the fauces. This becomes a superficial ulcer covered by a greyish slough. This ulcer spreads, destroying the adjacent tissue, soft and hard alike, so that in time the skin falls in allowing the nasal and buccal cavities to form one aperture. It may then afifect the face without or the larynx within. Vision may be destroyed. The odour given ofif is most offensive . Ulcers may appear on other parts of the skin which is uncovered by clothing. Ugly deformities are caused by the scarring and contraction. A chronic osteitis may set in simulating that of syphilis. SOME NERJ'OUS DISTURBANCES IN THE TROPICS 405 It mav go on from ten to thirty-five years, progressively or inter- mittently. Wassermann's reaction is always positive. As a rule the o-eneral health is little affected. It is rarelv fatal^ and all tend to recover ultimately. DIAGNOSIS. There are neither signs nor symptoms of s}'pliilis (Johnson does not agree). The spirocha?te cannot be found and iodides are useless. There are no leprosy nodules nor anesthetic patches. Hansen's bacillus has not been found. Its histological characters are not those of epithelioma. There are no metastases and its course is protracted. Tuberculosis is excluded by the absence of Koch's bacillus and other symptoms. Guinea-pigs cannot be inoculated successfully. TREATMENT. Nothing will stop its onward course. Application of iodine tincture or the actual cautery can be tried. Wash the foul ulcers with potassium permanganate or peroxide of hydrogen. Segregation is essential for stamping out the disease. SOME NERVOUS DISTURBANCES IN THE TROPICS. (1) TROPICAL NEURASTHENIA. This is a condition somewhat common in white people, and the better class coloured people residing in the tropics, especially where there is a moist warm atmosphere. There are many predisposing causes, such as malarial fever, or other illness, overwork and alcoholism. Perhaps 30 per cent, to 50 per cent, of white residents become semi- invalids from this malady. Palpitation with heat flushes is usually present. Phobia, especially with regard to diseases, is a common feature. Sleeplessness and irritability are common. The condition is the cause of many clerical errors and inaccuracies which lead to numerous petty worries and manifestations of bad temper. The patient should have a change of work and climate. Neither sedatives nor tonics have been much use in the writer's experience. 26 4o6 DISEASES OF UNCERTAIN ETIOLOGY (2) ENDEMIC PARALYTIC VERTIGO. This is seen in France, Switzerland, Shiivoku, Japan. The aetiology is unknown. An attack begins with the blurring of objects, ptosis, paralysis of the internal rectus causing diplopia, photophobia, affection of colour vision, hyper^eniia of the optic disc. vSpeech is disturbed, mastication difficult through paresis, and later paralysis of the muscles that operate those functions. The head falls forward as the neck and shoulder muscles are affected. The posture may be stooping. Weakness of arms, hands and legs is not uncommonly seen. The attack usuallv lasts ten to fifteen minutes. Between attacks the patient may be perfectly well. The disease is never fatal. Iodides and arsenic should be given. Remove the patient to a healthy climate and district. (3) ENDEMIC PERIPHERAL NEURITIS. This is seen upon the Central African plateau, 5,000 to 6,000 feet high. It is said to affect 3 per cent, to 5 per cent, of the Bantu people. There are shooting or pricking pains in the forearms and legs., accompanied by numbness, with an erythematous rash and local swell- ing of the affected area. Cold and damp increase the symptoms. Heat and dryness diminish them. The gait is peculiar, the patient having the appearance of walking upon his toes and heels. The whole body may be affected. The disease may spontaneously clear up or it may last for years. (i) LATAH. This is seen in the Malay Peninsula, Java, Sumatra, Siam, Burmah, Philippines, Siberia and North America. ETIOLOGY (Abraham). Auditory, an unexpected noise behind a person. Visual, some unlooked-for movement. Tactile, an unexpected sudden touch. SYMPTOMATOLOGY. The action seen, noise heard or words uttered may be repeated, with the addition often of foul language. ENDEMIC FUNICU LITIS 407 The patienl is conscious, bui cannot apparently control his actions. The hand spontaneously rises to the head. There is a loss of memory of what has taken place. The actions may be impulsive or mimetic. It is not unlike the " jumpers " or " jerks " seen in Europe during the Middle Ages. It is sometimes present during religious revivals of to-day. It has a medico-legal aspect of considerable importance. These subjects are often teased, irritated and made worse. Auto suggestion can be tried. Determination on the part of the patient is essential. (5) AMOK ( = an impulse to murder). This is a term applied to a condition, partly physical, partly psychical, following a period of depression. They are capable of self-violence and of wounding and killing others. Memory fails them as to what they have done. The attack is followed by a condition of stupor. It is seen in Malaysia, Trinidad, India and Liberia. The exciting causes are excessive smoking of Cannabis indica, or opium, or some strong emotion, such as anger, fear or sorrow. After this the patient broods over his wrongs for davs or w'eeks, then complains of the appearance of devils, and goes forth to kill them with his flame-shaped knife or his gun. The attack lasts but a short time. ENDEMIC FUNICULITIS. DEFINITION. An acute specific suppurative inflammation of the spermatic cord of uncertain aetiology. The theories of causation are legion. DISTRIBUTION. It is seen in Southern India, Egypt, West Indies, Ceylon. PATHOLOGY. The whole cord is wholly inflamed, infiltrated and swollen. It may be 3^ inches in circumference. On incising it transversely, yellow pus exudes from the veins of the pampiniform plexus and the vas deferens. The inflammation also attacks the epididymis. There is usually some oedema and a little clear fluid in the tunica vaginalis. 4o8 DISEASES Of UNCERTAIN /ETIOLOGY The microscope shows the veins of the pampiniform plexus dilated with pus cells and thrombi ; the coats of the veins and the vas deferens are infiltrated by small cells. SYMPTOMATOLOGY. The onset is sudden. The patient after a day of hard work feels tired, takes a bath, and has a shivering fit and a rise of temperature. There may be vomiting. There is pain along the cord and epididymis. The condition becomes rapidly worse. On the third dav there mav be continuous vomiting and some hiccough. The temperature is about 102° F., the pulse small and rapid. The cord is swollen, hard and tender. The skin over it is normal. The condition is usually unilateral. There are no signs of gonorrhoea or trauma. If left, a septic^emic condition sets in, the skin becomes jaundiced, cutaneous hemorrhages, the fever rises and the pulse cjuickens, the hiccough is worse, and death follows in a few days. Spontaneous recovery is the exception. TREATMENT. The only effective treatment is prompt surgical interference. The inflamed cord should be excised as high as affected. The testis loses its generative function in all but the mildest cases. EPIDEMIC GANGREXOl\S RECTITIS. (Ackers.) DEFINITION. A very rapidly fatal and spreading phagedasnic disease about the anus and the lower part of the colon, confined to the natives of the northern provinces of South America, Fiji and other islands of the South Pacific. It occurs amongst the children of poor natives and also in animals. SYMPTOMATOLOGY. There is anal itching, tendency to frequent defalcation, inflam- mation of the rectal mucous membrane, the latter developing in about three days, followed by acute dysenteric symptoms, mucus, blood, sometimes bile with much tenesmus. There is some fever, thirst and anorexia. A semi-liquid, slimy, foetid, blood-stained, greenish stool comes awav. INFANTILE BILIARY CIRRHOSIS 409 All food is refused. The thirst becomes intense. Prolapse is common. Gangrene sets in, spreads rapidly, and is fatal. TREATMENT. As practised by the natives. For animals. An enema of strong- lemon-juice mixed with diluted white rum (aguadiente) thrice daily. Dust tlie anus with wood ashes. An oil purgative is given. This appears to be successful in early cases. For children. Give an enema of juice from the stalks and leaves of Spigelia anthelmentica (Pasote). A decoction of the same is given bv mouth thrice dailv. (This mixture is also given as an anthelmintic.) A portion of roasled lemon inserted into the rectimi once or twice daily. It is said to be caused b}' children chewing the green tender stalks of unripe maize. INFANTILE BILIARY CIRRHOSIS. This is a rapidly fatal disease attacking young native children in Calcutta and some other large Indian towns. iETIOLOGY. Children are attacked in their first year during dentition as a rule. They are rarely attacked from the first to the third year. Hindoo children in Calcutta had a mortality of 1,616 (1891-1893), and Mahommedan children in the same citv had 80 dead during the same period. The children of the rich suffer more than those of the poor. It tends to run in families, and attacks them as the young are born. Nearly if not all of those attacked die. Alcohol, syphilis, and malaria have been excluded. The cause is unknown. Some suggest that it is a variety of kala-azar. SYMPTOMATOLOGY. The onset is insidious. The liver enlarges even to the umbilicus. There is nausea, sometimes vomiting, sallow skin, constipation, irritability and anorexia. Low fever sets in with jaundice, pale stools and dark urine. 410 DISEASES OF UNCERTAIN ETIOLOGY There mav be oedema of the feet and hands with ascites. Death from rholccmia ensues in a few weeks to a few months. PATHOLOGY. The bihary cirrhosis seems to be the resuh of some gastric irritant acting upon the hver cells. The cells at first become degenerate, then the intercellular connective tissue is increased, follow^ed by that of the portal sheaths. There is a marked attempt to form new bile ducts between the hepatic cells (Gibbons). TREATMENT. Early removal from the district has been suggested. A change of wet nurse and infant foods could be tried. GOITRE. In the Tropics this condition does not appear to be associated with any geographical or geological condition. Many authorities believe it to be of parasitic origin, and suspect an amoeba which is ingested with water. A new-comer to an endemic district notices that after a few weeks his neck begins to swell gradually. At times it may be stationary, at others progressive until a permanent hypertrophy results. The whole thyroid gland is usually affected. Later it may undergo cystic or adenomatous changes. Removal to another non-endemic district will cause it to diminish in size and to clear up in earlv cases. Salol and thymol arc sometimes given. CLIMATIC BUBO. DEFINITION. A painful gradual enlargement of the inguinal Ivmphatic glands with fever of uncertain as^^tiology. DISTRIBUTION. The East Coast of Africa, West Indies, Straits Settlements, China, Madagascar, Chille, Uganda, and many other places. iETIOLOGY. Hewlett has isolated a bacillus not decolorized by Gram and not unlike the B. pestis. Cantlie believes it to be a form of attenuated plague, pestis minor, Hewlitt's isolation supporting it. Others hold that the disease is a distinct entity. GOUNDOU 411 PATHOLOGY. The gland capsule is thickened. The lymphocytes are in great excess. Ha^morrhagic foci may be seen. There are numerous typical plasma cells that are absent in plague. The retractile cells of Recklinghausen are absent, but present in plague. SYMPTOMATOLOGY. The onset is gradual. Several days of malaise precede slight fever and pain in one or other or both inguinal glands. The inguinal glands are enlarged, hard and tender. These may become as large as a goose's ^gg- A.S a rule they do not suppurate. Lymphangitis is absent. Aspiration yields a little sterile fluid, but no pus. The fever is low and irregular, about 102° F. The disease may last a few days, weeks, or months. The general health is good. TREATMENT. This is symptomatic. Rest in bed. Lead lotion, ichthyol and belladonna ointment, and mild aperients. Incise when sepsis is present. GOUNDOU. This condition is a bony, bilateral, symmetrical swelling situated on either side of the root of the nose. It is rarely unilateral. Some observers assert that it is a general condition that affects the other bones of the skeleton also. It occurs in young people of native races and is commonest in the West Indies. The writer has seen it in the Kasai basin, Central Africa and on the Gold Coast. The condition has been reported in an European (Cantlie). The aetiology is unknown. PATHOLOGY. Outside the bony swelling is a thin layer of compact bone, all the remaining mass being spongy bone. The covering periosteum strips off easily and shows no sign of inflammation. The growth may be attached to the nasal bone, the nasal process of the superior maxilla, or to the maxilla itself. The skin over the tumour is always freely movable. 412 DISEASES OF UNCERTAIN .ETIOLOGY SYMPTOMATOLOGY. Gradual onset, pain in the nose, bloody discharge lasting six to eight months. As this disappears a swelling appears and increases in size. The vision may be interfered \vith. ' The deformity is sometimes hideous in the extreme. There mav be polvpoid-like excrescences protruding from the nasal mucous membrane. The growth ma}- stop at any time. TREATMENT. Surgical removal is easy and effective. Other treatment is symptomatic. BIG HEEL. This is a condition seen on the Gold Coast and Formosa. The aetiology is obscure. The attacks come in the wet season with sudden onset and fever. There is great tenderness over the os calcis so as to prevent walking or sleeping. In three to seven days tlie bone enlarges and increases progressively for two weeks or so, during which time the pain becomes less and the fever disappears. After a month the bone ceases to grow and remains like this for one or two months, when the patient is able to M'alk with some degree of comfort. The growth then gradually diminishes, but never wholly disappears. It usually affects both sides. The ankle-joint is never affected, and the tarsal bones but seldom. The bone should be trephined or gouged down to afford relief. AINHUM ( = to saw or to cut). DEFINITION. A chronic dystrophy of the fifth (rarel}- other) toes in native races, characterized by the formation of a furrow at the digito-plantar fold, which extends and deepens until the toe is severed. It is seen in man}' parts of the Tropics. PATHOLOGY. There is irritation of the cutaneous epithelium causing an internal proliferation, extending to the cutis, injuring the vasomotor nerves, causing spasm of the vessels, endarteritis obliterans, fibrosis of the cutis and rarefying osteitis which separates tlie digit. CHAP PA 413 No organisms can be found. ( The source of the irritation: why this pariicular spot should be cliosen, and why a fibrotic ring is caused, has not yet been made clear. SYMPTOMATOLOGY. There is no general disturbance. It begins on the inner side of the digito-plantar furrow. An ulcer may form that causes pain. The condition may last two to fifteen years until the toe is severed. In 10 per cent, of cases the fourth toe is affected. TREATMENT. No known treatment is of any avail. Some divide the fibriotic ring early so as to save the toe, but the condition usually progresses. CHAPPA. This is seen in Lagos. There are severe pains in the muscles and the joints of the ■extremities. After a few months the pain increases and the joints swell. Nodules, subcutaneous, the size of a goose Qgg appear in different parts of the body. The skin over them ulcerates, later exposing a fatty base. There may be one or many nodules. When ulcerating thev ma}' coalesce. Some of the nodules are absorbed without ulceration. The ulcers may last for years. The joints may become permanenll\- disorganized and the bones affected. It may be a tertiary phase of yaws (Manson). Mercury and iodides are useless. Scraping and antiseptics are good measures. Neosalvarsan could be tried. PONOS ( = pain). This disease, affecting young children of Spezzia and Hydra in the Grecian Achipelago, resembles infantile biliary cirrhosis of Indian towns in that — It is confined to very young children. It is endemic in particular districts. It tends to run in families. It is invariablv associated with the disease of an abdominal viscus. 414 DISEASES OF UNCERTAIN ETIOLOGY SYMPTOMATOLOGY. It affects children of the rich and poor alike. The onset is rather sudden in the first year of life. Sallow tint of skin and irregular fever are present. The spleen enlarges much and is tender, hence the name " ponos " = pain. Prostration is marked and emaciation progressive. Late in the disease oedema and ascites set in. Hcemorrhages from the gums and from other organs are not uncommon. Bronchitis, pneumonia, dysentery, peritonitis and meningitis are complications to be looked for. The disease lasts from two months to two years. A pronounced leucopenia has been found. Some suggest because of this that it may be of protozoal origin, related to kala-azar. TREATMENT. Nothing specific is known. TROPICAL LIVER. A condition of hepatic congestion brought about during the first two years' residence of Europeans in the Tropics. Chills, changes and excesses of food and drink cause hypera^mia of the liver, congestion, blood stasis and diminution of the function of that organ. SYMPTOMATOLOGY. There is frontal headache, malaise, nausea, dyspepsia, constipation and pale-coloured stools. The liver is slightly enlarged and tender, slight icterus, diminished urine, irritability, slight fever to ioo° F. TREATMENT. Rest in bed in acute cases. Calomel, 2 grains, followed by saline purges. Hot fomentations to liver region are good. Bland diet, no alcohol or spiced foods, moderate exercise, avoid chills. The following mixture has been found useful : — H Ammon. carb. ... ... grains 2-5 Sod. bicarb. ... ... ... ... ... ,, 20 Citr c acid „ 20 One ounce thrice daily. BOOMERANG LEG 415 BOOMERANG LEG. This is a bowing forwards of the bones of the legs occurring in young aduhs during the period of gro^\l]l. It is of uni^nown causation. DISTRIBUTION. It occurs among the natives of Western Australia, Northern Territory, North Queensland, Torres Straits and British New Guinea. AETIOLOGY. The post-mortem appearance suggests a chronic osteomyelitis of both tibia?. It begins as a rarefying osteitis, passing on to a con- densing osteitis, metaplasia of the fibrosed marrow, and a new peri- osteal formation. Syphilis and tuberculosis can be excluded as causative factors. SYMPTOMATOLOGY. There are tenderness and pain in the tibia' and fibuhe, the bones may become soft and bent until the}- graduall}- assume the boomerang curve with the convexitv outwards. The patient becomes flat-footed and walks w ith a shuffling gait. The subcutaneous tissues become inflamed and tender. There is some febrile disturbance. The symptoms gradually disappear, the bones resume their former hardness, but the deformity remains. WHITMORE'S DISEASE. DEFINITION. A septicasmic infection of insidious onset, characterized by nodules and abscesses resembling those of glanders in the lungs and viscera, occurring in morphino-maniacs usually and those addicted to the cocaine habit. A bacillus has been found, but not yet definitely classified. DISTRIBUTION. Rangoon. ^ETIOLOGY. It occurs in the adult males of the poorer classes. It has a close relation to the hypodermic syringe. The isolated bacillus has been differentiated from the B. mallei. The diagnosis is usually made at the autopsv. SYMPTOMATOLOGY. It is insidious in onset, usually occurring in broken-down morphine or cocaine victims. There is cough with pain, irregular pyrexia, furred tongue, slight ulceration of the tonsils, broncho-pneumonic S'gns and 4i6 DISEASES OF UNCERTAIN .ETIOLOGY symptoms, palpable spleen, subcutaneous abscesses, sometimes oedema of the arms or legs. The characteristic lesions are " nockiles " of the lungs, liver and kidneys, the former resembling patches of broncho-pneumonia. The abscess mav be subcutaneous or intramuscular, or in the lymph glands, liver or spleen. The mesenteric glands suppurate, the sigmoid colon becomes ulcerated; petechias have been seen in the endocardium. 1 ^HHI N| 1 ^^^^ ^^^^^ 1 ' H ^ H^^ ^^K ^ » ^ a 3 Arm infected and scarred from morphine injections. Both arms were in the same condition. (By Jefferys.) Diarrhoea has been noted. The duration of the disease is from one to three months. The disease is also known as Morphine Injector's Septicaemia. ONYALAI. DEFINITION. An acute infectious disease of unknown causation, characterized by the appearance of bulk-e containing blood, on the surface of the body, the tongue, soft palate, or buccal mucous membrane. AFEBRII.E SPLENOMF.C.ALY 417 iETIOLOGY. IMense tliinks that it may be some kind of poisoning, perhaps due to some species of the Euphorbiacea?. The disease was first described by Yale Massey in Angola, 1904, later on the Portuguese West Coast, East Africa and the Congo. SYMPTOMATOLOGY. The onset is sudden. There are lassitude, a dazed appearance, tender parotids, con- gestion of conjunctivas, slight fever, numbness and pain in various parts of the body. Bullae appear on the tongue, in the mouth and pharynx, oesophagus, stomach and bowels. The tongue is swollen and painful. There may be vomiting of blood, and diarrhoea has been noted. Haematuria and cerebral haemorrhage have been described with the usual signs. There may be haemorrhages in the viscera. The bullcT also occur on the skin. The disease may recur several times. TREATMENT. Arsenic in full doses should be tried. Massey recommends large doses of sodium bicarbonate and cod- liver oil. AFEBRILE SPLENOMEGALY. This disease is also known as Pseudo-Banti's Disease. DEFINITION. A chronic afebrile disorder characterized by splenomegalv and severe anaemia. DISTRIBUTION. Tropica] Africa, Ceylon, India, and probably elsewhere. SYMPTOMATOLOGY. The onset is insidious. It attacks children and adults alike. There is a painless enlargement of the spleen without enlargement, of the liver or other organs. There is a severe anaemia, but no parasites are found. It has been differentiated from other tropical maladies. TREATMENT. This is symptomatic. Iron and arsenic are useful. SECTION V. DISEASES DUE TO VENOMS AND POISONS INTRODUCTORY REMARKS. REPTILES. General Features. Classification. Distribution and Peculiarities. The Venom Apparatus. The Characters of the Venom. The Varieties of Venom. The Symptoms of Snake Bite. The Treatment of Snake Bite. Prophylactic Measures. FISHES. TOADS AND SALAMANDERS. ANEMONES, CORALS AND JELLY-FISHES. HELMINTHS. 5C0RPI0NS AND SPIDERS, MITES AND TICKS. CENTIPEDES. LICE AND BUGS. BEES AND WASPS. ANTS AND CATERPILLARS. MOSQUITOES. BEETLES, SNAILS AND LIZARDS. POISONS TAKEN ACCIDENTALLY BY MAN. ACKEE POISONING. THE VOMITING SICKNESS OF J.A.MAICA. POISONS USED IN ORDEALS, P IGHTING, FISHING, HUNTING. REPTILES 419 DISEASES DUE TO VENOMS AND POISONS. INTRODUCTORY REMARKS. Venoms are useful : — (i) To keep off enemies by discharging the venom into the sur- rounding medium, e.g., toads, salamanders. (2) To aid nourishment by the animal mixing the venom with its own digestive juices, e.g., snakes. (3) To serve as a means of attack or defence by inoculating the venom, e.g., snakes, scorpions, &c. Animals are venomous only when they are capable of inoculating their venom. Among these, reptiles form the greater part. Humanity has held strange and contradictory ideas with regard to reptiles all down the ages. For example : — In Genesis the serpent represented the Evil One. In Greece it symbolized wisdom and prudence. In Egypt it was the protector of crops and represented immortalit}-. In Rome its presence caused epidemics to cease. In India the living Xaja represents happiness and prosperity, the dead reptile, terrible calamity. There is an average of 25,000 deaths per annum from snake-bite in the Indian Peninsula alone. 300,000 vipers have been killed in Haute-Saone, France, during twenty-seven years (Calmette). It is interesting to note that the blood also of vipers, toads and salamanders is toxic and that the eggs too carry the venom. REPTILES. GENERAL FEATURES. A thick epidermis covering the skin is detached or moulted three or four times yearly in all except a few species of snakes, and these retain a few rings at the tip of the tail as in the rattlesnake, by means of which it makes the noise so characteristic of it. This moult is pre- ceded by several weeks of torpor during which the reptile does not eat. The epidermis becomes dull, dry and wrinkled, later cracking at the mouth after which the reptile awakes, shakes itself free from the remainder and goes once more in search of food. Their coloration, governed generally by mimicry, is not of much value for diagnostic purposes as it may be modified several times during the life of the same reptile. 420 DISEASES DUE TO VENOMS AND POISONS The scales and shield (ihe latter are simply large scales that do not overlap) serve to differentiate the species. The ventral scales, moved by the ends of the ribs, serve the purpose of locomotion. The tongue a, head u{ JVa/a bungariis, showing occipital shields; b, maxilla of Detidraspis ; c, Btin- garus candidits, showing enlarged vertebral scales ; d, laterally compressed tail of sea-snake '■> e, head of Cattsus rhombeatus, showing large shields ; f,Cerasles, showing oblique lateral scales > ,<,', head of Ancistrodon, s^howing large shields ; h, head of Bids, showing supra-nasal shield and small scales between nasal and rostral shields. is long, very retractile, forked at the tip, is capable of considerable protrusion but is harmless. Some large lizards also possess a similar organ. The eyes have no eye-lids; the cloaca! orifice is transverse; the mouth is most extensile. This latter feature is permitted largely owing REPTILES 421 to the lower jaw being attached to the upper by means of elastic ligaments which permit of considerable distension. The teeth are used for holding and poisoning the victim in some tn i. Head of Lachesis, showing loreal pit {/. /.) ; k, head of Vipera bertis, showing shields and scales ; /, skull of Crotalus, showing oblique maxilla and long transpalatine ; m, skull of Python, showing inter alia absence of mandibulai symphysis. instances but not for mastication. The victim is swallowed whole, even though it be three times the diameter of the snake, the mouth parts are drawn over it like a glove until the whole has disappeared. Deglu- 27 422 DISEASES DUE TO VENOMS AND POISONS tition is slow and painful, but digestion is powerful and rapid, so that the bones themselves are dissolved. There are some lizards that possess snake-like features, but on ' f a, Cranial skeleton of one of the non-poisonous Cohibridx {Ptyas mucosus) ; 3, cranial skeleton of one of the poisonous Cohihrida {Naja tripudians) ; c, cranial skeleton of one of the poisonous Coluhrida [Bungarus fasciaius) ; d, cranial skeleton of one of the Viperidce (Vipera russellii) ; e, cranial skeleton of one of the Viper idx Crotalina {Crotalus durussis) ; /, cranial skeleton of one of the Colubrida Hydrophiime [Hydrophis pelamis). examination it will be found that they do not have extensile jaws, but they do have eyelids and an external ear, which latter organ snakes do not possess. For details see a larger work. REPTILES <23 CLASSIFICATION. The Reptilia include two orders of importance to the tropical medical officer, viz. : The Ophidia and the Lacertilia. The former is all important as it contains the venomous reptiles. The Ophidia con- tains two important families, viz. : The Colubrid^e and the Viperid^. (I) The Colubridae. These form nine-tenths of the order Ophidia. All snakes other than pythons and vipers belong to it. There are three groups: — (i) Aglypha. These have solid ungrooved teeth. Their saliva is toxic to rats and mice but not to man. Among them are the common British snake (Tropidonatus natrix), the North American water Poison-gland and fangs of a venomous snake {Nafa tri- pudiatts, Cobibridct). (Natural size.) L, Lobe of the gland ; D, poison-duct ; F, fang attached to the maxillary bone ; G G, gland ; M, capsule of mucous membrane surrounding the fangs ; R, reserve fangs ; A A, muscular fascia covering the gland. (After Sir Joseph Fayrer.) mocassin (T. fasciatus), the Indian rat snake (Zamenis mucosus), and the African egg-eating snake (Dasypeltis scabra). (2) Opisthoglypha. {oTTLaOev = behind; ')\v 6 ounces 25 drachms 10 ounces 470 DISEASES OF THE SKIN Any pressure of the temporal arteries or veins of the scalp by hard unventilated hats. Profuse perspiration with bacterial invasion and decomposition of the hair. Chronic seborrhcea, and a Neurosis when it is local and follows the track of some nerve. TREATMENT. To remove the cause, e.g., clear up the syphilis, treat the febrile or general disorder, remove the pressure on the vessels, correct the nutrition, &c. Stimulate the blood supply of the scalp locally with mild irritant. Nourish the follicles externally by ointments. External Irritants. — There are endless varieties. A good one is : — R Borate of soda Salicylic acid Tinct. of cantharides ... Bay rum... Rose water Boiling water to ih pints. Nourishing Ointments. — A good one is : — ^ Acid salicyl ... 5 grains Sulph. praecipitat. ... ... ... ... 15 ,, Beta-naphthol ... ... ... ... ... 10 ,, Vaseline to one ounce. (2) Canities. A senile change usually causes greyness, but the condition of grey hairs may be congenital, the result of disease, nervous shock, or long-continued nervous exhaustion. In elderly persons, treatment other than dyeing is useless, while in younger persons cure is very doubtful. Black hair may result from pilocarpine injections given for any reason. Aniline dyes will cause a deep red brown colour of the hair in some dye workers. Green hair is caused by copper amongst copper smelters. Blue hair is caused amongst workers in cobalt mines. For the treatment of grey hair in young persons the follow- ing can be tried : Tinct. of jaborandi, internally, 15 minims t.d.s., or pilocarpine hydrochlorate, hypodermically, gr. ^^ to . (3) Dermatitis Papillaris Capillitii. An inflammatory process, commencing on the back of the neck and spreading upwards. The papules form large rasp- HAIR AFFECTIONS 471 berry-like vegelations, which bleed readily and give off an offensive odour and discharge. These vegetations are charac- teristic of the disease. Abscesses may form. Later the vegetations shrink and heal spontaneously by scarring. (4) Folliculitis Decalvans. A chronic folliculitis of the scalp leading to cicatrization and baldness. Use anti-parasitic ointments and stimulating lotions. (5) Leptothrix. Concretions upon the hairs of the axillary and scrotal regions. The hairs are very brittle and break readily. The origin is bacterial. Use cleanliness and anti-bacterial ointments. (6) Monilethrix. Beaded hair aft'ecting almost all the hairy parts of the body. The pigment is collected in the nodes, the hairs breaking off at the narrow parts. Young people are generally affected. It is probably due to atrophic changes at periodic intervals. A modification of this condition is known as "bayonet hair." (7) Overgrowth = hirsuties. This condition is usually associated with some anomaly of dentition, insanity, disorder of menstruation, barrenness, severe illness, local irritation and heredity. Treatment is of no avail permanently apart from electrolysis, by which means isolated large hairs are removed with the hair follicles. Local remedies simply scour off the hairs like pumice-stone applications. (8) Piedra. Small, black, gritty concretions that rattle on combing the hair. They are closely packed pigmented spore-like bodies, due in all probability to the Trichosporon giganteum. It is common in Colombian women. (9) Pseudopelade. Irregularly shaped patches of baldness which coalesce, cicatrize and destroy the follicles. Adults with coarse, dark, wiry hair are usually the victims. Treatment is of little avail. (10) Tinea Nodosa. A nodular concretion caused by fungus spores affecting the beard and moustache. Shave and apply antiparasitic remedies. 472 DISEASES OE THE SKIN (11) Trichomycosis Capillitii. Similar to Leptothrix, but due to a different organism. (12) Trichorrhexis Nodosa. Small bead-like whitish swellings resembling "nits" on the hair shaft causing the cortex to split, while the medulla remains unbroken. The condition is probably due to a diplo- coccus. TREATMENT. Epilation of diseased hairs, or Frequent shaving and anti-parasitic remedies. HERPES. A cluster of transparent vesicles the size of a pin's head to a pea, numbering from two to twenty, seated on an erythematous patch and surrounded by an inflammatory zone. There are two types, Herpes febrilis and Herpes zoster (Shingles). The former is designated Herpes labialis, facialis or progenitalis, according to its position. It is symptomatic of febrile disorders, but tvphoid fever is a noted exception. Herpes zoster is nervous in origin, and follows the distribution of one or more of the posterior spinal roots on the skin. These nerves correspond whh those nerves that become tender in visceral dis- turbances. TREATMENT. Menthol or collodion externally and morphia internally may be required ; otherwise for all herpes treat the general disorder and apply anti-pruritic lotions and ointments locally. HYPERIDROSIS. General or local excessive perspiration. It is often associated with prickly heat. Do not try to check the excessive sweating, a physiological action, by belladonna, but add cyllin to the daily bath, and dust the body with antiseptic powder. Change the clothing frequentlv. ICHTHYOSIS (c^ed<; =a fish). A dry, rough, scaly and sometimes warty skin of uncertain causation, usually congenital, but rarely acquired. VARIETIES. (1) Ichthyosis FoUicuIaris. Horny skin, patches of baldness, hair replaced in certain areas by pin-head papules which are surmounted by hornv spines. It is non-inflammatory. IMPETIGO 473 (2) Ichthyosis Hystrix {vaTpi^ =- a porcupine). A rare condilion. It consists of loni^iludinal patches on the limbs and transverse patches on the trunk, corresponding with the distribution of the cutaneous nerves and associated with a general xerodermia. Such ridges may rise half an inch above the surrounding skin. TREATMENT. Cure is exceptional. Improvement has followed thyroid extract, soft soap and warm baths with vigorous friction, lanoline or salicylic acid inunctions in the last variety. Some patches may require excision or scraping. (3) Ichthyosis Simplex. Extreme scaliness, may be horny like the hide of a crocodile and of a similar colour. The nails break easily. There is slight improvement in the summer. There is much itching, great sensitiveness to cold, and a tendency to " chap " deeply. (4^) Keratosis Pilaris (Xerodermia). This is the commonest form. The skin feels to be hard like a nutmeg grater, hence the name. There are dry skin, imperfect development of hair, and changes in the sebaceous and sweat glands. Give inunctions of myelocene ; also castor oil, followed by mag. sulph. and plain water enema. IMPETIGO. A pustular eruption caused by scratching, followed by inoculation of streptococci and staphylococci. The proximate lymphatic glands enlarge and may suppurate. The condition is contagious. Remove scabs by carbolized oil or carbolic acid lotion, i in lOO. Apply mercurial and other antiparasitic ointments. Vaccines may be required. Mag. sulph. and tonics are useful. INTERTRIGO SACCHAROMYCETICA. A rare inflammatory condition attacking the scrotocrural and axillary regions caused by a Saccharomyces. Antiparasitic lotions and inunctions will clear it up. JUXTA-ARTICULAR NODES. Multiple subarticular movable nodules about the elbow and knee- joints usually, probably caused by the fungus Nocardia carougeaui. The writer has seen many cases in the Choco, Colombian Republic, in some of which twenty-four nodules could be counted about the joints mentioned, many of them being the size of a walnut. Excision is advisable when thev interfere with articular movements. 474 DISEASES OE THE SKIN KAPOSI'S DISEASE (Xerodermia pigmentosum). A rare formation of numerous tumours, running a malignant course, and ultimately causing death by exhaustion. The condition commences as "freckles," which develops into a warty condition, and later into ulcerating fungoid masses, destroying all approximate tissue. The tumours are epitheliomatous in structure, but there are no secondaries. The disease commences early in life as a rule, and requires years for its development. Avoid the sun's rays. Excise patches and tumours. Try X-ra}S and electrotherapy. KERATOMA PLANTARE SULCATUM. A thickening of the epidermis of the heels and soles with deep furrows, at the base of which a whitish fungus can be found. Walking is often painful. The only known efificacious remedies are preparations of salicylic ointment, plaster and collodion. LEUCODERMA. A patchy, non-pigmented, white or pinkish condition of the skin ; chronic and incurable; found in coloured races. The patches are irregularly shaped and distributed; local or universal, but without any modification of the skin functions. The condition is chieflv of nervous origin, but occasionally fungi, burns, or injuries mark its onset. The hair over the patches is whitish. Exposure to the sun causes a burning sensation over such areas, and patients often complain of weakness or giddiness, making them unfit for any tropical outdoor work. Some have found arsenical preparations useful. The patches ma\' be darkened by silver nitrate, potassium perman- ganate, or tattooing. LICHEN CONVEX. A chronic, pruriginous, papular, non-inflammatory eruption, pinkish in natives and reddish in Europeans, leaving no excess of pigmentation on healing. The disease lasts three to nine months and may recur. There is no scaling, and the convex papules never show "plugs." There may be spontaneous healing. The general health is not affected. Internal remedies have no effect. Externally use a salicylic-alcoholic lotion, 2 per cent., followed by naphthol ointment, 5 per cent. LICHEN PLANUS 475 LICHEN PLANUS. The term "lichen" does not mean much more than '"papular," thus lichen simplex is really a phase of eczema, and lichen tropicus the same as prickly heat, &c. The word should be restricted to eruptions that are papular throughout and of a persistent typical form. Lichen planus consists of a violet or reddish eruption of small, irregularly shaped papules, flat on the top and sometimes umbilicated, carrying a small scale "in the centre. It is probably of an angio- neurotic origin. The papules may group themselves in lines, curves, or rings. Vesicles seldom, and pustules never, appear in adults. The mucous membrane may be affected, but the accompanying skin con- dition will assist the diagnosis. In acute cases there is much depression and irritability. Arsenic is useful given in increasing doses over long periods, but improvement is not to be expected until after the sixth week of treat- ment. Intestinal antiseptics are useful. Morris uses the following: — R Liq. hydrarg. perchlor. Potass, iodid. Decoct, sarsae. co. ... I ounce 40 grains 8 ounces Take one ounce thrice daily. y '— R Corros. sublimate roo gramme, Carbolic acid 20-00 ,, Simple ointment 500-00 „ Apply twice daily. LICHEN TROPICUS. See Prickly Heat. LUPUS ERYTHEMATOSUS. An inflammatory condition with cellular infiltration, terminating in atrophy of the affected skin. It is often symmetrical, and commences by primary spots having a red or pinkish elevated thickened edge and a depressed centre. The redness fades on pressure. The face is most commonly attacked in the " butterfly area." The disease lasts from ten to twenty years, when it clears up. Patients are most frequently women from 25 to 45 years of age. Anv slight wound causing a disturbance in the local circulation, such as a mosquito bite, will mark the site and time for its onset. To differentiate it from Lupus vulgaris : — Lupus erythematosus. Begins as small red spots. No ulcrration. Always superficial Develops after puberty. Lupus vulgaris. Begins as soft apple-jelly nodules. Ulceration frequent. Cartilage may be affected. Develops usually before puberty. 476 DISEASES OF THE SKIN TREATMENT. Avoid stimulanls, irritants and sea air. Examine for auto-inoculation, and deal ^vilh it when found. If intestine is affected give salol, ichthyol, &c. Tincture of iodine externally is often good. For chronic cases, carbon-dioxide snow, ionization with zinc or copper, high-frequency current and Finsen light. MONGOLIAN SPOTS. Mulberry coloured, smooth, non-elevated spots, occurring usually about the sacral region, the colour not disappearing on pressure. It is of unknown origin, and is found chiefly amongst the Chinese, Koreans, Japanese, Malays, Italians and Europeans. The spots may be single or multiple, one to six or more. They appear at birth, and spontaneously disappear about the third or fourth year. No treatment is necessar}^ MOSSY FOOT. A dense, warty, vascular, painful condition of the foot, occurring in masses, seen chiefly amongst the Amazonians. It is of uncertain origin and of chronic course. Cranston Low suggests that it is Tuber- culosis cutis verrucosa. The masses may be half to three-quarters of an inch high. THE MUCOUS MEMBRANE. Pathological skin conditions affecting the mucous membrane secondarily are dealt ^^•ith elsewhere. Disorders arising more or less primarily are dealt with here. Black Tongue (Hairy tongue). A dark brown or blackish hyperkeratosis, usually in front o'f the rircumvallate papillae, commencing in the mid-line, found usually in adult males, persisting for weeks and perhaps years, and then spon- taneously disappearing. Treatment, apart from mouth washes, is unnecessary. Cheilitis Exfoliativa. A persistent exfoliation, recurring, of the vermilion of the lips, accompanied by numbness or burning pain, probably caused by the liabit of gnawing and picking the lips in neurotic individuals. Radium may clear up the condition. Cheilitis Glandularis. A chronic inflammation of the lower lip with enlargement of the mucous glands, dilatation of the follicular openings, the formation of fistulous tracts which discharge a viscid secretion, sometimes fixing the lips together during the night. THE MUCOUS MEMBRANE 477 There is often a previous catarrh of tlie mouth and pharynx. Silver nitrate caustics, potassium chlorate gargle, and potassium iodide internally are most successful. Fordyce's Disease. Small whitish bodies affecting the lips and mouth, accompanied by a feeling of stift'ness. The condition tends to become permanent. Treatment is discouraging. Caustics and scraping may be tried. Glossitis Areata Exfoliativa. Small, greyish, well-defined, slightly elevated spots near the tip of the tongue, desquamation in the centre and spreading at the periphery, sometimes forming circles or festoons suggesting the " langue geographique." It usually occurs in children, and is frequently confined to families. Its origin is unknown. Treatment is disappointing. Grooved Tongue. Single or multiple grooves on the dorsum of the tongue in which food particles accumulate requiring the constant use of a mild anti- septic mouthwash. The condition is often congenital and confined to families. Treatment is useless. Ichthyosis Glossse. A condition of leucokeratosis of the tongue resembling tylosis (keratosis of the palms and soles). Kraurosis Vulvae. Atrophy of the vulv^, with stenosis of the orifice occurring: — (i) After the menopause, (2) As a sequel of oophorectomy, (3) In sterile young women (rare). Treatment is surgical when necessary. Leucoplakia of the Tongue. It may be Syphilitic, Parasyphilitic, or Idiopathic. Predisposing factors are : clay-pipes, tobacco-smoke, bad dentures, ragged tooth stumps. The ulcerating fissures may become the seat of epithelioma. Always exclude syphilis. Caustics make the condition worse. Hot fluids and spices are to be avoided. Radium can be tried. Excision may be necessary. Leucoplakia may also affect the penis, vulva and vagina. Use X-rays, radium and excision where necessary. 4/8 DISEASES OF THE SKIN Perleche. A chronic stomatitis usually afifecting the commissures; commonly seen in children. The fissure divides the two patches into equal parts at the commissure. The child frequently licks its lips, hence the term "pour lecher," perleche. The condition is probably caused by a streptococcus and is infec- tious. It lasts two to four weeks and then spontaneously clears up. Relapse is common. Cauterize with copper sulphate and appl_y zinc oxide ointment. MYCETOMA (Madura Foot). Madura was a district in India where the disease was very prevalent. It is an invasion of the hand, but more usually the foot, less fre- quently other parts of the body, by fungi belonging to the following genera : Aspergillus, Sterigmatocystis, Madurella, Indiella, Mono- Madura foot. sporium, Sporotrichum and Nocardia. These produce enlargement and deformity of the part, the condition being characterized by an oily degeneration and tissue fusion with cyst-like cavities and sinuses. The disease is chronic and progressive, terminating in death by exhaustion if not removed surgically. It is common in India, Asia, Africa, Europe and America. MYCETOMA 479 ETIOLOGY AND PATHOLOGY (Castellani). The causal fungi belong to the genera numerated above, the saprophytic life of which is quite unknown, except that of Nocardia bovis, which lives in cereals. Barefooted natives are usually affected, the fungus entering in at some wound about the foot, the wound heal- Mycetoma of the foot. ing, but enclosing the fungus which grows slowly within, without there being any real attempt at repair by the body except for some lymphocytic infiltration and the formation of some granulation tissue. Fibrous tissue is formed about the fungus; endarteritis and peri- arteritis cut off the blood supply; the cellular exudate becomes oily, often foul, discharges at the surface through sinuses, the exudate carrying witli it some of the parasites. As Nature thus tries to throw 48o DISEASES OF THE SKIN off the fungus, the latter forms special club-shaped persistent hyph^e which asexually propagate the disease in the part. Leucocytes then attempt to get rid of them by engulfing the parasites and succeed in carrying them to other parts, where the leucocyte is killed by the enclosed parasite, which latter again reproduces the disease where it may happen to be. When the fungus is surrounded by pus, a mass of debris contain- 'mr^ Mycetoma of the hand. ing granules — yellow, black or pinkish — is formed and exuded. The tissue adjoining, muscle, tendon, nerve and bone, degenerate and break down into debris; the body is drained and exhausted; emaciation and cachexia set in, and some intercurrent disease ends the scene. SYMPTOMATOLOGY. A small Avound, usually in the foot, heals, and a small swelling is noticed which is painless. After one month or so the swelling softens, ruptures, and discharges an oily blood-stained exudate containing MYCETOMA 481 minute coloured granules about the size of fish roe. The whole foot is much enlarged, especially in thickness, its shape is lost, anatomical points are obliterated, multiple sinuses reach the surface and discharge through their sinuses with distinctive odour. As the foot enlarges the leg atrophies from disuse, thus making the foot enlargement the more noticeable. Pain is usually absent; locomotion is difificult; the skin sensibility is normal ; pitting is not obtained, but the tissue is elastic. There is no spontaneous healing, and after eight to twelve years of exhaustion, diarrlura often carries off the patient. VARIETIES. (^4) The Melanoid Group. (i) Carter's black mycetoma. Parasite, ]\Iadurella mycetoma, Laveran, 1902. The sclerotia are small, hard and blackish. The parasite throws off a blackish debris. (2) Boufifard's black mycetoma. Parasite, Aspergillus bouffardi, Brumpt, 1905. The grains are larger and more elastic than the above. Curetting may cure this condition. (3) Nicolle and Pinoy's black mycetoma. Parasite, Madurella tozeuri, Nicolle, 1908. (4) Link's black mycetoma. Parasite, Penicillium glaucum. Link, 1915. (B) The Ochroid Group. (i) Carter's white mycetoma. Parasite, Nocardia madura?, \'incent, 1894. The sclerotia are whitish, mulberry-like and spherical. (2) Actinomycotic white mycetoma. Parasite, Nocardia bovis and Israeli, 1872 and 1896. The sclerotia are yellowish, sulphur colour and soft. It destroys bones and forms metastases throughout the bodv. (3) Nicolle's white mycetoma. Parasite, Sterigmatocystis nidulans, Eidans, 1883. The sclerotia are large, like peas, and smooth. It attacks bone. (4) Brumpt's white mycetoma. Parasite, Indiella mansoni, 1906. The sclerotia are small and white, occurring as hard bean- shaped granules. (5) Reynier's white mycetoma. Parasite, Indiella rejieri, 1905. The small white sclerotia occur in soft coiled masses. 482 DISEASES OF THE SKIN (6) Bouffard's white mycetoma. Parasite, Indiella somaliensis, 1905. The sclerotia occur as hard, small, spherical and polyhedral grains. It destroys bone. (7) Musgrave and Clegg's white mycetoma. Parasite, Nocardia asteroides, 1890. The sclerotia are first oval, then vary in shape. It invades the medulla of bone. (C) The Red Group. Pelletier's red mycetoma. Parasite, Nocardia pelletieri, 1906. It may attack other parts of the body. It occurs in Africa. TREATMENT. Amputation is the most certain cure, well above the ankle or wrist, rarely less than this. Scraping and cauterizing with potassium iodides internally may be successful in some cases. MYIASIS. The invasi(jn of the skin or other parts by the larva? of flies. (1) Dermatobia cyaniventris (Oistridae). This is found in Tropical America, and is present in cattle, pigs, dogs, monkeys, birds, and rarely in man. There is local pain, itching, swelling, oedema with a central sinus, in which the larva may be seen from time to time. The larva may attack any part. (2) Cordylobia anthropophaga (Muscid^e). It is common in Africa, where it is known as Tambu fly disease. In Europeans the thighs and buttocks are usually affected, the source of infection probably being the latrines. In natives, the forearms, axillae and head are more commonly attacked. The inflamed area is about three-quarters of an inch in diameter. Extract the larva and treat antiseptically. Some require a long time to heal. (3) Chrysomyia macellaria (Screw-worm). Common in America. The insect lays a mass of 300 to 400 eggs on the surface of wounds, in the ears and nasal fossas of persons sleeping in the open air. Offensive discharges will attract the flies. PEDICULOSIS 483 The larvas hatch in a few hours, and are about three-quarters of an inch long, with twelve segments carrying circles of spirally arranged spines giving a screw-like appearance. These burrow into and devour mucous membrane, muscle, cartilage, periosteum, bone, and may even reach the brain and cause death. Neglected, the patients die; treated, they live. Injections of chloroform, carbolic acid, turpentine, &c., are necessary. The frontal sinuses, antrum, and other bony cavities may require opening up. (4) Auchmeromyia luteola. A keen blood-sucker, the Congo Floor Maggot, common in Africa. The larva has eleven segments, at the posterior end of each are three short limbs provided with spines directed backwards; laterally each segment bears two or more protuberances with a small spine. The anterior segment bears the mouth and two black hooks, each surrounded by minute teeth. After feeding, the semitransparent body appears red to about the fifth seg- ment as a result of the blood taken. The adult fly corresponds in colour Avith the smoke-stained straw of native houses ; it rests under the roof ; is silent ; lays its eggs in the cracks of the mud floors, under native mats, and in soft moist earth. They feed at night. Those sleeping on beds and raised plat- forms escape as a rule. NODULAR LIPOMATOSIS. Innocent fatty, subcutaneous nodules, felt under the skin, which may at time be mistaken for enlarged lymphatic glands. No treatment is necessary. PEDICULOSIS. A condition, exceedingly common in the Tropics, resulting from the bites of Pediculus humanis, P. corporis and Phthirius pubis. The latter is less common among races that constantly shave the pubic region. PATHOLOGY. The mouth parts of the parasite consist of a double tube, one inside the other. The outer chitinous tube or proboscis is a fused labrum and labium armed with minute curved booklets. The inner membranous or suctorial tube consists of maxilla and mandibles. 484 DISEASES OP THE SKIN When biting the proboscis is inserted into a sweat duct, the small booklets everted and the skin thus gripped ; the suctorial tube is then protruded until it reaches blood, the salivary glands at the same time inject their venom causing the pruritus; the pharyngeal pump draws blood, the parasite falls off leaving a minute red spot and marked itching. This area is vigorously scratched and pyogenic infection may follow. This condition, when constant with some thickening of the skin and pigmentation, is known as "vagabond's disease." The parasites secrete themselves in the folds of the clothing, especially about the seams, and later attack the hairy parts. The eggs are attached to the hairs. TREATMENT. Shave off the hair and apply calamine lotion, or Soak the hair in petroleum, wash with soap and water every twenty- four hours, or Apply sulphur and resorcin ointment, wash with soap and water, soak in acetic acid, 25 per cent., comb with a tooth-comb to remove the eggs, and Avash again. All clothing must pass through steam sterilizers. Antiseptic baths and calamine lotions are always useful. PEMPHIGUS CONTAGIOSUS (Pyosis mansoni). A non-febrile, highly contagious disease of warm countries, charac- terized by large vesicles or bullae without inflammation or ulceration. The fluid is clear, then turbid ; the blister ruptures ; exfoliation of about one inch of skin takes place, and a pinkish scar forms. It may attack any part of the body, but in adults the axillae and groin regions are usually selected. The causative organism has not been proven ; it is probably a pyogenic organism. Keep the parts clean and dry. Use dusting powder of boric acid, zinc oxide and starch, equal parts. Mercuric lotions should be used- Iron, arsenic and strychnine internally. PYOSIS CORLETTI (1915). An epidemic eruption of bulla amongst English soldiers in Khartoum, probably identical with Corlett's " Impetigo contagiosa bullosa " in American soldiers. Bulla arise from apparently sound skin without fever or pruritus- and spread over the whole body and limbs. A diplococcus (Amococcus mollis) is always found. The soles are not attacked, there are no crusty lesions, and strepto- cocci are absent. It does not select moist folds of skin, and is not surrounded by an inflammatory zone. PENICILLIOSIS 485 Autogenous \accines and local antiseptics cure the condition. Isolation is necessary to stop the epidemic. PENICILLIOSIS. The hairs of the moustache, beard, or axilhe are attacked by the fungi, Penicillium barbae, and Aspergillus barbie = Aspergillosis. The condition tends to become chronic. The diagnosis is easy. The treatment is as for pediculosis. PHAGED^ENA (Tropical Sloughing Phagedaena). It is a rapidly spreading gangrenous condition of the skin and subcutaneous tissues, forming a large sloughing sore which ultimately ceases to spread, and cicatrizes or remains as a chronic ulcer. Men, physically depressed from other causes, are generally attacked, such as slaves, prisoners, soldiers, pioneers, &c. Any small injury or ulcer may develop into one. There is a large bleb which ruptures, exposing a foul, moist slough, which extends in all directions. The deeper structures are generally spared, but deformitv alwa3's results if the victim lives. Saprasmia and exhaustion or the rupture of a large blood-vessel will carry off the patient. Pyogenic organisms have been found. The bacillus of Vincent and an associated spirillum are commonly found. Correct the general health, give nourishing fresh food and vegetables, opium and general tonics. Cauterize the part under chloroform, irrigate continuously until healing takes place. Consider the patient as infective and isolate him. PIEDRA. A mycotic disease of the hair found in South America, especially Colombia, consisting" of one or more liard small nodosities on the hair caused by Trichosporon giganteum. The affected hairs are bent, twisted and matted together. The node)silies arfe groups of spores around the hair, leaving the latter intact. They can be seen with a microscope after washing with ether and soaking in liq. potass. Bathe the hair, sponge with salicylic acid in absolute alcohol, 5 per cent. This is good for the long hair of women. Otherwise treat as for Pediculosis. PINTA (Carate). A group of allied epiphytic diseases of the skin common in Tropical America, characterized by pigmented areas of skin, varving in tint, 486 DISEASES OF THE SKIN and caused by more than twenty species of the fungi : Aspergillus, Penicillium, Monilia and Montoyella. It is contagious, but Europeans are rarely attacked. The Aztecs of Peru prayed about it centuries before the Spanish conquest. SYMPTOMS. There is desquamation and itching of the patches, the first of which may be red, white, blue or black, the varying tints being due perhaps to the variety of the fungus. When the scalp is affected the hair turns grey, becomes thin and falls out. One person may show different tints, but the patches them- selves do not change in colour. The superficial type is usually blue or black and spreads rapidly. The deep type is usually red or white and spreads slowly, and is more difficult to cure. TREATMENT. Destroy all old clothes. Absolute cleanliness. Apply chrysophanic acid, sulphur, resorcin, liniment of iodine or other epiphyticides. PITYRIASIS. P. versicolor. See Tinea versicolor. P. rubra. See Dermatitis exfoliativa. PRICKLY HEAT. A papular or papulo-vesicular eruption with marked pruritus con- nected with profuse sweating so common in all hot climates. Anything resulting in perspiration in hot climates may cause it. The theories of its causation are as follows : — (i) Sodden cells of sweat glands swell and obstruct the orifice of the sweat duct (Pollitzer). (2) Acute distension of sebaceous glands by their own secretion (Pearse). (3) An infective disease caused by a very minute but active amoeba (Durham). Numbers (i) and (2) may both be present, and infection is not at all improbable through scratching. The disorder is not serious in robust people, but to weaklings it may be serious from loss of sleep, &c. TREATMENT. Avoid all causes of excessive perspiration. Avoid copious drinks and all alcoholics. PSORIASIS 487 Avoid warm and irritating clothing and close rooms; silk clothing may be necessary. Apply spirit lotion to the skin; antiseptic baths; antiseptic dusting powders, e.g., boric acid, zinc oxide and starch, equal parts. Calamine lotion is soothing. Keep the bowels active with salines. For spirit lotion use : — ^ Acid, salicyl i drachm Spirit, rect. ... ... 8 ounces Followed by dusting as above. PSORIASIS. A chronic recurring, dry, patchy eruption of unknown origin, occurring most frequently about the elbows and knees, characterized by silvery scales. The general health is but slightly affected. It is usually seen in young adults. It is frequent among Europeans but rare among tropical races. Irritation of the skin should be avoided. Arsenic should be given internally. Fowler's solution is most useful, 3 minims, t.d.s., increased gradually when tolerated, to minims 10, t.d.s. Locally : Remove scales with salicylate acid spirit 6 per cent, and treat when there is marked hyperjemia present with ung. hydrarg. ammon. or chrysarobin, 10 to 20 grains to one ounce. ment is usetui : — ^ Acid, salicyl . 10 parts Olei ricin . 20 „ Chrysarobini ... . 20 „ Sapon. virid . 25 „ Vaseline flavi ... . 25 „ PYOSIS PALMARIS. There are numerous discrete conical white pustules on the palms, ■containing the ordinary pyogenic cocci, but not surrounded by any marked inflammation. The cause is unknown, and treatment is not •encouraging according to Castellani. SCABIES. Ten days or more after the female acarus (Scabiei hominis) has .entered the skin a small vesicle appears usually between the fingers or toes, occurring amongst dirty people and those working amongst such. There is much itching, especially at night; secondary infection is ■common. Sulphur ointment, vigorously rubbed in every few hours for several days, followed by an antiseptic bath, clears up the condition. The clothes should be boiled and sterilized. 488 DISEASES OF THE SKIN Balsam of Peru is also fatal to the acariis. Paint the part affected and leave it on for one night. SEBORRHGEA. This condition is common amongst Europeans in the Tropics. It occurs especially about the chest. Sulphur ointment about 5 per cent, will clear it up. SKIN PIGMENTS. Skin pigment is a mixture of black, yellow and red pigments. A "white" skin may average a mixture of pigments as follows; black, 8; yellow, 9; red, 50; white or absence of pigment, t,t, per cent. A "black" skin mav average a mixture as follows: black, 68; yellow, 2 ; red, 26; white or absence of pigment, 4 per cent. These tints can be obtained by blending them on a rotatory disc. SPOROTRICHOSIS. There are subcutaneous nodules ^hich soften in two to three months, forming abscesses discharging a greyish yellow pus. The disease is caused by eight species or more of the fungus Sporotrichum. This fungus is readily cultured on Sabouraud's glucose, this being the best means of differentiating the disease from Tuberculosis, Syphilis, Glanders and Blastomycosis. The condition is ver}- chronic and requires vigorous treatment. Puncture the nodules in the early stages and inject i per cent, of iodine solution. Give iodides internally in all cases in large doses. The disease rapidly disappears under iodine treatment. Appl\- antiseptic dressings to ulcers. Operative surgical measures are not necessary. SYPHILIS. This is very prevalent in all its phases. It should not be confused with frambcx'sia iro]3ica. Treat as in luirope. TATTOOING (tattoo -. marking). The formation of indelible skin marks resulting from the insertion of pigments into slight or deep wounds. The term " tattoo " is also applied to the skin fu.ri'ows or "keloid" so commonh- seen in African natives. Tattooing is usually intended to be a permanent form of decoration, an advancement on the "painting" of uncivilized peoples. Extensive tattooing is very painful and recjuires \ears to complete elaborate designs as little can be done at a time. Sometimes several weeks are required for Avounds to heal; blood poisoning and even death has resulted from the process. The designs seen amongst Europeans and Asiatics probablv come from the Japanese, amongst whom it was introduced over 300 years ago. Charcoal and vanilla are the most common pigments. TINEA (RINGWORM) 489 TREATMENT. Small marks can be excised. Blistering and Finsen light has been used. Carbon dioxide snow leaves a scar. When gunpowder is used paint with di-iodide of ammonium, followed by dilute HCl. Persistent application of dilute acids and dilute alkalies may be effectual, but it is a tedious and painful process, eventually leaving a scar. Only a prolonged dermatitis will remove extensive tattooing. TINEA (Ringworm). A contagious inflammatory infection of the skin affecting the hair, nails and, rarely, mucous membrane, caused by one of the fungi to be enumerated later. Ringworm, which is derived from animals, is usually more inflam- matory than that of human origin. The appearance of the lesion varies according to the part aftected, as — (i) The hairy parts, e.g., the scalp = tinea tonsurans, so-called because it resembles in outline the priestly tonsure; tinea barbae, sycosis and palpebralis. (2) The non-hairy parts, e.g., the body = tinea circinata, the nails ^ onychomycosis, the mucous membranes of the mouth, vulva, inguinal, perineal and gluteal regions = T. marginata (eczema marginatum). There are two families of ringworm fungi : — (i) Trichophytons (large spores) (6'/?^^= hair, 0i;toj^ = fungus). (2) Microsporons (small spores). Of these there are many species of clinical interest which will be dealt with seriatim later. DIFFERENCES BETWEEN Trichophytons and Microsporons. Large-spored tinea Small spored tinea Square or oblong Round or ovoid Arranged in regular chains No definite arrangement Regularly jointed, short, mycelium Mycelium irregularly jointed, curved and branching Fungus first attacks root and grows up- Fungus lies about the hair as a visible wards, breaking the hair off short greyish sheath, destroys the shaft and eats down to the root The lesion commences in the epidermis in both cases. The Endothrix tinea develops exclusively within the hair structure, Endo-ectothrix tinea develops within the hair. 490 DISEASES OF THE SKIN EPITOME OF ETIOLOGY (Morris). Tinea tonsurans is mostly due to M. audouini and to the endothrix trichophytons, but the scalp, and especially the juvenile scalp, may be attacked by a great many of the fungi of both families. The beard is attacl'ced by trichophytons only. The hairless skin is seldom affected by microsporons. The nails are rarely involved ; in such cases the parasite is the T. acuminatum or T. violaceum. Adults are scarcely ever attacked except by endo-ectothrix tricho- phytons, which group is also responsible for much of the ringworm of the hairless parts. VARIETIES. (1) T. alba. Parasite, T. macfad3'eni. Attacks the arms, legs and any part of the body. Lesions are white, oval or irregular patches, margins slightly elevated and sometimes dotted with papules. It is a form of dhobie itch. Treatment. — Chrysarobin ointment, 2*5 per cent., and tincture of iodine. (2) T. albigena. Parasite, T. albicans. Attacks the palms and soles especially, also the nails, forearms and legs. Lesions, bullae which rupture, followed by a profuse keratosis until the palms and soles thicken considerably. White patches may develop on the leg and arm. Treatment as above. (3) T. barbae (Sycosis). Parasite, endo-ectothrix trichophytons from animals or children, shaving brushes, &c., less often. T. acuminatium, violaceum and nodoformans. Attacks the beard area, mostly confined to young male adults. Lesions, itching, chronic, scaly eruption, sometimes gyrated or pustular. In simple cases the hair is not damaged ; in severe cases the hair is permanently destroyed. Treatment. — Perseverance is essential for a cure. X-rays where possible if there is no suppuration. Epilation with forceps. Chrysarobin and sulphur ointment. All barber's instruments to be sterilized thoroughlv each time thev are used. TINEA {RINGWORM) • 491 (4) T. capitis (tonsurans). Parasite, Trichophytons violaceum, T. sudanense, T. poly- genum, T. exsiccatum, rarely also Microsporons. Incubation under two weeks. Attacks the scalp. Lesions, patches increase in size surrounded by an erythema- tous zone, sometimes vesicles appear, the patch is studded by broken hair stumps and debris at the roots, making the epidermis to resemble "goose-skin." A serious suppurative variety is known as "kerion," when the pus in the follicles loosens the hairs, but sloughing never occurs. The patches usually remain bald. Treatment. — X-rays, epilation by forceps, turpentine oil, tincture of iodine and weak chrysarobin ointment, 2 per cent. (5) T. circinata (Ringworm of the Body). Parasite, usually Trichophytons, rarely Microsporons. Attacks the face, neck, hands and wrists most frequently. Lesions, a small red spot enlarged in a ring form and may reach a considerable size, or several small coalesce and form festooned patterns. Sometimes the diagnosis is not easy but the presence of the fungus, when found, is conclusive. Treatment, remove superficial epidermis by iodine or liquor epispasticus. This may destroy all the fungi. It is best to follow it up with ointment as: — 1^ Chrysarobin ointment Salicylic acid Ichthyol Unguentum simplex (6) T. cruris (Eczema marginatum, Dhobie Itch). Parasite, Epidermophylon inguinale, peculiar to man, widely distributed in the tropical and sub-tropical countries. The term "dhobie itch" is loosely used in the East for epiphytic skin diseases which are supposed to be contracted from clothes returned by the dhobie or washerman. Attacks pubic, anal, perineal, axillary and other regions where skin folds are in contact, e.g., interdigital folds. It never attacks hair but remains in the stratum corneum. Lesions have a broad, well-defined margin, scaly and papular. They may assume an eczematoid character. Pruritus is con- siderable and pyogenic infection common. Treatment : — 5 parts 2 )i 5 ') 00 n ]?^ Chrysarobin Ichthyol Ungent. zinc oxide Acid salicylic. Vaseline ... )> ... 20 4 drachms 8 grains I ounce Apply morning and evening for fourteen days. 20 grams 492 DISEASES OF THE SKIN (7) T. decalvans. An anomalous form of mirrosporosis of tlie scalp or bald ring- worm. The hair falls out, leaving a bare patch in a place previously unaffected or on an ordinary ringworm area. The scalp is affected and the lesion resembles alopecia areata. (8) T. flava. Parasite, Malassezia tropica (Castellani, 1905). It is very common in all tropical countries. The mycelial threads are thick with numerous swellings and constrictions. The spores are rounded or oval and have a double contour, and often run into clusters. In chronic cases the fungus is not so readily found. It is common amongst the Russian poor. Attacks face, neck, chest and abdomen. Lesions begin as tiny spots, slowly enlarging, the tint varying from deep orange yellow to deep canary yellow. There is no itching or descjuamation. It tends to be very chronic. These " beauty " spots are liighly appreciated by some natives. Treatment. — Patience and perseverance are necessary for months. A cold climate hastens the process of cure. Apply turpentine daily. For exposed parts use : — ^ Resorcin i drachm Salicylic acid 10 grains For covered parts use : — Chrysarobin 20 per cent., or tincture of iodine. (9) T. imbricata. A form of body ringworm formerly peculiar to the East, but now rapidly spreading in damp equable climates of 70° F. to 90° F. It is produced by a trichophyton, and characterized by a concentric arrangement of closely set rings of scaling epidermis (Manson). It is not known in Africa. Parasite, Endodermophyton concentricum and E. indicum (Castellani). Incubation, nine da}s. Attacks the whole body, but avoids hairy parts, especially the scalp. The nails may be affected. Lesions commence as spots and develop into concentric rings of tissue-paper-like scales about i inch a)5art and having one free edge. Itching is generallv intense, but the general health is unaffected. The condition tends to become chronic without spontaneous recoyer\-. Relapses are common. TINEA (RINGWORM) 493 Treatment. — Strong iodine liniment or : — i\ Resoicin 2 drachms " Tinct. benz. CO i ounce Or, Chrysaiobin ointment 5 per cent., but it is necessary to examine the urine and watch the patient. Continue for weeivS. Improvement is frequently followed by relapse. (10) T. intersecta. Parasite, Kndodermophyton castellani, found on the inner surface of the scales; the mycelia are abundant, but spores are rare. The former are long, straight, articulated threads without fructifications. Attacks the arms, legs, chest and back. Lesions commence as small, round, elevated, ilchy patches, with minute black papules about the border. Several may coalesce. They are at first tense, then shrivelled, cracked with white lines on the dark sur'face. The cracks deepen and the scales are formed. Treatment. — Apply sulphur and chrysarobin ointments. (11) T. nigra. Parasite, Cladosporium mansoni, abundant in the lesions. The mycelia are short, bent, often banana-shaped with large spores. T. flava may co-exist with it. Attacks any part of the body except the face, usually on the neck and chest. Lesion is black, lustreless, with but little pruritus. Treatment. — Easily curable except on the palms. Small patches yield to 40 per cent, formalin. Large patches to salicylic-alcohol lotion, 2 per cent. Later apply resorcin ointment. (12) T. nigro-circinata. Parasite, Trichophyton cevlonese. It has large spores, not numerous, having a double contour. Attacks the neck and scrotum. Lesion, black rings with thick elevated margins. Treatment. — Spontaneous healing is common, leaving dark patches. Apply tincture of iodine. (13) T. nodosa (Morris). A nodular concretion containing a fungus, and its spores affecting the hair of whiskers, beard and moustache. The affected hairs split and break. It is not to be confused with piedra due .to T. giganteum. Cut the hair short and use antiparasitic remedies. 494 DISEASES OF THE SKIN (14) T. palpebralis. A rare form of ringworm that attacks the eyebrows usually by spreading from the face. (15) T. sabouraudi tropicalis. Parasite, Trichophyton blanchardi ; cultures of it cannot be grown . Attacks the legs. Lesions commence by erythematous patches covered with small pityriasic squama, later there is a circinatiform appear- ance with a dark brown base. Pruritus is marked. In chronic cases there is thickening of the skin. Treatment. — A cold climate causes it to disappear. Apply chrysarobin ointment, 2 per cent, to 4 per cent. (16) T. ungium. Parasite, Epidermophytons, Trychophyton and Endodermo- phytons. Attacks the nails of the fingers and toes. Lesions cause discoloration of the nails, brittleness, roughness and splitting of the free border. Treatment is difficult. Soften the nails by rubbing in liquor potassium. Apply wet dressings of hyposulphite of soda or -^ Pot. iodid. ... ... ... ... lo'oo grammes Iodine ... ... ... ... i"oo „ Water, ad. ... ... ... ... i"ooo c.c. If the accompanying condition is due to T. imbricata, use resorcin in tincture of benzoin, i in 16. (17) T. versicolor (Pityriasis versicolor) . Parasite, Microsporon furfur; cultures are grown with diffi- culty. The double contour spores are found in clusters. Attacks the trunk usually, less frequently the arms and face. Lesions are rounded, slightly raised, scaly patches with a well-defined border, often fused, of a brownish tint, some- times black. Pruritus is marked. Treatment. — Spontaneous cure ultimately. Wash with soft soap and warm water. Apply tincture of iodine. Naphthol ointment, i in 39, or sulphur ointment, i in 20, are efficacious. TRICHOMYCOSIS. A nodular affection of the hair, generally of the axillary regions, caused by a Nocardia which closely resembles, but is not identical with Leptothrix. The affected hairs have soft thickenings of yellow, black or red colour, easilv removed from (he hair. TUMOURS 495 Formalin in spirit will clear it up, i in 30. Apply sulphur ointment at night, 4 per cent. The principal nodular concretions of the hair are : — (i) Nodular trichomycosis. (2) Piedra (trichosporosis tropica). (3) Tinea nodosa. TRICHONOCARDIASIS (Nodules on the Hairs). See above remarks. TUMOURS. (1) Benign epithelial tumours. Epithelial moles are frequent. Hyperkeratosis is common in all barefooted tribes. Molluscum fibrosum. (By C. C. Elliott, Paoning.) Before operation. After operation. Molluscum contagiosum is not infrequently met with. Verruc^e are extremely common. Warts are very common. (2) Malignant epithelial tumours. Melanotic carcinoma is rare, but has been seen in half-castes. Paget's disease of the nipple is rare. Rodent ulcer is rarely seen. a o a o o i r/} !i 3 O S O t/3 3 .2 3 U o s o 1) C/3 u ^ o o o 3 V o .2 o B o u ■*-» (« rt u. TJ iM , rt s 3 cu O J3 (/> 3 C o O S s 0) rl > lU fl O c w aj n 3 O 3 H u p 5 ■q. V M 3 O e« S _o '5. c 3 >5 o E :/3 13 rt hfl "J a> '« iM ^t: c o hr 'So Cu j= O tr. 1-4 3 O P 5 32 502 DLSiiASliS (>/•" / ///: .S7\7.\ (3) Benign connective tissue tumours. .\ni,n()niatc-i arc fairl\- conimon. Fibroma mollusciini or neurolibrosis common. I'""ibroma pendulum and l-\ sinj^le are common. i'llaslorrhexis or of Recklinghausen, Molluscum tibrosum. (By M. Mackenzie, P'oochow.) pseudo- xanthoma has been seen in half-castes. Cheloid is extremely common ; ii follows tattooing in African natives and hypodermic in- jections in Chinese. L\ nii^hangiomata are very fre- quent. Multijile telangiectasis some- what common. Myomata are rare. Xanthoma diabeticorum is com- mon in India and Ceylon. Xanthoma planum and tubero- sum are fairly frequent. 4) Malignant connective tissue tumours. L\mplioderma perniciosum has been seen. Mycosis fungoides has been seen in a half-caste. Angio-sarcoma is to be fotind in the Cameroons. Multiple sarcomatosis is rare. The author has seen carcinoma of the cervix and of the pvloris in Colombia, South America, and carcinoma of the ovarv in Central Africa. ULCERATIONS. ihc majority of tropical idcera- tions are (he residt of some trivial scratch or bruise, but as a residt of neglect, underfeeding, moistness of the skin, exjx)sure and liability lo secondary infections, ulcers of enormous dimensi(jns may develop. In some cases the writer has seen both tibia and llbula of the same leg exposed on two sides by ulcera- tions, the vessels and nerves remaining isolated like strings plainly visible. ULCERATIONS 503 Various methods have been employed for the naming of ulcers as- Local names, e.g., veldt sore. Anatomical names, e.g., interdigital. Age, e.g., infantile. General disease, e.g., leprotic or elephantoid ulcers. Local pathogenic condition, e.g., varicose ulcer, ulcerating granuloma. Sarcoma of the Buttock. It will suit our purpose to use the alphabetical classification of common terms employed. Blastomycotic, see Blastomycosis. Cancerous, same as in temperate climes. Diphtheroid, has grey or blackish re-forming membrane, usually on the legs. 504 DISEASES or Tin- SKIS Elephantoid, see I-'lephantiasis. Framlxvsial, see I'rambccsia tropica. Gangosa, see Gangosa. Glanders, same as in temperate climates. Infantile, usually multiple and not severe. Interdigital, treat as for septic ulcers. Horny growth from the cheek. (I'robably a sebaceous hum.) Leprotic, see Leprosy. Oriental sore and espundia, see Leishmaniasis. Septic, antiseptic treatment. Syphilitic, treat the constitutional disease. Tubercular, treat the tubercular disease. Tropical, generailv chronic and sloughing; spiroclvTtes and Leishman-Donovan bodies have been found in them. ULCERATIONS 505 Ulcerating granuloma, see article on. Varicose, common among young rickshaw coolies. Veldt sore, a septic ulcer common during the Boer War. Ulcerations which are manifestations of general diseases must be treated accordingly; ulcers of local origin are dealt with according to their severity by antiseptic lotions, powders, ointments, cauterizations and other operations. Fomentations to clean them up, assisted by petroleum washings if necessary, followed by cleansing lotions of corrosive sublimate, lysol, cyllin, potassium permanganate, oxygen peroxide, boric lotion, eusol, followed by antiseptic dusting powders such as iodoform, i ; talc, I ; boric acid, 2. Chondroma. (By P. B. Cousland, Swalow.) Some may require cauterization by silver nitrate, pure carbolic, or the actual cautery; others may require scraping and cauterizing under anaesthetic; some may require excision, others X-ray treatment. Bier's passive congestion has not proved useful in the author's experience. Rest, nourishing food, correction of other disorders and the best hygienic conditions will hasten the process. VESICULAR DERMATITIS. An epidemic dermatitis occurring at Leopoldville, Congo, caused by a small beetle of the genus Polderus. There may be vesicles on an ervthematous patch or on long streaks with inflamed borders. 5o6 DISEASES Of THE SKIN The initial erythema of twenty-four to forty-eight hours is followed by the vesicles which soon become mucopurulent, persisting for four or five days, and ending in desquamation. Europeans are affected on the uncovered parts. The beetle is crushed by tlir vie (ini and the secretions ri:bbed into skin (Rddhain and Iloussiau). XANTHODERMA AREATUM. Clusters of yellow spots about the lower part of the legs which coalesce, forming a large, irregular, unraised patch. The disease is purely local and not of a serious nature, although it is chronic. Resorcin ointment assists the condition. SECTION VII. DISEASES OF THE EYE. GENEREAL REMARKS. BLINDNESS. LOCAL DISEASES OF THE EYE. CATARACT. OCULAR MANIFESTATIONS OF GENERAL DISEASES. THE TREATMENT OF EYE DISEASES. 5o8 D IS RASES 01- THE EYE DISEASES OF THE EYE. (;i:\i-:i<.\i. ki:m.\kks. \Vk do not projiose to consider the subject in detail, but only to mention those disorders of tlie eye that are more or less confined to the Tropics or are met with in an ajj^ij^ravated form or with greater frequencv than elsewhere. For example, quinine amblyopia and the advanced pathological conditions of the eye in leprosy are more or less confined to the Tropics, and conjunctivitis is more common than in an\ other jiari of the wcirlcl. due to the filthy dwellings and habits, the prevalence of dust and fly carriers, and the higher temperature favourable for bacterial development. HLIXDXESS. Blindness is very ct)mmon in the Tropics. In India (1901) there were twelve blind men and twelve blind women in every !o,fxx) adults of each sex, while for the same period and number there were in I*!ngland eight blind men and seven blind women. The causes are (tflen due to the neglect of slight injuries followed by septic infection. Dr. \'ell has classified the causes of blindness thus: — (1) Congenital, e.g., syphilitic affections of the optic nerve, retina .111(1 choroid, malformations of the eveball. (2) Local Eye Diseases, e.g., ophthalmia neonatorum, purulent ophthalmia in adults, catarrhal and granular ophthalmia, ulccrati(m of the cornea, severe paralyses of the ocular muscles, glaucoma. (3) Traumatisms, e.g., injuries from sticks and thorns, exposure to suniighi, eclipse iilindness. night blindness. (4) Constitutional Diseases, e.g., .syphilis, malignant tumours, leprosy, tuberculosis, typhoid fever. (5) Drugs, e.g., alcohol (most common), tobacco (rare), quinine and opium (very rare). LOCAL DISEASES OE THE EVE 509 LOCAL DISEASES OF THE EYE. (1) Traumatisms. Burns and scalds. The cornea may be injured and slough. Enucleation may be necessary. If by lime and acids there is often symblepharon. To treat such cases insert a neutral oil, as castor or olive oil. Foreign bodies such as pieces of steel. Apply 2 per cent, cocaine and remove the particle. If allowed to remain in the eye it may become encased in fibrous tissue and followed by vitreous degeneration and opacity, gross pigmentation of the choroid, iritis and optic atrophy. Flies may carry micro-organisms and cause conjunctivitis. Abrasions of the cornea from inverted eyelashes or scratches from baby's finger nails, &c. Contusions and concussion injuries (black-eye). Such may be followed by mydriasis, rupture of the ball, dislocation of the lens, haemorrhage into the anterior chamber, vitreous or retina, rupture of the retina or choroid, opacity of the lens, pigmentary changes in the retina, some optic atrophy, detach- ment of the iris; svmpathetic irritation and inflammation may follow. (2) Exposures. (a) To bright light. Eclipse blindness is an affection of the macular region of the retina from exposure to direct sunlight. The changes are probably of a chemical nature brought about by the ultra-violet rays. Night blindness occurs in badh' nourished individuals from exposure to indirect sunlight unaccompanied by any ophthalmic changes. The condition may be due to failure of the visual purple which has been bleached by the bright light. Bright light reflected from the snow will also cause blindness. Erythropsia. A red vision due to bright reflected light. It usually occurs in persons whose lenses have been removed. The cause is uncertain, it is possibly due to hyperaemia of the retina. Cataract. This is common where there is much reflected light. Arc lights will cause it. The condition is common in glass-blowers. Sponge-fisher's Asthenopsia. This is an hyperaesthetic condition caused by the scintillation of sunlight upon the water. iio />'y^y:.i.W:A i>j- J nil iiVE Li^htniu^, by means of its ultia-violt'i rnvs. may result in blindness tliroii^h : — 1 lie heat rays produtin^^ burns. Hlectrolytic action. Concussion causing a disturbance of the circulation. .Sunlight is al.so said to cau.se a spring catarrh which dis- appears in autumn and winter. (6) Wind and Dust. These will cause: — Pitiguccuhi, a yellow thickening of the outer conjunctiva: opposite to the palpebral fissure. Ptervf^ium, an extension of a triangular va.scular fold of conjunctiva spreading lo the cornea. Ophthalmic irritation and microbic infection. (3) Habits. &c. Xerosis among debilitated children is very common, esf)ecially in the Mast, where famine, cholera and dysentery are pre- valent. Keratomuhichi, an ulci rative condition, may ensue from the same cause. Cataract in India is chiefly senile, although diabetes is common amongst vegetarians. I'lonorrhaeal conjunctivitis is common as a result of unclean habits. Inflammatory conditions arise as a result of pilgrims bathing in infected water. Toxic amblyopia is caused by excessive smoking and drinking, as also is misty vision. Tiiere is a central colour scotoma for red and green especially. There must be immediate cessation of the causiitive factor. (4) Insects and Parasites. (a) Insects. .Stings cause ix'dema of the lids and conjunctive'^. Irritating secretions are troublesome, e.g., the eye-fly of India, the great-ant of Senegal, &c. Pediculis pubis may occur on the eyelaslies. Sarcopleri invade the free edges of the eyelids by burrowing beneath the skin. It is not uncommon in .San Domingo. Larva." may be deposited in or about the eye by Musca vomitoria, Dermatobia noxalis and cyaniventris, Sarco- phaga magnitica. Hairs or horns mav find a resting place here. Ophthalmia nodosi is due to the liairs of liombyx rubi. Infective discharge is not uncommonly carried to the eye as by .Musca domestica. Irritating pollen may cause vesicular eruption. LOCAL DISEASES OP THE EVE 511 (/*) Animal parasites. Filaria loa may cause trouble beneath the skin of the eyelids and conjunctiva as in West Africa. Filaria oculi humani may insert itself in tiie eyeball. Cysts containing Paragonimus westermanii have occurred in the eyelids and orbit. Dermanyssus gallina? in the cornea. Demodex folliculorum in the Meibomian glands. Cysticercus cellulos^e in the choroid, vitreous, retina or ciliary region. Amongst other parasites that have been 'found troublesome are : Agamodistomum ophthalmobium, Monastomum lentis, Sparganum rhansoni and Filaria palpebralis. (c) Fungi. These play an important part in local eye diseases as the following list will show. Ocular blastomycosis is caused by Cryptoccccus dermatitis and various Saccharomyces. Papules, pustules and an ulcerative warty condition of the eyelids is produced. Ocular tinea is caused by the Microsporon lansomum and the Trichophyton tonsurans. There are crusts and pustules about the cilia. Ocular aspergillosis is caused by Aspergillus fumigatus. There are pain, abscess and ulcer formation. Ocular nocardiasis is caused by Nocardia bovis, N. israeli, N. foersteri, N. dassonvillei, all which produce actinomy- cotic conjunctivitis, corneal ulcers, miliary metastases in the choroid and lachrymal concretions. Ocular moniliasis by Monilia albicans, the organism of " thrush " and perhaps of sprue. Ocular genosporosis by Genospora graphii (rare). Ocular sporotrichosis by Sporotrichum beurmanni infecting the eyelids, conjunctivae, lachrymal sac and iris. (5) Local eye conditions not previously dealt with. Congenital defects are not uncommon, such as anophthalmos, microphthalmos, coloboma, albinism and errors of refraction. Conjunctivitis. (a) Conjunctivitis catarrhalis. Acute : this is caused by the Koch-Weeks bacillus and is nearly always severe, also by the IMorax-Axenfeld bacillus which causes a mild type, also by the pneumococcus and staphylococcus less com.monl\-. This latter may occur in epidemics. 112 DISEASES OE THE EYE Chronic, caused l)y wind, dust, eye-strain, alcoliolic ex- cesses, foreign bodies and ilic Morax-Axenfeld bacillus, P'ollicular, this variety occurs in epidemics. Ii may be bacterial and acute or non-bacterial and chronic. There are small round jKile pfranulcs the size of a pin's head found chiefly about the inferior fornix. In trachoma the g"ranul('s are larijfcr and in the superior fornix. (6) Gonorrhwal Conjunctivilis. This is met with in babies and adults. A streptococcus may also cause a similar condition in ciiildrcn. Gonococcus. x 950. (By Hansel! and Sweet.) Pneumococcus. x 950. (By llansell and Sweet.) bacillus laciinatis Mora\-.\\enfeld. x 950. (I'.y Hiinscll and Sweet.) Kocli-Woeks bacillus. x 950. (liy llansell and Sweet.) (c) (iraiiuhir Conjunctii'itis or Truchowa. Seventy per cent, of the children in Monq^-kong are infected. It is al.so common in India, Japan, South America, North .\frica, especially in F.u^ypt, South .Africa and other parts. LOCAL DLSEASES OF THE EYE 513 ETIOLOGY. IVachoma is found among- the poorer classes. Certain races seem predisposed to it, as the Jews from Russia, the Germans, Austrians and the poorer population of the Balkan States. Some affirm that the causative organism is a fungus, Microsporon trachomatosum, others affirm that it arises from chronic urethritis and vaginitis, the organisms being carried by towels, hands, &c., to the eyes. Cell inclusions of a chlamyzoan nature have been found in these discharges and also in the trachomatous nodules. The disease is important because of its disastrous complications and sequelas. DEFINITION. An acute or chronic inflammation of long duration, accompanied by hypertrophy of the conjunctivae and the formation of " granules " with subsequent cicatricial changes. SYMPTOMATOLOGY. Photophobia, lachrymation, itching and burning sensation, pain, visual disturbance, swelling of the eyelids, narrowing of the palpebral fissure, drooping of the upper lid from weight, swelling and stiffness; muco-purulent discharge, marked in recent, scantv in chronic cases. The conjunctiva of the larsus and fornix is reddened, thickened and uneven on account of the hypertrophy and granules. These granules are rounded collections of lymph corpuscles in a connective tissue reticulum. Papillar}-, granular and a mixed form are recognized. Cicatrical changes occur Axhich ma\' cure the trachoma but which unfortunately give rise to the sequelae. The disease often manifests intermissions and exacerbations. Relapses are common and treatment is often discontinued too soon. COMPLICATIONS AND SEQUELAE. Pannus is common. It consists of a newly-formed vascular tissue often covering the upper part of the cornea, the vessels springing from the conjunctival vessels at the limbus. The entire cornea mav be covered. The condition is not merely due to mechanical irritation but also to changes like those of the conjunctiva. Iritis and corneal ulcers may be present, the latter having opacities interfering with the vision. Corneal opacities when chronic leave a permanent layer of con- nective tissue causing the opacity. Cicatrization leads to : — Trichiasis : the cilia are turned backwards and mav touch the cornea. 3^A SM DISEASES Of THE EYE nintropiun which is more pronounrod in tlic upper lid. The distorted ciha may cause corneal ulcer. The ed^e of the lid is turned inwards. Kclropion when the etl.i,n* of ihc lid is everted and the lower lid is usually affecieti. li is the result of ihe cicatrization of the conjunctiva ami the hypertrophy and contraction o'f ihe orbicularis muscle. Symblepharon is le.ss common. The foi-nix is obliterated and the eve movements limited. ^v r:^T^ X^fh8^i^e M/II , Trachoma bodies of Prowazek-Greeff. (Giemsa stain.) Courtesy of Dr. Brown Pusey. (From "Webster's Diagnostic Methods.'') Staphyloma is rare, and when present is of the cornea. Xerosis is a dry scaly conlracteil condition of the conjunctiva with changes of the cornea in severe cases due to loss of the secreting powers of the conjunctivae TREATMENT. For local a|)plicaiion use copj)er sulphate pencil once daily followed by an eye wash of warm boric acid and iced compresses. This can be pursued for months. Silver nitrate, i lo 2 per cent, solution is g(^)d when there is much discharge, followed by .siiline eye washes. LOCAL DISEASES OF THE EYE 515 Glycerine of tannin, 5 to 25 per cent., and alum stick are also used. Carbon dioxide snow applied once fornightly is good but it requires cocaine for its application. Surgical remedies are : — Expression, perhaps the most popular. Use Knapp's roller forceps for squeezing out the granulations. Wash after- wards with mercury bichloride. General anaesthesia is usually required. Native Chinese operation for lower-lid entropion, pinching the skin between two small sticks. In this case the compression was not complete and two curious tumours resulted. (By Jeffreys.) Grattage, which consists of scrubbing the granulations with a stiff tooth brush, followed by an eye wash of mercury bi- chloride with or without previous scarification. Excision, to remove the conjunctival fold containing the granules. The conjunctiva is often injured in this process. Curetting is popular with some surgeons. 5i6 DISEASES 01- J HI: liYE LUrtroly.sis, X-rays, racliuin and tin- j^Mlvaiin-cautci y an- iist^ul in the hands of skilled operators. Whatever the treatment it must he coniiniitd until every trace of hvpertrophy has disappeared. Prophvlaxis is most im|xjrtani and necessiiry warning with appropriate advice must be given to those concerned. An epidemic of trachoma is a .serious matter. (d) Spriufi Catarrh or Conjuuclivitis ccstivalis. This varietv, which resembles trachoma, occurs in tiic spring- and summer. Tiu- conjunctiva' may be covered with flattened jiapilla' of a bluisii tinge. The intermittent and recurrent nature of the disease with the reappearance of the granules will difi^erenliate this from trachoma. The letiology is unknown. The condition mav last for years and then dear up. There is no known cure and the treatment is symptomatic. (e) Epithcliosis desqiiamaliva or Samoan eye disease. There is a milkv secretion from trachoma-like bodies. Some of the.se are intracellular and form a cell inclusion of small granules or " elementary bodies " which stain violet-red with Giemsa's stain. The extracellular bodies are tiiose that are more mature. True granules do not develop. The conjunctiva atrophies. The disease is common in Samoa as is indicated by its name. The suggested para- site is a chlamydozoon, Lycozoon atrophicans. (/) Phlyctenular conjunclivitis and keratitis. This is fairly common in China. There are small reddened projections (phlyctenuki?) consisting of accumulated hniphoid cells which .soften at their apices forming a small ulcer. They nia\- occur on the conjunctiva? or the cornea. Sometimes they appear in crops, each phlyctenule from two days to two weeks. Relapses are common. This di.sease is found in chiklren of .so-called scrofulous diathesis and seems to be caused by some constitutional or dietetic error. For treatment, dust with calomel daily or use yellow oxide of mercury, i to 2 per cent. Corneal ulcers are not uncommon. Treat with the actual cautery and atropine. ( )ne p<'r cent, xeroform ointment, mois; warm compresses, hydrogen peroxide, formalin 1 in 40. \-c. Cocaine is nece.s.sary for the actual cautery. Perforations require iridectomy. M >> >> CATARACT 517 CATARACT. This is an opacity of the lens or its capsule. NOMENCLATURE. If the opacity commences about the centre of the lens it is a nuclear cataract, if about the periphery il is a cortical cataract. The former tend to develop in old age, the latter during middle life. The hard variety are senile, common after the forty-fifth year and can be extracted, but the soft may occur from childbirth to the thirtieth year and require needling, &c. All cataracts occurring under the thirtieth year are soft. Cataracts are primary when independent of any other ocular condition. ,, ,, secondary when other ocular disturbances are present. lenticular when in the substance of the lens. capsular when affecting the capsule. capsulo-lenticular when involving both. ,, ,, stationary when they remain incomplete. ,, ,, progressive when they spread and tend to affect the whole lens. ,, ,, congenital when they are due to faulty intrauterine development or inflammation. These include the anterior and posterior polar, lamellar and sometimes the complete cataract. ,, ,, traumatic when the capsule is pierced or ruptured by a foreign body or bv a simple concussion allowing the lens to absorb the aqueous humour. We shall follow a classification of May and Worth and deal with each seriatim. A. Stationary Cataracts. (i) Anterior polar. (2) Posterior polar. (3) Lamellar. (4) Uncommon forms. B. Progressive Cataracts. (i) Senile, cortical and nuclear. (2) Congenital, juvenile. (3) Traumatic. (4) Catarrhal eye complications. (5) After cataract. 5i8 n/sf-ASFS 01' rur. rye A. (1) Anterior Polar or Pyramidal Cataract. ii is an opacity situaU-d ai llic anterior pole of the lens beneath ihe capsule. It may be conp^enital or acquired. In the ac(|uired form, a corneal ulcer perfigmentosa. These remain stationary for years and may become complete. Vision is impaired and treatment useless. Deal with the accom pa n y i n g condition. A. (3) Lamellar or Zonular Cataract. These are congenital or infantile. They are most commonly seen in children and usually alTect bd perception of liglil ; that is to say, he must appreciate the covering of the eye. (4) His peripheral vision should be good. The jxjsition of- a lighted candle when placed in varying |)ositions in a darU r(M)m should be appreciated by the patient when looking straight forward. H.Nlraciion can be carried out with or without iridectomy as follows : — (i) The Corneal Section. Cocaine with a few drops of adrenalin are necessary, rarely general ana'Sthesia. Tlu' patient looks downwards, fixation forceps are applied, the (Iraefe knife enters the cornea, with the cutting edge upwards, a knife's breadth above the hori- zontal meridian, and the corneal flap completed. The knife must not be twisted, the aqueous humour must not escape, and the iris must not be cut. (2) The Iridectomy. The conjunctival ilap is turned forwards on to the cornea, curved iris forceps are inserted and grasp the upper margin of the pujDil, which is gently drawn out and a small portion removed with scissors. (3) Opening of the Capsule. The cystotome is inlrtxiuced flatwise into the anterior chamber, its point turned towards the capsule, which is gently cut. The incision may be T-shaped, A-shaped, or +-shaped. (4) Delivery of the Cataract. Gentle pressure is exercised upon the lower part of the cornea towards the centre of the globe w ith the back of the spoon ; the section opens and the lens presents. (5) The ]]'ound Toilet. Stroke the cornea upwards to remove any cortical remnants and blood-clots. The edges of the section must be clear. The lids must not touch the wound. The coloboma is flattened out with a spatula; adjust the flap, insert a drop of atropine and close the lids. (6) The Dressings, ^'c. Cover with gauze, both eyes, and add cotton wool soaked in antiseptic and fix with a binocular bandage. The patient must remain upon his back, quiet, anodynes are best given, straining is to be avoided, the wound examined and atropine instilled daily, the iris excised if prolapsed; liberate the unoperated eye on the fifth day when the patient may sit uj). In two weeks smoked glasses are worn. CATARACT 521 Later, in four weeks, the hypermetropia is about 10 D., with some astigmatism of 2 to 3 d. due to the incision. Give therefore a convex spherical lens of 10 d. with a convex cylinder of 2 to 3 d, for distant vision, wi'th an additional convex sphere of 3 to 4 d, for reading. Previous errors of refraction will modify this correcting lens. Some operators omit the iridectomy, thus avoiding prolapse of the iris, but the capsule is more liable to be left in the wound. Soft and traumatic cataracts are evacuated by tearing the capsule with a c}'stotome. In India many surgeons remove the cataract in its capsule. In such cases the suspensory ligament is ruptured, capsulotomy omitted, and the lens expressed bv corneal pressure with a squint hook. The grave risk of the lo5S of vitreous is the chief danger. Complications of extraction include : — Loss of vitreous, lens dislocation, wounding prolapse of the iris, incomplete evacuation, intraocular haemorrhage, striated kera- titis, glaucoma, iritis, iridocyclitis, cyclitis, suppuration and panophthalmitis. B. (2) Congenital and Juvenile Complete Cataract. These are uncommon; always soft; bluish white with a pearly lustre in one or both eyes. The eye may be other- wise normal, or there may be other eye complications. There is often a history of heredity, convulsions and other mal-intrauterine developments. Treatment is that of discission (needling). This should be done early, and needs to be repeated a number of times. If the patient is young give a general anaesthetic, if older a local anaesthetic is sufficient. Dilate the pupil, introduce the speculum, steady the eye with fixation forceps, divide the cornea and the lens capsule, making two superficial cross cuts, break up the lens matter by rotating a needle so that the lens matter will be absorbed. Repeat this after several weeks. The discission must be deeper each time, and finally include the posterior lens capsule. Three operations are usually required. Keep the pupil dilated with atropine. B. (3) Traumatic Cataract. This is the result of a wound involving the lens capsule, or more rarely after concussion. Swelling and cloudiness 522 DISEASES OF THE EVE of the pupil last for srvrral days when ihr lens becomes absorbed. Often the cure is spontaneous, but part may remain behind, become opacjue, and recjuire operation. Iritis and j^laucoma are not uncommon. Treat on /general Unes indicated. B. (4) Cataracts of Eye Complications. 1 lie t(jilo\\ in^ condiiii-ns may lead lo cataracts : — Iridocyclitis, choroiditis, severe corneal ulcer, glaucoma, retinitis pigmentaresis. Cerebrospinal meningitis to conjunctival (vdema, ocular paresis, strabismus, ptosis, nystagmus, keratitis, optic neuritis and atrophy. Dij^htheria to paralysis of extrinsic muscles and optic neuritis. OCULAR MANIFESTATIONS OF OENERAL DISEASES 523 Erysipelas to orbital cellulitis, &c. Influenza : asthenopia, corneal ulcer, paresis of ocular muscles. Pneumonia: corneal herpes and ulceration. Septicaemia and pyaemia : retinal haemorrhage, emboli, purulent choroiditis. Syphilis : iritis (25 per cent, of all iritis cases), choroiditis, chorio- retinitis, optic neuritis and atrophy, gummata of the iris, ciliary body and periosteum, interstitial keratitis, paralysis and paresis. Tuberculosis : deposits in the iris, choroid, sclera, conjunctivaj and lids. Variola : pustules of the lids, conjunctivas, keratitis and ulceration, complete destruction of the globe, ectropion, entropion and trichiasis. Nephritis : oedema, albuminuric retinitis and amblyopia. Diabetes : cataract, retinal haemorrhage, retinitis, optic neuritis, retrobulbar neuritis, pareses, paralyses and myopia. Gout : episcleritis and scleritis, dry catarrh, marginal ulcer of the cornea, glaucoma and ha?morrhagic retinitis. Rickets : congenital zonular cataract, interstitial keratitis, phlyc- tenular keratoconjunctivitis. Scurvy : haemorrhages of any part, temporary night blindness, apoplexv and retinal haemorrhage. Friedreich's disease : nystagmus, ocular paralyses, optic neuritis. G.P.I. : irregular pupils, miosis, mydriasis, Argyll-Robertson pupil, impaired or loss of accommodation, optic atrophy, paralysis of the third, fourth and sixth nerves leading to diplopia, strabismus and ptosis. Coma : choked disc, mydriasis (organic brain disease), miosis, inequality of pupils, conjugate deviation (cerebral haemorrhage), albuminuric retinitis (uraemia), dilated pupils and pareses (alcohol), extreme miosis (opium). Epilepsy : transient flashes of light, coloured sensations, hemi- anopia, complete loss of vision, muscular spasm, conjugate deviation, distension after narrowing of the retinal arteries. Poisonings : retrobulbar neuritis, optic atrophy (tobacco and iodoform, lead, arsenic, e.g., atoxyl in trypanosomiasis, carbon- bisulphide and nitrobenzol). Heat-stroke : amblyopia and optic neuritis. Typhoid fever : convergence, impaired accommodation and mydriasis. Relapsing fever : iridocyclitis and iritis. Cholera : focal necrosis of cornea and conjunctiva with ulceration, dry catarrh, enophthalmos from loss of fluid, subconjunctival haemorrhage. 524 I) IS RASES OF THE EYE Dysentery : keratitis, iritis, iridocyclitis. Beri-beri : irdenia of lids, lymphatic spaces in opiic nerve and retina distended, defective central vision, loss of central colour vision, axial retrobulbar retinitis, spasm and paralysis of ocular muscles. Kala-azar : retinal luemorrhag^es with deposits of pigment emboli. Snake bite : iridocyclitis, intraocular luemorrhages. Oriental sore : cicatricial contraction, ectropion, epiphora, spasm of the orbicularis. Yellow fever : amblyopia, hyjx'raMiiia of conjunctiva?. Trypanosomiasis : iritis, keratitis and retinal changes in untreated cases; cataract and optic atrophy in treated cases. Plague : photophobia, lachrymation, conjunctivitis, deepened anterior chamber, punctate keratitis, iritis, contracted pupil, serous exudate, later plastic, posterior synechia, increased tension of eyeball, later diminished tension, shallow anterior chamber, vitreous exudates, retinal haemorrhages, optic neuritis, optic atrophy and panophthalmitis as in order given. Leprosy : eyelashes lost early, frontalis muscle paralysed, nodular lepromata and ulceration of eyelids with destruction later, conjunctivitis leading to lagopthalmitis, ectropion, xerophthalmia, infiltrated epi- sclera, whitish grey masses spreading round cornea, keratitis punctata, leprosa, anterior and posterior uveitis, nodules in ciliary bodv or in spaces of Fonlana causing iridocyclitis and chronic glaucoma. Ihe optic nerve, retina, lens and vitreous humour are rarelv attacked. .\ plastic exudate may cause posterior svnechia, i.e., adhesions between the iris and lens and cau.se occlusion of the pupil and consequent blindness. This may be broken down in earlv cases by an effective mydriatic, pyelitis causes impaired accommodation and diminished vision, llceration and ])erforation of ihe anterior chamber are not uncommon in bad cases. X'ision will be affected bv the .scar if in the pupillary area. Hypopyon is not an uncommon sequel, i.e., pus, llbrin and leuco- cytes with pus organisms in the anterior chamber. In cases of per- foration the pyogenic organisms enter the eyeball and cause total destruction by panophthalmitis. See article on Leprosy. Malaria : eye troubles are due to circulatory disturbances more than to inflammatory conditions. There are conjunctival congestion, photo- phobia and lachrymation. Keratitis dendritica, a herpes cornea zoster, giving rise sometimes t(. ulcers, branch-shaped with knobs on them; nine out of ten are Of malarial origin. Keratitis profunda, a central infiltration of the cornea which is OCULAR MANIFESTATIONS OP GENERAL DISEASES 525 brought on by a chronic malarial cachexia. These are opaque greyish dots. It abates in from four to eight weeks. Vitreous opacities are due to hjemorrhages and serous effusion. Amaurosis is due to atrophy of the optic nerve. In retinochoroiditis the papillae are obscured and the retina hazy. The condition is due to the parasites in the vessels. A pigmented retina is left. If there is embolism of the central artery, less rare, there is sudden loss of vision. Optic neuritis and oedema may be caused by the blockage. Paralysis of the accommodation is not uncommon in malarial con- ditions, but secondary iritis is rare. Supraorbital and ciliary neuralgia are common. Amblyopia is less frequent and may be caused by the disease or the treatment of it, i.e., malaria or quinine. The points of differen- tiation are set forth in the following table : — QUININE AND MALARIAL AMBLYOPIA. (After Manson.j QUININE History — Quinine must have been taken in large doses, not less than thirty grains. Onset — Sudden, accompanied by deafness ; both eyes are affected Pupils Widely dilated, and whilst loss of vision continues they do not react to light Vision — Completely lost for a time Ophthalmoscopic appearances — A white haze over fundus; cherry-red spot at macular; optic disc pale; retinal vessels markedly constricted Termination — Usually some permanent defect in the field of vision or in colour vision. Central vision recovers first ; optic disc is unusually white, and retinal vessels small Treatment — Stop quinine. Amyl nitrite has been recommended to induce dilatation of retinal vessels MALARIA Quinine may have been taken but not necessarily in large doses Not usually sudden, but it may be so if haemorrhage has occurred in the macular region. There is no deafness, and both eyes are not necessarily affected React to light Never completely lost There is optic neuritis ; optic disc is of characteristic greyish - red colour; le- tinal haemorrhages and sometimes vitreous opacities Some cases recover completely; in others greater or less permanent defect of vision remains Give quinine Quinine causes buzzing in the ears with partial or complete deaf- ness. It is usually temporary, but is sometimes permanent. 526 DISEASES OF THE EVE Persons tuntemplaling residence in malarial tropics should undergo a course of heavy doses of tjuinine in luiroi>e first. Persons unable to take the dru^ well should not be permitted to reside in the tropics. .Some are su.scep'.ible to the drui; in small doses, 4 j^rains producinj^- unpleasant symptoms. rill-: rKi:.\ r.\ii:\ I oi- l■.^ i; I)I.sj:.\si:.s. The treatment of eye diseases is local and j^^eneral, but we are only concerned here with local remedies, which will be dealt with on general lines. (1) Eye Rest. Correct errors of refraction hv suitable lenses. Give temporary cessation from all work involving eve-strain. Paralyse the accommodation with atropine, homatropine or hyoscyamine. Prescribe protective goggles or glasses, eye-shades or bandages. Green glasses cut out the ultra-violet rays. Smoked ,, ,, glare of light. Blue ,. ,, heat rays. (2) Cleansing and Antiseptic Solutions. All solutions must be warm. For washing the eyeball and removing discharges use : — Sterilized warm water. .Saturated .solution of boric acid. Physiological saline. Mercuric chloride, i in io,ooo to i in 6,ooo (one grain to a pint), formalin, i in S,ooo (one minim to a pint). Condy's fluid pure, i in 2,(kx) (four grains to a pint). Carbolic acid, oin per cent. (3) Stimulating and Astringent Remedies. For conjunctivitis: — v„„ J .11 . , Give two drops twice daiy. AquiL- deslill.... ... ... i ounce ) '^ ' R Acidi tannic! \ grain ) Zinci sulph \ „ ■• „ „ „ Aquic deslill. ... ... ... i ounce ' K Zinci sulph ... \ grain | Sodii biboras ... ... ... 3 grains \ „ ,, „ Aqu.x destill. i ounce ) 9i Acid, tannic \ grain j Zinci sulph. ... ... ... \ ,, I Aquic camphora- ... ... 2 drachmsl " " " .Aquai destill. ... ... 6 „ / THE TREATMENT OP EYE DISEASES 527 Silver nitrate can be used, grain ^ to i to one drachm. This can be painted on the lids in chronic cases, or stronger, grains I to- 5 to- one drachm. Wash well later with saline solution. Keep solution in a stoppered bottle and in the dark. Protargol is commonly used, 10 to 25 per cent. Copper sulphate, grains }^ to one drachm. It is usually used as a pencil in trachoma. In blepharitis, conjunctival interstitial phlyctenular keratitis use yellow oxide of mercury. For persistent ulcerative blepharitis use : — ^ Ichthyol 10 grains Ung. zinc. ox. 2 drachms When vasoconstrictors are required for the absorption of exudates use : — ^ Adrenalin chloride (i : rooo) i drachm Aquae destill. ad i ounce ^ Acid boric 10 grains Suprarenal (i : I'ooo) ... i drachm Aquas camph. ... ... h ounce Aquae destill i ,, Both these are contra-indicated in corneal ulcer. In iritis, keratitis, glaucoma and corneal ulcers use : — Dionin, a derivative of morphine, 2 to 4 per cent, solution, two drops every two minutes for ten drops. It relieves pain, induces local anaesthesia, is a vasodilator and a lymphagogue ; it is a counter-irritant and will assist in dilating the pupil and breaking down the posterior synechia caused by the iritis which so often ends in blindness. This drug loses its effect in a few days, so that it cannot be used over long periods. (4) Disinfectants (so-called). These are for restricted use only and required to be followed by excess of bland solutions to remove any disinfectant left behind. In cases of purulent conjunctivitis and corneal ulcers use : — Mercuric chloride i : 5,000. i : 5,000 has been used upon the conjunctiva after trachoma. Chlorine water diluted with 10 to 20 parts of water, freshly made. Carbolic acid, 3 per cent, and pure carbolic to infected corneal ulcers. Formalin, i : 1,000 to i :2,ooo. i :50o to in'fected ulcers. Tincture of iodine for infected ulcers. 528 DISEASHS OJ- THE EYE Silver nitrate, i to j per rent. Protargol, lo to 25 per cent. Ii has a feeble action. The actual cautery for corneal ulcers, conical cornea and epithelioma of flie lid. (5) Mydriatics and Cyclople^ics. These are to tlilaie the |)upil and paralyse the accommodation. Indications. To dilate the jiupil for ophth.ilmic examination. To prevent adhesion in iritis. I'or central ulcer of the cornea. To j)arahse the accoinmodation in order to estimate the refraction. For lamellar and nuclear cataract. After some operations. In certain diseases of the cornea and deeper structures. Remedies. Atropine in solution or oininieiu, i j)er cent. The effect lasts for a week or more. It may jirecipitate an attack of glaucoma in a predisposed eye. Some patients are sus- ceptible to its use and show toxic symptoms. Give morphine as an antidote. Homatropine hydrobromate is milder and almost as useful. The effect lasts one day onl} or a little more. Use 2 per cent. soluiit)n, one drop every five minutes for three to four doses. Kuphthalmin for examination purjxjses. 5 to 10 per cent, solution ; two drops onlx . The effect passes off in a few hours. Cocaine hydrochlorate, one or iwo chops of a 4 per cent, solution. The effect passes off in about one hour. It will usually diminish intraocular tension. (6) Myotics. To contract the pupil and diminish intraocular tension. Useful in cflaucoma and f>eriplieral corneal ulcers, lilserine salicylate J to .] per cent. It may cause irritation. I'ilocarpine nitrate (muriate) I to i per cent, is milder. l\ Eserine sulph. 1-| yrain Cocaine miir. ... ... 2 ,, Ac|ii;e destill. ad ... ... i ounce (7) Anaesthetics. General. Chloroform for children; ether for adults if possible. Cocaine hydrochlorate, 2 to 4 per cent. It a.ssists the action of mydriatics and miotics, (^ne drop is sufficient for the removal of a foreign body. THE TREATMENT OF EYE DISEASES 529 Holocain hydrochlorate, i per cent. It acts quickly and penetrates deeply. It keeps well. Eucaine B. This is best used hypodermically, 5 per cent. solution is not toxic. Novocain, 3 per cent, in adrenalin chloride, i : 1,000 for hypodermic use. (8) Various. Hot compresses, frequently renewed for affections of the cornea, iris and ciliary body are useful. Cold compresses in conjunctival inflammation. Lint laid on ice, then to the closed eyelid, frequently renewed is soothing. Electricity. Distorted eyelashes are removed by electrolysis. Ionization is employed for corneal ulcers, interstitial keratitis, trachoma, rodent ulcer, &c. It is painful and the results are not very encouraging. Blood letting by leeches in cases of iritis and deeper affections is a favourite remedy with some. Apply two to four to the temple. Massage in cases of interstitial keratitis, glaucoma, corneal opacities, &c., has done good. Place a small portion of ointment in the conjunctival sac, close the lid and massage. (9) Native Treatment. Fumigation is done for inflammatory conditions. Wheat grains are also inserted under the deltoid muscle for these affections. Powders are commonlv used made up of sugar, alum and lime which, when mixed, are blown into the eye. In Arabia they give a " drop of mother's milk." Ectropion is treated by removing or pinching up the skin and retaining it with matches. It sloughs and a cicatrix results Some cannot close the eyelids at all afterwards. Black antimony is used to beautify the eyelashes. This is inserted with a feather, which latter is a suitable vehicle for carrying the gonococcus from one to the other. Cataract is treated by the dislocation of the lens or couching. A needle or thorn is passed through the sclera to the pupil and the lens is pressed down ; the patient jumps slightly and the lens falls. Some recover and others become septic. There is much iridocyclitis, loss of vision and secondary glaucoma. SI'C'l'loX \III TROPICAL HYGIENE, SANITATION, ETC. HYGIENE. Climate. TKMI'ERATURE. Rainfall. Sott. Constructional Hygiene. Physiological Effects of Hot Climates on Europeans. Patiioiocical Effects of Hot Climates on Europeans. The Relation of Climate and Hygiene to Tropical Diseases. Some General Rules for the Maintenance of Health in the Tropics. Epidemiology. WATER. Amount, Sourcfs, Transport, Pathology, Control. Contamination, Purification. FOOD. Nutrition. Adulteration of Foods. So.ME MoRuiD Disturbances caused by Food. Examination of Meats. Examinatio.n of Living Animals. Meat Preservation. Vegetarianism, Infant Feeding in the Tropics. Concentrated Foods. Drinks. SANITATION". Refuse, its Collection, Removal and Disposal. Disinfection. Quarantine. IMMUNITY, VACCINES AND SERA. Some Propiiylactic Measures for Common Infective Diseases. HYGIENE 531 TROPICAL HYGIENE, SANITATION, ETC. HYGIENE. CLIMATE. Castellaxi defines climate as " the combined effects of tlie sun, the atmosphere, and the earth at any one place of the earth's surface." The sun exercises its influence by its heat, light and chemical ravs. The atmosphere by its chemical composition, temperature, dia- thermacy, humidity, pressure, motion (winds) and electric conditions. The earth by its latitude, relative proportion of land and water, ocean currents, soil vegetation, configuration of the surface and altitude. TEMPERATURE. Climates known as tropical and subtropical lie between 35^^ X. and 35° S. (approximately) of the equator, the northern parallel being the Tropic of Cancer and the southern being the Tropic of Capricorn. The sun is always vertical over some part of this broad belt, the average mean temperature of which does not go below 68° F. (30° C). When the sun's rays are vertical, 80 per cent, of the sun's heat that enters the atmosphere reaches the earth. As the sun's ravs become more oblicjue less heat reaches the earth until probably none reaches it, when the sun's rays are horizontal to it. The highest temperatures are reached over the two parallels men- tioned above, because the sun remains vertical for the longest periods over those parallels. The superficial land temperature may rise to 200° F. (93*3° C), while superficial water temperature rarely exceeds 90° F. {^^'2'^ C). The mean temperature of the earth increases with its depth, about 1° C. per 28 metres. Thus mines in temperate zones may become tropical or subtropical, and consequently tropical diseases, such as ankvlostomiasis, may flourish there under suitable conditions, e.g-., the tin mines of Cornwall. A daily range of temperature of more than about 20° F. (11° C.) is apt to be dangerous if precautions are not taken. Short journeys 53-2 TROI'ILM. IIYCIEMi. SAMTATIOX, RTC. from (»nc jjlact* to another with a incin tempera lure of considerable variation must be done at intervals. Health resorts can be found in the troi)ics at hij^jh altitudes. It is useful to know that approximately the temjierature decreases 1° F. for everv ,V)() ffet of heij^'ht, or i° C\ for every iSo metres, hut here aLfain if the mean average temperature is much lower than that of a previous residence, sick people must approa( h it j^Madually, in stages, no matter how beneficial that altitude may be. This has been manifested verv forcibly during the late war in connection with aviation. When aviators move very rapidly through varying atmo- spheric pre.ssures there are such results produced upon the vital organs of the bodv that only selected persons can become aviators. Atmospheric pressure is much less on the equator than about the parallels of Cancer and Capricorn, because the constant heating of the air, more or less loaded with a(|ueous vajxiur, ascends to high altitudes with considerable force. This expansion and rising of air is followed bv an inrush of cool air from the north and south to fill the space, hence if heat were universally uniform there would not be any winds. The currents of air on either side of the equator, not across the ocean, meet at the ef|iiator and produce calms or " doldrums." The easterly direction of winds is due to the rotation of the earth. The air over the land is heated more rapidly than that over the sea, hence the land air rising is replaced by the cooler moist sea air, and is known as the " sea breezes." At night the land, having given off its heat verv rapidiv, is cooler than the sea, hence the conditions are reversed and we get " land breezes," when wind comes from the land to the sea. Hence the pre.sence of large tracts of water have a cooling inlluence over the adjacent, land. 'J'he land breeze, being dry, is apt to extract too much moisture abruptly, and cau.ses a cooling process which may cau.se serious chills and .so reduce one's resistance to disea.se. The \.I{. and .S.W. nionscrons of India are explained by Dove as follows: Owing to the heating of the great plains of .Asia, where the air ascends during the months from May to .\iigust, the south-east trade wind, which is blowing .south from the equator, is drawn north- wards, at the .same time being deflected to the west, thus forming the .S.W. mon.soon. Conversely, when the plains cool from November to March, there is a breeze from the north-east towards the equator which, though known as the X.F.. mon.soon, is really a trade wind. The .S.W. mon.soon is laden with moisture. .\ failure of the rain from this monsoon means a .serious Indian famine accompanied by tens of thou.sands of deaths. HYGIENE 533 RAINFALL. Rain is always cooling, and may be abundani in tropical countries. Tropical rains are usually very heavy, so that they predispose to floods and the formation of swamps. In India the prevailing winds regulate the rainy seasons. Generally there are two rainy seasons each year between 5° and 10° from the equator, one when the sun is on the zenith and going away from the equator, and the other when it is returning. Otherwise there is but one rainy season during the year. The violence of tropical rains is caused bv the additional amount of water that warm air can take up, thus at : — 20*^ F. ( 7"5'^ C.) air takes up \';^ grains of water per cubic foot 60° F. ds-S" C.) „ S77 85^' F. (29f/' C.) „ 1278 When saturated air at 85° F. (29-6 C.) is cooled to 60° F. (15-8° C.) every cubic foot will yield seven grains of water (Hill). Owing to the excessive heat and moisture in the tropics, putre- faction and fermentation are very rapid and often dangerous to man. SOIL. Soil affects the temperature by its power of absorption and radiation and its vegetation. Sandy soils are hottest and emit a glare which is very trying to the eyes. Clayey soils are coolest because of the water they hold. They cause a high atmospheric humidity, retard evaporation and radiation. The climate in consequence is made more ecjuable, but more oppressive and predisposing to rheumatic troubles and chest diseases. Soil temperature varies but slightly at a depth of 8 feet below the surface, and is not affected at all at a depth of 40 feet (Galton). Trees and shrubs intercept the sun's rays and check evaporation from the soil and thus render the ground cooler. Evaporation, however, is great and takes much moisture from the soil. In Algeria the Eucalyptus globulus absorbed and evaporated twelve times the rainfall. Grass renders soil cooler, drier, and of more equable temperature. When soil is permanently damp it is injurious to health. In order to keep the subsoil water at a low level subsoil drains must be put in, periodically cleaned and relaid. A permanent dampness mav be due to : — (i) Clayey soils that do not drain themselves readily, thus forming swampy and mosquito breeding grounds. (2) By an impervious layer approaching the surface at a given place and bringing the subsoil water-level higher than it otherwise would be. This level should always be 5 feet below the surface. 534 TROI'IL.IL HYGIRXE. SAX IT ATIOX , HTC. (3) I>\ ((b.siriiciccl dr.iina.ijr rcsiiltiii}^^ Irom railway fmbaiikmenls, excavations, &r., resuliin.tr from such cunsiruriional works. Also by sand pits and clay holes. (4) 15v the backwater from obstructed rivers, blocking up the house drains by its refu.se. (5) Bv sullaj^e water when a water .system has been provided with- out the nece.s.sary drainage for waste water. (6) At (tr near the irregularities of the earth's surface, as at the f(X)t of hills and low-lyinj^ country. Such |)Iaces are often flooded for months after the rains. (7) Hv tile effects of lar<^e-scale irrijj^alions, unaccompanied b\ efticient drainaj^e. To correct this latter fault the Indian Sanitary jx)wers have laid down the following regulations: — (i) The irrigation canals to be constructed along the line of the watershed. (2) The smaller canals to be so constructed as not to be carried across tiie natural lines of drainage. (3) Drainage cuts to be constructed along the natural lines of outfall. (4) The supply of water to be limited lo the amount required, and to the particular time needed to secure the success of the crops. The Government of (he Soudan have introduced the following regulations in regard to irrigation : — (i) Irrigation channels should be constructed on a higher level than the surrounding ground, so that when :he flow of water in them ceases they may drain dry. (2) Thev should be constructed of such material, and in such a manner as to prevent leakage. (3) Their banks and beds should be kept in good repair and the beds even to |>revent the formation of pools. (4) " Dead ends " of irrigation < hannels should be reduced to liie smallest size compatible with efficiency, so that water will not stagnate in them. (5) \ egetation should be pericxlically cleared out of the channels. (6) Sluices should be ccjnslructed so that there is no leakage to form stagnant puddles. (7) Where possible fish should be introduced, and kept in the main channels to destroy larv.e. (8) Lands where water is apt to stand should have proper surface drains. (()) Crops, such as sugar cane, rice, or others, which require to stand in water, should not be grown within a mile of any town or village. HYGIENE 535 (lo) In the event of an engine or jDump breaking down, particular care should be taken to deal with stagnant pools, and petroleum should be used where necessary. (ii) Malarial fever and excessive numbers of mosquitoes should be notilied to the Governor of the province by the manager of the concession. Rice-bearing ground must be closely watched and well controlled lo avoid mosquito breeding, otherwise cultivation decreases the healthiness of the soil. Ground air must be cut off from tropical dwellings by having a basement or foundations in cement or other impermeable material. Loose sand mav contain 50 per cent, of ground air. Ground air contains moisture, organic matter of animal origin, sometimes of vegetable origin, also, in consequence, ammonia, hydrogen sulphide, marsh gas and carbon dioxide in excess. The ground air is in constant movement as a result of the wind, percolation of the rain, varieties of temperature and barometric pressure, also by the rise and fall of the ground water level. Organisms exist in the soil in abundance, nitroso bacteria (nitrous organisms), nitro bacteria (nitric organisms). These are found within I J inches of the surface. B. tetanus is world-wide. B. anthracis, bacillus of malignant oedema and B. typhosus may survive twenty weeks in the soil. The B. coli exists in the soil, but for shorter periods. CONSTRUCTIONAL HYGIENE. Building Site. In selecting a site for a house, choose the side of a hill awa}' from the native quarters and secure natural drainage. Tablelands are always good. Avoid all depressions, feet of hills, ravines and narrow valleys. Avoid a luxuriant fertile soil which means dense vegetation. What is good for vegetation is bad for man. Select a dry site, granite if possible; " build your house upon a rock." Good water should be accessible. Clear all bush for 200 metres from the nearest dwelling. Leave high trees. Plant Bahama or Kasai grass, but keep it cut short or it will harbour mosquitoes. There should be a slope from the house in all directions if possible, with small, shallow, open drains to carry off the water. The House. Mosquito-proofed brick houses, raised from the ground, \\\{\\ a broad verandah are most suitable for the tropics. The rooms and verandahs should be ceiled to form a ventilated air space under the roof. The rooms should be lofty and boarded. 34 536 TROPICAL HYGIENE, SANITATION, ETC. If there is any glass in the windows it should be shaded from the direct sunlight by screens. Through ventilation is essential in all good houses. There must be a very good damp course in cement around all the walls. It should be remembered that an ordinary brick holds 1 6 ounces of water. One must insist on the instant removal of every impurity and household refuse bv burial or fire. One should avoid windowless cubicles and narrow passages. The kitchen should be built apart. Villages, Camps and Stations. The houses should be built along the lines indicated as far as possible. Always plan and plot as for a larger settlement. Construction must be controlled or every cluster of dwellings will become a death-trap. Make all streets of one-storeyed houses 30 feet wide (10 metres), and those for double-storeyed houses 50 feet wide (18 metres). The principal streets should be 60 to 100 feet wide (22 to 36 metres). All streets should be parallel to or at right angles with each other and shaded by suitable trees. All ordinary houses should be in alignment with one of the streets. If a township is anticipated plan for a large population, and allow for open spaces, gardens, recreation grounds, schools, hospitals, ceme- teries, latrines, wash-houses, &c. All proposed buildings should be submitted b^' plan to the responsible authorities before their con- struction. Consider the possible demands for tram lines, rail roads, &c. Provide a lane 15 to 20 feet (5 to 7 metres) wide for sanitary purposes at the back of each row of houses. This will also serve for drainage, scavenging, air space, &c. It will also prevent encroach- ments and will facilitate alignment. Native villages should be on a health v site, well av\ay from any European dwellings. The huts should be of brick, daub or ant-hill clay with a grass roof. Such are cool, but the usual iron buildings are insufferably hot, even to a native. There should be permanent openings below the wall-plates for ventilation. The houses should not be more than 16 feet in height (5 metres) and built along a road- way, 30 feet (10 metres wide). Nine feet (3 metres) should be allowed between detached huts. They should be properly constructed with a latrine for each, and a back lane, parallel with the road, 15 feet (5 metres) wide. Jails. Formerly they were the endemic centres of bacillary dysentery. At the present time much improved buildings are being erected. The site area should be 50 square yards (50 square metres) for each prisoner. The dormitories should be 20 feet (6 metres) wide and 12 feet (4 metres) high with two rows of beds, one on either side and HYGIENE 537 a good passage bet^veen them. Each bed should have 36 square feet (4 square metres), for the hospital 54 square feet (6 square metres) each (Bengal Jail Code). Solitary cells should have 75 superficial feet (8 metres) and a cubic space of 1,000 feeto Drinking water must be sterile. Latrines must be well controlled. If a prisoner loses more than four pounds in weight in two weeks he should be sent to the Medical Officer. PHYSIOLOGICAL EFFECTS OF HOT CLIMATES ON EUROPEANS. The effects of hot climates upon individuals vary according to the humidity, altitude, sedentary occupation, town or countrv life, habits, &c. The climate has been blamed for much that has been due to insanitarv conditions, alcoholism and other excesses, but when all pathological conditions are ruled out the following generally hold good until acclimatization has taken place, a process requiring two to four years : — (i) There is a greater supply of blood to the surface of the body accompanied by excess of skin functions, e.g., pigmentation and increased perspiration. Persons who cannot perspire should not reside in tropical countries, as perspiration is the chief means of main- taining a normal body temperature. (2) The body temperature of an European in the tropics is slightlv above the normal until thoroughly acclimatized. It is increased o"05° F. for every 1° F. increase above the average normal temperature. Exercise, tight-fitting and unsuitable clothing will raise the body temperature. (3) Owing to the modified distribution of the blood, the capacitv of the lungs increases, more blood is drawn out and more air enters, thus reducing the weight of the lungs. As respirations are decreased in number the lungs actually do less work than in temperate countries. One must also remember that tropical air is rarefied and contains less oxygen than cold air, consequently less carbon dioxide is taken off in a given time, and there is a tendency to retain carbonaceous matter in the blood. Nine per cent, less oxygen in inspired at 80° F. (27° C.) than at 32° F. (0° C). (4) As the pulse is slowed and respiration slightlv impaired the heart's action is weakened and the vital organs are less well nourished; hence there are diminished vigour, general debility, anaemia, irritabilitv, nervous depression, sleeplessness and irritabilitv (the tropical fury of Phehn). (5) O'Connell in 1909 sought to show that exposure to a damp- tropical climate could cause an intermittent fever with haemolysis. 538 TROPICAL HYGIENE, SANITATION, ETC. poikllocytosis, melanjemia and enlarged spleen. This is not commonly- held. (6) The urine is diminished in quantity and in solids. (7) The generative organs act more vigorously. (8) Menstruation begins one year earlier with European girls living in the tropics. (9) The children of European parents residing in the tropics during the active stages of growth are generally weaker than their brothers and sisters of temperate climes. (10) The effects of the sunlight are dealt with elsewhere. During the two to four years of acclimatization tropical residents are especially liable to disease from diminished resistance of both body and mind. Acclimatization for permanent residence of Europeans in the tropics does not take place. Anderson's views upon this subject are as follows : — (i) When a white species is well adapted to the conditions which environ it, it flourishes; when imperfectly adapted, it decays; when ill adapted, it becomes extinct. (2) When a white man, a native of the temperate zone, goes to the tropics, there occurs a biological reaction of his system to the new environment, and a readjustment of co-ordination between his vital processes. (3) In the tropics the white man, individually, can exist ; racially, he cannot exist. (4) Acclimatization is not possible. (5) No superior race can successfully govern an inferior race superior in numbers with equality before the law. (6) Onlv by partial enslavement of the coloured natives, superior in numbers, can the white man rule and govern the tropics, and it is only by relays of fresh representatives that he can continue his sovereignty. {7) Xo colony of northern origin has ever been able to lead a permanent and independent existence in the tropics. To obtain the best results all excesses must be avoided, while daily baths and exercise should be carried out religiously. PATHOLOGICAL EFFECTS OF HOT CLIMATES ON EUROPEANS. Those effects not due to parasites are of congestive or nervous origin. The abstraction of heat by the cool evening breezes often causes congestion leading to chills and predisposing to disease. At such times the blood leaves the surface of the body and concentrates in the viscera, such as the spleen and liver, causing congestion in them. Excessive exercise and alcohol will produce the same effects. HYGIENE 539 The sun's ra}'s will cause congestion of the skin, followed by increased pig-mentation, sunburn, dermatitis, and probablv xeroderma pigmentation. Heat exhaustion is perhaps due directly to meteorological con- ditions, but sunstroke and siriasis are not so easy to explain. For details of these two disorders see separate section. Neurasthenia is almost universal. Loss of memory is common, especially on the West Coast of Africa, where it is known as " Coast Memory." THE RELATION OF CLIMATE AND HYGIENE TO TROPICAL DISEASES. A few of the outstanding features onlv will here be dealt with as these diseases are described elsewhere. Asiatic Cholera. This disease often subsides or disappears in the winter and in temperate climates, but it reappears witli the warm weather without fresh introduction; hence heat is an important predisposing cause of the disease. Heat is not all, however, for if the temperature is rising, as in Calcutta during April and May, and the rainy season sets in, cholera is diminished, but when the rains cease in November it again increases, for at this time the temperature again falls. A moist soil, prolonged heat and drought are the best conditions for the spread of the disease. It is a water-borne disease; hence no water should be allowed to become polluted, and all water should be sterilized before drinking. Insanitary conditions of air, water, food, soil, drainage and housing determine the point of attack. Yellow Fever. This disease is endemic only where the mean temperature reaches 68° F. (20° C). Frost always arrests it. I'nless the temperature is very low, atmospheric humiditv and rainfall favour it. It is limited to the sea coasts and the mouths of great rivers. It is seldom found over 700 feet high. The disease commences usually in the most crowded and filthiest quarter of the town or ship if similar conditions prevail. As the ultra-microscopic virus is mosquito-borne (Stegomyia calopus), all conditions favourable for mosquito breeding are favour- able for the spread of the disease, e.g., no mosquitoes, no yellow fever. Plague. This is an infectious disease of filtli that has robbed India alone of more than 7,000,000 of its inhabitants. It is fostered by filth, overcrowding, lack of ventilation and destitution. 540 TROPICAL HYGIENE, SANITATION, ETC. Malarial Diseases. Given the parasite and the mosquito, malaria tends to increase with the temperature. Atmospheric humidity favours it by encouraging mosquito breeding and by predisposing to chills in European residents. Clay soil is bad on account of the high subsoil water which encourages mosquito breeding. Complete temporary flooding or good draining will reduce its incidence anywhere. Its prevalence decreases with altitude, other things being equal. Relapsing Fever. Neither soil nor climate affect this disease. Destitution, tilth and overcrowding are powerful predisposing causes. These conditions favour the presence of the soft ticks, e.g., Ornithodorus moubata and Argas persicus, which are blamed as carriers of the disease. Leprosy. Climate and tropical conditions exercise but little influence upon this disease. Sanitary improvements in habits and surroundings will certainly assist in suppressing it. It has been called a disease of semi-civilization. Undulant Fever. This disease is carried largely by the infected milk of infected goats. It is also carried by water. Pellagra. The eruption recurs each spring and autumn. Exposure to the sunlight is a strong predisposing factor of the eruption. The symptoms abate during the summer and almost disappear in winter. Agricultural classes are most aft'ected. It is almost world-wide in its distribution. Trypanosomiasis. Insanitary conditions favour the breeding of the Glossin^e which are necessary for its propagation. Destitution predisposes to the disease and raises the case incidence and mortality. Dysentery. Personal cleanliness is absolutely essential on the part of the patients and carriers. Excreta are the chief factors of its spread. Poverty, overcrowding and debility give good ground for bacterial dysentery. Beriberi. This is a deficiency disease in all probability. The best food under the best hygienic conditions will prevent its onset and spread. HYGIENE 541 Dengue. Its prevalence is greatest in the hot season. It affects maritime towns and seldom spreads inland. Low-lying, filthy and overcrowded quarters are the first attacked. SOME GENERAL RULES FOR THE MAINTENANCE OF HEALTH IN THE TROPICS. All defective teeth should be corrected by a qualified dentist before the traveller leaves Europe. It is preferable to abstain absolutely from alcohol. If alcohol is taken it should be in great moderation after sunset. Take a dail_v tepid bath, preferably at sundown, before food. Cold baths are tmsafe for all who have any bowel weaknesses. Judicious exercise is of great value, taken in the earl}- morning or the late afternoon, such as golf, cricket, croquet, polo and tennis. Chills afterwards should be avoided. The great temptation to lead a sedentary life must be overcome. A muslin mosquito net, twenty strands to the inch, tucked under the mattress one hour before sundown, and kept in good repair, is essential. High boots, leggings, or puttees are of great value for all travel- ling through bush for the protection of the legs from snake and insect bites. Light khaki clothes with spine pads for the bush and white drill for the stations and evenings are best. Wool is irritable to the skin. A mixture of wool-silk is comfortable, e.g., Anglo-Indian gauze. Silk next to the skin may be necessary for those whose skins are irritable as a result of perspiration, &c. All personal servants sliould take a daily bath and be free from infectious disease. All water should be boiled and filtered. It is a good plan to drink weak tea or coffee instead of water, as this ensures the water having been boiled. If a filter is not obtainable a little alum added to the water is useful. Boil it after standing. Keep all food supplies awav from flies in a gauze receptacle. All fresh milk must be boiled. Take Cjuinine; hvdrochloride is better than the sulphate, 5 grains daily, except Sundays, when take 2 grains of calomel, followed by half an ounce of Epsom salts. Jaeger sleeping sacks are useful for those sleeping out. Always dress according to the temperature, and not according to appearances and the " climate." After perspiring change clothes frequently. 542 TROPICAL HYGIENE, SANITATION, ETC. Take an hour's rest during the hottest part of the day. Food should be well cooked, excess of meat and fat avoided, fresh fruits, salads and vegetables should be sought after and substituted for the salted meat and rum of olden days. The effects from over indulgence of alcohol are m^u'ked. If possible, it is advisable to spend the hottest months at a greater elevation. The next best thing is to use fans and punkahs to avoid heat debility. Cholera bells are not necessary for healtliy individuals, and to such are often a source of discomfort A\hen worn. It is absolutely essential to protect oneself from the sun's rays. The measures to be adopted are as follows : — Wear a light, well-ventilated pith or rubber helmet or topee with a broad brim and a prolongation for the neck. A white covering is best as it reflects the heat, but does n<3t absorb it. The helmet may transmit chemical rays, and hence it is best that it should be lined with coloured material. For those stooping at their work spine-pads are essential. Broad verandahs should be added to all buildings. Reflection of tlie sun's rays from the floors must be avoided. There should be ventilated ceilings to all dwellings. The roads should be shaded with trees having spreading branches. Plots of green grass will prevent the glare from the sun. Alcohol is the most predisposing cause of sunstroke. Smoked glasses are very comforting from the glare. The_y will often prevent the onset of troublesome eye symptoms. EPIDEMIOLOGY. Communicable diseases may manifest themselves in one of four ways when one of the following terms is applied to it : — (1) Sporadic. A disease is sporadic when cases occur singly or in small groups in scattered communities, e.g., typhoid fever, undulant fever, &c. Such sporadic cases may precede endemic or epidemic manifestations, and should always be closelv watched and controlled. A sporadic disease may at certain times and places become endemic, epidemic and sometimes pandemic, such as undulant and typhoid fever. The divisions are purely arbitrary. (2) Endemic. A disease is endemic A\hen the cases attach themselves more or less to a certain district or localitv, e.g., cholera in the delta of the Ganges; leprosy in parts of Norway, &c. HYGIENE 543 These are often considered by those residing in the endemic area to be some of the unavoidable ills to which man is heir. (3) Epidemic. A disease is said to be epidemic when the cases are widely prevalent over a larger or smaller area. Epidemic diseases, as a rule, tend to spread rapidly and to attack fresh communities. Examples are small-pox, \'ellow fever, cholera, plague, dengue, trvpanosomiasis, relapsing fever, anthrax, &c., though some of these are limited in their distribution by the prevalence of their carriers, e.g., the mosquito, glossina\ rat and rat flea, bugs, &c. (?) Pandemic. A disease is said to be pandemic when the cases become diffused over most parts of the world, as influenza from Russia and plague from India. The study of the modes of the transmission of communicable diseases increases much with the opening of new means of intercourse between countries and continents, e.g., the Suez Canal, the Trans- Siberian Railw^ay, the Panama Canal, &c. For example, plague may be brought from Guayacjuil on the Pacific Coast, where it is endemic, and introduced via the Panama Canal into countries where it has been obliterated, e.g., England. The arrival of one plague-infected rat in Liverpool from Japan caused a consternation in that cit}' only a few^ months ago. There were eight cases of plague brought to London in October, 1919. When studying the question one has to consider the carriers and conditions under which the disease thrives. For example, if there are no mosquitoes (Stegomyia calopus) in the country of arrival, one need not be over-anxious about importing a case of yellow fever, just as one does not hesitate to send to Europe cases of trypanosomiasis from infected areas to places where there are not any Glossin^e. There are many other factors to be considered as locality, climate, season, surrounding's, age and sex of those exposed. The spread of ankylostomiasis needs heat and moisture; cold will cut off the epidemic at once and define its margins. Likewise, bil- harzial disease requires molluscs; no molluscs, no bilharzial disease. The old theories of air dissemination are in the main exploded, they being but a cloak for our ignorance, as the old term " eczema " was for skin diseases in general. The whole facts affecting the spread of these diseases are not yet ^\ell understood even in advanced countries. We do not know why scarlet fever should tend to become epidemic at intervals of five years in temperate climates where it has become established. The same applies to measles, which tends to be epidemic every two 544 TROPICAL HYGIENE, SANITATION, ETC. years. Whooping-cough of uncertain causation shows no marked periodicity, but tends to become epidemic every two years on an average. WATER. WATER— AMOUNT. One should estimate for about 15 gallons per head per diem for personal and domestic use, made up as follows : — Domestic washing... ... ... ... 4 gallons Ablutions ... ... ... ... ... 3 „ General baths ... ... 4 ,, W.c 4 M One should allow for a little waste in excess of this. In towns ID gallons per head should be allowed daily for municipal purposes, and if trade processes are at all numerous another 10 gallons should be added. Hence, roughly, one may say provide : — 12 gallons per head per diem where there are no w.c.'s. 16 „ „ ,, are w.c.'s. 36 „ ,, in large towns generally WATER— SOURCES. All natural waters, springs, rivers, lakes, &c., are derived ultimately from rainfall, which is water taken up from humid surfaces of the earth, distilled under the influence of the sun's rays and distributed to the earth afresh. Part of the rainfall is quickly evaporated. Some of it flowing above an impervious layer finds its way into shallow springs, streams and lakes. The remainder sinks below the surface below an imper- vious layer, when it may form deep springs. Bodies of water may lie in large " pockets " either just above or below an impervious stratum ; in the former case surface wells can be dug, and in the latter deep wells will be required in order to obtain it. A deep well, however, may not be so deep as a shallow well, the difference being according to the nearness to the surface of the imper- vious layer. Ninety per cent, of rain water sinks below the soil surface in sandy and gravel districts, while a clayey soil permits of an exceedingly small filtration. In places where rainfall is scanty, as at Aden, or only salt water is available, as on the ocean and on salt lakes, drinking water is obtained by the distillation of the salt water. This process is carried out for the European residents and troops at Aden, for the miners on some Australian mines and on board war and other vessels. WATER 545 Distilled water can be aerated at the same time by a Normandy's condenser. On British warships five gallons per man per diem is distilled and aerated. In land districts where there are no rivers, wells, or storage tanks for the rainfall, boring should be carried out. This should be done in a hillv country for preference. The required depth will depend upon the distance from the surface of the impervious layer. Select the following places for experimental borings : — (i) Under dry river beds. (2) At the junction of ravines and valleys. (3) At the foot of hills. (4) In a thickly w^ooded country. When a country is cleared of vegetation and timber, the rain water flows away very rapidly and permanent streams are few. (5) Examine along the line of any geological fault in the part. (6) Test localized areas over \vhich fogs or swarms of insects are noticed in the early morning. (7) Limestone and sandstone districts are good for deep wells, but unfortunately there are large inland areas where such do not exist. We will now deal with the subject under three heads, viz. : Rain Water; Surface Water; Subterranean Water. Rain Water. Rain water is soft, well aerated and pure, apart from the impurities taken up by it from the atmosphere. It also absorbs atmospheric gases, such as carbon dioxide, oxygen and nitrogen, the last two in the proportion of 8 and i6'5 per litre. Tropical rain water varies much in quantity, from 600 inches per annum at Cherrapunji, in India, to rainless desert tracts. At Aden rain may not fall for several years. Rain water may be collected from the roofs and stored in tanks, or from large surface areas made impermeable by cement, &c., and stored as at Gibraltar. When collected from iron roofs the latter should not be painted, as the paint, containing lead, may lead to lead poisoning. In some parts, as in the Choco, Colombia, there is nearly one inch of rainfall every night all the year round, so that permanent storage is not required and fresh w-ater is always available. Birds should ahvays be kept off collecting roofs as they pollute the water. Wires should be placed above and along the ridges and the guttering to keep them off. In rainy districts pollution from the dust and decayed vegetation does not arise. To determine the rain water available it is necessary to know two things : — 546 TROPICAL HYGIENE, SANITATION, ETC. The annual rainfall in inches as ascertained by a rain gauge. The sc|uare inches of sectional area of the building (not the slant surface of the roof). The annual rainfall in inches multiplied by the square inches of sectional catchment areas equals the cubic inches of water per annum. This multiplied again by 0*0036 gives the number of gallons per annum. The storage of rain water is often a problem. In Venice the system is good, e.g., the soil is excavated, and the reservoir thus formed is lined with brick and puddled clay. In the centre of this a brick well is built, with openings in the sides towards the bottom of the shaft. The remaining part of the reservoir is filled with sand, into which the rain water first flows. In other countries there are underground tanks (Buenos Aires), stone vaults (Jerusalem), or large galvanized vats on pillars (Demerara and South Africa). Probably the best is a tank of galvanized iron or in brick and cement, raised from the ground, pro- tected bv a roof and made mosquito proof. All such, whatever their construction, must be under the constant observation of a Medical Officer of Health to control fly breeding, &c. When preparing storage tanks the longest duration of the dry season must be known with the accurate rain returns and the amount of water required daily. The average during twenty years, less one- third, is about the rainfall in the driest year, and plus one-third in the wettest year. Onlv a little more than one-half of the rainfall should be considered available for storage. First washings from the roof should be rejected. This should be by a small receiving tank with a float and plunger which, when the tank is full, diverts the flow into the storage tank. A simple method is to have the elbow of the tank supply pipe half-way between the roof and the waste gully at the bottom. When the rain has flushed the roof, plug the bottom of the pipe, the water then rises up to the elbow, when it passes down into the tank. Some suggest that it is always better to pass the water through a sand filter before running it into the storage tank. All pipes should be protected by mosquito copper gauze. To ascertain the dimensions of supply pipes needed and the possible discharge of cubic feet in a given time through a given pipe is often troublesome. The following formula will be a guide : — If water with a head of H feet flows through L feet of pipe D inches in diameter, the discharge W will be in cubic feet per minute : — W, = 472 / H X D' hence D = -538 -^ /JI^^ ^' L '^ H WATER 547 Surface Water. We have stated that rain water flows in part over the surface of the ground into natural drainage channels, such as rivers and lakes. The water becomes polluted according to the media through which it passes. Lakes. These when natural or artificial form the purest supply Avhen containing upland waters. Their purity is the result of : — (i) The action of light, destroying surface bacteria. (2) The subsidence of suspended matters entangling bacteria. (3) The draining of underground waters which have already undergone filtration discharge into it. (4) Its free oxidation. Alg^e are apt tO' form in all standing waters and should be removed by screening and filtration. It is better to store underground w^ater in covered reservoirs, 12 feet deep at least, witli perpendicular sides to diminish the growth of alga^ when this is troublesome. Copper sulphate can be added also in the strength of i in 1,000,000. The catchment area should be cuUi^'ated and be as free as possible from dwellings of man or animals. Open conduits for water conveyance should be immediately condemned. There should not be anv peat in the catchment area, for not only does it make the water brackish but it is particularly solvent of lead. If the presence of peat cannot be avoided, add lime to the water. Rivers. Tropical rivers are usually of greater volume and are less polluted than rivers in luirope, hence the water is purer. The fouling of the water by dead bodies in India and Africa is becoming a thing of the past. The purity of these waters is due to : — (i) The great dilution of any pollution that reaches them. (2) The great volumes of filtered water that reach them. (3) The gradual subsidence of organic matter to the bottom and sides where it undergoes disintegration. (4) The oxidation and bactericidal influence of sun and light. There is no river long enough in the United Kingdom to become pure by oxidation alone. The water from small shallow rivers is always dangerous and should be avoided. In any case a pipe to draw river water should have its intake as near to the middle of the bed of the river as possible and above any villages that may be on or near its banks. The water should always be boiled and filtered. Tanks and Ponds. Water from surface drainage is often directed into tanks and ponds as is the case at Calcutta, but they are ahvays 548 TROPICAL HYGIENE, SANITATION, ETC. subjected to much pollution. They should not be encouraged especially amongst the native peoples of a country. They form a good growing ground for all kinds of parasites, worms, cyclops,, cholera and typhoid bacillus, mosquito larvae, &c., &c. Subterranean Water. When rain water falls upon permeable soil much of it percolates through the first impermeable stratum, the depth of uhicli may vary much. The water flows on the surface of this layer in the direction of its fall and may : — (i) Become collected in the indentations of its surface and form shallow wells, (2) Form a reservoir at the foot of the fall, (3) Find a place where the impermeable layer comes to the surface when the water passes beneath it, forming deep reservoirs of water, deep springs, constant or intermittent or when tapped deep wells are formed. This deep water may also pass into a river, lake, or into the sea, its movement being fairly constant but slow. The level of this underground water varies much according to the rainfall, adjacent springs, river level, &c. Subterranean water is then classified according to its relation tO' the first impermeable stratum thus : — {A) Ground Water above the impermeable layer forming : — (i) Shallow wells, (2) Surface springs. (jB) Deep-seated TTV/ier beneath the impermeable layer forming: — (i) Deep wells. (2) Nearly all springs, (3) Artesian wells; in these the water must be under sufficient hydrostatic pressure, to force itself to the surface when the well is bored. Shallow Wells and Springs. The depth varies from 2 to 50 feet according to the depth of the upper impervious stratum and the depth of the water lying upon it. The area drained and affected by pumping from it varies according to the nature and lay of the surrounding soil, but it may be from 20 to 200 times the area of the depression. The water mav be pure while the drainage area is free from- contamination as was the case in the South African War before men and horses were picketed upon it, and as at Maidstone before the hop-pickers squatted upon it, and as in certain districts of India prior to their occupation by pilgrims. WATER 549 As the water percolates tlirough the soil it becomes charg-ed with carbon dioxide from the air interstices of the soil, after which it may dissolve out lime, mineral salts and organic matter. The soil tends to filter and remove this while the oxygen present in the soil may oxidize it with the formation of nitrates. The water may be contaminated by : Cesspools, privies, manure heaps, sullage water, stables, burial grounds, latrines, and as the result of men and animals residing on the area. The contamination Well with hath and washhouse on one side. These are covered with old galvanized iron, old rail, &c. Tubs where horses and cattle stand and drink. The drainage runs back into the well. mav not be obvious until the rains have washed the filth into the water or until the water has risen in level until it reaches the filth, or carries water with the pollution over eminences of the impervious layer contaminating the wells and springs beyond. In India and China infected natives often wash themselves neai to a well or spring, so tliat the ablution water will drain back again into the well or spring in a polluted condition. A native will bathe thrice daily, yet he will drink water unhesi- tatingly which is obviously filthy. 550 TROPICAL HYGIENE, SANITATION, ETC. A large proportion of typhoid epidemics is due to the use of shallow wells. Any well should have the brick'-work run up to a height of several o 4) u E u .2 U. V z 3 4 5 6 7 ,. 1-4 weeks ... 4 weeks to 3 months 3-6 months ... 6-9 ., 9-12 ,, •3 3 3 3 3 3 3 z. 60 5° 40 30 24 20 16 12 12 12 12 1 oz. i^ oz. 2 oz. 3-4 oz. 5-7 oz. 7-9 oz. 8-iooz. 2 2 2 2 2 2 2 2i 3 3 4 No. of diluent feeds daily 6-8 boiled water 8 )> 10 >> 10 >» — 10 » — 10 it 8 >i 7-8 !> 7 >) 6 barley water S » Note : X. y- z. equals sweet condensed milk ,, unsweetened condensed milk ,, boiled water, or after six months of age, barley water The contents of every bottle should be tasted first by the mother to see that no alteration has taken place in the contents. FOOD 581 A proper tubeless feeding buttle, kept scrupulously clean, is essential. To make the barley water : take one tablespoonful of pearl barley and wash it. Add one pinl of cold water. Soak for ten to tw^elve hours and strain. Boil slowly for two hours. Add water from time to time so as 'o have one pint of the finished product. Season with half a teaspoonful of salt and strain through muslin. To make oatmeal jelly : — This food is useful after the child is nine months old when there is a tendency to constipation. Take one cupful of rolled oats, soak in two cupfuls of water for ten to twelve hours, and strain through muslin. Add one cupful of cold water. Boil for two hours and stir frequently. Add half a teaspoonful of salt, when cool a jelly is formed. Add two to four teaspoonfuls to each bottle. When the child is one year old give one hen's egg daily in milk or boiling water when it jellies. Afterwards thev may be lightly boiled and given with a rusk or toasted bread and butter. The child should not have more than five feeds daily. After fifteen months old, give two eggs daily, and four feeds in all. After eighteen months old, give a light general diet with a little green vegetable. After twenty-four months old, feed thrice daily and give water only between meals. From age three months the child may have fresh unsweetened fruit juices. Sugar is usually given to babies in excess and should be but minute in amount. The majoritv of prepared infant foods contain a large carbohydrate content, e.g., powdered biscuit, &c. No child's digestive juices can deal with it adequately until more than one year old. If the child takes too much of it there will be fatness, inactivity, slow dentition, constipation and occasional diarrhoea. Generally such foods should be avoided. Probably the most useful of all are Allenbury's. The better nourished the baby the less disturbance may one expect during teething. If there is vomiting, absolute anorexia, high fever and sometimes diarrhoea, in all probabilitN- milk poisoning is the cause. Examine and jealously guard the milk supply. 582 TROPICAL HYGIENE, SANITATION, ETC. Excess of sugar and other carbohydrates may cause : — Fever, enteritis, entero-colitis, eczema, enuresis and rheumatisms, recurring bronchitis, pustular dermatitis and dry histreless hair. Curds in the stools (fatty acid soaps) are not important. Banana flour is a useful food. Add one ounce (31 grm.) to one pint of water. Boil for five minutes. The methods here advised are cheap, sterile and efificacious (W. E. Deeks). CONCENTRATED TABLET FOODS. The food tablet will never become universally used. Science will never request that we should sit down to a lozenge lunch or tablet tea. Sugar is almost essential as a food but it cannot be compressed. The solids of our normal diet, daily, when all gases and water have been driven off, will occupy three-quarters of a pint. If we take this in 5-grain tablets we should require about 1,700 dailv. But these we could not digest without water and six pints would be required for these tablets only and water cannot be com- pressed. The question of taste, smell, &c., are all important to stimulate the digestive juices to flow. There would have to be some definite w:ay of distinguishing the itablets to know when one was about to partake of the meat or pudding course. Some dried foods can be prepared and are useful, as evaporated milk, casein, &c. DRINKS. Water. There is nothing to equal Nature's first thirst quencher, viz. : cool, pure water. Mankind, however, requires variety. Tea. Tea (Thea sinensis, &c.) has an odour due to essential oil, a nerve stimulant due to caffeine, 2 to 5 per cent., and an astringent due to tannic acid, 7 to 15 per cent. Indian and Ceylon teas contain about twice as much tannin as the China teas, and tannin is prejudicial to digestion, forming with proteins a leathery substance which is insoluble. Strong tea or an excess of weak tea induces indigestion, nervous- ness and irritability. The nervous breakdown of tea-tasters is due to this. Tea should be drunk within ten minutes of its being made. Coffee . Coffea arabica contains half to three-quarters as much caffeine as tea. Black coffee as a common and frequent indulgence produces a FOOD 583 deplorably neurotic state. In moderation it is a good muscular and mental tonic. Dyspeptic persons should not take coffee after dinner. Chicory, previously considered harmless, is now said to have an unfavourable effect upon growth and development. Cocoa. Cocoa (Theobroma cacao) powder, commonly known as cocoa "essence," is pure cocoa deprived of part of its fat, which originally amounts to 50 per cent, or more of the whole. This fat is not extracted when the cocoa powder is to be used for chocolate. For this latter sugar and flavourings are added, and the whole is ground in a hot mill. Cocoa powder contains 27-33 per cent, of fat, 12-15 P^r cent, of proteins, of which 60 per cent, is not assimilable. There are also traces of caffeine. In pure cocoa nibs there is o'9-2'7 per cent, theo- bromine. Cocoa powder forms a pleasing, mildly stimulating beverage, but is not a food. When starches are added cocoa is more assimilable. Cocoa contains too many solids for it to be a good solvent of other foods when they are taken at the same time. It is estimated that 80-90 per cent, of the cocoa bean is insoluble in water. The so-called soluble cocoas are not soluble, but potassium carbonate is added, which saponifies some of the fat and keeps the particles longer in suspension. This chemical does not aid the digestion, especially of invalids and children. Alcohol. Alcohol is made from malted and unmalted grain, potatoes, maize, rye, grape, beetroot, molasses, palm tree sap, coal and coke gases, &c. The total effect of small quantities is to favour gastric digestion, but excess is a common cause of acute and chronic dyspepsia and many other ailments. Alcohol is a source of heat and energy, but it reduces the activity of metabolism and stimulates, but later depresses the circulation and the nervous system independently of its action on tissue changes. It is not a food because, while it is oxidizable, it acts detrimentally on the nervous tissues. Men soon get thirsty in the tropics, and excesses seem to be the rule. Alcohol is not generally necessary and strenuous work can be done without it. Taken medicinally it is of great value. The alcoholic average contents of common drinks are : — Whiskies ... ... 50 — 60 French wines ... ... 8 — 11 Brandies ... ... 45 — 65 British wines ... ... 20 — 25 Gin 35 — 45 Champagne 10 — 12 Rum ... 35 — 70 Beer ... 3—5 Koumiss 1-3 per cent, alcohol is made from mare's or cow's milk. The body manufactures about two ounces (62 grm.) of alcohol 37 584 TROPICAL HYGIENE, SANITAl^ION, ETC. daily, or an amount equal to that contained in about four ounces of whisky or brandy. Mineral Waters. Soda water contains little or no soda at all, but carbon dioxide gas. It is useful for some invalids. Lemonade from fresh limes, not the chemically made article, is a refreshing beverage. Commercial articles contain saccharin which has a sweet taste, but no nutritive value. It is a drug and not a food, and is forbidden in the United States except for medicinal purposes. Sugar is not desir- able as a substitute in these instances because it would ferment. Saponin is a hjemol^ytic poison which is used in drinks and should be prohibited. This produces the "head " so well known in beers. Gum arabic could be substituted, but why should a " head " be required at all ? Coal tar colouring matters are sometimes used, some of which are poisonous. SANITATION. * REFUSE, ITS COLLECTION, REMOVAL AND DISPOSAL. An outline only of this subject is attempted here. The systems to be adopted vary according to the population, the nature of the surrounding country and the local tribes for which provision is to be made. A medical ofificer is often placed where there is no legal enforce- ment of hygienic measures, and he must adopt that system, most hygienic, which the particular people with whom he has to deal are prepared to use. All waste products and refuse decompose much more rapidly in the tropics, and must be removed and disposed of daily. This consists of domestic refuse, human excreta, solid and liquid, slop water, animal excreta and waste. In large towns sewers are in existence for dealing with human excreta, but in villages and small towns manual labour is required for its removal and disposal. The amount to be removed is one and a half times as much for tropical natives as for Europeans, the latter being largelv meat eaters and the former vegetable feeders. For each vegetable feeder one could estimate as a maximum 8 ounces (225 grm.) of solids and 40 ounces (ri2 litres) of liquid excreta per man per diem, or if ablution water is to be included 80 ounces (2*25 litres) of liquids. Hence for 1,000 people there would be 500 lb. (226 k.) of solids and 500 gallons (2"268 litres) of liquids to be removed daily. SANITATION 585 Now 1,000 ounces of solids equal i cubic foot, and 6*25 gallons of fluids equal i cubic foot. One adult yields 14 cubic feet of solids and liquids per annum without ablution water. If the latter is added it is best to double the amount given above, then one can ascertain the amount of land necessary for its disposal. For its removal use buckets of i cubic foot capacity and carts of 12 cubic feet capacity. Now 1,000 persons yield per diem 500 lb. of solids or SQ'^ ^ i^ or 1. 000 8 cubic feet of solids and also 500 gallons or J^? or 80 cubic feet. This 6-25 equals eight\'-eight buckets daily. Now each scavenger carries two buckets and goes twice daily to the trenching ground, hence to remove the total excreta of 1,000 persons there would be required twenty-two men with forty-four buckets of i cubic foot capacity each. Each man to make two trips daily. LATRINES. (A) For Natives. (i) The Bush. — All primitive natives in small communities use the bush. If a small hole is made in the ground and the excreta covered, the method would be hygienic for districts where there are small communities and extensive bush abounds. (2) Pits. — Some natives dig pits about 2-6 metres deep and 2-4 metres in diameter; the sizes are by no means con- stant. These holes are covered over with sticks and clay, leaving a small aperture at the top. When one is nearly full it is covered with earth and another prepared. It is surprising what a minimum amount of nuisance such pits cause. (3) Shallozv Trenches. — These are useful in certain small bush communities where there is ample supervision. An area is screened off and divided for the sexes. The trenches are half a metre deep and a quarter of a metre wide. They are made as long as required. The native squats astride. Earth is thrown on daily, and the whole trench is filled in when it is within a short distance from the top. A fresh trench is then prepared in front of the old one, and so on until the whole screened area, is exhausted. The screens are then removed to another part. In some instances the excreta is mixed with earth and removed daily. 586 TROPICAL HYGIENE, SANITATION, ETC. (4) Deep Trenches. — These are often used, but are very un- satisfactory and should be condemned. They are 3-4 metres deep, 1-2 metres wide, with sticks thrown across at intervals. The sides are nearly always fouled. (5) Prepared Trenches. — These are useful in certain instances close to works for the use of the native workmen. The floor of the latrine is covered over with dry earth, the excreta covered with another layer immediately, and the whole removed daily. Constant attendants are required. A double public latrine. Exposure to the sun is advantageous, but rain and flood water must be excluded in the rainy season. (6) River Latrines. — These are often used by companies for their employees, but the practice fouls the river banks and the river bed at low water, and in any case pollutes the water for the villages downstream. The practice should be condemned. (7) Deep Pit Latrines. — For better class natives one has found useful a latrine as follows : A hole is dug about 6 metres deep and 0*5 by 075 metres in diameter. A box seat is fixed over it with a lid to make it fly-proof. A small house with a locked door is built over this, say of corrugated iron and made movable. SANITATION 587 A small portion of earth is thrown doAvn daily from a box of loam kept in the little house for the purpose. A latrine like this may last a family for a year or more, after which time it is filled in, another hole dug, and the house removed over it. This method can only be adopted where there are small communities, and where there can be no possibilit}^ of drainage affecting the water supply. Flies do not descend deeply to breed. There is no nuisance with latrines of this kind when kept properly. (8) Chinese Latrines. — Men use public latrines; the women and children use vases and pots in the house, which are emptied dailv. The public latrines may be platforms over fish ponds or raised masonry reservoirs with holes over which the user squats. The use of petroleum will remove all objections to these masonry latrines, and they are useful. These can be made elaborate and the system applied to private dwellings. It is always much better to use pails beneath holes so that the excreta can be removed daily from outside the house. The floor and sides of the recess for the pail should be cemented. The buckets should have a special lid to prevent splashing. A double number of pails is required to replace those removed. The pails should be washed out with cyllin before being replaced. Some of these latrines are modified so as to separate the solid from the fluid excreta. The former can be applied to the land, and is of more value than the fluids. When they are not separated decomposition sets in more rapidly and gives rise to liberated ammonia, carburetted hydrogen and foetid organic gases. The solid matter is mixed with •earth, the urine passing down an inclined plane in front of it and treated separately, but in the same way. The solids are removed, deposited in pits on the farms, covered with earth, kept three to six months, and then used upon the land. The urine is used for manuring soon after collection. The Chinese are the most careful people in the world in the conservation and profitable disposal of sewage, and the most careless with regard to personal cleanliness. Solid excreta is often used in the production of silkworms by applying it to the mulberry trees and also for breeding maggots for the fattening of ducks. 588 TROPICAL HYGIENE, SANITATION, ETC. (9) Indian Latrines. — The separation system is commonly used. The urine and washings are led by a pipe to a special receptacle and are not immediately mixed with earth. There are many modifications of platforms both Avith regard to material and pattern. They are made in iron, stonework, glazed ware, &c., and may be so con- structed as to avoid splashing. Instead of a seat there are the necessary foot rests for squatters such as are employed in all oriental latrines. Pails for the removal of the excreta should have a tight, well-fitting lid. They are taken away in carts or carried by coolies. Their contents should not be emptied into carts near to dwellings. (B) European. (i) Deep Pit Latrines. — These are useful for small communi- ties, with a box seat over a pit, and a small movable house over the whole as previously described. (2) The Bucket System. — This is good when the natives attend-' ing to them are reliable and the supervision sufficient. Loam should be used and the bucket emptied daily and washed out with cyllin. No nuisance need arise. The receptacle for the bucket should be so constructed that it is not necessary for the scavengers to enter the dwellings. (3) Water Closets. — These are the best of all where a water supply is laid on and the drainage is good. They should be outside the house, as in the tropics the evaporation of water allows the best of traps to leak sewer gas. (4) A Che7nical Method. — For troops in the field the system suggested by Myer Coplans and James Menzies has found favour with the War Office, and is useful for the purpose for which it is intended. The writers describe it as follows : — "The apparatus consists of: — " (i) A partitioned chamber for reception of excreta, " (2) A condenser, " (3) A receptacle for the condensed products. " The tank into which the excreta, mixed urine and faeces are introduced is cylindrical in shape and divided into several sections by horizontal partitions. The sewage is poured in through a hopper and broken up by a revolving comb ; it passes on from above downwards through the successive partitions, being exposed all the time to a high temperature. As a result there ensues complete disintegration. The solid residue comes out at SANITATION 589 the bottom carbonized into charcoal ; the volalihzed products are led through a condenser and received into a chamber, where they settle out into : — " (i) A heavy ammoniacal liquor, " (2) A layer of oil, " (3) Gaseous products. " These last are piped off to a burner, where their com- bustion provides the heat required to produce the dis- integrating action on the sewage that takes place in the partitioned chamber. " The ammoniacal liquor forming the lowest laver in the receiver contains pyridine bases, which are of value as an insecticide and as a bactericide. The laver of oil is collected and used for working the motor that actuates the revolving comb or scraper in the cvlinder first men- tioned. The solid carbonized residue is practically pure carbon, which may be used as fuel or for many other purposes. Hence these excretory products can be ren- dered innocuous and disposed of at a very minimum of cost, or even at no cost at all ; it is quite possible that the residue charcoal may come to be a source of profit. At any rate, it seems proved that the working expenses are covered. The fact of the apparatus being self-contained and self-supporting — viz. : (i) That the heat required for the destructive distillation of the excreta is provided by the gas which is set free; (2) that the petroleum oil for running the motor is also obtained from the results of the same distillation — distinguishes it from all other chemical processes or methods of disinfection depending on heat. " It is stated that no fuel is required at all except for the commencement of the working. That an insecticide and a bactericide should be obtainable from the condensation liquor is also much in favour of this method, if in practice it can be recovered without difficulty. In camp life such a substance would be most useful for the destruction of flies, fleas and vermin generally, as well as for its more important disinfectant applications to contagious patho- genic material." Cesspools. Cesspools or receptive tanks for houses or blocks of buildings are generally difficult to keep clean and to emptv. To correct these nuisances several methods of emptying cesspools 590 TROPICAL HYGIENE, SANITATION, ETC. have been adopted, the most recent being the " Tonne Vidangeuse Pneumatique," but it is a costly method. No town with a population of over 15,000 can deal efficiently with its excreta other than by a pipe-water system. The Disposal of Excreta. Apart from what has already been said generally on this subject one may include the following remarks: — (i) Excreta may be collected into cesspools and pits and then used for agricultural purposes on farms as previously stated. (2) It may be carried to an incinerator and destroyed completely, but such is regarded generally as being a needless waste. (3) It can be carried by a water-carriage system in the case of larger towns and discharged into large rivers, or by a pipe out to sea. The failings of the latter system are waste, offensive odours and troubles from the ebb tide. (4) After a water-carriage system it can be treated by precipitation .with or without filtration, intermittent filtration through land, broad irrigation, or bacterial treatment. Special works should be consulted for technical details. The principles have been dealt with under Water Purification. (5) Chemical processes are used apart from the one mentioned above proposed by Coplane and Menzies. The " Poudrette " method is fairly well known. After fermentation by urea, volatile ammonium carbonate is formed which is usually fixed with calcium sulphate. The sewage is then desiccated by evaporation in numerous shallow pans. The resulting powder is known as " Poudrette," and is sold to farmers for manure. The process is costly and the demand is usually small. Two tons of excreta yield about two hundredweight of poudrette. The system is unsuitable where there is much rain. There are various modifications of this system. (6) Trenching and cultivation are perhaps the methods most com- monly employed in hot climates. The trenching ground must be high, well drained, with a loamy soil, to the leeward of the village or town, and well screened from the public view. The area should be large enough to deal with all excreta from the population and divided into twelve monthly plots for trenching. Tiie trenches should be o'6 metre wide and o'4 metre deep. They should be 0*3 metre apart. Each trench should receive o'2 metre of excreta. The area required for a population of 1,000 persons would be 14 square metres SANITATION 591 per diem, or for the same number 5,110 square metres per annum. This affords twelve months' rest for each trench. Where the soil and all conditions are particularly favourable Disposal of Excrement as Manure. Chinese Method. (l) Chinaman taking from public latrines in a Government receptacle fresh human ordure. (3) Filling his private bucket with the contents of manure pit, consisting in part of fa;ces kept sufficiently long for eggs to be destroyed, but in part sufficiently fresh for eggs to retain their vitality. To the contents of this bucket water is usually added. (2) Decanting into his manure pit where, if kept long enough, the eggs of most entozoa will be destroyed. It is rarely kept long enouiih. (4) Watering vegetables, including those used for salads or eaten raw, with the contents of this bucket. The great prevalence of " flukes " (trematoda) amongst the Chinese is probably due to the general use of some such method. the land can be retrenched in six months. It is al^va^•s best to arrange it so that one trench takes one day's supplv, thirty- one trenches for a month's supply. The earth should be raised dome-shaped when covering them in to allow for sinking. 592 TROPICAL HVGIEXE, SANITATION, ETC. After three months plough up each plot and sow with rye grass, sugar cane, or tobacco. After the first crop, vegetables can be grown and sent to the market for sale and consumption. Swarms of flies about a trenching ground indicate improper management. Such trenches could be dug at the base of cocoanut or palm trees, a safe, effective and profitable means of disposal. S ullage water should be taken to trenching grounds in special slop carts where there are no good drains. Storm water requires surface drainage. Wells must be protected and sewage controlled. Dry Refuse. — This always exists in large quantities. In Calcutta, with its population of three-quarters of a million, there are nearly 1,500 tons daily. There are 900 carts employed making three trips daily. For disposal incineration is always the best. Failing this, hollows can be filled up, covered with soil and planted, but the system is not to be recommended. It should not be thrown into ponds or marshes. The putrefaction, fermentation and formation of gases thus produced will go on for years and mav escape, proving deadly to man and beast alike, even though the refuse mav be covered with several feet of earth. DISINFECTION. Disinfection is the destruction of the specific virus and is equivalent to a bactericide. The term should not be applied in a general manner to antiseptics which arrest or impede the growth of organisms. Dis- infection means destruction of the agents of infection. Deodorants, of course, only oxidize and destroy or mask the effluvia. Much money is wasted in the purchase of disinfectants, while the inefficient application of them engenders a false feeling of security and often prevents simple means of purification. Whenever possible one should employ a simple and useful method, namely, of exposing articles to direct sunlight, or rather, to the ultra- violet rays of white sunlight. This is sufificient to destroy ultimately most pathogenic organisms. Desiccation only will kill cholera vibrios. Disinfection by heat or chemicals should always be preceded by thorough cleansing, e.g., stripping the paper from the walls, scraping and washing the walls and floors, allowing plenty of air and as much sun as possible to enter the apartments, washing, brushing, beating and suspending all garments, blankets, &c. The chief means of disinfection are heat, hot air, steam and chemicals. SANITATION 593 Heat. This is the most efficient means of disinfection, but unfortunately it is not of universal application. For example, infected garments^ articles of small value, native huts, &c., should be destroyed com- pletely by fire, and in the latter case killing all the rats as thev attempt to escape. Hot Air. This is sometimes used for clothes and bedding, but it is slow and not very efficacious owing to the poor penetrating power of dry heat. Some articles may be scorched. It is useful for books and leather goods. The air temperature should be 230^-250° C. for four to eight hours, but steam should be substituted wherever possible. Steam. Steam is more rapid and efficacious because of its increased pene- trating power. The essentials of its application are that the steam under pressure shall permeate the whole article to be disinfected. The steam temperature must be 221° to 270° C. After the steaming, hot dry air should be passed through the articles for drying them. Steam is inadmissible for leather objects, such being destroyed by it. All fusible substances such as glue and sealing wax are ruined by steam in any form. The Current Steam Disinfector is the best. The machine is light,, has no heavy boiler, is of easy construction, the cost is low and the management of it is not expensive. The Washington Lyon apparatus by Manlove and Alliott is good. It has doors at both ends. The steam in the jacket is at a pressure of 30 lb. to the square inch and in the chambers at 20 lb. It is not superheated. Elliott and Paton's vacuum apparatus is an improvement owing to the greater penetrating power and its increased efficiencv and rapidity. Ten to twelve minutes will suffice for the disinfection. The articles are dried in a current of hot air. Thresh's Disinfector has been extremely useful in the colonies and the tropics. Chemical. The chemical disinfectants used are legion. The most common are: Corrosive sublimate, i in 1,000; Cyllin, i in 200; Izal, i in 100 ; Carbolic acid, i in 20 ; Potassium permanganate and Lysol. A good chemical disinfectant should have the following characters : (i) Germicidal within a reasonable time. (2) Its chemical properties should not unfit it for ordinary use. 594 TROPICAL HYGIENE, SANITATION, ETC. (3) It should be soluble and emulsible in water. (4) It should not produce injurious effects on human tissue. (5) It should not be too costly in proportion to its germicidal value. (6) Heating "should not affect it. Corrosive sublimate is poisonous, acts on metals, is thrown out of solution by alkalies and organic matter, is acted on by oxides, sulphur and sulphuretted hydrogen, loses its efficiency when mixed with sputum, faeces, &c., because a harmless albuminate of mercury is formed. Its use is therefore limited. It is usually mixed with other chemicals to overcome some of these difficulties. Carbolic acid is not so widely used as in former times because its bactericidal power is sixteen times less than cyllin and kindred prepara- tions. Cyllin, lysol and similar preparations have the advantages of form- ing a permanent emulsion with water, they do not act on metals, they are less toxic than carbolic acid and are sixteen times stronger than carbolic acid. They are compatible with soap. They should not be mixed with anything markedly acid. Lysol and cyllin are the routine disinfectants used by the author. The former gives a clear solution for instruments, &c., for opera- tions, the latter being used for general sanitary purposes. For general use one may use the following : — For washing drains, courtyards, &c., pot. perman., i in 250; cyllin, I in 200. For disinfecting walls, floors, furniture and clothing, cyllin, ij oz. in a three-gallon bucket, or lysol, i in 40. For cowshed floors, dung-heaps, privies, cesspools, dust-bins, use the above but double strength. For solid and liquid excreta use as above or chloride of lime, 4 per cent. For oxidizing organic matter in water, pot. perman. until a pink colour remains. For douches, ] per cent, lysol. For hand lotions, i per cent, solution of lysol. For surgical instruments, i per cent, lysol. For Insecticides Castellani recommends : — For body lice, kerosene, vaseline, guaiacol, anise preparations, iodo- form, lysol, cyllin, carbol solution, naphthaline, camphor in the order mentioned for efficiency. Sulphur, corrosive sublimate and zinc sul- phate are useless. For bed bugs, kerosene, guaiacol and pyrethrum. For moths, naphthalene, menthol powder. The latter is repellent to lice, fleas and mosquitoes. For patients entering the hospital with lice, &c. : strip off all clothes. SANITATION 595 sterilize clothes, shave patient completely, bath in soft soap each night for three nights, put powdered naphthaline down the shirt collar next to the skin. The heat at night will dissolve it and kill any remaining bugs. For houses and dosed spaces fumigatiofi is usually resorted to. The means used are usually sulphur dioxide and sulphurous acid gas, formaldehyde, chlorine gas, bromine gas and nitrous acid. (i) Sulphur Anhydride and Sulphurous Acid Gas. This is generated by burning rolls of sulphur in an iron vessel with a little spirit to commence the burning.' Three pounds of sulphur are used for each 1,000 cubic feet of closed air-space yielding theoretically I'l to s'3 pcr cent, of sulphurous acid gas in the space. The Clayton apparatus is in common use for extensive fumigations with this gas. As in other methods the essential factors are to stop up completely all the air holes in the place to be disinfected. It is useful for large rooms, stores, ships, &c. Three per cent, of this gas for two hours will kill anv pathogenic bacteria in exposed spaces, also rats, mice, insects, weevils, beetles, cockroaches, lice, bugs, moscjuitoes, the eggs and the larvae of insects. Anthrax spores are not destroyed. Air saturated with from 6 to 8 per cent, of the gas for six hours destroys : — The bacillus of plague, diphtheria, cholera, typhoid bacillus, tubercle bacillus, the smallpox infective agent and vaccines. For a loaded ship's hold use 3 per cent, for eight to twelve hours and leave closed until next day. 0*5 per cent, will kill rats and insects in two hours but the 3 per cent, is needed for the penetration. The gas destroys fruits and potatoes. It injures wheat in bags but not in bulk, neither maize, rice, nor other grains in bulk. It will kill the weevils in these. The method is more applicable for houses than any other because the articles need not be removed from the house. It is easier to take ,a Clavton apparatus to the house than to take the articles to the dis- infector. Everything is disinfected in situ. (2) Formic Aldehyde. Formic aldehyde vapour by the alformant lamp is good. It burns 30 tablets per 1,000 cubic feet. The exposure is for five to ten hours. Trillat's autoclave for formalin is more efficient but much more costly. Singer's apparatus uses formalin 30 per cent, with glycerine 10 per cent. This is vaporized and is ejected as a fine spray. One needs 20 ounces of formalin for each 1,000 cubic feet, i per cent, of vapour or o'5 per cent, solution will kill most organisms. It is more rapid. 596 TROPICAL HYGIENE, SANITATION, ETC. penetrating and diffusible than chlorine. It is harmless to colour but iron is affected. Other means of using formalin are as follows : — Mix I42i grammes of permanganate 285 ,, formalin Put it in a metal tray 7 inches square and 3-4 inches deep for the combustion The Formanganate process consists of : — 16 oz. of 40 per cent, formaldehyde solution 240 grammes of permanganate for each 1,000 cubic feet Warmth to 63'' F., and moisture to 60-65 per cent, humidity are essential. A " homely " method is to use 8oz. of permanganate for each pint of formaldehyde for every 1,000 cubic feet of air space. Suspend wet sheets in the room. All fires should be extinguished as the gas is slightly inflammable. (3) Chlorine. Chlorine is produced by adding crude hydrochloric acid to calcium chloride, ij to 2 pints of the acid to each pound of lime. Two pounds of calcium chloride with three pounds of the acid for each 1,000 cubic feet are generally used. Nitrous fumes are generated by adding copper filings to nitric acid. Some medical officers have found useful the following for the destruction of mosquitoes : — Crenyl or creolin vaporized by a spirit lamp. Use 600 c.c. for a room of 100 cubic metres with 270 c.c. of alcohol. It is not necessary to paste up all the cracks. It should be left for eight hours. It is cheap, there is no smoke, it does not damage objects and does not have the bleaching effect of sulphurous acid. In Great Britian rats do an enormous amount of damage reaching the sum of ;^' 10,000,000 per annum. For rat extermination viruses are sometimes used, e.g., the Liver- pool virus, the Danysz virus and Ratin at a comparative cost of i, iJ and 2^, but they rapidly lose their virulence in the tropics. Barium carbonate, i in 4 of meal on fish or bread, is effective against rats and mice. Warehouses and stores should be disinfected with Clayton's apparatus every two months. QUARANTINE. Land quarantine was abolished in Europe some time ago but the governments have the right to close the frontiers if necessary. The International Regulations of the Paris Convention of 1903 were formed to prevent the importation of cholera, plague and yellow fever. These are the onlv diseases as vet under international control. SANITATION 597 For large seaports the Convention recommends as follows : — (i) A properly organized port medical service and permanent medical supervision of the health of the crews and of the population of the port. (2) Suitable accommodation for the isolation of the sick and for keeping suspected persons under observation. (3) A bacterial laboratory and buildings with the necessary plant for efficient disinfection. A supply of drinking water of quality above suspicion at the dis- posal of the port authorities and a system of scavenging that offers sufficient guarantee for the removal and disposal of excrement and refuse. .4// arriving ships arc classified as : — (i) Infected when there is a case of plague or cholera on board or has been on board within seven days of arrival in port. The sick are immediately disembarked and isolated. The other persons disembarked, and if cholera they are kept under observation either on a ship or at a sanitary station before being allowed "free pratique"; or they may be placed under *' surveillance "for five days after arrival in port. Such as have "free pratique" are watched by the local authorities in the districts where they go. With regard to the ship the bilge water and drinking water are replaced. If it is a case of plague observation may be followed by surveillance for five days. The soiled linen, wearing apparel and personal effects of crew and passengers are disinfected by the sanitary authorities. Parts of the ship are also disinfected. All rats must be destroyed within forty-eight hours. (2) Suspected when there has been a case of plague or cholera on board at the time of departure from port or during the voyage, but when there has not been a new case within seven days of arrival in port. Passengers and crews of suspected ships are subject to surveillance for more than five days after arrival of the ship in port. Soiled linen and personal effects are disinfected and such parts of the ship as have been occupied by persons infected are also disinfected. For plague, all rats are destroyed and for cholera the bilge water is removed and good drinking water substituted for that on board. (3) Healthy when there has been no case on board of plague or cholera either before or during the voyage, nor on arrival in port. The passengers and crews of healthy ships from an infected port are subjected to five davs' surveillance after departure of the ship from the infected port. The authorities may require the disinfection of clothes, the destruction of rats or the complete emptying of the bilge nyater. 598 TROPICAL HYGIENE, SANITATION, ETC. In tropical countries it is more difficult and costly to carrv out these measures althoug'h the dangers are greater. At ports where large numbers of coolies or immigrants are arriving, there is usually a strict quarantine for fourteen days at a quarantine station. This is followed by the disinfection of the clothes and the bathing of the bodies of natives. For English Regulations in detail see the Local Government Board Order of September 9th, 1907. IMMUNITY, VACCINES AND SERA. SOME PROPHYLACTIC MEASURES FOR COMMON INFECTIVE DISEASES. . Vaccines and sera are administered in order to produce partial or complete immunity against given diseases. The fundamental principle of vaccine therapy is "to exploit in the interest of the infected tissues the unexercised immunizing capacities of the uninfected tissues " (Wright). Immunity depends upon some property in the living blood serum which opposes or annuls, in part or wholly, the products and action of the infecting organisms (Whitelegge and Newman). Natural Immunity denotes natural resistance to some given disease, e.g., white rats are immune to anthrax; the lower animals are immune to cholera and typhus fever; man is immune to swine fever. Acquired Immunity may be acquired as the result of a natural attack of a disease, e.g., smallpox, or it may be after an artificial attack of the disease, e.g., inoculation. Active Acquired Immunity is produced as the result of inoculating attenuated bacteria into the tissues, e.g., as for rabies. Passive Acquired Immunity is produced by inoculation of anti- toxins into the tissues, e.g., diphtheria. Vaccination is an inoculation by an attenuated virus. Vaccines are prepared from laboratorv bacteria or bacteria from the patients about to be treated. These latter are known as autogenous vaccines. The bacteria are isolated, cultivated, killed by heat or anti- septics, tested for sterility, counted and preserved in antiseptics. Imported vaccines do not keep at all well in the tropics. To pre- serve them for the longest time possible cut a portion of banana stem, clear out the central core, insert the vaccines, plug up the ends of the banana stem with a piece of the same material and keep in a cool place. The internal temperature of a banana stem is 23° to 25° C, and is fairlv constant for some davs. When becominsf drv make another. The interior can be cooled dailv by sprinkling it and its contents with ethvl chloride. IMMUNITY, J'ACCINES AND SERA 599 Some medical officers use a tube of asbestos cloth surrounded by coKon silicate, the whole placed within a wooden or bamboo lube. Others have found thermos flasks useful. TABLii; OF Vaccines and their Doses. Vaccine Appt'oxijiia/e Dose Acne bacillus 5 million initial, to 20 million Acne bacillus with staphylococcus 5 million with 100 million increased IJacilius septus 50-500 million Cerebro-spinal meningitis 5-10 million initial Cholera No. i followed by No 2 Coli bacil'us 10-25 initial up to 500 million Diphtlieria 10-100 million Friedliindei's bacillus 50 million initial to 1,000 million Gonococcus 25-50 million to 1,000 million Micrococcus melitensis 25-250 million Pneumococcus 25-500 initial to 500 million Staphylococcus 100-5,000 million Streptococcus Up to 500 million Typhoid 500-1,000 million. (Broth cultures) Dysenteiy In four strengths, for immunizing and curative in chronic conditions Mallein f 10-15 minims in humans 1 I c.c. for diagnosis in animals Plague 75-80 million or i c.c. Vaccines are : — (i) Killed or attenuated org^anisms with or without toxins. Such are known as Bacterial Emulsions. (2) The toxins only as in Mallein. (3) The fluids of animals suffering from an infectious disease, e.g., calf lymph. (4) Sensitized vaccines. Antitoxic Sera are usually obtained from the horse. A healthy one is reared, tested for tuberculosis and glanders, inoculated with atten- uated serum, later with increasing doses of virulent toxin until a higii degree of tolerance has been obtained. The horse rests a few days, 16 to 20 pints of blood are then drawn ofif from the jugular vein into sterile flasks, the serum is decanted after coagulation and mixed with anti- septic, it is tested for sterility and toxicity and then standardized. A standard dose is sufficient to neutralize a given minimal lethal dose in an animal of known weight. A unit dose of antitoxin will exactly neutralize 100 minimal lethal doses. In diphtheria a unit dose of loxin will kill a 250 grm. guinea- pig in four days; this is considered as a minimum lethal dose. The former or unit dose of antitoxin will neutralize the latter or animal lethal dose and prevent symptoms. Sera have been used for diphtheria, tetanus and bacterial dvsentery> with high value, and in snake bite and plague with some value, iXx. cholera with little value, and in tuberculosis and leprosy with doubtful value. 18 6oo TROPICAL HYGIENE, SANITATION, ETC. The Protection afforded by these sera and vaccines is accounted for along the lines of live principal hypotheses as follows : — (i) The Exhaiislion (Pabulum) Theory. During the first attack the invading organisms remove certain chemical substances necessary for their own growth and in consequence the same species cannot later reinvade the tissues with success owing to shortage of essential chemical food. This view is not widely held. If correct, each specific disease must have a specific chemical pabulum as one disease is only protective against itself. (2) The Antidote or Retention Theory. It is assumed that after a bacterial atack some product is left behind which inhibits any further multiplication of the organism. This theory preceded the antitoxin and antibacterial theories. There is experimental evidence in support of it. Some of the bodies being formed are known as Agglutinins, which agglutinate bacteria or corpuscles, Cytolysins which destroy living cells and Precipitins which precipitate the albumin of the serum. They have been summed up as follows : — Antibody Antigen Action Antitoxin Toxin Neutralization Precipitin Coagulable protein Precipitation Agglutinin Cells, bacteria, &c. Clumping Cytolysin, including bacte- Cells, bacteria, &c. Prepares cells, bacteria, &c., riolysin and haeniolysin for solution by complement Opsonin Cells, bacteria, &c. Prepares cells, bacteria, &c., for ingestion by leucocytes Some authorities stale that opsonin should not be classed as an antibody. Possibly all antibodies may play the part of an opsonin. (3) The Acclimatisation Theory. This is a condition of increased cellular resistance following a bacterial attack. The cells acquire a tolerance of the poison so that ordinary symptoms do not manifest themselves. (4) The Phagocytic Theory. The phagocytic cells, polymorphonuclear leucocytes, mono- nuclears, &c., absorb and destroy the invading bacteria. The inoculation of an attenuated virus is said to stimulate the cellular activity in this direction. Metchnikoff's views were based on this theory. Opsonin (opsono = I cater for) is a chemical substance in the blood stimulating the leucocytes to ingest bacteria. The extent of its action, known as the opsonic index, is a valuable test in estimating the trend of immunization. This opsonic index is estimated by comparing th? number of bacteria ingested by a given number of leucocytes in a normal serum and in a " stimulated " serum. IMMrXITV. J'ACCINES AND SERA 6oi (5) Ehrlich's Side-chain Theory. Antitoxins and antimicrobic substances are assumed to be normally present in the blood, which when stimulated by the introduction of toxin become increased. A central or mother cell is imagined which throws off two varieties of small cells. These are receptor cells capable of com- bining with food-stuffs for the nourishment of the mother cell. One variety links up with simple food substances, the other breaks down compound bodies preparatory for assimilation. Toxins also have two varieties known as haptophores and toxophores. One becomes fixed to one variety of the receptor cells and the other remaining free, and if in sufBcient numbers, produces toxic changes. If the dose of toxin injected is small the mother cells throws off the receptor cell \\ith the toxin attached, such passing free, and now being without harmful effect because it is '' locked up " by the attached receptor. The mother cell produces more receptors so as to exhaust the toxins if these latter are not too excessive. The mother cell then continues to throw off receptor cells into the circulation unfixed, seek- ing toxin cells to fix, but if these latter are exhausted the excess of receptor cells constitutes antitc^xin molecules which are ready to render innocuous or non-toxic an\' new toxic substances of that specific nature which may enter the system. Hence immunity is established, partially or completely, for that specific disease. The toxins may be of the nature of albumoses, and the a.ntiloxins are probably of the nature of globulins. The immunity afforded may be feeble and of short duration — weeks, months, or vears. In small-pox seven years or thereabouts. After an inoculation there is an increased susceptibility for several days, a condition known as anaphylaxis or a negative phase, conse- quently just after an inoculation there is increased susceptibility towards the disease. Because of this negative stage inoculations should not be given within seven to ten days of the former one. Inoculations should be given before the disease is established, during the prodromal period if it is known, or antisera may be given therapeutically during the disease. As to plague vaccine, Ilaffkine claims that the case mortality is reduced to less than one-half after inoculation. Cholera vaccine gives a marked protection against an attack, but the case mortality amongst the inoculated is not much diminished. Antityphoid vaccine reduces the case incidence and case mortality as confirmed in the Great European War. It was only on its trial during the South African War. The protection is not permanent and lasts but from six to twelve months. One could not expect an inoculation to be permanent, really knowing that all the body cells are renewed entirely every seven years or so. 6o2 TROPICAL HYGIEXE, SANITATION. ETC. Bacterial dysentery vaccines for chronic cases are most useful where there are epidemics of chronic dysenter}^. The sera are more useful in the acute stage. Combined vaccines are used and recommended by Castellani. One vaccine made and used by him was for Cholera, Plague, Typhoid. Paratyphoid A and B and I'ndulant Fever together. The inoculation was harmless. Time and experiments alone will indicate their thera- peutic and prophylactic value. SECTION IX. LABORATORY HINTS. THE EXAMINATION OF THE BLOOD. INCLUDING: — The Preparation of Slides. The Choice of Stains. The Fixing of Films. .A. Differential Leucocyte Count. Abnormal Blood-cells. The Estimation of Red Blood-cells and ILemogloein. To Demonstrate Living Malarial Parasites. To Stain Malarial Parasites. Their Varieties. To Demonstrate Micro-filari.^2. The W'assermann and Widal Reactions. To Estimate the Specific Gravity of the Blood, Spectroscopic Examina- tion, and the Tonicity of the Blood. Spectroscopical Examination. The Tonicity of the Blood. TFIE EXAMINATION OF MICRO-ORGANISMS : — Staining Methods. Diagnostic Features of Micro-organisms. The Preparation of Cultures and Culture Medla. THE PREPARATION AND STAINING OF SECTIONS. MALARIAL PIGMENT, WHERE IT IS AND HOW TO FIND IT. THE TRICHOMYCETES. THE HYPHOMYCETES (MOULDS). THE BLASTOMYCETES (YEASTS). THE EXAMINATION OF F.ECES. Macroscopical^ Microscopical, including Ova. Diagnostic Features of Ova. THE DISSECTION OF MOSQUITOES. THE EXAMINATION OF WATER. Biological, Bacterial, Physical, Chemical. THE EXAMINATION OF SEWAGE. THE ANALYSIS OF MILK. 6o4 LABORATORY HINTS LABORATORY HINTS. THE EXAMINATION OF THE BLOOD. To Clean Slides. Slides should be of the medium, not the best, quality for the tropics. Boil in strong soda Avater for five minutes. Wash well in running water. Place in 50 per cent. ILSOj fur ti\e minutes. Wash thoroughly to remove all acid. Drain and place in methylated spirit. To Clean Cover Slips. These should be of the best quality. Boil for ten minutes in bichromate soluiion with a low flame. Wash well and remove all traces of yellow colour. Drain and place in methylated spirit. CHOICE OF STAINS. Basic stains do well for newly growing cells, but more mature and permanent ones as red cells take acid stains better. Hematoxylin and eosin are good in the tropics and do not fade. Leishman's stain is better at first but fades later. Hematoxylin should be matured in (|ua1ily by light and air. Leave the bottle in the sun with the cork loose. To stain for blood changes, use hematoxylin and eosin, but use Leishman's for unfixed blood films. To stain for bacteria, use Loefifler's methylene blue or carbol fuchsin (dilute, four minutes). To stain for animal and vegetable parasites, use carbol thionin or carbol fuchsin. Another film must be used for the acid-fast test. To stain for tissue changes in sections, use hematoxylin two and a half minutes, eosin ten .seconds. If for protozoal parasites use : — Hematoxylin, fifteen minutes, acid alcohol ten seconds, or Carbol thionin or \^an Gieson stain. TIJE EXAMINATION OF THE HLOOD 605 TO FIX BLOOD FILMS. Agents. — Time, lieat, Ilg- perchloride, formalin, csmic acid, absolute alcohol. The best is absolute alcohol and ether, equal parts. Place blood films in it from ten minutes to ad lib. This solution does not lose its fixative power. Blood films to be stained with Leishman's need no fixing at all. A NORMAL DIFFERENTIAL BLOOD COUNT WILL SHOW :— Some '' blood dust " which must not be taken for parasites, though Brownian movement may be present. Leucocytes. — 6,000-8,000 per c.mm. Lymphocytes. — 15-25 per cent. They have a large deep staining nucleus with little protoplasm. Large Mononuclears. — 5-10 per cent. These are larger cells with a larger and paler nucleus with more protoplasm. Polymorphonuclears. — 65-75 P^*' cent. There are several nuclei which are connected by nuclear filaments. Eosinophiles. — 1-3 per cent. The granules show an affinity for acid stains. Transitional. — Few. These have a horseshoe-shaped nucleus. Remember that: — (i) The lymphocytes are increased during digestion, scurvy (60 per cent, are Ivmphocvtes), lymphatic leukaemia (70-85 per cent, are lymphocytes), enteric and Malta fever, but these latter are not constant. (2) The large mononuclears are increased during malarial fever (15-20 per cent.). This is not reduced after taking quinine. Quinine may have cleared up the parasites, but the above condition will assist the diagnosis. (3) The polymorphonuclears are increased physiologically during youth and pregnancv, and pathologically during suppuration and pneumonia. (4) Eosinophiles are increased during worm infections, e.g., trichiasis, bilharziasis, filariasis, &c. Trypanosomiasis, verminous conditions, asthma and bronchitis, urticaria, pemphigus, and after dietetic errors, such as " high " cheese, venison, &c. (5) The total leucoc\'tes are diminished in trypanosomiasis and knia-azar (,^,000 or less). ABNORMAL BLOOD CELLS. White Cells. Mast cells are degenerated leucocytes of the polynuclear type. The nucleus stains poorly. The granules are coarse and are called meta-chromatic granules, because they neither take h^ematoxylin nor eosin well, but stain better with a combination of the two. 6o6 LABORATORY HINTS Leishman's is good and gives them a brownish lint. They are sometimes found in normal blood. Their significance is not known. In lymphatic leukc\?mia the leucocytes are irregular in size, shape and staining qualities. Tlie}- are increased to 14,000 per c.mm. From 70 to 98 per cent, are lymphocytes. The red cells are diminished in number and hb. In spleno-medullary leukcemia, myelocytes are found. The cell may be very large or smaller than normal, the nucleus stains poorly, and it is sometimes studded (U'er with eosinophilic granules. These cells are pathognomonic of this disease. As a rule they are more numerous and larger than any other leucocyte. The nucleus is never horseshoe-shaped. The blood looks milkv. The red cells are reduced to 700,000 per c.mm., some are nucleated. There are also polychromatic and mast cells. Red Cells. Variation in colour usually indicates the amount of hb. A rough indication of anasmia is thus given, Poikiloc^^tosis as seen in pernicious auccmia ma}' be imitated artificially in making the film by drawing the cells down one slide with another, but the elongation is in the same direction in all the cells. To avoid it in making a blood film \\\\h two slides, the drop of blood should be drawn away from the operator and not pushed awav with the second slide. Nucleated red cells may appear in normal blood, ]3rimar\- and secondary ana?mia. The nucleus may be divided, or it may appear as two rounded bodies. Polychromatic cells are not uncommon in the ana?mias, especiallv in malaria. They are degenerated red cells and take up both eosin and methylene blue. Some red cells are basophilic; thev show slippled dots peripherally which may be polychromatic. Thev indicate a degenerative process. They are very common in lead poisoning. They do not indicate latent malaria as Plehn supposed. COUNTING BLOOD CELLS AND ESTIMATING HB. To Count Red Cells. Use Gowers's hfemacytometer. Draw into the pipette blood from a small needle wound in the lobe of the ear or finger-lip up lo the mark on the stem near the bulb. Fill to mark above the bulb with Hayem's solution. Shake well, then place one drop on special slide provided. Place on this a cover slip. The drop should cover the central disc, but should not run over this so as to come between the cover slip and THE EXAMINATION OF THE BLOOD 607 the main slide. Practice will soon enable one to estimate the size of drop required. Use i-in. lens and Xo. 4 eye-piece and focus so that a set of sixteen squares is seen. Count the red cells in each square and on two sides of it. Count up four sets or more of sixteen scjuares each and divide the stun bv the number in each. Thus sixty-four squares contain 768 red cells = 12 in each scjuare. The content of each square is 4o x 2^5 x t\t = 40V0 c.mm. Hence one c.mm. of the solution contains 473750 ^ 12 red cells. lUit the solution was diluted 100 times with the sodium sulphate solution. Hence i c.mm. of blood contains '"" = 4,800,000 red blood ,, 4COO X 12 cells. For White Cells. l\se I per cent, acetic solution and a drop of methj-lene blue. A separate pipette giving a 10 per cent, dilution is better. In estimating the Hb. in the Tropics. A book \\ith stained papers and corresponding blank blotting papers is used. A little of the latter is touched with the blood, and then is matched with the stained paper, which gives the percentage of hb. A small book costing 5s. will last five vears. TO DEMONSTRATE LIVING MALARIAL PARASITES. Take a small drop of blood on centre of cover slip. Edge the cover slip with vaseline and place it on a slide. Examine middle zone with a T^-'n- objective. In the outer zone are rouleaux. In the middle zone are single red cells. In the central zone very few red cells. A dull light is required as corpuscles are colourless. The parasite will be seen in a red cell and pigment in the parasite. If the field is flooded with light the pigment is still clearly seen, but the granular leucocyte is not clearly seen. The parasite shows amoeboid movement ; the males will throw out long pseudopodia which lash the red cells, and eventually become free to enter the female cell. The actual entry has not been witnessed. TO STAIN THE MALARIAL PARASITE IN THE BLOOD. (i) Leishman's stain is the best. It is polychrome. No fixing is recjuired. The eosin stains the red cells. 6o8 LABORATORY HINTS The red methylene blue stains the chromatin. The blue methylene blue stains the nucleus. The soloids are dissolved in pure metliyl-alcohol and put up in phials. The film should be fresh and imfixed. Stain half to one minute. Add distilled water in drops as 2 to i of stain and move about gentlv five to seven minutes. One can see under l^ in. when it is stained sufiliciently. Flush ofif with distilled water. Dry and mount with Canada balsam and cover slip. Unmounted blood films will keep a long time. Other methods are : — (2) Borax meth^dene blue. Fix in alcohol and ether, ten minutes. Dry and stain with borax methylene blue, thirty seconds. Wash well, dry and mount. This will not differentiate the chromatin. It is not so good for the white cells. It is better than Leishman's for old films. (3) Haematoxylin and eosin. Fix in alcohol and ether, ten minutes or more, and dry. Stain with haematoxylin, seven minutes. Flush off with tap water for five minutes. vStain with eosin, thirty seconds. Wash, dry in air, mount. (4) Carbol-thionin. Fix in alcohol and ether, ten minutes. Dry and stain with dilute carbol thionin, ten minutes. Wash, dry and mount. Strong solutions are used for sections. This will keep. This is diluted with three parts of water for blood films. This soon degenerates — twent}'-four hours. One cannot over-stain with it. The older the film the less time required for staining. (5) Eosin-azur. No fixing required. This stain shows up the crescents well. Stain as with Leishman's; onlv use three times the distilled water from twelve to fifteen minutes. Dissolve one soloid in 10 c.c. of methyl alcohol. It is tw^ice the price of Leishmnn's stain. This is good for the trvpanosome and halteridium. THE EX.IMIXATION OF THE BLOOD 609 THE VARIETIES OF MALARIAL PARASITES. There are three to look for : — The benig^n tertian parasite full\' i^r.nxn in fort\-eight hours. The subtertian, t-estivo-autumnal or malignant parasite, fully- grown in tliirty-four to forty-eight hours. The quartan parasite full^' grown in seventy-two hours. There may be several " crops " of one parasite, so that the same slide may show two or three groups at different ages. There may be a multiple infection, two varieties of parasites in the same film. One family of parasites may be so few in number that there will be no corresponding rise of temperature. If there are two infections of the same varietv the rises of tempera- ture are seldom equal. In benign tertian the red corpuscle is enlarged and pale. Schiiffner's dots ma\' be seen, which, consist of peculiar granular degeneration staining brick red and diagnostic of benign tertian. Parasites are plentiful in the peripheral blood, but tend to sporulate in the deeper organs; the gametocvte is rounded or ring-shaped, fifteen to twenty-five spores, yellow brown, pigment coarse. Active amoeboid movement. Life-cycle forty-eight hours. In the subtertian the red cell is smaller, no St-liiiffner's dots. Young ring forms are seen in the peripheral blood, but not always; it matures in the deeper organs. The sporulating form found in the spleen ma}' be seen in the peripheral blood just before death. The corpuscle becomes yellow — " brassv bodA-." The gametocyte is crescentic in shape, pigment black and fine. It is very amoeboid. Life-cycle is variable, perhaps thirty-four to forty-eight hours. Spores, 7-8, rarely 20. Very active, but small processes. The male and female cells can be distinguished. Male, has pigment and chromatin more scattered. Female, one central mass of chromatin with the granules arranged around it. There ma}- be two or three or more small, clean-cut ring forms in 'one cell which is rare in benign tertian or quartan. Some subtertian parasites mav be seen that have not penetrated the red cell which is uncommon in benign tertian. The chromatin is more flattened, and not knob-shaped as in benign tertian. A second slide taken twenty-four hours later \\-\\\ show parasites enlarged if benign, but the\- will be little altered or gone to the deeper organs to sporulate if subtertian. In benign tertian and quartan there are usuallv a few earlv or late sporulating parasites which would not be seen in subtertian. 6io LABORATORY HINTS The finding of crescents establishes the diagnosis. A sporulating subtertian fills about one-third of the red cell. A sporulating quartan fills the cell. The crescents or subterlian gametoc^^tes are especially interesting. The sexes are differentiated. They do not produce fever, 'i'hey undergo no change in man's blood. The}^ appear one week after the fever has commenced and persist for six \\eeks after quinine has been given. Although the patient has no fever, he is infective as long as these crescents remain in the blood. In the quartan parasites the red cells are never enlarged. The affected cell is darker than the normal ones, it requires longer to develop, seventy-two hours; it has fewer spores, five to twelve, than benign tertian, but they are the largest of all. Sporulates in the peri- pheral blood. Corpuscle becomes smaller and darker. Gamete rounded, the pigment is black, and granules coarse. There is little amoeboid movement. The parasite may be stretched out across the cell "cigar-shaped," when it is called an "equatorial " parasite;. The pigment of the male dances about, throws off flagella which are very active. In ten to fifteen minutes they break off and swim freely in the blood until they pierce a female cell. The female cell is quiescent after the polar bodies have been extruded. The fertilized female or zygote becomes oval " ookinet," and later when it moves it is known as a travelling vermicule. The leucocvtes gather around the male cell when the flagella have been thrown off and remove them. This process can be seen under the microscope in specimens of fresh blood. TO EXAMINE FRESH BLOOD FOR MICROFILARIAE. Make a thick film of several drops of blood and let it dry. Place it inverted in a watch-glass of water so as to remove hb. from the blood. Fix it in alcohol and ether. Stain ^\•ith hot hc'ematoxylin five minutes, then flush with water. Examine while wet. Repeat stain if not well blue. Dry and mount. THE WASSERMANN REACTION (FLEMING'S MODIFICATION). This important diagnostic reaction of the blood depends upon the l^rinciple of hiemolwsis. If the case for diagnosis be really a case of syphilis, then no hasmolvsis will occur. A control experiment is carried out at ihe same time, using normal serum. The substances required are: — - (i) An alcoholic extract of heart muscle. It is made from i grm. of heart muscle (guinea-pig) rubbed in a mortar with 25 c.c. absolute alcohol, heated to 60° C. for an hour and filtered. THE EXAM I SAT ION OF THE BLOOD 6ii (2) Sheep's corpuscles washed and dihited with normal sah'ne. (3) vSerum in an ordinary blood tube. Use a throttle pipette with a long- stem and rubber teat. Half an inch from the capillarv end mark with a grease pencil. 'J'his equals one volume. Permit a bubble of air and draw up another volume, and so on until all required are drawn up into the pipette. Prepare the following : — (i) Extract of heart muscle ... ... 4 volumes Syphilitic serum ... ... ... i ,, (2) Heart muscle 4 ,, Normal serum ... ... ... i ,, (3) Normal saline ... ... ... 4 ,, Syphilitic serum ... ... ... i ,, (4) Normal saline 4 ,, Normal serum i ,, (5) Heart muscle 4 ,, Incubate all these for one hour at 37*^ C. Add then to each tube one volume of sheep's corpuscles. Incubate again for one-and-a-half to two hours. The results should now be : — No haemolysis in tubes (i) and (5) Haemolysis in all the others. The heart contains a syphilitic antigen which serves the same purpose as a syphilitic foetal liver. To discuss the whole biochemical process is not our purpose, but the explanation of the reactions in each tube is here given in brief. (i) Syphilitic antigen in extract + syphilitic serum (svphilitic amboceptor + complement) + sheep's corpuscles. The complement is fixed, therefore there is no hcemolysis. (2) Syphilitic antigen + normal serum (non-specific amboceptor + complement) + sheep's corpuscles. The complement is not fixed, therefore hcemolysis. (3) Xormal saline + syphilitic serum (amboceptor + comple- ment) + sheep's corpuscles. The complement is not fixed, therefore haemolysis. (4) Normal saline + normal serum (amboceptor + complement) + sheep's corpuscles. The complement is not fixed, therefore ha?moIvsis. (5) Antigen + sheep's corpuscles (no amboceptor, no complement). Therefore there is no haemolysis. THE WIDAL REACTION. An important diagnostic blood reaction for tvphoid and allied fevers, depending upon the agglutination of the bacteria. Clean the lobe of the ear with ether. Collect a few drops of blood in a sterile capillary tube. Seal the ends in a flame with blood in tlie central part. 6i2 LABORATORY HINTS Centrifuge or let it stand several hours, break off end, and blow out serum when required. Use a pipette as for the Wassermann reaction. Draw seven volumes of normal saline into pipette. Express one volume on each of seven clean slides or one large slide. Take one volume of serum to be tested and place on a clean slide. Take another volume of serum to be tested and place on a slide with one volume of saline. 71iis serum is now diluted i in 2. Take one volume of this latter, mix with another slide with one volume of saline. This is I in 3 dilution. Repeat this process through the series excepting the seventh slide, as this last is of normal saline for a control. Take a thick emulsion of typhoid bacilli from an agar culture. Add one volume of this to each of the slides and mix well. Examine under a i-in. objective. The reaction is positive if complete agglutination occurs imme- diatelv in the i in 2 dilution and within half an hour in the i in 6 dilution. These can be examined by drawing them up into a long pipette separated bv an air bubble, or separate fluid drops on one large slide or on separate slides. THE SPECIFIC GRAVITY OF THE BLOOD. From 1035 to 1068. To estimate it prepare a fluid of glycerine and water or chloroform and benzol in known proportion about the normal specific gravity of the blood. Place in it one drop of blood, and alter the specific gravity of the .fluid bv adding glycerine and water or chloroform and benzol until the drop neither floats nor sinks. The specific gravity of the fluid is then that of the blood. THE SPECTROSCOPIC EXAMINATION. A small direct vision spectroscope is the most useful. Dilute the blood with distilled \\aler. Focus the spectrum, closing the slit as much as possible so as to bring out Fraunhofer's lines distinctly. Oxy haemoglobin and reduced haemoglobin can be obtained from the same specimen by shaking it up with air to oxidize it and adding ammonium sulphide to reduce it. Oxyhiemogkjbin shows two narrow une([ual dark bands between the lines D and E. THE EXAMINATION OF MICRO-ORCANISMS 613 Reduced hcTmoglobin shows one broad band between lines D and E. Metha^moglobin sliows two equal bands between D and I{ and one between C and D. The urine is brown. It is often seen in mild cases of blackwater fever. Urobilin shows one broad band between E and F. THE TONICITY OF THE BLOOD. Some specimens of corpuscles have the power of retaining hb. better than others. Distilled water will remove the hb. but saline solution over a certain strength will not remove it. The resistance or tonicitv can be measured by the strength of that saline solution which is just sufiticient to prevent the solution of the hb. This solution is said to be " isotonic." Normal blood is hypertonic. Normal saline solution, 75 per cent., prevents the solution of the hb. Make a series of weaker solutions differing o"02 per cent. Place one drop of blood in this, shake and allow to stand. The weakest saline solution that does not cause solution of the hb. is the index of the tonicity of the blood used. The normal is o"46 to 0*48 per cent. A decrease of tonicity often precedes a h^emolytic attack. Persons of a normally low tonicity should not be allowed to live where blackwater fever is endemic. THE ENAAIINATIOX OF ?^IICRO-ORGAXISAlS. TO STAIN MICRO-ORGANISMS. The Gram method is important. To Stain Smears. Stain witli aniline gentian violet, five minutes. Pour off, treat with Gram's iodine solution, two minutes. Pour off, treat with alcoholic eosin until the colour ceases to come out freely. Wash, dry and mount. Gram's iodine is i part of potassium iodine and 300 parts of water. Jo Stain Sections. Stain with aniline and gentian violet, ten minutes. Stain with Gram's iodine, two minutes. Pour off and blot. Stain with alcoholic eosin, thirty seconds. Oil of cloves and xvlol. 6i4 LABORATORY HINTS Important Differentiations. Gram-positive G?-ain-jiei^a/ive Staphylococcus, all varieties Bacillus i mallei Streptococcus pyogenes n coli communis Micrococcus tetragenus )' coli dysenteria? Fraenkel's bacillus n enteritidis (Gartner) Bacillus acne >) pestis ,, anthracis )> pyocyaneus ,, botulinus )' influenza' „ diplitheri?e )) Friedlander's pneumo „ enteritidis (Klein) J» malignant oedema „ Oppler-loas u prodigiosus ,, pseudo-diphtheriae > proteus vulgaris „ xerosis ■)1 fluorescens ,, tuberculosis 51 smegmne „ smegtn?e ? )t soft sore „ leprs Di plococcus intracellularis meningitidis ,, subtilis D iplococcus catarrhalis „ welch ii Gonococcus ,, tetani Sp irillum cholera asiaticre Aspergillus Spiroch ietes of syphilis, relapsing fever. Sarcinas, all varieties Vincent's angina, and other para- Yeasts (blastoniycetes) sitic protozoa Ringworm fungi M icrococcus melitensis Streptothrix of actinomycosis „ madura disease Most organisms when stained with fuchsin are readily decolorized by weak solutions of mineral acids. The exceptions are : Tubercle bacillus, bacillus leprcC, smegma bacillus, the bacillus of timothy grass, the dung bacillus and others less important. If an organism retains its stain after treatment by 25 per cent. H2SO4 or 30 per cent, nitric it is acid-fast. The Acid-Fast Method. Stain with warm carbol fuchsin, five minutes. (To warm, heat a penny over a Bunsen flame and place slide upon it. Repeat the process during five minutes.) Decolorize with 20 per cent, strong HoSO,, HXO3 or HCl. Wash well, dry and mount if a film; dehydrate, clear and mount if a section. Some organisms are so rapidly decolorized that they are not seen, as the pneumo-bacillus. For these use aniline oil instead of acid alcohol. Weigert's Method. Aniline gentian violet, five minutes. Gram's iodine, two minutes. Pour off, treat with aniline oil, then stop its action with water. Counterstain other Grams with Bismarck brown one minute, or aqueous eosin 20 seconds. Wash, dry and mount. THE EXAMINATION OF MICRO-ORGANISMS 615 To Find the Diplococcus pneumoniae stain thus: — Aqua eosin, twenty seconds. Wash, treat with aniline gentian violet, ten minutes. Pour off, treat with Gram's iodine, two minutes. Pour off, blot, and treat with aniline oil until colour ceases to come out freely. Treat with xylol to stop the action of aniline oil. To Stain Spores. Hot carbol fuchsin, five minutes. Wash, treat with 20 per cent, acid, two dashes. Wash well to get rid of the acid. Stain with Loeffler's blue, four to five minutes. Wash, dry and mount. In examining a micro-organism ascertain its : — Motility, morphology, acid-fast or not, Gram-positive or not, does ir form spores or not. Remember that no acid-fast organism is motile, no coccus is acid-fast or forms spores, all acid-fast organisms are Gram-positive, Gram-negative organisms are non-sporing except the bacilli of malignant oedema. Thus a cholera vibrio would be motile, hence it would not be acid-fast nor would it form spores. Motility depends upon flagella but the extent of movement does not depend upon the number of flagella. These latter are difficult to stain and readily break off. Brownian movement can be performed by inanimate matter as well as by some micro-organisms. TO DIAGNOSE MICRO-ORGANISMS. One must know their morphology. The chief ones from the acid-fast group are : — (1) The Tubercle Bacillus. A non-motile slender rod with rounded ends, often slightly curved, 2'5 to 5 /x long. Some portions do not stain well and hence it often presents a "beaded " appearance. It is acid-fast. The culture is aerobic and facultatively anaerobic. Grows slowly at blood heat. In glycerine broth it develops as a floating pellicle. On glycerine agar it gives a creamish. dry and wrinkled film. It does not liquefy gelatin. 39 6i6 LABORATORY HINTS Pure cultures can be formed by inoculating a guinea-pig from tubercular sputum. (2) The Bacillus pseudo-tuberculosis of Pfeiffer. It grows rapid! V and readily forms a creamy growth on agar very different from that of tubercle. On gelatin a whitish growth without liquefaction. It is not acid-fast. Is Gram-negative. Found in milk and sewage. Pathogenic to guinea-pigs and rabbits. (3) The Bacillus leprae. A long slender straight rod, with somewhat pointed extremities, non-motile, does not form spores. Gram-positive. Acid-fast. Stains more rapidly and decolorizes more readily than the tubercle bacillus. Attempts to grow cultures have not been very successful. (4) The Smegma Bacillus. Shorter and flatter than the tubercle bacillus in cultures. Grows readily, acid-fast. Non-pathogenic in small infections. (6) The Bacillus of Timothy Grass. Acid-fast. Resembles tubercle bacilli, but is harmless. It grows readilv in any ordinary medium. It is found in fodder about cow-sheds, and when in milk may be taken for the tubercle bacillus. The chief ones from the spore-forming groups are : — (1) The Anthrax Bacillus. It is aerobic and facultatively anaerobic. 5 to 6 /a long. Non-motile, scjuare ends, occurs in short chains and singly in blood. Some segmentation may be seen on staining. It is surrounded by a sheath in which it divides; this process may continue, forming chains. In the presence of much oxygen and a temperature of 20° to 38° C., spores are developed, but only after death when the blood dis- charges come into contact with the air. In cultures it liquefies gelatin in two days. In a stab, fine branching filaments grow outwards from the needle track called the " inverted fir tree growth." Liquefication begins at the top. In both a focculent growth forms at the bottom. On agar a thick grey-white sticky growth. The bacilli are Gram-positive. To stain spores heat them for twenty minutes in warm carbol fuchsin. THE EXAMINATION OF MICRO-ORGANISMS 617 (Heat a penny over the flame, remove it, place upon it the slide witii spores and stain. Repeat several times.) (2) The Tetanus Bacillus. Short straight slender rod with rounded ends, slightly motile with man^' flagella, forms spherical spores at one end, giving the " drum- stick " appearance. Gram-positive. Not acid-fast. A strict anaerobe. Liquefies gelatin. In glucose-agar stab, a feathery radiated growth with slight gas formation. Spores very resistant. Nearly pure cultures obtained by heating ordinary earth to 80° C. on two to three successive days and then preparing agar shake cultures. Produces two alkaloidal toxins, tetanotoxine and spasmotoxine, which both produce convulsions. Readily destroyed by heat and light. Natives bury carcases in order to produce this toxin for arrow poison. (3) The Bacillus oedematis maligni (Bacillus septicus). A motile slender rod (4 jx long), with several flagellce. Gram- negative. Stains readily. Forms spores in a central position. Tends to grow in long filaments. A strict anaerobe. Gelatin liquefied with pro- duction of foul smelling gas. Blood serum liquefied. (4) The Bacillus botulinus. Large (4 to 6 /i), with rounded ends, slight motility, four to eight flagella, forms terminal spores, an obligatory anaerobe. Gram- positive. Does not curdle milk, ferments glucose with production of acid and gas, lactose not fermented. In glucose gelatin yellowish- brown translucent colonies are formed surrounded by a liquefied zone. Causes botulism. (5) The Bacillus welchii. A long (3 to 6 jx'), thick bacillus in ones, chains and clumps, often has a capsule, forms spores only in serum cultures, strictly anaerobic, Gram-positive. Non-motile. Licjuefies gelatin slowly, produces gas in dextrose and lactose, a honey-combed curd in milk with gas in twenty-four hours. Cultures are stronglv acid. Found in septicaemic and pyasmic infections of the gastro-intestinal tract. The important ones from the Coli Group are : — (i) Bacillus coli. (2) The capsulated bacilli." (3) The bacillus enteritidis group. (4) Bacillus typhosus. (5) Bacillus dysenteric. All are as a rule short, stout with rounded ends, form no spores. 6i8 LABORATORY HINTS Gram-negative. Do not liquefy gelatine. On gelatin plates form ithin, irregular, notched colonies (see table for dififerentiation). Class Motility Glucose Lactose Litmus paper Indol Production Neutral red Typhoid ba- Actively mo- Acid formed; No action Permanent No indol No change cillus tile ; 8 to 12 flagella no gas acidity; no other change Intermediate Ditto Acid and No action Kirst acid, No indol Becomes or Gartner gas formed then alkaline, as a rule yellow group no other change Colon group Feebly mo- Ditto Acid and gas Permanent Indol Ditto tile ; 3 to 4 formed acidity with formed flagella curdling Dysentery Non-motile Acid formed ; No action First acid. Sometimes No change bacillus no flagella no gas then usually becoming alkaline formed (1) The Bacillus coll. Short (2 to 4 fi) rounded ends, sometimes almost oval, three to four flagella, feebly motile, no spores. Gram-negative. It never liquefies gelatin, produces permanent acidity in milk which is curdled within seven days at 37° C. Ferments glucose and lactose with acid and gas, forms indol, a thick yellow-brown growth on potato, reduces nitrates. • (2) The Capsulated Bacilli. Bacillus pneumoniae, or the pneumo-bacillus of Friedlander. A short rod (i to 2 /a) with rounded ends, encapsulated, frequently in pairs, non-motile, non-sporing, aerobic and facultative anaerobic. Gram-negative. (The pneumococcus is Gram-positive.) It loses its capsule when cultivated, a nail-shaped growth in stab gelatin, milk slowly coagulated. Bacillus lactis aerogenes, non-motile, does not ferment dulcitol, milk rapidly curdled with formation of capsules, forms " nail-head " growth in gelatin. (3) The Enteritidis Group. The enteritidis group includes such as Gartner's bacillus which causes meat poisoning epidemics. The pneumonic group such as bacillus psittacosis causing epidemic pneumonia in parrots and a fatal broncho-pneumonia in man. The paratyphoid group causing paratyphoid fever. The non-pathogenic group (to man), as the bacillus suicholeras or hog cholera bacillus and the Danysz's bacillus for exterminating rats. They all resemble the typhoid bacillus, morphologically being Gram-negative, activelv motile, multi-flagellate, non-sporing, but they THE EXAMINATION OF MICRO-ORGANISMS 619 differ in cultures. They reduce neutral red, do not curdle milk, pro- duce acid and gas from glucose, do not attack lactose. Litmus milk is first acid then alkaline. The agglutination test is often necessary to differentiate them. (4) Bacillus typhosus. Short (2 to 4 ^), thick, rounded ends, no spores but granules and vacuoles are sometimes seen. Involution forms 10 ' to 30 yu on repeated sub-culture are characteristic. Aerobic and facultative anaerobic. Gram-negative. Not killed by drying. Direct sunlight kills in five ho'urs. On agar a thick greyish-creamy growth, on gelatin a thin white growth without liquefaction, turbidity in broth with some deposit, milk made slightly acid, no curdling, ferments glucose with acid but no gas, lactose not affected, neutral red not affected, forms little or no indol. Infects humans through water, shell-fish, dust and air, flies, vegetables, soil, milk (dirty), filters, contact with carriers. (5) The Dysentery Bacillus. Fifteen tvpes are said to exist. The Flexner and the Shiga-Kruse varieties are the best known. All resemble Bacillus coli and typhoid bacilli in morphology and staining reactions. Generall}' said to be non-motile. Grow well in milk without clotting, with acid then alkaline reaction. In a few days ferments glucose with acid but no gas. Agglutination identifies the variety. The Flexner type ferments mannitol with acid but no gas. The Shiga-Kruse bacillus has no action on this polyhydric alcohol. Other important micro-organisms are : — The Bacillus diphtheriae. The Klebs-Lofffer bacillus is a slender (3 to 5 /^ ) non-motile, non- sporing rod with rounded ends. A parallel arrangement is common and club-shaped forms are frequent. Not killed by drying. Aerobic and facultative anaerobic. Shows segmentation on staining with Loffler's blue. Gram-positive. Shows growth on gelatin with- out liquefaction, rapid growth on agar and blood serum at blood heat, does not coagulate milk, forms acid therein but no gas. The Bacillus pestis. A short, thick rod, usually linked in pairs, like a cocco-bacillus. Gram-negative, non-motile, no spores, bipolar staining. Grows best from 25° to 20° C. Easily killed by disinfectants, cultures lose their virulence quickly. In broth with a little butter flocculent tapering masses of growth are seen depending upon the oil droplets floating on the surface — Haffkine's stalactite growth. On gelatin a thick whitish punctate growth without liquefaction. It does not coagulate milk. 620 LABORATORY HINTS The Staphylococcus pyogenes aureus. Occurs as a diplococcus in grape-like masses, non-motile, no spores. Gram-posilive. General turbidity in broth, liquefies gelatin with an orange-yellow sediment, on agar and blood serum a pale, then later a golden streak is formed. Staphylococcus pyogenes albus pro- duces a white and Staphylococcus pyogenes citreus a lemon-yellow growth on agar and blood serum. The Bacillus pyocyaneus. A small bacillus found in blue-green pus, very motile. Non- sporing. Creamy growth on agar with greenish fluorescence, liquefies gelatin rapidly. Gram-negative. The pigments, pyocyanin and pyo- xanthin, can be extracted with chloroform. The Streptococcus pyogenes. In chains, ten to fifteen bacteria in pus, thirty to forty bacteria in broth cultures. Gram-positive. Grows well with or without oxvgen. Produces turbidity in broth, but growth ceases after four days owing to the production of an inhibitory metabolic substance. Slow growth on gelatin without liquefaction. Coley's fluid is from Streptococcus pyogenes and Bacillus prodigiosus, grown together for two weeks and sterilized by heat 65° C. The Gonococcus. Small coffee-bean in shape, usually in pairs, a strict parasite. Does not grow on ordinary media, but can be cultivated on blood or blood serum agar. A pure culture has a raised greyish-white mulberry appearance. The Meningococcus. The Diplococcus intracellularis meningitidis is Gram-positive. Grows on blood agar at blood heat, occurs within the pus cells as a diplococcus, produces epidemic cerebrospinal meningitis (or spotted fever). The Diplococcus pneumoniae. Usually seen as a diplococcus, but sometimes in chains of pus. The cocci are oval or lance-shaped in a gelatinous capsule. Gram-positive. Grows well on blood serum, but not readily seen. Does not grow well on gelatin. In cultivation the capsule is lost. No growth on potato. Produces curdling and acid with milk. The Micrococcus melitensis. Small, in pairs or singly or short chains with active Brownian movement. Slow growth, in three to four days small semi-transparent droplets on agar, which later become yellowish-orange. On gelatin a dirty white streak without liquefaction. Gram-negative. It occurs in the blood and milk of goats. THE EXAMINATION OF MICRO-ORGANISMS 621 The Glanders Bacillus. The Bacillus mallei is a short rod (2-5 /a) with rounded ends. Bipolar or beaded in stained preparations, no spores. Non-motile, but active Brownian movement. A creamy growth on glycerine agar, does not liquefy gelatin. On potato, four days, looks like drops of honey, but later darkens to chocolate colour, but the potato remains unstained. Gram-negative. Does not readily stain at all; methylene blue, and then 4 to 5 per cent, acetic for ten seconds is the best stain. The Spirillum cholerae asiaticsB. Koch's comma bacillus is a curved rod (2-.-; ^) vS-shaped in liquid media, actively motile, one flagellum, no spores, desiccation and sun- light rapidly fatal. Gram-negative. Readily stained with aniline dyes, grows readily on most media, but a slight alkaline reaction is necessary. Forms indol rapidly, creamy growths on agar. General turbidity in broth and H2S in both. Occurs in flakes in a "fish in stream" position. For bacterial diagnosis, see Cholera. The Finkler-Prior spirillum may be confounded with it. These are thicker and longer than the Koch's comma bacillus, and it can be differentiated by the cultural reactions: — Cultural Characters KocK s Comma Bacillus Vibrio Proteus (Finkler-Prior Spirillum) Gelatin stab culture ... Slow liquefaction Rapid liquefaction Potato at 37°C Slow light greyish brown Rapid slimy yellow growth growth ... Peptone water Indol reaction marked Indol reaction feeble or nil within twelve hours ... in three days t TO PREPARE CULTURES. For nutrient media, test-tubes, Petri dishes and other vessels are used. Wash all with 25 per cent. HCl, rinse well with water and drain, rinse with alcohol and dry, plug test-tubes with cottonwool, sterilize at 140° C. The common media are : — Beef Broth. Use I lb. of beef steak, free from fat and connective tissue, mince, add 1,000 c.c. of water, boil and stir well for thirty minutes. Strain through muslin, add water up to 1,000 c.c, add sodium chloride, 5 grm., and peptone, 10 grm., boil for five minutes, carefully neutralize with sodium hydrate solution, make it slightly alkaline to litmus, then boil for ten minutes, shaking well, filter it into flasks plugged with sterile cottonwool. 622 LABORATORY HINTS Glucose and Lactose Broth. To each loo c.c. of above i to 2 grm. of line g"lucose or lactose. This is used for anaerobic bacteria. Nutrient Gelatin. To one litre of acid beef broth add 100 grm. of gelatin, 10 grm. of peptone, and 5 grm. of salt. Place in water bath until solution is clear, make faintly alkaline with NajOH, cool to 50° C, add the white of an egg, after stirring steam for an hour, filter, and run into test- tubes. Sterilize for fifteen minutes on three successive days. Agar-agar. 15 grm. of powdered agar-agar well boiled with one litre of nutrient broth for two hours until dissolved, replace the water .lost, see that it Hot-air sterilizer. is faintly alkaline, clear with egg-albumen, filter through a " Chardin " filter paper. It remains solid at 40° C, and only melts completely at 90° C. Glucose and Lactose Peptone Waters. 10 grm. of peptone and 5 grm of salt dissolved in 1,000 c.c. of dis- tilled water, boil well, neutralize in the usual way, boil and filter, run into tubes and sterilize thrice. Add I to 2 per cent, of glucose or lactose to this, tinge it with litmus solution to indicate production of acid and alkaline. It is a useful media for determining the fermentative power of organisms. This medium is best placed in Durham's miniature test- THE EXAMINATION OE MICRO-ORGANISMS 623 tubes, which will become filled during the sterilization. During fermentation these become gas-holders. Blood Serum. Take blood from the jugular vein, operation wound, or placentc'e with aseptic precautions, let it stand, draw off with large pipette into test-tubes set on a slant. The serum sets after heating in hot-air sterilizer to 65° C Hearson's incubator, working with petroleum lamp. Gelatin Plate Cultures. Place three test-tubes containing nutrient gelatin in boiling water until liquid, then cool to 40° C. Introduce into tube a sterilized platinum loopful, a mere trace, of a culture of the organisms to be examined, and mix well. Sterilize the loop, and put one loopful from tube I to tube 2 and shake, put two loopfuls into tube 3 from tube 2. Pour the contents of each into Petri dishes. In these the colonies may be seen and counted without removing the lid. Agar plates are prepared in the same way, but it is necessary to 624 LABORATORY HINTS work more quickly as the agar soon solidifies and the organisms are not evenly distributed. When the agar has set invert dishes to prevent water of condensation spoiling colonies. " Streak " Cultures. An oblique slope of agar or nutrient gelatin in a test-tube is taken, and with a sterilized platinum loop a trace from the culture is drawn up the slope. "Stab" Cultures. A test-tube of solid media is taken, and the straight platinum wire with the growth on the tip is introduced down the centre of the medium. " Shake " Cultures. Liquefy the gelatin in a test-tube by putting it in a beaker of water at 40° C, and inoculate the medium with the organism. Gently mix to distribute the organisms; gas producing organisms form bubbles. "Anaerobic" Cultures. Glucose agar or gelatin is most frequently used. A tube three- quarters full is kept in boiling water for five minutes to soften the medium and expel the oxygen. After the stab is made, warm the top of the medium to seal the needle track. For fluid media place thereon a layer of olive oil, and then inoculate with a sterile pipette. In diflFerentiating growth note: — If the colonies are separate, rounded, minute or large indefinable masses. Plague bacteria grows in small rounded masses, but Coli form one creamy mass. Notice if any colour is produced and if the medium is stained as with Bacillus pyocyaneus. Does the growth spread aw^ay from the line of inoculation, and if so, what kind of an edge does it form ? Is gelatin liquefied, broth rendered turbid? Does a scum form on the surface? Is the deposit at the bottom ? Does it produce acid or gas or both in a sugar medium ? Is milk clotted or acid formed in it? Will it grow on potato, and if so, is any colour produced ? THE PREPARATION OF SECTIONS. (1) Fixing the Tissues. Place the piece of tissue in 10 per cent, formalin, twelve to twenty-four hours. Wash in running water and then proceed to harden it. After it is hardened the tissue must be prepared for section cutting. This is by freezing or embedding in paraffin. THE PREPARATION OF SECTIONS 625 (2) Hardening of Tissues. Place the tissue in three strengths of alcohol successively, viz. : 50 per cent., 75 per cent., and absolute, the tissue remaining in each twenty-four to forty-eight hours. If one desires to keep the tissue, place in 70 per cent, alcohol. Cut from the tissue small blocks 10 to 20 mm. square and immerse in alcohol. (3) Freezing of Tissues. Place the blocks of tissue in an open vessel and allow water Microtome, Cathcart's, with spray bellows. to run into it for two hours to remove the alcohol, then soak in a syrupy m.ucilage of gum acacia with a little carbolic acid. Place it on the plate of the freezing microtome, a little mucilage is added and the whole frozen. The sections are cut by the knife moistened with A\ater and brushed into tepid water with a camel-hair brush. These can now be stained or preserved in 70 per cent, alcohol. (4) Embedding of Tissues. After hardening place in absolute alcohol twelve to twenty- four hours, then in pure xylol for the same time, then in a 626 LABORATORY HINTS bath of melted paraffin wax six to eighteen hours ; the paraffin must be kept melted. The paraffin that is most useful for all purposes is that having a melting point of 50° to 60° C. Skin tissues become friable if kept long in the melted paraffin. After impregnation of the tissue it must be embedded. Pour a little paraffin wax into a small (pill) box, place the block of tissue in the centre and fill the box with wax. When set remove the box and attach to the plate of the microtome. (5) Mounting Sections on Slides. Place section in a dish of warm water so that the paraffin is softened but not melted, then the sections become flat. Introduce a slide into the water under the section and raise it out of the water, adjusting it with a needle. Dry in warm incubator for two hours. If the sections are thick it is preferable to smear the slide first with egg albumen mixture to make the section adhere sufficiently for staining, For individual sections place a few drops of water on the slide, float section in it, and warm over a flame until it straightens out. Pour off the water and the section will adhere. To Stain Sections. Remove paraffin with xylol and the xylol with spirit and the spirit with water. This is unnecessary if it is not a paraffin section. Stain with haematoxvlin two and a half minutes, and flush with water until blue. Stain with eosin ten seconds and wash with water. Treat with spirit to remove water, then with clove oil. Treat with xylol and mount wilh Canada balsam. Never let the section dry. To tell if completely dehydrated when using clove oil place on a dark slab, when it will appear milky as long as water remains in the section. To show Parasites and Bacteria. Remove the paraffin with xylol, spirit and water as above. Stain with strong carbol-thionin ten minutes. Pour off and blot lightly. Treat with spirit rapidly, two dashes only. Treat with oil of cloves until transparent. Treat with xylol and mount with Canada balsam. THE PREPARATION OF SECTIONS 627 Van Gieson's Stain. Treat as above to remove paraffin. Stain with hjematoxylin fifteen to twenty minutes and blue well in tap water. Stain with van Gieson half to one minute (picric acid i| per cent. of acid fuchsin). Treat with spirit, oil of cloves, xylol and mount. The haematoxylin stains the nuclei and parasites blue. The picric acid stains the protoplasm of the cells yellow. The fuchsin stains the fibrous tissue red. To show Malarial Parasites in the Brain. Remove the paraffin. Stain with haematoxylin twenty minutes and blue well in tap water. Treat with acid alcohol one to four seconds, wash well. Treat with spirit, oil of cloves, xvlol and mount. To Embed in Celluloidin. Celluloidin is a product of gun cotton and looks like glass cotton . It must be packed in water for transit. It is a gummy transparent substance, and is useful for holding the brain tissue and the malarial parasites together in subtertian cases. It must be dried before using. Place the section in spirit twenty-four hours, in another solution of spirit for the same period, in absolute alcohol twenty-four hours, in alcohol and ether for twenty-four hours, in thin celluloidin twentv- four hours. Pour some thick celluloidin on a wooden block and place the tissue on it; leave it in the air for a few minutes. Place in 60 per cent, spirit to harden it until it is cut. To mount and stain the Section. Place in a watery haematoxylin stain twelve minutes. (Watch glasses are the best for these processes.) Wash and blue well in tap water. Treat with acid alcohol until red, five seconds. Wash well and stain Vvith alcoholic eosin three to four minutes. Pass through three baths of spirit. Clear in carbol xylol and mount. A low power shows the brain capillaries plainl\' because of the malarial pigment present in subtertian cases. 628 LABORATORY HINTS MALARIAL PIGMEXT : WHERE IT IS AND HOW TO LOOK FOR IT. This pigment is found in the parasites, rarely in the polymorpho- nuclears and in large mononuclears. When in the latter it is ])athognomonic of malaria. The pigment is carried by the cells to the liver and spleen. The endothelial cells of the capillary also take it up and may then become detached. If pigment is found elsewhere it is not malaria. The pigment is nearly always intracellular. The mononuclears soon give it up again, so that to find these cells carrying it indicates that malaria was progressing at Jhe time. In the liver it is found in the small cells of the connective tissue type with a dark staining nucleus which penetrates between and into the liver lobules. The containing cell becomes degenerate, the nucleus stains faintly, and the pigment appears in larger clumps. Later, the pigment alone remains, lying in the connective tissue. This latter stage is reached from the twentieth to the thirty-second day, so that from the examination of the liver one can tell how long the malarial process has been going on, and it indicates that the liver was active at the time of death. In the spleen pigment is always present, chieflv in the macro- phages, which may give a dark appearance to the organ on section according to the number of malarial attacks and the amount of pigment deposited. A slaty-black colour is almost diagnostic. Malarial pigment consists of : — (i) Melanin, which is diagnostic. (2) H^emosiderin, not diagnostic. (3) Iron-bearing granules, not diagnostic. Melanin contains iron, but in such firm combination that it does not give the iron reaction. It is insoluble in acids, soluble in alkalies, insoluble in alcohol. H^emosiderin is insoluble in acids and alkalies, but soluble in alcohol. It does not require staining to be seen. It is said not to contain iron. Carbol thionin stains it violet. The iron-free granules contain iron in inorganic combination, so will give the reaction for free iron. The more acute the hsemolytic process, the more numerous the iron granules ; the more chronic the process, the more numerous are the yellow granules. In blackwater fever there is much blue pigment; and in anky- lostomiasis much yellow pigment. The haemosiderin and the iron- free granules are seen in any disease causing haemolysis, as pernicious THE TRICHOMYCETES 629 anemia, blackwater, &c. They are found in the true secreting cells Hning the first portion of the convoluted tubules of the kidney. Rarelv the three kinds may be found in the same cell. To show the three Pigments: — Stain with carmine ten minutes. Stain with acid alcohol three minutes. Stain with potassium ferrocyanide five minutes. Stain with acid alcohol until blue. Treat with spirits, oil of cloves, xylol and mount. This is a chemical process, and Prussian blue is formed. The potassium ferrocyanide and acid alcohol can be repeated several times until the part is sufficiently blue. The pigment in the lung is chiefly carbon ; treat the section with an alkali if suspicious, carbon will not be dissolved, but melanin will. The pigment in the skin of the dark races is not like that of malarial pigment. It contains no iron whatever, and is dissolved in weak acids, which distinguishes it from true melanin. Tattoo pigment is deposited very irregularly, and can be diagnosed at once under the microscope. Between bacteria proper (Schizomycetes) and the moulds (Hypho- mycetes) comes a group known as — THE TRICHOMYCETES. This group is divided into : — The leptothrix, no branching. The cladothrix, false branching. The streptothrix, true branching. The Actinomyces. This ray fungus is a streptothrix consisting of filaments, cocci and clubs. The filaments are long and thin, interlacing in the centre of the colony forming a network. In older filaments the protoplasm is broken up into coccoid bodies which may break out from the sheath. The clubs are involution forms perhaps produced by resistance of the tissues. In actinomyces from human tissues : — The threads are Gram-positive, the clubs Gram-negative, but from cattle the threads are Gram-negative and the clubs are Gram-positive. Man may be injected with the bovine type. In artificial media the clubs are not found. Il grows well on potato and glycerine agar. On potato it forms a thick, grey, raised, wrinkled growth of sulphur yellow or light chocolate colour. It causes actinomvcnsis in man and cattle. 630 LABORATORY HINTS Streptothrix madura. This fungus produces in Cyprus, India, South America and Egypt the white form of madura disease or mycetoma, which is much more common than the black or red varieties. It does not form yellow or black pigments in cultures, and does not liquefy gelatin. It is not infective for rabbits. The clubs do not stain by Gram. Stain with hsematoxylin and acid or carbol thionin. THE HYPHOMYCETES. The moulds or mycelial fungi are multicellular organisms composed of filaments which interlace, forming a mass of mycelium. (1) Mucorinal. The end of a filament or hypha swells into a knob around which a spherical seed capsule forms. When ripe, the spores burst the enclos- ing membrane and thus become free. It occurs in any decomposing material and in man ma}- occur in the ear, old abscesses and bron- chiectatic cavities. (2) Aspergillinae. The heads of the filaments are covered with a number of spore carriers (sterigmata), each sterigmata bears a chain of spores. They may invade the lung, blocking up the acini, giving rise to symptoms much like phthisis. (3) Penicilliacese. The filaments are branched, from these basidia arise the sterigmata from which in turn chains of spores arise. Thev will soon overrun any exposed agar plate. Penicillium glaucum is the commonest mould and is seen on moist bread, damp boots, &c., as a bluish-green fur, giving off a musty odour. To mount moulds remove the thin layer of fat that normally covers them, with alcohol and a little ammonia. Then mount in glycerine. They can be stained with Loffler's methylene blue, which stains the mycelium and livph^e, the spores remaining unchanged. Another method of showing moulds is to : — Stain with aniline gentian violet, five minutes. Pour off, blot, treat with Gram's iodine, two minutes. Treat with aniline oil and iodine until differentiation is com- plete, about fifteen minutes. Treat with xylol and mount in Canada balsam. Ringworm. This is a kind of mould. It has the power of living on the keratinized products of skin which it breaks up and digests. THE BLASTOMYCETES 631 Most forms disappear before the human host has reached twenty years of age. (i) Microsporon andouini. Met \\\t\] in cliildren. Xever attacks the scalp of aduUs. Never affects the beard and nails. Very intractable. It occurs as a whitish sheath around the stumps of broken hairs. They are round or oyoid spores, 3 to 4 /Lt. (2) Trichophyton megalosporon. The endothrix variety is exclusively of human origin : the spores are seen in the interior of the affected hairs. The ectothrix variety which affects the beard and nails is derived from animals, the spores lying on the exterior of the hair. The spores are large, 4 to 12 m. To facilitate examination soak the hair in 10 per cent, caustic potash and then alcohol and ether as for moulds. THE BLASTOMYCETES. These yeasts are round or oval unicellular organisms having hyaline protoplasm in healthy, and granular protoplasm in old cells, surrounded by a wall of cellulose. The torulas multiply by budding. The saccharomycetes by budding and spore formation. Spores are formed when the food materials are exhausted. They must have moisture and plenty of fresh air, temperature above 25° C. is best while fermenting nutrient liquids facilitate the formation of spores. S. cerevisias. There are two typical brewery yeasts, the typical English, a " top " fermentation variety, and the yeast of the Continental lager beer, a " bottom " fermentation. The " top " and " bottom " are also known as the " high " and " low " as they develop in high and low tempera- tures respectively. They are 8 to 9 /a in diameter. Three to four spores form in one mother cell. There are " wild yeasts " as : — 5. pastorianiis. There are three varieties with peculiarly shaped cells and having two to four spores in each mother cell ,, No. I is a bottom form and causes a disagreeable smell and a strong bitter taste in beer. ,, No. 2 is a feeble top form of little importance. ,, No. 3 is a dangerous " top " form causing tur- bidity and disease. Bulgarian sour uiilk is used for therapeutic purposes. 40 632 LABORATORY HINTS A yeast attacks tlie milk sugar after lactic acid has been formed, inhibits the gro\\th of pathogenic and putrefactive bacteria and im- proves tiie taste. The yeast may get the upper hand and carry the fermentation too far. Pathogenic ycasls cause blastomycetic dermatitis as sometimes seen in man. They have also been recovered from tumours, lung diseases, sprue and dysentery cases. To Stain Yeasts. Use Gram or an}- :?imple stain. Remember that they stain mahogany brown and not gentian violet with Gram. THE EXAMINATION OF F.ECES. MACROSCOPIC. This is a very necessary routine practice in the tropics. Note the number, bulk, colour, odour, consistency and the reaction of the stools. Note the presence or absence of gaseous fermentation. The presence or absence of blood, mucus, pus and their degree of admixture whh the stool. Any visible £inimal parasites, undigested food materials, &c. Remember that mucus from the small intestine is stained with bile and is not frequent) \' seen, but mucus is common from the lower bowel and may be caused by anything tliat sets up inflammation in it such as bilharzia, chronic ulcerations as from ulcerated haemorrhoids, nic'ilignant and granulomatous gro^\•ths and chronic dysentery. In acute dysentery the mucus is usually clear, not mixed with faecal matter, and may be streaked with bright red blood. If it comes awa}- in condensed hard masses with much debris and epithelial tissue ^\ith pus the affection is usually of the rectum. If bowel casts are passed (membranous colitis) they may be twisted, these should be floated out in water as they may resemble worms. If bright red blood is passed it does not necessarily mean that it has come from tiie rectum, such mav come from the small intestines. If the stools are numerous, pale, frothy, it is suspicious of sprue. Remember that in the tropics the caecum and upper part of the colon may be ulcerated acutely and extensively without passage of either mucus or blood or with tenesmus. Such may be rapidly fatal. Remember that rice and plantain eating peoples pass much larger stools normally tlian do meat eating peoples. The people of the East eat excess of carboh^-drate food to obtain sufBcient protein. THE EXAMINATION OE FJECES 633 Europeans in the tropics give an average stool per diem of 130 grni. Natives give an average stool of 2t,t, grm. per diem. The reaction of a normal stool is nearly neutral to litmus, acid on fasting, faintly alkaline when taking milk. In most cases of diarrhoea they are decidedly alkaline. All stools should be examined as soon as possible after being passed. Macroscopic mucus usuall}' means catarrh in the large intestine. Microscopic mucus usually means catarrli in the small intestine. Earth eaters pass pale stools which may in this respect resemble obstructive jaundice. Those who eat coal-dust and take iron or bis- muth have blackish stools which may resemble mekena. The stools are dark blue after taking metlu'lene blue and brick \'el1()\\- after ipecacuanha. Bile acids are recognized by Pettenkofer's reaction. Mix a little fiscal matter with a little sugar on a \\hite dish, add a little HsSOj. A crimson colour indicates the presence of bile acids. To Estimate Nitrogen. Weigh a portion of fajcal material. Add 20 c.c. of ^^ H2SO4 to prevent loss of ammonia. Dry in a water bath. Complete desiccation in a drying chamber at 10° C. over H.SO,. Weigh out I grm. Mix with 25 c.c. of strong ILSOi and i grm. of sodiimi h\])(v phosphate. Permit to stand four hours, then boil cautiously. The nitrogen now is converted and ammonium sulphate is formed. Allow to cool. Add 600 c.c. of water. Add sodium hydrate solution till strongly alkaline. Add a few pieces of granulated zinc to prevent bumping. Distill this, passing it into ^-^ H2SO4. Some of the acid is neutralized by the ammonia. Titrate the H0SO4 to estimate the amount of the ammonia distilled over. To Estimate Fat. Dry faeces over H2SO4. Treat with i per cent, of HCl to split up the soaps. Add ether to dissolve fat. Add more ether and pour off and add to former. For bile pigments, bilirubin and biliverdin employ : — (i) Schmidt's reaction. Add to faeces a saturated solution of Hg perchloride. A bright green indicates their presence. 034 LABORATORY HINTS (2) Giuelin's reaction. Add a few drops of yellow nitric acid to faeces. A display of colours including green is positive. (3) Huppert's test. Add slaked lime suspended in water to the faeces. Filter, wash and dry the precipitate. Make an extract with hot alcohol and a little HoSOj. Bile pigment gives a green colour. A complete absence of red or green colouring shows absence of bile when icterus is present. When the latter is not present it indicates temporary suspension of bile secretions. In fresh brown stools giving no red coloration there is usually intestinal decomposition. When green colouring is macroscopic it indicates too rapid a passage through the colon. Urobilin is ahvays present in small quantities 0*03 to o"o6 grm. per diem. Any h^emolytic disease increases the amount, especially malaria. In subtertian it may go up to I'yi grm. or more. It is one of the final products of destroyed hb. The smell is due chiefly to indole and skatol. Food materials are absorbed principally in the latter half of the small intestine. In the event of increased peristalsis or catarrh of this part the contents are hurried through without benefiting the patient. Water is absorbed from the large gut, increased peristalsis or inflammation hastens the contents through and gives loose stools, while diminished peristalsis or constipation from any cause means hard fseces due to their remaining too long in the colon and too much water being absorbed. The water in an average stool is 75 per cent. Weigh before and after drying. Dry over H2SO4 as volatile substances are present and do not heat over 60° C. Evaporate ether from bath. Weigh residue = total fats. To Examine for Macroscopic Parasites. Place the stool in a muslin or fine wire gauze strainer, add water and stir well. Repeat with a finer mesh each time and use fresh water. The entozoa are readily found. For diagnosing helminths and amoebae see section on : " Diseases due to Helminths " and " Amoebic Dysentery." MICROSCOPIC. Use water with firm stools, but as little water as possible. Cover with a cover-slip and spread out the material by pressure on the slide. To distinguish mucus from connective tissue add a drop of acetic acid : fibrous tissue is dissolved and mucus is more distinct. THE EXAMINATION OF FJECES 635 Muscle fibres looking like brown splinters of wood will indicate the powers of protein digestion in the small intestines. Connective tissue indicates gastric indigestion and that organ should be minutely examined. A normal stool contains 23 per cent, of fat of the dry substance, slight variations from this are unimportant ; a morbid increase gives a clay coloured sour copious stool, and the sebacic acid flocculi in a cold acetic acid preparation are much increased as are also neulral fat drops, salts of lime and soap crystals. If bile is absent and fat increased the disease is in all probability in the biliary duct system. If \\ith excess of fat there are muscle fibres and hydrobilirubin present and mucus is absent the pancreas is the* seat of the disease. When biliary and pancreatic disorders are excluded the excess of fat may be due to severe intestinal disease such as tuberculosis, amyloid disease or tabes mesenterica. Errors in the examination of faeces are not uncommon. Banana fibres may be mistaken for tapeworms, especially T. nana and T. diniinuta, owing to the fact that they are made up of segments resembling tapeworm strobilje. Orange debris resembles certain trematodes, liver flukes, &c. Celery shreds may be mistaken for hookworms. Oatmeal may simulate the segments of worms. Undigested pollen grains might be mistaken for eggs. The ascus of a mould mistaken for an egg-shell. The oncospheres for a dividing ovum. Always consider the patient's vegetable diet first. Bacteria, &o. The microscope will demonstrate mild infections due to staphylococci from the more dangerous streptococcal infections. Typhoid, cholera and dysentery bacilli can be detected by culture. These are dealt with under their respective headings. The amoebae can be seen in fresh stools and when the slide is kept warm their movements can be recog- nized. Water kills them and should not be added in examining them. Free moving larva? in fresh stools are never ankylostomes but probably Strongylus stercoralis. Blood. Blood in small quantities and altered blood can be recognized by Weber's test : — Extract the fat with ether. Rub the stool up with water. Add one-third bulk of acetic acid and shake up the whole Avilh ether. 636 LABORATORY HINTS a, Ascaris hunbricoiJes ; b, Trichocephalus dispar ; c, Oxyuris vermiciilaris ; t', c'^, Ankylostomum diiodenale ; d, oncosphere of Cestode ; e,f,g, xarious Fasa'o/idir ; /i, Schis- tosomum (?) hainatobiiiin (from faeces) ; ?, Schistosovmm haviatobium (from urine). THE EXAMINATION OE EJECES 637' An ethereal solution of acid hiemalin is obtained. If altered blood is present it is seen by means of the spectro- scope, THE DETECTION OF OVA. This is all-import£int. Their appearance is described in the section on " Diseases due to Helminths," but to facilitate laboratory work a concise description will be given here. A moist stool needs no water; to a dry one add a little water and place a small portion on the slide, and press it out gently with a cover glass. As eggs are heavier than \\ater more will be at the bottom of a water stool. Many eggs of Ascaris matter little as a rule, and those of Tricho- cephalus dispar less, but a few ankylostomes are of considerable importance. A § objective should diagnose all. (i) Ascaris lumbricoides. — Ovoid or round with a double contour. Thick clear yellow shell. May or may not be surrounded by an irregular protective coat of stained albumin, granular yellow contents not completelv filling interior. The shell resists formalin. (2) Trichocephalus dispar. — Small oval yellow eggs, double con- tour, a distinct " plug " of mucus at each end, a granular interior and a very thin unstained inner capsule. (3) Oxyuris vermicularis. — Xot unlike the ankylostome ^gg, but somewhat flattened, and contains a well-formed embryo when freshly passed. (4) Ankylostomum duodenale. — Unstained, a single thin trans- parent capsule, segmented nuclear matter into two to forty- eight cells, does not fill cavity, an embryo in about forty-eight hours. (5) Trematodes. — These are yellow, small, and have a lid or operculum, which may be split olT. Their size differentiates them. (6) Chlonorchis sinensis. — This has a " jug " shape, with a distinct lid above and a small spine below. (7) Schistosoma haematobium (from urine usually). — Large ter- minal sharp spike, thick shell containing embryo. Add a little water to the slide and the embryo will come out. Schistosoma mansoni as above with a lateral spine. Schistosoma japonicum has a knob laterally, no spine and no operculum. (8) Oncosphere of Cestode. — A radical striation of the thick capsule with three pairs of booklets in the central embryonic matter readily distinguishable from other ova. 638 LABORATORY HINTS (9) Bothriocephalus. — The only egg outside the trematode eggs with a lid. Oval, cellular contents, but little stained, other- wise much as trematode eggs. Later it becomes encysted, and ciliated for swimming about in water. THE DISSECTION OF MOSQUITOES. To kill the mosquito, if alive, put it in a test-tube and tap the tube on your arm. Remove legs, mount and dry, fixing cover slip with gummed paper having a window in it. Study well the complete structure. buccal cavity pharynx dorsal reservoirs oesoph. valve and caeca midgut begins stomach . malpiqhisn tube - midgut ends - - ileum - - colon rectum Internal anatomy of the mosquito THE EXAMINATION OE WATER 639 Remove wings at right angles to the body and mount likewise. Transfix the thorax with a fine needle and remove the head by pull- ing it away from and backwards off the thorax; in this way the salivary glands may be withdrawn from the thorax, and they can be examined under the microscope for parasites. Then take the remainder, bruise the abdomen across the last seg- ment, and draw it away with another needle; in this way the internal viscera will be dra^^■n out also, and if one is fortunate the salivary glands, if not already removed, will be withdrawn. The stomach, rectal glands, spermathecae, &c., will be well shown. Examine the gastric contents for malarial parasites. If the salivary glands are not removed, tease the thorax into very small portions in a drop of saline and examine. There is much debris resulting from this method, and the glands may be lost. Stomach of mosquito showing malarial parasites. The parts not being examined should be kept in saline, or better, liquor potasscu in a watch-glass. Press the proboscis out under a cover slip and examine; several of the elements may be seen in each specimen thus treated. Examine the base of the proboscis and the thoracic muscle for filarial embryos. THE EXAMIXATIOX OF WATER. Good waters are spring, deep well, and upland service waters. Suspicious waters are stored rain and surface water from cultivated land. Dangerous waters are shallo\\- well and river water to which sewage has access. There are four examinations : — Biological, Phvsical, Bacterial, Chemical. 640 LABORATORY HINTS (1) THE BIOLOGICAL EXAMINATION. This enables us to determine the absence or presence of lowly organisms, bacteria, jDrotozoa, larvae, &c. The following are common and should be looked for : — In impure water In sewage Vorticella Rotifera Carcliesium Cienothrix Ulothiix Oscillatoria nigra Asterionella Alg.=e Leptomitus Diatoma Spirilla Sphterotikis natans Actinophrys Spirogyra Beggiatia Protocoeccus Gammarus pulex Ulva latissinia Euglena Cyclops Enteromorpha Oscillaria Water bear Infusoria Desmids Bomina longitirastis (2) THE PHYSICAL EXAMINATION. The reaction should be neutral. Add a little neutral litmus to the sample. COn will turn it red. Remember that acid waters attack lead and iron pipes. The colour should be a pale blue or green. Half till a two-feet tube and la}- it upon tlie table. Look through the upper lialf which is colourless. Look through the lower half ^\'hich assumes the colour of the water. It should be odourless. To test it warm to about 37° C. Certain mineral waters contain HoS, also given off by beggiatoa and crenothrix. Volvox and uroglena give a fishv odour. Anab^ena and rivularia give a grass v odour. Asterionella and diatoma give an aromatic odour. There should be no sediment. If there is such it should be examined under the microscope. (3) THE BACTERIOLOGICAL EXAMINATION. This indicates the presence or absence of pathogenic and other bacteria and the number thereof. These are : — (i) Normal inhabitant bacteria. (2) Accidental soil bacteria. (3) Intestinal bacteria. Sunlight reduces their number if the water is shallow and the exposure prolonged. Cold inhibits their growth and warmth stimulates it. Presence of food materials stimulates their growth. Most bacteria tend to settle at the bottom and so thus assist in self-purification of the water. Typhoid and cholera organisms die out if stored long, about twelve weeks. THE EXAMINATION OF WATER . 641 To Collect the Sample. Use sterile glass-stoppered bottles and immerse in the water 12 in. below the surface before removing the stopper. If from a tap, let it run for five minutes before taking sample. Remember that a local cistern contamination gives a fallacy not to be applied to the water supply in general. For deep wells Sclaver's "smash" bottles should be used. These are small vacuum bulbs, let down by a string and mechanically broken when under water. Examine the sample within three hours or pack it in ice. To Examine the Sample. Until recently bacteriological examinations of water supplies in tropical countries have been few and far between, owing to the lack of well equipped laboratories. When sufificient statistics are 10 hand we shall be able to appreciate the difference of the bacterial content of tropical waters and to modify existing standards of bacterial impurity. To one already accjuainted witli the subject in a temperate climate there will appear dilficulties innumerable. He will find that standards of impurity cannot be applied generally and that the local water con- ditions vary enormously. For example in the tropics : — (i) The rains are torrential and periodic, so that the bacterial flora of districts where vegetation is rank will be brought down. The surface organisms of sandy districts, where much vegetation is absent, mav give an altogether different flora from the above. (2) The sun and soil kill off all the H. coli communis, where it has existed, but other resistant types persist, new probably to the sanitary worker. Their significance as infectious and danger- ous agents in water supplies has to be ascertained. (3) A clay subsoil, instead of acting as a lifter in purifying the water, in some measure may provide a culture media for its increased pollution, oAving to the organisms being held up, cultured, and swept away into surface waters during the first shower. (4) The sanitarian will be frequently called upon to deal with the bacteria persisting after the action of sun and soil, which residual bacteria may not include the notorious B. coli com- munis, the presence of which forms a basis for a standard of impuritv in temperate countries. (5) Animals residing in a catchment area will give a very distinct bacterial flora from that in temperate climates where the pollution is largelv from human fcccal bacteria from the large towns on the river banks. 642 . LABORATORY HINTS (6) The bacterial flora of human origin is very different to that of animal origin and reasoning based upon the formisr and applied to the latter in tropical climates may often lead one into very serious error. (7) The worker will find that high winds laden with dust will gain access to his plates and colonies and repeatedly ruin his works. Each district water supply must be judged on its merits. Data from many different parts of the tropics must be provided before standards of impurity can be generally recommended and adopted. The first data came from : — Daniels in Malay. Balfour and Archibald in the Soudan. Clemesha in India. (A) Daniels working in the Federated Malay States (1908) proposes the following as a basis : — (i) The number of organisms (exclusive of known, easily recog- nized, non-pathogenic organisms, e.g., B. subtilis, B. megaterium, B. violaceus, and some of the organisms which form characteristic yellow colonies) which have been proved to be non-pathogenic to lower animals, (2) The amount of the water required to react, forming acid and gas, with MacConkey's medium, from o'2 to 2 c.c. being employed in the tests. (3) Indol formation in forty-eight hours in peptone water with 10 c.c, 5 c.c. and i c.c. of the water to be tested. As a standard Daniels and Finlayson suggest that : — (i) Not more than 100 organisms, exclusive of those mentioned, should be present in i c.c. of the water. (2) That no acid and gas should be formed in twenty-four hours in MacConkey's medium at 37° C. with 2 c.c. of the water. (3) That no indol should be formed in peptone water in forty-eight hours with 5 c.c. of the water added. They remark that the standard is not a high one but it is exceptional to find a natural water that will pass all three tests. In unprotected shallow wells liable to be polluted bv surface wash- ings, they found the average bacterial count to vary between 300 to 900 per c.c, while in twenty-three out of twentv-seven wells examined, acid and gas forming organisms were present in 3 c.c. and usually in 4 c.c. of the water, and indol formers in 5 c.c. in the case of ten of the wells. B. pyocaneus was found in one instance, and in two cases organisms indistinguishable from B. coli communis. (B) Balfour and Archibald have done good work in the Soudan in connection with river and shallow well water in Khartoum. THE EXAMINATION OT WATER 643 Dealing with river water, B. coli was found present in o'5 to i cc. of the water taken near the bank but only in 5 cc. taken from mid- stream. In shallow well water B. pyocyaneus was found and dysentery was observed to follow the use of this water. Deep well water was examined by Captain Archibald with the following results : — (i) The colony count in i cc. This was always carried out with agar plates as the heat prevented the use of gelatin. The percentages of the various constituents of the agar was the same throughout all the tests. The acidity was plus 10 to phenol-phthalein. One cc, o'5 cc, and 02 cc of the water sample is taken and run into melted agar at a temperature of 41° C. This was then placed out in Petri dishes, incubated at 37° C. for forty-eight hours, and all colonies visible to the unaided eye counted. (2) Sporogenes Test. Twenty cc of the sample of water are pui into sterile milk con- tained in tubes. The milk is then heated up to 80° C. for twenty minutes, and a laxer of hot vaseline is run on to the surface of the milk so as to render the latter anaerobic. The milk tubes are then incubated at 37° C. for forty-eight hours. Evidence of the presence of the spores of B. enteritidis sporogenes is shown by the clotting of the milk. (3) The test for the presence of the lactose-fermenting organisms and their subsequent isolation. Lactose bile-salt-neutral-red-broth is used and, as varying quantities of \vater are inoculated into tubes containing this medium, the latter is made up in single, double, and triple strength. One tube is inoculated with 20 cc of the water, two tubes with 10 cc, four tubes with 5 cc, five tubes with i cc, and five tubes with o'oi cc All are incubated at 37° C, only tubes that give both acid and gas being counted as having given the reaction. If only one tube in the first seven of these gives a reaction, then faecal bacilli are present in 60 cc, and if three out of the five i cc tubes gives a positive reaction, then fascal bacilli are considered to be present in i cc The same applies, more or less, to the o'l cc and the o'oi cc groups. The next step in the procedure is to isolate the various f^cal organisms present; and in order to do this satis- factorily, the tube containing 10 cc of water or more, that has given a positive reaction in forty-eight hours, is taken. Of this, three to five platinum loopfuls are removed and inoculated into 10 cc of sterile water. The latter is then vigorously shaken, and one loopful of this 644 LABORArORV HINTS mixiure is then plated out on lactose bile-salt-neutral-red agar, which is incubated at 37° C. for forly-eight hours. At the end of that time fifteen to twenty colonies are found to be present on the plate. Two colonies are in any case picked off, and eacii single colony is inoculated into a tube containing a few drops of sterile water. From these tubes further inoculations are made into broth, glucose-peptone, and four different special sugars are incubated at 37° C. The inoculated broth ttibe is examined at the end of eighteen hours for motility and the production of indol. The glucose-peptone is inoculated for forty-eight hours and at the end of that time, if a strong growth is present, a few drops of a very concentrated solution of caustic potash are added for the purpose of finding if the \^oges-Proskauer reaction is given. If this is present a bright ^range-red colour is produced. It may take twenty- four hours before this colour is apparent. The four sugars that are inoculated are saccharose, sulcite, adonit and inulin. In these a positive reaction is represented at the end of forty-eight hours' incubation at 37° C\ by the production of acid and gas. It was assumed that the same species of bacillus ahvays fermented the same sugar. In connection with the indol test the paradimethyl benzol- dehyde reaction was alwa'ys used, as it seems to be a very delicate and reliable test. With regard to the \\)ges-Proskauer reaction consider- able difference of opinion exists, but there can be but little doubt that it appears a good test for the B. cloacae, B. lactis aerogenes, and Oxytocus perniciosus group. The term B. coli was only applied to Escherich's organisms. Experiment (i). Sample taken from the Blue Nile, two metres from the bank. Local rainfall nil. River steadilv rising for three weeks. Temperature of water, 27° C. Total colonies on agar al 37° C. were 218 per c.c. F'iecal bacilli present in 01 c.c. Sporogenes test plus in 20 c.c. Experiment (2). Sample from same place. Local rainfall nil. River steadilv rising for two months. Temperature of water, 24*5° C. Total colon}- count in agar at 37° C. was 700 per c.c. Faecal bacilli present in o"i per c.c. Sporogenes test plus in 20 c.c. Experiment (3). vSample from shallow well sittialed in a native vard about a quarter of a mile from the Blue Xile. The water was at a depth of 19 metres from the surface. The water temperature was 30° C. THE EXAMIA'ATION Of WATER 645 Total colony count in agar at 37° C\ \\as 700 per c.c. Fsecal bacilli present in o'oi c.c. Sporogenes milk lest plus in 20 c.c. Experiment (4). Sample from well Xo. 7 of the Khartoum water supply. Gas was present in MacConkex's medium when the latter was inoculated with 50 c.c. of the sample. Sporogenes milk test negative in 20 c.c. Remarks on these and other Tests. The observations have been too few to justify any definite con- clusions being arrived at with regard to the position that the B. coli occupies in this country as an indication of recent pollution. Experiments should be carried out every month of the vear to determine the effects of external natural forces, such as sunshine and rain on all organisms of faecal origin. There was more faecal pollution present in a " falling " than in a "rising" river, although the colony count in the latter was nearly four tinies as great as in the former. Experiments have demonstrated that there are different types of lactose fermenters present in human freces in different months of the year. Experiments also go to prove that B. coli communis is extremely susceptible to the bactericidal eft'ects of sunlight, and that B. cosco- roba, I?, schaefferi, B. neapolitanus, and B. vesiculosis are extremely resistant. B. coli were not found in trenches seven days old, hence soil destroys them. The chief bacilli found in the faeces of animals were : — B. coli, B. clcaccC, B. neapolitanus and others in goat fceces. B. schaeft"eri and B. neapolitanus in cow faeces. (C) Probably the best methods and the best data yet given come from Major Clemesha of the Madras Presidency. He states that there must be considerable doubt as to whether the standards of purity in common use amongst sanitarians in England were suitable to India. Most Indian waters are loaded with fa?cal contamination that no analyst in England would dream of passing as fit for human con- sumption. And yet it is remarkable that the evil effects of using such water as drinking-water are not al\va\s apparent. The resulting diseases are not in proportion to the cause at all times. In England a cautious Medical Ofificer would condemn water for drinking which contained true coli in i c.c, but in India the B. coli 646 LABORATORY HINTS communis is a very rare organism in its waters, while other organisms are particularly common. Clemesha comes to these conclusions : : — (i) That standards in use in cold climates are useless, and worse than useless, in tropical climates. (2) That il is necessary lu separate the individual species of bacilli by well-established tests and to study their characteristics and their position in nature. (3) That it is advisable to classify all lactose fermenting organisms according to their ability to resist the action of sunlight, and on this to base the standard of bacterial purity. The general conclusions of his experiments are : — The Bacteriology of Earth. (i) B. cloacae, B. grunthal, B. Xcn 75, and to a less extent B. coscoroba, are capable under favourable conditions of remain- ing alive in the soil for a considerable length of time, probably up to three to four years. (2) Faical organisms of an}- kind do not appear to exist in large numbers after they have been in the earth for longer than one to two years; night soil buried in the ground, even in large quantities, loses most of its organisms in this period. (3) Sporogenes enteritidis spores are capable of remaining alive in the ground for a period of something between three to four years. (4) B. coli communis has never been isolated from the trenching ground samples, hence it is j^robable, though not certain, that this organism does not remain alive in the ground as long as the more resistant organisms like cloacae, &c. It has been proved in one experiment to exist in the ground for a period of ninel}'-seven days. The Bacteriology of ]]'ater and Fccccs during Monsoon Weather. (i) The conditions obtaining during a heavy monsoon when fresli faeces mav find their way easily into water, the whole country being submerged, is in some ^\ay connected wiih the appear- ance of a set of rare micro-organisms in all the water supplies over a wide area. This fact has not been noticed with previcHis and subsequent heavy rain. (2) These and allied bacteria may suddenly become extremely common in the faices of animrds and man. The cause of this increased prevalence is unknown. THE EXAMINATION OF WATER 647 (3) The flood conditions having passed away, the bacilli very rapidly disappear from all waters. Consequently this supports the suggestion that these organisms are especially susceptible to natural forces inimical to bacteria. The Bacteriology of Water from a Shallow Well. (i) In common with most other water supplies, including rivers, lakes, springs, &c., B. cloaca would appear to be the pre- dominating organism in a well after prolonged drought. (2) Even a small downpour of rain, after a prolonged spell of dry weather, has a very marked influence in increasing the number of fascal bacilli in wells situated in porous soils. (3) Early showers, following on a long period of hot weather, have caused an increase in the number of Coli communis in this well. It is not by any means certain where these coli come from, but it is unlikely that they come from the surface of the ground, and probable that they remained alive in (he lower layers of the soil, (4) After heavy downpours of rain, in consequence of which it is certain that surface contamination has penetrated deep into the layers of the soil, a mixture of fjecal organisms is usually found in the water obtained from wells. Coli communis appears to be present after early rains, but disappears as the rains become more plentiful. (5) Plentiful rains improve the quality of the subsoil water after the contaminated surface water has run off" the land. (6) Shallow wells are a most unsatisfactory source of water supply, especially if they are situated in a highly porous soil, and unless the greatest possible care is exercised in protecting a large space of ground in the immediate vicinity from all chances of pollution. The Bacteriology of Hitman and Animal Fceces. (i) The flora of the intestinal tract of men and animals are subject to very considerable changes due to influences which are at present unknown. These influences have been proved to operate over very wide areas. (2) Within certain very wide limits, these forces appear to affect man and animals equally, both as regards number and kind of micro-organisms. (3) Under well-defined conditions, such as heavy rainfall, the water supplies contain the same organisms as the fasces of man and animals at that particular time, but this similarity of bacterial flora is also noted occasionallv when rain is absent, and there is no apparent cause for it. The explana- tion of this occurrence is at present unknown. 41 648 LABORATORY HINTS (4) Having regard to the variation in tiie bacteria in fceces, botli in quantitv and kind, no constant approximate composition can be arrived at. Even in the large groups, suggested by ]\IacConkey, variation in percentage composition in the same animal is considerable. (5) Xo lactose-fermenting organism has been isolated by us that has been proved to be the inhabitant of the intestinal tract of cattle or man only. (6) The numerical relation of the organisms constituting Mac- Conkey's groups in the intestines of cattle in India is entirely dififerent from that in England, while in the intestines of man it appears to be very similar in the two countries. (7) A study of the organisms present in faeces at different times of the year is necessary for the proper interpretation of the results obtained from water analyses. The Bacteriology of Lake Water. (i) The action of the sun is powerful in destroying all faecal organisms in water, particularly where they are " naked " and not surrounded by mucus derived from the intestine. (2) All f^cal organisms do not possess the power of resisting the action of sunlight to an equal degree. (3) It is possible to divide f^cal organisms, with a reasonable degree of accuracy, into the following classes : — (a) The delicate organisms or those that are very susceptible to the action of sunlight. (b) An intermediate class containing a very large number of organisms which occupy an intermediate position between the two extremes, and (c) The resistant organisms or those capable of resisting the sunlight for a considerable length of time. (4) The surface layers of any large volume of water are in conse- quence purer than the deeper ones. (5) Consequently the outlet from the reservoir should be arranged as near the surface as possible. (6) In the Red Hills lake, B. cloacae is by far the commonest faecal organism isolated from the bottom. (7) Coli communis even in large numbers, in a huge volume of water, disappears with great rapidil\'. The organisms never survived longer than six days. (8) There is some evidence that the middle layers of water in the lake of over 12 ft. deep contain more water organisms and more faecal bacilli than the bottom or the surface. When taking samples the depth should be stated from which they are taken. THE EXAMINATION OF WATER 649 (9) The B. cloacae and B. grunthal will persist in water exposed to the action of sun and storage for many months, and may therefore be looked upon as resistant to these forces. (10) The rareness (^)f su(~h organisms as CoH communis in the samples analysed demonstrates the fact that organisms very susceptible to the action to sunlight do exist, Coli communis being the commonest of these. (11) Storage in the tropics is capable of rendering a highly con- taminated water exlremelv pure, and of killing a large number of the faecal organisms present after gross pollution. In estahlishlui^ bacterial standards, for drinking-water in India, a preliminary grouping is given to us thus : — Class (i). — See (3), (a) above. Those Avaters containing Coli communis and the members of the susceptible group. The contamination is recent and dangerous. These are not commonly found. Class (2). — See (3), (c) above. Those Avaters containing such resistant organisms as B. grunthal, or B. cloaca? or both. These represent a pollution months old from a water supply becom- ing exhausted. Class (3). Those waters containing both the above organisms. This condition is to be expected in rainy weather and flooded rivers. In general be guided by : — The number of faecal organisms present. The number of different species present in the ten colonies isolated. To which group the organisms tend to belong most. In fresh samples of fa?cal contamination the Lactis aerogenes is not often present, hence if it is found it may be considered as evidence that a considerable amount of purification of the water has taken place. Clemesha proposes to classify river waters thus: — (i) Good river water. This should not contain more than 100 colonies on a (jar at o Ftecal organisms should not exceed one in 10 c.c. No organisms in Class (i) should be present in 50 c.c. Ffecal organisms present should belong to either Class (3) or the more resistant group of Class (2). (2) Fair or usable river water. This should not contain more than 300 colonies on agar at o 7° C. 650 LABORATORY HINTS It should not contain more fc'ecal organisms than one in i c.c. There should not be any organisms of Class (i) in less than 29 c.c. The fecal organisms present should consist mainly of mixtures of Class (3) and Class (2), and there should be a tendency for one organism to preponderate. (3) Bad river waters to be condemned. When the total colonies are more than 800 on agar at 37° C. When lactose fermenters are present in number of 10 to 100 per c.c. When organisms belonging to Class (i) exceed one in 5 c.c. When the faecal organisms isolated (Class (i) being absent) are rich in varieties such as occur in an emulsion of faeces. For Well and Spring ]]\iters. A good water should contain no f^cal bacilli in 20 c.c. No Class (i) in 100 c.c. Total colonies under i^ft^' per c.c. For the details of this excellent ^^'ork one must see "A Study of the Bacteriology of Drinking Water Supplies in Tropical Climates'* (1909), by W. W. Clemesha. Sanitarians are recommended to adopt similar methods. Unfortunately he has not told us anything of deep wells. It seems to be agreed that if experiments are carried out along the lines adopted by Clemesha, in most tropical countries, sufificient data will be available for suggesting some standard for a tropical water supply fit for drinking purposes. We venture to give, however, for comparison, the standards as adopted by British sanitarians. (a) Enumerate the bacteria capable of growth at room temperature (18-22° C). (b) Identify and enumerate the bacilli coli present. (c) Enumerate bacteria capable of growth at blood heat (36° to 38° C). (d) Enumerate the streptococci present. (e) Detect the typhoid bacillus. (/) Detect the cholera vibrio. (a) To enumerate bacteria grown at room temperature. Nutrient gelatin is most often the medium used. (In countries with a high temperature nutrient agar should be used, but it is not as useful as nutrient gelatin in showing the presence of liquefying organisms (Simpson).) Professor Hewlett prefers beef broth. The percentage of gelatin should be increased with the temperature. THE EXAMINATION OF WATER 651 ]\Ielt the gelatin in three tubes in a water bath or incubator at blood heat. Inoculate three sterile Petri dishes with 0*5, o'3, 0*2 c.c. of water well shaken. Pour the contents of a gelatin tube into each Petri dish. ]\Iove quietly to mix the water and gelatin. Allow to solidify on a flat surface. Count the colonies at the end of seventy-two hours, but inspect daily. 1,000 organisms can be counted on a 10 cm. dish, but 200 colonies should be the maximum. In pure water less than 10 per cent, will liquefy gelatin. In the purest upland streams i c.c. contains often under 100 bacteria, while in town sewage the same quantity contains millions. In deep well water over 100 organisms per c.c. is conclusive evidence of contamination. 500 per c.c. and above is suspicious water, 1,000 or more means condemnation of the water for drinking purposes. (b) To enumerate bacteria grown at blood heat. Inoculate two sterile Petri dishes with i and o'l c.c. of the sample. Melt two tubes of nutrient agar and allow to cool to 45° or 40° C. and pour into the dishes. Mix quickly and place to cool. Count them at the end of forty-eight hours. (c) To enumerate Bacillus coli present. The most important datum of bacterial examination. The sample should be 50 c.c. of shallow well and surface water. The sample should be 100 c.c. of deep well water. Add a medium that contains a substance fermented by the Bacillus coli, and also a substance to inhibit the growth of other water organisms as Pake's method, glucose-formate broth. Savage's method, neutral red glucose broth. MacConkey's method, bile-salt broth, generally used. In this is lactose, the Bacillus coli ferments giving acid gas. Sodium taurocholate... ... ... ... o"5 per cent. Wittes' peptone ... ... ... ... 2*0 „ Lactose ... ... ... ... ... ro „ Agar 2-0 „ Made with tap water and i per cent, solution of neutral red added. A double strength is also made. Bacillus coli gives bright red colonies, and Bacillus typhosus white colonies without fermentation. Inoculate four tubes containing 5, 10, 15, 20 c.c. of this double strength medium with 5, 10, 15, 20 c.c. of the water sample. Incubate at 42° C. for twenty-four to forty-eight hours. 652 LABORATORY HINTS If acid and gas is produced it is presumptive evidence of Bacillus coli. Take a loopful of liquid from the tube with the smallest amount of water, and add it to a test-tube of 10 c.c. of sterile water. Shake and inoculate a similar tube \\\{\\ one loopful of this. Repeat from the second to a third tube. Smear one loopful of each dilution over a gelatin or agar slope. One of these is sure to give discrete colonies. Subculture these into tubes of nutrient broth, and later examine for motile organisms and do a Gram stain. From the broth, culture inoculations are made into the various media necessary to identify the organism and the attributes of the organism thus collected. If typical Bacillus coli have been found in the tube to which 10 c.c of the w^ater had been added and not in that of 5 c.c, it would be stated that Bacillus coli was present in 10 c.c, but absent in 5 c.c. Those waters showing no Bacillus coli in 50 c.c. are of a high degree of purity. Spring waters should not show them in 50 c.c In upland surface waters their presence in 10 or 40 c.c. means contamination, but not necessarily dangerous, as it may be from animals grazing, and not pathogenic human excreta. If there are more Bacillus coli than 500 per litre the water is suspicious. {d) To enumerate streptococci. As above, but use glucose broth or glucose neutral red broth, and incubate at 37° C. for four hours, and then make a hanging drop preparation. The primary Bacillus coli tubes can, of course, be examined for them. Streptococci do not multiply after sampling, but Bacillus coli do. Their numbers should not exceed that permissible for Bacillus coli. {e) To detect the typhoid bacillus. This is difficult. Remember that as the incubation of typhoid fever is twelve to fourteen days, the organisms ma}- have disappeared from the water before the examination is started. Water containing typhoid bacilli will contain large numbers of Bacillus coli also. Other organisms may overgrow those of the typhoid bacilli. There are many wavs of concentrating the agar in the water, such as filtering through a porcelain filter, adding a little alum, entangling them in the aknninium hvdrate, centrifuging, &c. THE EXAMINATION OE WATER 653 To isolate the organism from the concentrated deposit : — Plate in Conradi-Drigalski agar or litmus lactose bile-salt agar. Subculture the colonies into broth and work out their attributes in other media. Try agglutinating (Widal) reactions in each subculture. Do a Pfeiffer's test, depending upon bacteriolysis to clinch a diagnosis. (/) To detect tlic cholera vibrio. (See " Cholera.") (5) THE CHEMICAL EXAMINATION OF WATER (after Stewart). The results of water anahses are expressed in parts per 100,000 or as grains per gallon = parts per 70,000, since there are 70,000 gr. per gallon. 100 c.c. is a convenient quantity to work with for certain estimates. When one is using standard solutions of a strength I c.c. ^= o'ooi grm., the number of c.c. used in the titration gives the result in parts per 100,000. Likewise, if 70 c.c. are taken of the sample, the actual titration gives the result in grains per gallon. This much facilitates the work as is demonstrated in a simple example thus : — In estimating chlorine in a water sample, 3*4 c.c. of standard silver nitrate solution (i c.c. = o'ooi grm. of chlorine) were required to reduce it. Hence there were 3*4 parts of chlorine in 100,000 parts of the water because : — 3"4 X o-ooi X 100,000 =3"4 100 To convert grains per gallon to parts per 100,000 multiply the result by 10 and divide by 7, and conversely to multiply bv 7 and divide by 10 gives grains per gallon. One is required to ascertain the (1) Total solids (6) Nitrates (2) The degree of hardness (7) Oxidizable organic matter (3) The metals present (8) Saline ammonia (4) Chlorine (9) Albuminoid ammonia (5) Nitrites (10) Degree of aeration in the ordinary drinking-water and sewage. These will be dealt with seriatim, applied to drinking-water first. (1) To Estimate the Total Solids. Weigh a small porcelain dish. Take 200 c.c. of the water sample. Evaporate to dryness in dish over a water bath, pouring water in as it evaporates until 200 c.c. have been poured in. Dry the dish in a water oven for an hour. Cool, weigh the dish and residue. 654 LABORATORY HINTS ' Deduct the weight of dish, remainder equals total solids in 200 c.c. Simply calculate how much in 100,000 c.c. Example : — Dish + total solids — 27*848 grm. Dish alone = 27797 ,, Weight of residue = o'05i grm. x 100,000 = 25'5 parts 200 per 100,000 (2) To Estimate the Hardness. The hardness of water is largely due to the presence of bi- carbonates, sulphates and chlorides of calcium and magnesium. (i) Total Hardness. In a stoppered bottle of 150 c.c. capacity place 100 c.c. of sample. Run in from a burette standard soap solution (i c.c. = o"ooi grm. CaCOg), shaking vigorously until a permanent lather of \ in. is obtained. Exaynple. 13*8 c.c. of soap solution is required. Hence I3'8 x cooi is contained in 100 c.c. of water. I3'8 X 001 X 100,000 = I3'8 parts per 100,000. 10 If 100 c.c. are used this latter calculation is avoided as the c.c. used, i3'8 in this case, indicates the parts per 100,000. (2) Temporary Hardness. This can be removed by boiling. It is due to the bicarbonates of lime and magnesia. On boiling the COo is driven off and the carbonates are precipitated. Commercially it is removed by adding lime. The degree of temporary hardness is calculated by subtracting the permanent from the total hardness. (3) Permanent Hardness. This is due to the sulphates and chlorides of calcium and magnesium. They are soluble in water and cannot be precipitated by boiling. To estimate them : — Boil 100 c.c. in a beaker for fifteen minutes. Filter when cold and make up the filtrate with distilled water to 100 c.c. Shake well. Run in soap solution as described. Example : 4*2 c.c. required. Hence 4*2 parts per 100,000. But the total hardness was 138 = 9'6 parts per 100,000 temporary hardness. The permanent „ „ 4-2 THE EXAMINATION OF WATER 655 (3) Detection and Estimation of Poisonous Metals. To 100 c.c. of the water add a few drops of acetic acid. Pass in H2S. A light clear brown deposit = copper. A dirty granular deposit = lead. Copper. To another 100 c.c. add a little acetic acid. To this add 2 c.c. of fresh solution of potassium ferrocyanide. To estimate the amount of copper present : — Match this chestnut brown colour by a standard copper solution. Copper solution (i c.c. = o'cooi grm. Cu) as is described in Nesslerizing the ammonia solutions. Lead. To 100 c.c. of water add a little acetic acid. To this add a few drops of potassium chromate and stir well. A yellow turbiditv (of lead chromate) indicates lead. If lead is in excess a yellow deposit will be formed. Pass H.S in 100 c.c. of the sample. Match the brown coloration wilh a standard lead solution (i c.c.=o"oooi grm. Pb) to estimate lead. Example, 12 c.c. of the standard solution are necessary to match the colour in the given sample. Hence there is o'oooi x 12 grm. of lead in the 100 c.c. of the sample, there is qooqi x 12 x ico.o r-2 grm. Pb in 100,000 parts. ICO Iron. If neither copper nor lead is present test for 'won. Take 100 c.c. of the sample. Add 5 c.c. of nitric acid, i in 5. Then 5 c.c. of 10 per cent, potassium sulphocyanide. A red coloration indicates iron. Match this colour with a standard iron solution (i c.c. = o'cooi c.c. grm. Fe) to estimate the amount. If the colour is too intense to be matched conveniently take a smaller amount and dilute to 100 c.c. with distilled water. (4) To Detect and Estimate Chlorine, This is present in most waters as sodium, potassium or calcium chloride. Its presence may be due tO' : — (i) The water passing through saline compounds in the strata, e.g., sandstone, greensand. (2) Pollution bv organic matter, especially urine. (3) Deep wells near the sea coast. (4) Tidal rivers. 656 LABORATORY HINTS Place 100 c.c. of the water in a large porcelain dish. Add a few drops of 5 per cent, potassium chromate. Run in from a burette standard AgXOg solution (i c.c. =^o"ooi grm. of CI) until a reddish tint remains. Silver chromate is formed which is red. If sa}' r; c.c. are required then these are the parts per 100,000. Since 17 x q-coi x -100.000 = j--, lOD To obtain the results in terms of sodium chloride multiply the result by i'647 since CI x r647 = NaCl. This factor is obtained from the ratio li^^^i _ 5^ = i'647- t-i 3S-5 (5) To Detect and Estimate Nitrites. These generally indicate recent organic pollution. Nitrites are eventually oxidized to nitrates. Sometimes nitrates are reduced to nitrites by ferrous salts or in deep wells due to the metal of the bore pipes, but these are the exceptions. Nitrites are usually found in sewage effluent. Test (i). Place 100 c.c. of the water in a Nessler cylinder. Add 6 drops of dilute HCl. Add 6 drops of naphthylamine hydrochloride. Add 6 drops of sulphanilic acid. Stir with a glass rod. A pink colour indicates nitrites. If no coloration in fifteen minutes nitrites are absent. Test (2). Place 100 c.c. of water in a Nessler cylinder. Add a few drops of H2SO4. Add I crystal of KI and mix well. Add 5 c.c. of fresh starch solution. A blue colour indicates nitrites. Test (3). To 100 c.c. of water add a few drops of diluted HCl. Add 5 c.c. of metaphenylene-diamine solution. Mix and allow to stand. A yellowish-orange colour indicates nitrites. If the reagent is not colourless, shake it with a little animal charcoal and filter. To estimate the amount match this colour by using a standard sodium nitrite solution (i c.c. = o'ooi grm.). (6) To Detect and Estimate Nitrates. These are usually present. Strata containing red sandstone, &c., impart them to the water. THE EXAMINATION OE WATER 657 They are also the final products of completely oxidized organic nitrogenous matter. Test (i). Fill a large test-tube with the sample. Add a few c.c. of diphenylamine solution. Pour concentrated H2SC)4 carefully down the side of the tube. A blue ring at tiie junction of the two licfuids = nitrates. Test (2) Repeat the above using a solution of brucine in H2SO4. A red ring is formed ^\hicll turns yellow, then brown. Both these tests are given ^\ilh nitrites also, hence nitrites should be excluded or Test (3) applied, which does not react with nitrites. Test (3). Evaporate 50 c.c. of the water to dryness in a water bath. Add I c.c. of phenolsulphonic acid. ]\Iix well Avith a glass rod. Heat on a water bath for one minute. Transfer the fluid to a 100 c.c. Nessler glass, washing the basin and rod with water, adding same to the glass. Add 10 c.c. of concentrated ammonia. Stir and make up to 100 c.c. with distilled water and shake. A yellow coloration denotes nitrates. By this method the nitrates are converted into picric acid. The ammonia forms ammonium picrate which has an intense yellow colour. To Estimate. Method (i). Retain the above yellow fluid and match it. Take 5 c.c. of the standard KXO3 solution (i c.c. = o"oooi grm. N). Evaporate to dryness and treat it exactly as the above solution. There are now two cylinders of yellow fluid that are not of similar tints. Suppose the Sample is the darker of the tzvo Solutions. Pour out some of the darker, say 15 c.c, and make up the 85 c.c. to 100 c.c. with distilled water. If now too dark pour out more, say 10 c.c, and make up the 90 c.c. to 100 c.c with distilled water. Suppose the tints now coincide we get : — looj^oo X 00005 X loo.ooo _ J. ^^^^ ^ ^^ j^ijj.^^fg . 100,000. 85 X 90 X 50 ^' ^ ^ 658 LABORATORY HINTS Suppose the Water Sample is the lighter of the two. Pour out some of the darker, say first 15 c.c, then 10 c.c. as above, then the amount of the orif^inal solution remain- ing- in the standard cyHnder is - ^ ^ '^° ° -^ 100 X 1 00 Therefore in the sample we have : — 85 X 90 X 00005 X 100,000 ICO X 100 X 50 Method (2). = 0*766 parts N as nitrate per 100,000 parts. Dissolve 2 grm. of sodium hydrate in 100 c.c. of distilled water. This is a pure solution of caustic soda free from nitrates. Add 100 c.c. of the sample water and a piece of aluminium foil. Permit to stand for twenty-four hours in a dark place. Then all the oxidized nitrogen is converted into ammonia. Distil this solution and Nesslerize as above. Before distilling test for nitrites to see that all have been reduced to nitrates. Method (3). Coat some zinc foil with copper by exposing it to copper sul- phate until it becomes black. Put zinc foil copper-coated into a bottle with 250 c.c. of the sample water, add 0*5 grm. oxalic acid and leave for twenty- four hours. All oxidized nitrogen is converted into ammonia. Distil and Nesslerize. (7) To Estimate the Oxidizable Organic Matter in Water (Oxygen absorbed) . This can be done in three hours at 37° C, or in four hours at 80° F. The putrescent organic matter is chiefly oxidized in the first thirty minutes. Oxygen may be absorbed by nitrites, HoS, ferrous salts, &c. In a stoppered bottle of 400 c.c. capacity place 200 c.c. of sample and add 10 c.c. of KMnO^ solution (i c.c. =o"oooi grm. of available Add 10 c.c. of H2SO4 (i in 4). Place in incubation at 37° C. for three hours. If the pink colour quickly fades add more KMnO^ always counting the c.c. used. At the end of three hours at 37° C. a pink colour should be present. Cool under the tap. Add 5 c.c. of KI 10 per cent, solution. Run in from burette sodium thiosulphate solution (i grm. in 1,000 c.c.) until the yellow colour has nearly disappeared. THE EXAMINATION OF WATER 659 Add 5 c.c. of fresh starch solution. Add more thiosulphate until the blue colour has disappeared, shaking constantly. We will suppose that 15*5 c.c. were necessary. We must now find out the strength of the thiosulphate in terms of O,. For this we do a blank experiment. Fill a similar bottle to the above with 200 c.c. of distilled water. Add at once 5 c.c. of 10 per cent. IvI, 10 c.c. of HoSO^ (i in 4) and 10 c.c. of KMn04 a? above. Run in the thiosulphate solution from the burette until the yellow colour has nearly disappeared. Then add 5 c.c. of fresh starch solution and add more thiosulphate until the blue colour has disappeared. Suppose 20'5 c.c. are necessary. Thus blank experiment requires 20'5 c.c. of thiosulphate. Water sample recjuires i5"5 c.c. of thiosulphate. Therefore the difiference is 5 c.c. of thiosulphate. Now 20"5 c.c. of thiosulphate = 10 c.c. of KjMnOi or o'ooi grm. of Hence 5 c.c. of thiosulphate ?:^^^L^iil^= 0-00026 of O,. In 200 parts of sample water 0*00026 parts of O, are absorbed. .". in 100,000 parts of sample water o'l^ parts of Oo are absorbed. Water cannot be judged on this experiment alone as peaty waters absorb much oxygen and they are not as detrimental as waters ab- sorbing the same amount due to the presence of nitrites. Those not exceeding o'l = good organic purity. Those not exceeding 0*3 =- medium organic purity. Those not exceeding 0*4 = doubtful organic purity. Those more than o"4 = polluted organic purity. If other than upland surface waters are examined use half the amount for the experiment. (8) To Estimate Free and Saline Ammonia. During decomposition of organic matter, X combines with H and forms ammonia. This may combine with the saline constituents of the water forming saline ammonia or remain free. As this ammonia — the product of decomposing animal matter — is verv small, all vessels, &c., used in the experiment must be ammonia free. Place 300 c.c. of distilled water into a flask and distil it over. Test the distillate with 2 c.c. of Nessler's solution until it does not give a yellow colour. Then the vessel is ammonia free. (Nessler's solution is caustic potash with potassio-mercurio iodide.) 66o LABORATORY HINTS In the emptied flask place 500 c.c. of the water sample. Add a pinch of calcined sodium carbonate. The ammonium carbonate thus formed yields ammonia readily on boiling. Distil and collect the distillate in 50 c.c. Nessler's glasses suc- cessively. Add 2 c.c. of Nessler's solution to the first cylinder, stir and let it stand three minutes. Match this tint with a standard solution of ammonium chloride (i c.c. = o'ooooi grm. of NHg). In a Nessler's glass place 50 c.c. of distilled water. Add 2 c.c. of Nessler's solution. To this add o'5, or i, or 2 c.c. of the standard ammonium chloride until the tint is the same as the first cylinder distilled. If the tint does not match make a fresh standard or have, say, six cylinders containing known and varying amounts for matching. Treat the other cylinders the same as thev are distilled over. Two or three are usually sufificient and contain all the ammonia. Thus the first cylinder recjuires 3*0 c.c. of ammonia chloride solution. And the 2nd cylinder requires o"8 ,, ,, ,, And the 3rd cylinder requires nil. >> 3-8 c.c. Hence amount of NH3 in 500 c.c. of water is 3'8xo-ooooi. Hence amount of NH3 in 100,000 c.c. of water 3"8 X O'OOOOI X ico,ooo = o'O076 500 = 0*0076 parts per 100,000. Save the resulting solution for estimating albuminoid ammonia. Good water does not usually contain more than o'oi parts per 100,000. (9) To Estimate Albuminoid Ammonia. When nitrogenous organic matter is heated with an alkaline solution of KMnO,,, it is oxidized and part of the On present is con- verted into ammonia. If the albuminoid ammonia exceeds the saline ammonia it indicates vegetable pollution. If the saline ammonia is high and the albuminoid ammonia above 0.005 ^vith high figures for saline ammonia it indicates animal pollution. There may be free ammonia in deep well water, the metal of the bore pipes reducing the nitrates. Boil in a beaker fifteen minutes 50 c.c. of alkaline permanganate solution with 100 c.c. of water. THE EXAMINATION OE WATER 66i Pour iliis into the flask with its contents left from the above experiment. Add a few pieces of pipe stem to prevent bumping. Distil over about four 50-c.c. Xessler glasses. Xesslerize and estimate as for saline ammonia. The amount in good water does not exceed o'oi part per 100, oco. (10) To Estimate the Aeration of Waters (O2 dissolved). Measure exactly the volume of a stoppered bottle about 250 c.c. Fill completely with water sample, avoiding air bubbles. By means of a long pipette, the rod inserted close to the bottom of the bottle : — Add I c.c. of 40 per cent, manganese chloride. Add 3 c.c. of (50 per cent NaOH and 10 per cent. KI) solution. Insert stopper, avoiding air bubbles, shake. Subtract 4 c.c. from volume of bottle for reagents used. Allow to stand ten minutes. Run in 5 c.c. of concentrated HCl, holding pipette just above the precipitate. Insert stopper and shake. Free iodine is liberated and a clear reddish brown fluid obtained. Transfer this fluid to a flask. Rinse out old flask with 10 c.c. of distilled water and add to new flask. Run in this from a burette sodium thiosulphate solution (4 grm. per 1,000 c.c.) until a faint yellow colour remains. Add 5 c.c. of fresh starch solution. Continue with thiosulphate until a blue colour is discharged. Now do a blank experiment : — In a flask place 50 c.c. of KMnO^ solution (i c.c. =o'oooi grm. O^). 20 c.c. of H2SO4 solution (i in 4). 10 c.c. of KI solution (10 per cent.). Titrate the liberated iodine as above. Suppose the blank required 25 c.c. of thiosulphate. Suppose the sample recjuired 15 c.c. of thiosulphate. 50 c.c. KMnOj 50 X o'oooi = 0*005 grm. oxvgen. Hence 25 c.c. thiosulphate solution 0*005 grm. oxygen. Hence 15 c.c. thiosulphate solution oto5_x^j^ ^ p^^-, 25 ^ "" The volume of the bottle = (224 - 4 c.c.) 220. In 220 parts of the sample there are grm. 0*003 of O^;. T . r .1 1 .^1 o-ooi X 100, oco r . . In 100,000 parts 01 the sample there are — = i 30 oxvgen absorbed. A good water should have about I'l parts per 100,000. 662 LABORATORY HINTS Certificate of Analysis of a Sample of Water. Date received : From : Particulars on label : London tap water. Taken at Laboratory Physical characters : Colour in 2 ft. stratum : clear pale blue. Suspended matters : nil. Taste. Odour when warmed to 37° C. : nil. Reaction : alkaline. Chemical characters : — Total solids dried at loo*^ C... Loss on ignition (after recarbonating) Chlorine... Chlorine x 1,647 — sodium chloride Nitrites (as N2O3) Nitrogen as nitrates ... Saline ammonia Albuminoid ammonia ... Oxygen absorbed in 3 hours at 37° C. Hardness — Total „ — Temporary ,, — Permanent Poisonous metals — lead !> —copper ,, — iron TO EXAMINE SEWAGE AND SEWAGE EFFLUENTS. The same processes as for water with a few modifications. The Ammonias. Dilute sewage five times when estimating the ammonias. Make 100 c.c. up to 500 c.c. with ammonia-free water. When distilling collect 200 c.c, mix well, Nesslerize, and multiply the result by 4. It is best to collect 50 c.c. more to see that no more ammonia remains. The Solids in Suspension. The estimation of these is required. Filter 1,000 c.c. of the effluent through a weighed filter paper. Wash and dry the residue and weigh again. The Rate of O, Absorption after Filtration. Do this as for estimating the aeration of water, p. 661, but tested at different times : — O, absorbed in four hours at 60° F. O, absorbed in twentv-four hours at 60° F. O2 absorbed in forty-eight hours at 60° F. O, absorbed in five days. Parts per IOD,000 Grains per gallon 2 9 '60 2072 2*50 175 2-1 1-47 3-45 Nil 2-41 0'12 0-074 Q-OGI 0-0007 0'007 0*0049 0-04 0-028 12-5 8-0 875 5-60 4-5 Ml 3-15 Nil Nil THE ANALYSIS Of MILK 663 The Ro)al Commission on vSewage Disposal recommended ihat an effluent "should not contain more than 3 parts per 100,000 of sus- pended matter; after being filtered it should not absorb more than o'5 by weight of O2 per 100,000 in twenty-four hours. I'o b\' weight of O. per 100,000 in forty-eight hours. r5 by weight of O2 per 100,000 in five days." Chlorine should not exceed 10 parts per 100,000. O2 absorbed in four hours at 60° F. (or two hours at 80° F.) and the saline ammonia should not exceed 1*5 per 100,000. The albuminoid ammonia not more than o'i5 part. Incubation of final effluent when at 37° C, and for five days should be odourless. Generallv high nitrates are a good feature. THE ANALYSIS OF MILK. The Average Composition of Cow's Milk is : — Total Solids I2"6 per cent. Water ... 87*4 per cent. Fat ... 373 ., Lactose ... 4*50 ,, \ Proteins ... 3"62 ,, - Solids not fat 8"87 per cent. , Mineral matters 075 ,, ) The specific gravity is about 1032 at 15° C. (1) To Estimate the Total Solids. Weigh a small porcelain dish. Put therein 10 c.c. of milk and reweigh. Evaporate to dryness on a water bath for one hour. Dry in an oven for one hour. Cool in a desiccator and weigh. Dish+ 10 c.c. of milk = 36*320 grm. Dish + total solids = 27722 grm. Dish = 26"4oo „ Dish = 26*400 „ Milk weighs ... 9*920 grm. Total solids ... 1*322 grm. Hence 100 grm. of milk will contain : — = 13*32 per cent, of total solids 1*322 X 100 9*920 (2) To Estimate the Ash or Mineral Matter. Heat the residue from the above to a white ash on a porcelain triangle. Stir with a glass rod meanwhile. Cool in the desiccator and weigh. Suppose ash is o"076. 100 grm. of milk contains about o'76 per cent. 0*076 X 100 9*920 (= weight of milk) = 76 per cent. 42 664 LABORATORY HINTS (3) To Estimate Fat. Weigh lo c.c. of milk. Place it into a Stoker's graduated tube. Add lo c.c. concentrated HCI and heat cautiously till brown. Cool and fill up to the 50 c.c. mark with ether. Shake Avell and allow ether to settle out. Read off the volume of ether, say 26 c.c. Pipette out 10 c.c. of ether solution into a small weighed glass flask. Evaporate ether, dry flask in oven for one hour. Cool and weigh. If a Stokes tube is not available heat the milk in a large test-tube, and transfer when cool to a graduated 100 c.c. cylinder. Wash out the tube with ether and place same in the cylinder, and the volume is now made up to 50 c.c, and the process continued as described above. Example : — Flask fat 2y^yi Flask 23-421 o'i5o In 10 c.c. of ether there is o"i5 of fat In 26 c.c. of ether there is o"i5 x 26 = 0-39 10 The amount of fat in io"2i3 grm. of milk (10 c.c.) = 0*39 The amount of fat in loo grm. of milk 0*39 x o"ioo = 3"8i per cent. IO"23I (4) To Estimate Solids not Fat. Subtract the fat from the total solids. Example : i3'32 — 3"8i = 9"5i per cent, of solids, not fat. (6) To Estimate Lactose (Fehling's method). Pipette 20 c.c. milk into a 100 c.c. graduated flask. Add a few drops of acetic acid. Mix well, place on a water bath for a few minutes. Cool and make up to 100 c.c. with distilled water, shake and filter, Fill a burette with this solution. In a porcelain basin place 10 c.c. of Fehling's solution. Add 40 c.c. of water and boil. Run in milk solution from the burette slowly. Continually try a few drops of liquid from the dish with a starch and KI paper. When it ceases to give a blue colour stop burette flow. Keep the liquid gently boiling during the process. For the indicator it is handy to have a series of test-tubes. In each place 2 c.c. of the indicator and one drop of acetic acid. THE ANALYSIS OF MILK 665 To make the indicator : — Dissolve o'5 grm. of starch by boiling in water. Dissolve 10 grm. of KI in water. Mix and make up to 100 c.c. Example : j'l c.c. of diluted milk were required But 7*2 c.c. of diluted milk = g"o678 grm. lactose Since 10 c.c. Fehling's solution = o"o678 grm. laciose Hence 100 c.c. of diluted milk = o"678 x 100 grm. lactose 7-2 But this is in 20 cc. sample of milk .•. In 100 c.c. sample of milk = 0*0678 x 100 x 100 = 47 per cent, lactose 7-2 X 20 (6) To Estimate the Specific Gravity. This can be estimated by Westphal's balance, the Sprengel tube lactometer, or the specific gravity bottle. The lactometer is best for tropical use. It is usually between 1028 and 1034. (7) To Estimate Amount of Added Water and Deficiency of Fat. These are obtained from two simple formulse. (A) 8-5 - S.N.F. X 100 per cent, added water 8-5 S.N.F. solids not fat found in sample, e.g., 27 E.X8-5 - 7-5 X 100 = 107 per cent, of added water 8-5 {B)3-F X 100 = per cent, deficient in fat. F. = fat in sample, e.g., 27 J^X o 2"7 ■ X 100 = 10 per cent, deficient m fat 3 (8) Common Preservatives are: — (i) Boric Acid. Acidify 3 c.c. of milk in a test-tube with distilled HCl. Mix well and place a drop on a turmeric paper. Dry same on watch glass in oven. A red spot indicates that boric acid is present. This turns green instead of black on adding caustic potash. (2) Formaldehyde. In a test-tube place 10 c.c. of milk. Add 10 c.c. of concentrated HCl and one drop of ferric chloride. Stir well, heat to boiling. A violet colour indicates formaldehyde. 666 LABORATORY HINTS Sale of Milk Regulations. The solids not fat must not be less than 8'5 per cent. The milk fat must not be less than 3 per cent. No preservative is allowed in milk of any kind. To Analyse Condensed Milk. Employ the methods already mentioned with a few modifications. Use a ID per cent, solution of the condensed milk. For the total solids and proteins take 15 c.c. of this solution. For the fat take 10 c.c. of this solution. The fat, ash, proteins and lactose subtracted from the total solids give the cane sugar. An average analysis should yield : — Water ... 25-2 per cent Fat iro „ Proteins ... 9-07 „ Ash rgo ,, Lactose ... i3'4o „ Cane sugar • •• 39-43 I OO'OO APPENDIX. FALLACIES IN BLOOD EXAMINATION, THE GENERAL TREATMENT OF FEVER. EMBALMING. SOME HINTS ON TROPICAL SURGERY. COMPARATIVE NORMAL TEMPERATURES. PRINCIPAL REFERENCES. 668 APPENDIX APPENDIX. FALLACIES IN BLOOD EXAMINATION. Conditions leading" to fallacies may be dealt with in two classes: — (1) External. Insect hairs may simulate filariae. Low and Stiles took this view of the F. gigas described by Proiit. Cotton fibres once led to a wholesale diagnosis of filarije cases. Care and cleanliness should exclude these. Films sent from the tropics may contain yeast cells or spores which may cause considerable confusion. Less troublesome are pollen grains, animal and vegetable debris found in the dust fouling the specimen. Films made from the blood of shot or slaughtered beasts or birds may contain parasites carried from the gastro-intestinal tract, skin, hairy hides or feathers of the cadaver. A piece of blotting paper may be used to dry one slide in staining and in blotting a second with the same paper some of the parasites from the first may be carried to the second slide. Flaws and cracks in the glass should always be anticipated, especially as "seconds" are better than "firsts" for tropical work, as the best quality slides "fog" readily. (2) Internal. Fresh Blood. Crenations of red cells are readily differentiated from parasites as a rule. Vacuoles are a little more troublesome. They are highly refractive, never show granules in their interior and exhibit no movements. Splits and cracks in red cells have received many names and as they appear more frequently in pathological specimens they may be more readily taken for hsematozoa. They have no amoeboid movement but the contraction and the coagulation of the protoplasm may cause them to change their position slightly. They have probably been mistaken for bodies occurring in pernicious anaemia, leukaemia and lead poisoning. The so-called Cropper's bodies may be of a similar nature. Granules from broken-down leucocytes may overlie red cells and cause trouble. They are easily differentiated by focusing. A raised temperature may cause a peculiar degeneration of red cells that must be watched. They are most often seen when one is working with a hremostat. A blood platelet lying on a red cell may simulate a malarial Plas- modium. These can soon be diagnosed by altering the light and by focusing. Blood dust may be confused with granular debris from leucocytes THE GENERAL TREATMENT OE EEVER 669 or with micrococci. They sometimes appear like minute fat droplets, which may be correct, as such do appear after a meal. Under artificial conditions lymphocytes and myelocytes may become flagellates, induced by excitants such as atropine, methylene blue and a cancerous plasma. Normal blood has shown bodies with pseudopodia supposed at one time by Koch and Kliene to be associated with piroplasmosis. They are only altered blood cells. Bodies like vesicles in red cells have been mistaken for a special form of intra-corpuscular spirochsetal inclusion. Stained Blood. Blood platelets on red cells must be differentiated from the malarial parasite, and a mass of platelets from a crescent or a clump of spores or Leishman-Donovan bodies. The corps en pessaire and corps en anneau of French writers should be differentiated from pathological findings in malarial cachectics. In such patients anticipate endoglobular and anaemic degeneration of the red cells. The degeneration and vacuolation of leucocytes may make the student almost unaware of their origin. Experience alone will aid in the process of differentiation. Oval and round rings occur in the cytoplasm of lymphocytes, probably under the influence of alkaline stains, &c. When animal blood conditions are considered the subject becomes much more comprehensive. For details upon this subject the student is recommended to : " Fallacies and Puzzles in Blood Examination," by Andrew Balfour, M.D., in the Fourth Report of the Wellcome Tropical Research Labora- tory, Vol. A, Medical, of which the above is an abstract. That article will be found sufificient for general purposes. THE GENERAL TREATMENT OF FEVER. In this outline of treatment the specific cause of the fever is not dealt with. This should be known and treated accordingly, but in all fevers there are so many things in common that the general treatment may be along similar lines for all. When death takes place probably the chief source of weakness is the heart, hence one must consider those factors telling against the circulation as : — Under and improper feeding. Insufficient water. Vomiting because it withdraws food and water from the patient, is exhausting and prevents rest and sleep. Diarrhoea for the same reasons. The breathing of foul air. Insufficient oxygen. The interference of oxygenation due to hmg troubles. The impairment of the renal secretion. The loss of sleep and rest due to noises, bright light, pain, toxaemia and pyrexia. The elevation of the head. 6/0 APPENDIX The main thing's one must watch and deal with are diet, vomiting, diarrhoea, constipation, pure air, the maintenance of oxygen for the blood, sweating, renal secretion, rest and sleep, the control o( pain, pyrexia, elevation of the head, sustenance of the heart and care during convalescence. These will now be dealt with seriatim. (1) Diet. It should consist of carbohydrates, proteins, fats, water, sodium chloride and vegetable salts, in a word it must be complete. The feeding must be adapted to the condition of the patient thus: — The patient may not be able to take food by the mouth or rectum owing to diarrhiea and vomiting, hence one must feed by giving salines intravenously or subcutaneously at a temperature of 100° F. in the funnel. Give at least one pint in twelve hours. This is, of course, not a complete food or anything like it, but it is the best that can be done for the time. The patient may not be able to take food by the mouth owing to vomiting but can take it by the rectum. Then give peptonized milk, 100 c.c. for an infant, 125 c.c. for a child and 250 c.c. for an adult every six hours. If rejected give a suppository and repeat the food. Raise the buttocks to assist by gravity the entrance of the food. Rectal feeds vary enormously as regards constituents and each will use that which in his experience has proved most useful. There is much controversy as to the absorption of foods per rectum but in such cases as those mentioned it is best to give them. When the patient can take some food by the mouth it must be an incomplete food at first, such as junket, raw meat juice, white of egrg. Beef teas and broths are not good foods. A little alcohol in special cases, albumen water and whey. When this can be retained begin with complete foods as follows: — No. I Diet. Milk about four pints in twenty-four hours. For infants during the first six weeks of life 2 water and i milk. ,. ,, second six weeks i ,, i ,, ,. ,, next four months i ,, 2 ,, For adults ... ... ... ... ... i ,, 5 >> If curds are formed add barley water, rice water, arrowroot water, aerated water or lime water. Add sodium bicar- bonate, 10 grains (o"65 grm.) to the pint of milk. The milk may be boiled or prepeptonized. Allenbury's food may be given. A'egetable juices, as lemon squash, lime juice, &c. Nasal feeding may be required in some cases. No. 2 Diet. Milk, two pints daily with arrowroot, cornflour, rice, tapioca and bread. Egg- albumen, cream and butter. Stewed apples, fresh fruit, tea and weak coffee, pounded raw meat. Beef tea and soups. THE GENERAL TREATMENT OF FEVER 6yi No. 3 Diet. No. 2 diet plus fish, vegetables, raw oysters, sweetbread, tripe. No. 4 Diet. No. 3 diet plus meat, as pigeon, chicken, mutton, beef, and rarely pork. Yomiting. Provide digestible food. Reduce the quantity. Feed per rectum. Apply a mustard poultice over the stomach. Wash the stomach with stomach tube and sodium bicarbonate. Diarrhoea. Examine the stools for foulness, undigested food, faction, worms' eggs, parasites and treat accordingly, good. Constipation. Give a mild laxative. Enemata are useful. Petroleum jelly is good. Give — excessive putn- Salol is alwavs R Salol OI. ric. Muc. acac. .. Aq. chlor. ad OI2 grm. o'3o CO. 090 CO. 30"oo grm. Thrice daily Pure Air. Open air treatment is always good. Prevent draughts. Skilful nursing is required. Maintenance of Oxygen for the Blood. Keep the air passages open. Use the steam jet when there is laryngeal obstruction. A cold douche or bath is good with pulmonary collapse with children. Tracheotomy may be necessary. Sweating. This is of minor importance, but the patient should be washed down with tepid water when the perspiration is finished and chills prevented by suitable clothing. When there is a persistent dry skin with a high temperature then induce sweating by hot drinks, blankets, hot bottles, &c. Renal Secretion. Apply large poultices over the loins every four hours. Dry cupping can be tried but it is less effective. Give fluids in sufficiency. Salines per rectum, i to 2 pints each twelve hours. If children, seat them in a hot bath. If adults, foment the abdomen. Test the bladder with a catheter. For Haemog'lobinuria, see p. 380. 6y2 APPENDIX Rest and Sleep. Exclude noise. Have a dull light in the evening. For insomnia give phenacetin 0*30 to 0'6o grm. at eight o'clock, or ^ Pot. brom i grm. Chlor. hydrat. ... i ,, Aq. ment. pip. ad ... 30 ,, For a child, 15 to 30 grm. ; for an adult, 30 to 60 grm. at eight o'clock. Trional is useful, i to i'5 grm. at eight o'clock. Morphia may be necessary at times but it is often followed by depression. Control Pain. Give aspirin, o'30 to i grm. every six hours; or opium, 0*02 grm. every six hours. Pyrexia. If the temperature is above 103° F. reduce it. If it is above 106° F. reduce it immediately. Keep the wards cool for typhoid, warm for measles, diphtheria and whooping-cough. Give — I^ Quin. hydrochlor. ... 0-30 — I'oo grm. Phenacetin ... ... o*i8 — 0*50 „ Thrice daily. Hydrotherapy. Sponge the whole body with hot water in four minutes to dilate the blood-vessels. Or a tepid sponge in fifteen minutes. Or a cold pack twenty minutes. This is more active and is used at once in high temperatures or when sponging is useless. Or a continuous pack. The sheet is kept moistened v/ith water at 90° F. for several hours daily. Mackintosh baths can be given. Ice bags can be applied. Children and the aged do not stand baths well owing to the tendency to cardiac weakness. As a last resort some give pilocarpine nitrate subcutaneously. Depress the Head. Avoid the elevation of the head. It not only causes muscular stress but as the Ijrain is not well supplied with blood owing- to gravity and heart weakness, depression, fainting and syncope may ensue. Sustain the Heart. This should l)e done with digitalis, strophanthus. strychnine, camphor and alcohol. Raise the foot of the bed. Give salines. Hot bottles. Some omit digitalis and strophanthus. Watch the Heart during Convalescence. After luemoglobinuria. beriberi, typhoid, diphtheria, &c., sudden heart failure may occur. SOME HINTS ON TROPICAL SURGERY 673 Watch the rate and rhythm, a weak first sound at the apex and an accentuated second sound in the aortic area. Exercises should be very gradual. The blood count must be over 3^- millions per c.mm. EMBALMING. In order to preserve bodies for autopsy inject 300 c.c. of 5 per cent, solution of formalin. The fluid can be injected into the large arteries, e.g., the femoral and brachial towards the extremities, the common carotid in both directions and the cavities and organs by trocar and cannula. A more elaborate method is as follows : — Prepare 10 litres of a 10 per cent, solution of mercuric chloride. Expose the abdominal aorta and both iliac arteries. Incise the aorta and tie a large cannula and syringe in the opening. Inject 3 litres into the upper part, slowly and resting when the pressure is great. Ligature both sides of the opening. Inject I litre into each leg through the common iliac artery. Ligature the mesentery and intestines from the jejunum to the sigmoid, divide and remove them. Open and wash them. Put into them a i per cent, solution of mercuric perchloride, replace them wrapped in sublimate wool,, or better, cremate the lot. Wash the stomach, duodenum and rectum in the same way and pack with sublimate wool. Treat in the same way the bladder, vagina, external ear, nostrils, &c. Clean out the abdominal cavity, dry it and sew up the incision. Wipe the surface of the body with the same solution and dry it (the hair excepted). Some also inject into the axillary and carotid arteries. SOME HINTS ON TROPICAL SURGERY. All surgical instruments and appliances must be of the best quality obtainable. People at home sometimes send out those goods not readily disposed of at home, much to the chagrin of the tropical surgeon abroad. It is awkward indeed, if when attempting to remove a stone from the bladder, one of the jaws of the instrument breaks off or bends consider- ably. Vulcanite and gum-elastic goods should be avoided. Rubber rapidly perishes, but if kept in water in a dark place it will last longer. Rubber gloves can be kept in a glass jar, in powder, well stoppered. Catheters should be rubber or metal, preferably the latter. Rubber tourniquets are often useless when most urgently needed. Good metal ones are now made. Syringes should be all metal or all glass. If they are made of two or more kinds of material, the unequal alternate contraction and ex- pansion will cause fracture of the instrument. All needles should be of irido-platinum. They keep their points well and do not become oxidized. Microscopic slides should be of second-class quality, as the best quickly "fog" and are useless. The cover-sHps should be of the best quality. Take duplicates of fragile instruments likely to be used by native 674 APPENDIX assistants, as these latter are usually careless, and fresh supplies of instruments may require months to obtain. .Ml metal goods should be well plated, vaselined, and well packed in a tin-lined soldered case for dispatch. The Customs authorities usually open them and leave them open, but protection has been afforded for the ocean passage. " Air-tight " boxes are not usually air-tight, air escapes about the fastenings owing to expansion from heat, and is usually reabsorbed in a moist condition when the atmosphere becomes cool. All cases should be tin-lined and well soldered. ^^e]vet-lined cases of instruments are only welcomed by cockroaches and other insects. The anaesthetic of choice is chloroform. Although given by native assistants over thousands of administrations very few accidents occur. Ether is used at the Ancon Hospital, Panama, a fresh small tin being opened for each case. Tropical workers as a rule find that ether evaporates too quickly. Chloroform should be dispatched in glass bottles, with glass stoppers well .sealed. Cork perishes, and unsealed glass stoppers become loose in transit. Intraspinal ansesthesia is coming to the fore. Boyd and Young report on over 6,000 cases at the Santo Tomas Hospital, Panama Canal Zone. It was used for all operations below the umbilicus and sometimes for the upper abdomen. The mixture was Stovaine o'l grm.. Sodium chloride, o'l grm. in i c.c. of distilled Avater. Five c.c. were usuallv given for operations of half an hour or less. Anaesthesia is complete in three and a half minutes and lasts fifty to sixty minutes. It was preceded by an injection of morphia. Cases showing a low blood-pressure from shock following loss of blood were excluded. The sepsis of wounds is much more prevalent in the Tropics than in Europe, as conditions are much less perfect and operations are carried out in theatres open to air currents. The treatment of fractures is difficult. The patients are usually restless, the skin is moist, and may be shed in cases requiring prolonged extension. Adhesive plaster i.s. seldom adhesive, and plaster-of-Paris seldom hardens sufficiently. One is often consulted as to when the spleen should be removed. The writer follows Cantlie's list : — (i) Rupture of the spleen. (2) Primaiy hydatids. (3) ,, malignant growth. (4) M abscess. (5) >» massive tuberculosis of the spleen. (6) Chronic splenic anaemia. (y) ,, hsemolytic (splenic) jaundice. (8) Banti's disease. SOME COMPARATn^E NORMAT. TE^FPERATURKS. Man 37'oO C. Cow 39"=^.^ C. ' Cat 38-80 C. Sheep 39-600. Dog 39-20 C. Pigeon 42-0° C. Goat 39-30 C. Duck 42-2O q Rabbit 39-50 C. Chicken ... 42-5O C. PRINCIPAL REPERENCES 675 PRINCIPAL REFERENCES. " A Manual of Tropical Medicine "... "Tropical Diseases" ... "Tropical Medicine and Hygiene" ... "The Principles of Hygiene" " Laboratory Studies in Tropical Medicine " Yellow Fever and its Prevention " " The Prevention of Malaria " " Sleeping Sickness in the Island of Principe " Trypanosomes and Trypanosomiasis " " Venoms, Venomous Animals, &c." "Medical Entomology" " Recent Advances in Tropical Medicine" " Review of Recent Advances in Tropical Medicine" "Diseases of China" " Amoebic Dysentery " ... "Sprue and its Treatment" ... "Beriberi" "Human Intestinal Protozoa" "Researches on Egyptian Bilharziasis " ... " The Animal Parasites of Man " "Gnats or Mosquitoes " "Hygiene Coloniale " "The Etiology of Relapse in Malarial Fever" " Notice sur les Glossines ou Tsetses " " Infant Feeding in the Tropics " "Manual of Bacteriology" " Hygiene and Public Health " "Diseases of the Skin" "Nutrition" " Diseases of the Eye " "The Extra-Pharmacopoeia" " Food Analysis " "Food and Hygiene" " Reports of the Sleeping Sickness Com- mission " The Classification and Pathology of Beri- beri " " Album of Photographs." B.M.A. Indian Section. Annals of Tropical Medicine and Parasitology. Tropical Diseases Bulletin. Transactions of the Society of Tropical Medicine and Hygiene. Journal of Tropical Medicine and Hygiene. Castellani and Chalmers. Manson. Daniels. Simpson. Daniels and Newham. Boyce. Ross. Bruta da Costa, &c. Laveran and Mesnil. Calmette. Alcock. Balfour and Archibald. Balfour and Archibald. Jefferys and Maxwell. Carnegie Brown. Carnegie Brown. Vedder. Wenyon and O'Connor. Leiper. Fantham, Stephens and Theobald. Giles. Alliott, Clarac, 8:c. James. Hegh. Decks. Hewlett. Whitelegge and Newman. Morris. Sohn. May and Worth. Westcott. Woodman. Tibbies. Mott. Wright. 676 INDEX I NDEX. Abdomen in typhoid fever in the tropics, 217 Abscess, evacuation, in filarial lym- phangitis, 281 Abscesses, filarial, 282 site of, 282 Abyssinian well for shallow Avater in tropics, 551 Acanthokeratodermia, 459 Acariasis, infected barley causing, 459 symptoms, 459 Acarina, order of, ticks, largest speci- mens of, 19 Acclimatization theory of protection formed by vaccines and sera, 600 Acid-fast method for staining micro- organisms, 614 Ackee poisoning, aetiology, 455 high mortality in, 456 pathology, 456 • prophylaxis, 456 symptomatology, 455 {vomiting sickness of Jamaica), 455 Acne-like eruption, produced by spar- ganum, 261 Acnitis, treatment, 460 Acrodermatitis chronica atrophicans, 460 vesiculosa tropica, 460 Acrodermatosis, 460 Actinomyces, diagnosis of, 629 Adrenalin in sprue, 360 injections in snake bite, 445 Aeration of waters, methods of estimat- ing, 661 Africa, poisonous snakes in, 431 West, mortality from yellow fever in, 370 West Coast of, loss of memory in, 539 .... After cataract, discission for, 522 Agar-agar, preparation of, 622 Agarsidae (tick), spirochaetes of Miana fever, &c., transmitted by, 19 Agglutinins, action of, Coo in snake venom, 440 Aglypha, 423 Ainhum, definition, 412 pathology, 412 symptomatology, 413 Air, hot, as means of disinfection, 593 "Alastrim" and chicken-pox, differentia- tion between, 401 symptomatology, 403 Albinism, 461 Alcohol, effect of, in Tropics, 459 medicinal value of, 583 Alcoholic drinks, avoidance in sprue, 359 stimulants, strong, avoidance in yellow fever, 371 Alga;, growth of, in standing water, method of removal, 547 Alimentary tract of fleas, 178 Alkalies, effect in sprue, 360 Alopecia, 469 treatment, 470 by external irritants, 470 by nourishing ointment, 470 Alum, rectal injections in oxyuriasis, 313 stick in trachoma, 515 Amblyopia, quinine and malarial, dif- ferentiation between, 525 toxic, 510 Ammonia, albuminoid, in water, method of estimating, 660 and ether in snake bite, 445 free and saline, in water, method of detection of. estimating, 659 Ammonias in sewage, method, 662 Ammonium chloride in treatment of tape- worms, 269 Amocbiasis, urinary, 41 Amok, 407 exciting causes, 407 Amputation in treatment of Madura foot, 482 Anaemia and intestinal irritation in Hymenolepis nana infection, 263 grave, in blackwater fever, 387 in African trypanosomiasis, 142 in verruca peruana (severe type), 364 severe, with fever produced by Dibothriocephalus latus, 260 Anaerobic cultures, 624 Anaesthetics in eye diseases, 528 Anderson, effects of hot climates on white men, 538 Anderson's process, sterilization of water ^3y, 556 Anemones, venomous, 448 sting from, symptoms, 449 treatment, 449 Aneurism, late manifestation of yaws, 25 Angio-fibroma contagiosum tropicum, 461 Angiomata, 502 Angio-sarcoma, 502 Animal matter in water, danger from, 552 Animals, epidemic gangrenous rectitis in, 408 living, examination of, 573 Ankylostoma duodenale, points of differ- ence between, and the Necator ameri- canus, 320 Ankylostomes, 314 Ankylostomiasis, blood examination in, 317-8 INDEX 677 Ankylostomiasis, complications, 318 life-history, 3i() prophylaxis, 318 spread of, factors necessary for, 543 ■ symptomatology, 317 treatment, 318-g Ankylostomum duodenale, 314-5 ova of, 637 Anopheles maculipennis, larva of, 295 Anthrax bacillus, diagnosis of, 616 Anti-bacterial action, how produced, 164 Antibactericidal substances, probability of, in snake venom, 441 Antibodies, 600 Antidote, or retention theory of protection afforded by sera and vaccines, 600 Antidysenteric serum, summarizing of work by Flexner, 201 Antifibrin ferment in snake venom, 441 Antigens, 600 Antihasmolysins in snake venom, 441 Antimony in kala-azar, 61 preparations in treatment of African trypanosomiasis, 148 Antitoxic sera, 599 Antitoxins, 163 Antityphoid vaccine, effect on case in- cidence and case mortality of typhoid fever, 601 protection afforded b\-, length of, 601 Antivenene in snake bite, 446 Ants, venom of, symptoms, 452 Anuria in yellow fever, treatment, 371 Appetite perverted in cerebral stage of African trypanosomiasis, 145 Archibald's fever, definition, 397 symptomatology, 397 Archibald and Balfour, bacteriological examination of river and well water in Khartoum, 642, 643 Archoplasm in protozoa, 3 Argas persicus (tick) attacks poultry and humans, 21 Arm, elephantiasis of, 293 Arrow poisons, treatment, 457 Arsenic emetic in treatment of African trypanosomiasis, 149 in afebrile splenomegaly, 417 in lichen planus, 475 in onyalai, 417 in psoriasis, 487 Arsenical poisoning in zetiologv of beri- beri, 337 preparations in treatment of African trypanosomiasis, 148 treatment in rat-bite fever, 398 Artesian wells, 551 Aryan races, vegetarianism of, 566 Ascariasis, definition, 309 geographical distribution, 309 parasite causing, 309 symptomatology, 311 treatment, 311 Ascaris lumbricoides, examination of faeces for eggs of, 311 life-history, 309, 311 morphology, 309, 310 ova of, 637 parasite causing ascariasis, 309 Asia, poisonous snakes in, 428 Aspergillinas, diagnosis of, 630 Aspergillosis, 461 ocular, due to fungi, 511 Aspirin in filarial lymphangitis, 281 in phlebotomus fever, 361 in yellow fever, 371 Asthenia in African trypanosomiasis, 142 Asthenopsia, sponge-fishers', 509 Atoxyl in pellagra, 336 in treatment of African trypano- somiasis, 148 Atripliasmus, 454 symptoms, 454 Antigens, 600 Auchmeromyia luteola, larvae of, causing myiasis, 483 Auto-intoxication in aetiology of beriberi, 340 Aviation, dangers of atmospheric changes in, 532 Babesia hominis, 6 Bacilli, 162 capsulated, 618 characters of, 1C2 Bacillus asiaticus fever, symptomatology, 397 botulinus, diagnosis of, 617 coli, diagnosis of, 618 — ■_ in water, quantity of, testify- ing to measure of purity of, 652 enumeration by method of British sanitarians, 651 diphtheriae, diagnosis of, 619 lepras, 180 diagnosis of, 616 mallei, diagnosis of, 621 oedematis maligni (Bacillus septi- cus), diagnosis of, 617 of timothy grass, diagnosis of, 616 paratyphosus A, geographical distri- bution, 215 - paratyphosus B, geographical distri- bution, 214 - pestis, behaviour of, 168 carried by fleas, 177 characters, 168 cultures of, 170 diagnosis of, 619 habitat, 168 — pseudo-tuberculosis of Pfeifl'er, dia- gnosis of, 616 — pyocyaneus, diagnosis of, 620 — typhosus, diagnosis of, 619 vibrio in flies, transmission of cholera by, 206 welchii, diagnosis of, 617 Ascites, chylosus, 284 ■ in filariasis, 279 Bacteria, death of, how produced, 163 demonstration of, in laboratory work, 626 detection in faeces, 635 diseases due to, 161, 162 distribution, 164 entrance into tissues, 165 general features of, 162 in aetiology of pellagra, 331 in waters, examination by methods of British sanitarians, 650, 651 infection by, conditions necessary for, 164 life of, conditons necessary for, 163 678 INDEX Bacteria, mclliods uf locomotion, 162 non-pathogenic, in water cause of muco-enteritis, 553 physiology, 162, 163 reproduction by simple fission, 162 by spore formation, 162 resistant to effects of sunlight, 645 ■ shape of, 162 staining for, 604 susceptible to effects of sunlight, 645 Bacterial activity, products of, 163 • emulsions, 509 Bacteriolysins, 164 Balantidium coli, 7, 40, 45, 46 parasite of ciliary dysentery, 44 — — minutum, 7, 46 Balfour and Archibald, bacteriological examination of river and well water in Khartoum, 642, 643 Balkan War (1913), vaccination against cholera during, results, 213 Banana flour in infant feeding, 582 Bandaging in elephantiasis of legs, 286 Barcoo rot, 461 Basic stains, 604 Beans causing favism, 389 Beef broth as nutrient medium for cul- tures, preparation of, 621 Bees and wasps, sting of, symptoms, 452 treatment, 452 venom of, 451 Beetles, venomous, 453 Belladonna, application in climatic bubo, 4" . . Benzoic acid and sodium benzoate as pre- servative, test for, 577 Beriberi, aetiology, 2:^7 atrophic, dry or paralytic variety, 343, 344 deficiency disease, 337 definition, 336 diagnosis, 347 dietetic causes of, 571 geographical distribution, 336-7 history, 337 hypertrophic, wet or oedematous variety, 345-6 infantile variety, 347 mixed variety, 346-7 oedematous variety, 344 pathology, 341 post-mortem examination, 341, 343 prognosis, 349 resemblances to and differences from epidemic dropsy, 348-9 spread and onset of, prevention, 540 treatment, 349-50 varieties, 343 wet, acute, 346 Berkefeld filter, 558 Beta-naphthol treatment of ankylostomia- sis, 319 Beverages, kinds of, causing pain in sprue, 357 Big heel, course of, 412 geographical distribution, 412 treatment, 412 Bile, leaking tumour discharging fluid giving reaction of, 501 Bilharzia Mission (1Q15), conclusions as to prevention and treatment of schisto- somiasis based on, 249, 250 Bilharziasis, transmission of molluscs essential for, 543 Binary fission, asexual method of repro- duction in protozoa, 3 Biotripsis (life-wear), 461 Bismuth-milk treatment in amoebic dysentery, 43 iodide (emetine) in amtebic dys- entery, 43 Black tongue, 476 Blackwater fever, blue pigment in, 628 diagnosis of yellow fever from, 370 ■ — presumed cause of, 6 see also H anioglohinnric fever Bladder, post-mortem appearance in schistosomiasis, 245, 246 stricture in schistosomiasis, 248 Blastomycetes, diagnosis of, 631 Blastomycosis, diagnosis, 462 ocular, due to fungi, 511 symptomatology, 461 treatment, 462 Blindness, 508 • • causes classified, 508 due to lightning, 510 Blood, acidity of, in cerebral stage of African trypanosomiasis, 145 cells, abnormal, 605 red, abnormal, 606 • counting of, 606 ha^mophilic, 606 nucleated, 606 transitional, 605 white, abnormal, 605 counting of, 607 of, changes in, 173 staining for, 604 condition in verruga peruviana, 364 condition in yellow fever, 367 count, differential normal, results 605 counting of_, 606, 607 in varieties of malarial fever, 609, 610 — detection in faeces, 635 — dust, 60; — effects of tropical climates on, 537 — examination of, 604 in ankylostomiasis, 317 — films, fixation of, 605 — fresh, examination of, for micro- filariae, 610 — in blackwater fever, 387 — malaria-infected, injections of, re- sult, 72 — malarial parasites in, 72, 73 — serum, as nutrient medium, prepara- — specific gravity of, method of estimating, 612 — spectroscopic examination of, 612 — state of, in sprue, 357 tonicity of, 613 tion of, 623 Boiling in sterilization Boils, treatment, 462 tropical, 462 of water, 558 INDEX 679 Bone-marrow in blackwater fever, 386 microscopical appearance in African trypanosomiasis, 139 Bone sarcoma, cystic (myeloid ?), of lower jaw, 4gg Bones and joints, how affected in chappa, 413 Boomerang leg, aetiology, 415 geographical distribution, 415 symptomatology, 415 Borax methylene blue for staining malarial parasite in blood, 608 Bore well, drill for producing, 551 Boric acid and borax as preservative, test for, 578 Bothriocephalus, ova of, 638 Botryomycosis hominis, 462 Boyce's summary of prophylactic measures against yellow fever, 372 Brackish water, ill-effects of, 553 Brain, amoebic suppuration of, 40 malarial parasites in, manner of demonstrating in laboratory work, 627 — ^ — pernicious manifestations of malaria in, 74 Breast, elephantiasis of, 2gi, 293 British sanitarians, methods of examina- tion of bacteria in waters, 651 Bromidrosis, 462 Bronchocele, fibroid, 498 Bubo, climatic, aetiology, 410 bacillus isolated from, 410 definition, 410 geographical distribution, 410 pathology, 411 symptomatology, 411 treatment, 411 see also Plague bubo Bucket system and European latrines, 588 Bugs, venom of 451 Building sites, suitable in tropical dis- tricts, 535 Burns and scalds of eye, 509 Bush, the, as latrines for natives, 585 Butter, adulteration of, 571 Butter-milk, ^68 Buttock, elephantoid tumour of, 287 C^COSTOMY in amoebic dysentery, 43 Caecum, section from, in case of amoebic dvsentery, 33 Caffeine injections in snake bite, 445 Calabar swellings, definition, 299 geographical distribution, 299 symptomatology, 299 treatment, 300 Calcium carbonate in sprue, 360 hypochlorite, use in purification of water, 555 lactate for viper venom, 445 Calomel in oxyuriasis, 313 Calorie value of foods, 565 Canities, 470 in young persons, treatment, pre- scription for, 470 Cantlie, Sir James, nature of climatic bubo, 410 Cantlie's treatment of sprue, 359 Carbohydrates, food value of, 563 43 Carbol fuchsin, use of, as stain, 604 Carbol-thionin for staining malarial parasite in blood, 608 Carbolic acid as disinfectant, 594 Carbon dioxide poisoning in aetiology of beriberi, 337 Carbonates, alkaline, excess in water, eft'ects of, 553 Carcinoma, melanotic, 495 of cervix, 502 of ovary, 502 of pylorus, 502 Cardiac and vascular tonic, probability of in snake venom, 441 insufficiency in yellow fever, treat- ment, 371 symptoms in South American try- panosomiasis, 157 Carrion's fever, see Verruga -perjiviaiia (severe type) Cassava plant, varieties of, 564 Castor oil in amoebic dysentery, 42 in ciliar dysentery (Balanti- dium coli), 46 seeds, poisoning by, 454 Cataract, 509, 510 • classification, 517 congenital and juvenile, complete, 521 discission (needling) for, 521 extraction of, complications, 521 operation, 520 ■ in India, 510 ■ lamellar or zonular, 518 nomenclature, 517 polar, anterior, or pyramidal, 518 posterior, 518 ■ senile, 518 stages in growth of, 519 tests for time of operation, 519 • treatment by extraction, 519 traumatic, 521 uncommon forms of, 518 Cataracts, eye complications leading to, Catarrh, intestinal, resulting from Stron- gyloides stercoralis infection, 271 Catchment areas for water supply, 547 avoidance of peat in, 547 Caterpillars, venom of, symptoms, 452 treatment, 452 Cauterization of tropical ulcers. 505 Celluloidin, embedding In, of section of malarial parasites in brain, 627 Centipedes, venom of, mortality in chil- dren, 451 symptoms, 451 treatment, 451 Centrosomes, in protozoa, 3 Ceratophyllus fasciatus, transmission of plague by, 171 Cercomonas hominis, habitat, 5 vaginalis, habitat, 5 Cerebral stage in African trypanoso- miasis, 144-6 Cerebrospinal system, microscopical apoearance in African trypanosomiasis, 138 Cesspools in tropics, 589 68o I^'DEX Cestoda, classification, 258 life-history, 258 morphology, 257 pathogenic to man (human tape- worms), 257 Cestode, onchosphere of, 637 Cestodes, preservation of, 323 Chappa, pathology, 413 treatment, 413 Chaulmoogra oil in leprosy, 188 Chaulmoogric acid in leprosy, 188 Cheek, epipthelioma of, fungating, papil- lomatous, 500 horny growth from, 504 Cheese, whole milk, most nutritious of all foods, 567 Cheilitis exfoliativa, 476 glandularis, 476 Cheiropompholyx, 463 treatment, 463 Cheloid, 502 causes of, 502 Chemicals used for testing water sus- pected of contamination, 553, 554 Chicken-pox common in India, 401 Children, Davainea madagascarensis in- fection in, 263 intestinal ulceration and anaemia resulting from infection by, in chil- dren, 263 men and women, food necessary for, compared, 564 of natives, epidemic gangrenous rectitis, in, 408 very young, alone affected by ponos, 413 fever in, 368 Chlamydophrys stercorea, habitat, 5 Chloasma, causative agents of, 463 varieties of, 463 Chloride, cold, in snake bite, 446 Chlorine as disinfectant for horses, jjgC in water, detection and estimation of, method, 655 sterilization of water by, 557 Cholera, aetiology of, 205 carriers of, 213 transmission of cholera by, 206 collapse of, treatment, 210, 211 complications of, 208 — definition of, 203 — development of, climatic conditions best suitable for, 539 — diagnosis of, 208-Q bacteriological, 2og epidemics in Europe, 203-4 relation of, to wars, 204-5 — geographical distribution of, 203 — modes of infection, 205 -— or plague on infected ships, cjuaran- tine measures respecting, 597 — organisms, removal from Avater, chemical process for, 556 — pathology of, 206 — post-mortem appearances, 206-7 — prophylaxis against, 212 — spirilla, 2oq — symptomatology of, 207-8 — treatment, 20Q, 210 — - by Rogers' method, 210 Cholera, treatment, indications for, 209 old and new methods com- pared, 211 vaccination against, results, 212, 213 vibrio in milk, tests for, 570 vomiting in, treatment, 210 Chondroma, 505 Chondrosarcoma of humerus, 498 Chromidiosomes in protozoa, 3 Chrysarobin ointment, application in various forms of tinea (ringworm), 490, 491, 493, 494 Chrysomyia macellaria (screw-worm), larva of, causing myiasis, 482 Chrysops dimidiata and silacea, carrier of Loa loa. Chyle, double conjunctivitis discharging, associated with hlaria infection, 294 Chylocele, 284 Chylous extravasations, 282, 283 in frlariasis, 279 Chyluria and lymphuria, symptomat- ology, 283 treatment, 284 natural immunitv to vellow in filariasis, 279 Ciliata, 5, 7 (infusoria), 5 Cimex lectularius (bed-bug), carrier of parasite of European relapsing fever, 10 Cirrhosis, biliary, pathology, 410 infantile, 409 ■ aetiology, 409 cause of death in, 410 symptomatology, 409 treatment, 410 resemblance of ponos to, 413 treatment, 410 Clarke's process for softening water, 555 Clayton apparatus, use of, for extensive fumigations with sulphur anhydride and sulphurous acid gas, 595 Clemesha, Major, methods of bacterio- logical examination of waters in India, 645, 646 classification of river waters for drinking purposes, 649, 650 Climate, definition, 531 effect of, on skin, 458 relation to tropical diseases, 539 Clonorchis sinensis, ova of, 637 Coast memory, 539 Cobra seizing prey, photograph of, 424 Cocci, shape of, 162 Coccidium oviformis, diseases caused bv, 6 habitat, 6 Cocoa, ciualities of, 583 Cod-liver oil in onyalai, 417 Coffee, qualities of, 582-3 Collargol in five-day fever, 398 solutions of, in treatment of African trypanosomiasis, 149 Colon, dysenteric ulceration of, healing, ^35 . Colubridae, 423 orders of, 423 Colubrine venom (snake bite), post- mortem, 442 symptoms, 441, 442 Coma in ackee poisoning, 456 INDEX 68 1 Comma bacillus, cause of cholera, 205 Koch's, 621 differentiation from Fink- ler-Prior spirillum (Vibrio proteus), 621 Compound tablet, sterilization of water by, 557 . . . ,. , . Conjunctivitis aestivalis (spring catarrh), 516 and keratitis, phlyctenular, 516 ■ , treatment, 516 astringent remedies for, 526, 527 — catarrhalis, 511 . double, discharging chyle, associated with lilaria infection, 294 gonorrhoeal, 510, 512 resulting from unclean habits. 510 . , . Connective tissue tumours, benign, 502 malignant, 502 Continents, new means of intercourse between, opening of, increasing study of transmission of communicable dis- eases, 543 Convulsions in ackee poisoning, 456 Coolie itch, treatment, 463 Copper in water, method of estimating, sulphate, test for, 579 pencil in trachoma, 514 sterilization of water by, 557 Copra itch, 463 Corals, venomous, 448 • sting from, symptoms, 449 Cordylobia anthro])haga, larvre of, caus- ing myiasis, 482 Cordylobiasis, 464 Cornea, abrasions of, 509 Countries, new means of intercourse be- tween, opening of, increasing' study of transmission of communicable diseases, 543 Cover slips, method of cleaning, 604 Cox's method of treatment of cholera, 211 Craw craw (nodular dermatitis), treat- ment, 464 Creeping disease or erui^tion, difficulty of treatment, 464 Crocidura coerulea (Indian musk rat), resistent to plague, 171 Crotalinae, 426, 431 in America, 435 Crotaline venom (snake bite i43 symptoms, mottled Crotalus confluentus (Pacific or rattlesnake), 429 terrificus (dog-faced rattlesnake), 428 Culex fatigans, breeding places, 295 carrier of filaria, 294 larvse and pupae of, 294, 295 morphology, 294 transmission of dengue by, 376 Cultures, differentiating growth, 624 preparation of, 621 Current steam disinfector, 593 Cycloplegics in eye diseases, 528 Cyclops quadricornis, intermediate host of Dracunculus medinensis (guinea- worm), 301 Cyllin as disinfectant, 594 Cytolysins, action of, 600 in snake venom, four groups of, 440 Daniels, diagnosis of microfilaria, 277 tests for bacteriological examination of water, 642 Darling, discovery of Histoplasma capsu- latum by, 6 IDavainea madagascariensis, infection in children, 263 Dengue, aetiology, 377 definition, 376 diagnosis, 378 of phlebotomus fever from, 361 ■ of yellow fever from, 370 • geogra])hical distribution, 376 incubation period, 377 insects transmitting, 376. leucopenia in, 377 seasonal prevalence and general habitat of, 541 seciuelas and complications, 378 symptomatology, 377 treatment, 378 Dermatitis bullosa plantaris, 464 difficulty in treatment, 465 cupoliformis, difficulty of treatment. 46: 46c exfoliativa, local applications in, — (pityriasis rubra), treatment, 465 ■ macrogyrata, 466 nodosa rubra, treatment, 466 papillaris capillitii, 470 rimosa of the toes, treatment, 466 Solaris, 466 venenata, classification, 466 treatment, 466 vesicular, 505 Dermatobia cyaniventris, larvse of, caus- ing myiasis, 482 Dermatophiliasis, 466 symptoms, 467 treatment, 467 Diamond drill, Sullivan's, for producing bore well, 551 DiarrhcEa, chylous and lymph, 284 dysenteric, infantile, symptomato- logy of, 199 hill, setiology, 351 — — ■ definition, 351 diagnosis of sprue from, 358 pathology, 351 symptoms, 352 theories of, 351 ■ treatment, 352 • infantile, treatment of, 202 Dibothriocephalus latus (human worm), 260 morphology, 266, 261 produces severe anaemia fever, 260 Diet, articles average, hard work. tape- wit h of, causing pain in sprue, not engaged in male for m pellagra, 336 in sprue, 358, 359 articles to be in typhoid fever avoided, in the 359 . tropics, 222 in yellow fever, of natives, 565 371 682 INDEX Diet of natives of India and of Euro- peans contrasted, in relation to in- cidence of typhoid fever, 215 Voit's standard, 565 classification, 5C5 Digestion in cerebral stage of African trypanosomiasis, 145 Digitalis, tincture of, in heat stroke, 304 Dionin in iritis, keratitis, glaucoma and corneal ulcers, 527 Diphtheria, antitoxic serum in, value, 599 Diplococci, arrangement, 162 Diplococus pneumonia?, diagnosis of, 620 stain, method of finding, 615 Dipylidium caninum, parasite found in dogs and cats, 262 Diseases, general, ocular manifestations of, 522 Disinfectants, chemical, 595 characters of, 593-4 in eye diseases, 527 Disinfection, 592 • chief means of, 592 Distillation of water, 558 Dog, Schistosoma japonicum from, 251 Dogs and cats, infection from, to man of Dipylidium caninum, 263 Double continued fever, low mortalit\ in, 396 ■ • symptomatology, 396 Dover's powder in dengue, 378 Dracontiasis, geographical distribution, 301 parasite causing, 301 pathological lesions, 304 prophylaxis against, 305 symptomatology, 304 treatment, 304-5 Dracunculus medinensis (guinea-worm), host and intermediate host of, 301 ■ life-history, 301, 304 ■ morphology, 301, 302, 303 parasite causing dracontiasis, 301 Drawer's ointment, in psoriasis, formula ^0'''.487 Drinking water, boiling and filtration, in prophylaxis against dracontiasis, 305 distillation from salt water, 544 in India, bacterial standards, ^.49 Drinks in tropics, 522 Dropsy, epidemic, aetiology, 350 definition, 350 diagnosis, 351 geographical distribution, 350 resemblances to and difi"erences from beriberi, 348-9 symptoms, 350-1 treatment, 351 Drug-takers, Whitmore's disease common in, 415 Drugs in typhoid fever in the tropics, 222 useless in hypcrpyrexial fever, 395 Dusting powder, antiseptic, application, in filarial lymphangiectasis, 282 Dysenteries (the), causes, 29 classification, 29 history, 27 of Ancon hospital, classification, 29 protozoal, 29 Dxsenterics, pseudo-dysenteries, most common in temperate climates, 29 verminous, 29 Dysentery, amoebic, 146 acute, symptomatology, 36 chronic, 39 complication of African try- panosomiasis, 146 ■ • complications in, 41 cysts in stools of, 30 definition, 30 diagnosis, 42 geographical distribution, 30 histology, illustrations of, 33, 34, 35 36 m lesions in great intestine, — • liver abscess in, 50 method of search for cysts stools of patient suffering from, 41 parasite of, 30 pathology, 32 macroscopic, 34 section from intestine in case of, showing ulcer of Harris, 38 treatment, 42 — antitoxic serum in, value, 599 — ■ bacillary, 29 acute, symptomatology of, 198 and amoebic, diflferentiation be- tween, 42 — ■ aetiology of, 196 — ■ chronic attacks, treatment of, symptomatology of, 199 complications of, 199 definition of, 196 diagnosis of, 200 geographical distribution of. 202 196 358 of pathology of, 197 prognosis of, 200 sequelae, 200 spread of, factors in, 540 symptomatology of, 198 treatment of, 200 bacilli, main types, ig^ bacillus, diagnosis of, 619 types of, 619 cause of, 553 chronic, diagnosis of sprue from, ciliar (Balantidium coli), parasite 44 treatment, 46 (Lamblia intestinalis), treat- ment, 46 mortality from, 44 — • (Tetramitus mesnili), 47 — ■ spread of, factors in, 540 vaccines, bacterial, 602 Dysidrosis exfoliativa, 467 Earth, bacteriology of, 646 Echinococcus granulosus causing cystic form of hydatid disease, 267 dangers of, to man, 268 geographical distribution, 267 life-cycle, 267 morphology, 267 pathogenicity, 268 INDEX 683 Echinococcus multilocularis, geographi- cal distribution, 268 morphology, 268 pathogenicity, 26g producing multilocular form of hydatid disease, 268 Eclipse blindness, 509 Eczema, definition, 467 symptomatology, 467 treatment, 468 varieties, 468 Egypt, percentage of population infected with Schistosoma haematobium, 242 Ehrlich's side-chain theory of protection afforded by sera and vaccines, 601 Elapinse, 423, 428, 431 in America, 434 in Australia, 433 Elapine venom (snake-bite), symptoms, 442 Elaps fulvius (harlequin or coral snake), 427 Elastorrhexis or pseudo-exanthoma, 502 Electrical methods of sterilizing Avater, Electricity and iodides in dengue, 379 Electrolysis in hirsuties, 471 Elephantiasis, 284 arabum, reasons why due to Filaria bancrofti, 287, 288 causes of, 279, 280 ■ of arm, 293 ■ of breast, 291, 293 of legs, 284-287 ■ after operation 286 ■ before operation, 285 symptomatology, 284-287, 293 treatment, 286 of localized areas, 293 of prepuce and legs, 288 of scalp, 293 of sci^otum, 289, 290 complications following opera- tion, 292 291 operation for removal of mass, symptomatology, 290 treatment, 291 of vulva, 292 post-mortem findings, 280 Elephantoid tumour of buttock, 287 Emaciation in cerebral stage of African trypanosomiasis, 14:5 Emetine in amoebic dysentery, 43 in ciliar dysentery (Balantidiam coli), 46 in liver abscess, 54 in sprue, 360 Endemic diseases, 543 , Endo-ectothrix tinea, 489 Endothrix tinea, 489 histolytica in tissues, 37 tetragena of amoebic dysentery, life- history, 31 binary fission, 31 — reproduction by reproduction by — reproduction by spore formation, 31 parasite of amoebic dysenterv. gemmation, 31 Enteritidis group of bacilli, diagnosis of, 618 Eosin-azur for staining malarial parasite in blood, 608 use of, as stain, 604 Eosinophiles, diseases during which in- creased, 605 percentage in normal blood count, 605 Epidemic diseases, sporadic, 543 Epileptiform, a complication of African trypanosomiasis, 146 Epinys norvegicus (Norway rat), plague in, 170 rattus (brown rat), plague in, 170 Epithelial tumours, benign, 495 malignant, 495 Epithelioma of cheek, fungating papillo- matous, 500 Epitheliosis desquamativa (Samoan eye disease), 516 Ergotism, 453 causes of, 572 Erysipelas, treatment, 468 Erythasma, 468 Erythema of verruca peruviana, 364 solare, 468 Erythematous eruptions in African try- panosomiasis, 140 Erythropsia, 509 Espundia, 68, 504. See also Leish- maniasis, naso-oral and oro-pharyn- geal Eucalyptus treatment of ankylostomiasis, 3ig Europe, cholera epidemics, 203-4 Europeans first entering Tropics, liability to typhoid fever, 215 in India, diet of, in relation to in- cidence of typhoid fever, 215 pathological eft'ects of hot climates on, 538 physiological eft'ects of hot climates on, 537 Excreta, chemical method in disposal of, 588, 590 disposal of, 590 Exhaustion (pabulum) theory of protec- tion aftorded by sera and vaccines, 600 Eye conditions, local, resulting in blind- ness, 511 contusions and concussion injuries of, 509 diseases of, 507, 508 local, 509 native treatment of, 529 remedies, various, in, 529 stimulating and astringent remedies in, 526 treatment, 526 142 526 29 lesions in African tr>-panosomiasis, rest in treatment of &\e diseases, traumatisms affecting, 509 F.ECAL carriers of typhoid fever, 214 contamination of waters in India, excessive, 645 F?eces and water, bacteriology during monsoon weather, O46 684 INDEX F.TCcs examination for eggs of Ascaris lumbricoides, 31 1 diagnosis of diseases from, 632 • macroscopic, 632 microscopic, 634 errors in, 6315 helminth ova in, preservation of. 323 648 human and animal, bacteriology of, in sprue, 357 paleness of, causes, 358 Fat, deficient, in aetiology of beriberi. 339 estimation of, in faeces, process, 633 Fats, food value of, 563 Favism, aetiology, 389 definition, 389 distribution, 389 symptomatology, 389 treatment, 389 Febrile or glandular stage in African trypanosomiasis, 140 Fever, daily, in cerebral stage of African trypanosomiasis, 145 in African trypanosomiasis, 140 Fibrin ferment in snake venom, 441 Fibrolipoma, pendulous, of back of neck, 407 , ■ • r Fibrolysin injections in elephantiasis of legs, 286 Fibroma molluscum, 502 multiple, 499 of neck, 495 pendulum, 502 Fibromatous condition of skin, curious example of, 496 Field rat, reservoir host for spirochsetes, Filaria bancrofti, adult, 273 carriers of, 278 cause of elephantiasis arabum, reasons explained, 287, 288 embryo, 274. See also Micro- filaria nocturna life-history, 273 morphology, 272 ovum, 273 carriers of, 294 infections associated with double conjunctivitis, discharging chyle, 294 Filariasis, clinical manifestations, 279 geographical distribution, 278 historical notes, 271 — ; — pathology, 278, 279 Filaridsc, diseases caused by, 271 Filtration of water, 558, 559 Finkler-Prior spirillum, 621 Fish venom, effects of, 447 high mortality from, 448 ■ symptoms, 448 treatment, 448 Fishes, venomous and poisonous, 447 which poison after their consump- tion as food, 448 symptoms, 448 by sjnnes, mortality from wounds of, 448 pain severe after wound from, 448 Five-day fever (\'olhynia fever), 398 Flea, species infesting rats and convey- ing plague, 171 Fleas, alimentary tract of, 178 carriers of plague bacillus, 177 destruction of, 179 external appearance, 177 families of, 179 larvas of, 179 reproduction, method of, 178 Fleming's modification of Wassermann reaction, 6io, 611 Flexner type of dysentery bacillus, 619 Flcxner's process of preparing anti- dysenteric serum, 201 Flies and disease, 223 danger of, to health, manner of infection by, 223 transmission of cholera by, 206 ■ ways in which dangerous to health, preservative test for food, 223 Fluorides, as 579 Fly, biting, in aetiology of pellagra, 332 carriers of typhoid fever, 214 Folliculitis decalvans, 471 treatment, 471 Fomites, transmission of cholera by, 20*5 Food adjuncts, 563 deficiency in aetiology of beriberi, 338-9 in aetiology of pellagra, 329-30 morbid conditions caused by, 571 poisoning in setiology of beriberi, 338 Foods, adulteration of, 569 calorie value of, 565 essential consituents of, 562 tinned, dangers from, 575 Foot, amputation of, for perforating ulcer in lepers, 185 Fordyce's disease, 477 Foreign bodies in eye, 509 Formaldehyde, as preservative test for food, 577 Formalin in sjiirit, a])plication in tricho- mycosis, 495 solutions of, in treatment of African trypanosomiasis, 149 Formic aldehyde for disinfection of houses, 595 Framboesia tropica (yaws), diagnosis, 26 ■ causation, 22 • contagious disease due to Tre- ponema pertenuis, 21 • histopathology, 22 • incubation, 23 infection of by direct contact, 25 primary stage, 23 prodromata, 23 ■ secondary stage, 23 ■ symptomatology, 23 • tertiary stage, 24 three stages in, 23 treatment, 26 Fungi, eye diseases, local, due to, 511 in fEtiology of pellagra, 331 ocular aspergillosis due to, 511 blastomycosis due to, 511 gonosporosis due to, 511 moniliasis due to, 511 INDEX 685 Fungi, ocular nocardiasis due to, 511 sporotrichosis due to, 511 tinea due to, 511 producing madura foot, 478 Funiculitis, endemic, definition, 407 geographical distribution, 407 pathology, 407 symptomatology, 408 treatment, 408 must be surgical, 408 Galvl in framboesia tropica, 27 in treatment of African trypano- somiasis, 148 Gangosa, definition, 404 diagnosis, 405 distribution, 404 late manifestation of yaws, 25 (rhino-pharyngitis mutilans), 404 symptomatology, 404 treatment, 405 Gastro-enteritis, ha^morrhagic febrile, of children, prognosis grave, 403 Gelatin, nutrient, preparation of, 622 l)late cultures, 623 Gemmation, asexual method of reproduc- tion in protozoa, 3 Genosporosis, ocular, due to fungi, 511 Ghee, 568 Glanders, 504 Glanders bacillus, see Bacillus mallei Glossina bocayei, 151 fusca, 151 longipalpis, 151 longipennis, 151 morsitans, 151 carriers of Trypanosoma pecorum, 135 food of, 152 habits of, 152 reproduction of, 15: — pallicera, 151 — pallidipes, 151 — palpalis, 151 food of, 152 habits of, 153 reproduction of, 15: of tachinoides, 151 Glossinae, notes on, 15 1-3 Glossitis areata exfoliativa, 477 Glottis, oedema of, complication African trypanosomiasis, 146 Glucose and lactose broth, preparation of, 622 peptone Avaters, preparation of, 622 Glycerine of tannin in trachoma, 515 Gnathostoma spinigerum rarely found in man, 271 Goitre in the Tropics, 410 Gonococcus, diagnosis of, 620 Goode, Norman, method of cleansing washing water, 560, 561 Goundou, definition, 411 ■ geographical distribution, 411 pathology, 411 symptomatology, 412 treatment, 412 Grain itch, 469 treatment, formula for, 469 Gram-negative and Gram-positive organ- isms, important differentiations in staining, 614 Granules, metachromatic, volutine, and metaplasmic, in protozoa, 3 Granuloma inguinale, treatment, 469 ulcerating, 503, 505 Green, protective colour in prevention of sunstroke, 392 Grooved tongue, 477 Ground-nut, common (Arachis hypogoea), nutritive value of, 564 Ground squirrel, spread of plague by, 171 Guinea-worm, see Dracnncuhis medineti- sis Gynocardic acid in leprosy, 188 H^MADIPSA in a-tiology of hirudiniasis, 324 Hsemato-chyluria, 283 in filariasis, 279 lymphuria, 283 Hsematoxylin and eosin for staining malarial parasites in blood, 608 use of, as stain, 604 Haemoglobin, estimation of, in Tropics, 607 reduced, demonstration by spectro- scope, 612, 613 Haemoglobinuric (blackwater) fever, aetiology, 381 ■ definition, 380 • • distribution, 380 pathology, 384 post-mortem appearances, 386 ■ • symptomiatology, 387 theories relating to, 381 treatment, 388 Hsemolysins in snake venom, 440 Haemolysis due to parasites of malaria, 74 Haemoptysis, endemic, see Paragono- viiasis Haemorrhage in yellow fever, treatment, 371 Haemorrhages, rectal, causing sudden death in spirochaetosis ictero-haemor- rhagica, 18 Hasmorrhagin in snake venom, 441 Haffkine's prophylaxis against plague, 175, 176 vaccine in proph\laxis of plague, 176 Hair affections, 469 colour of, changes in, causes of, 470 poor development of, in natives of Tropics, 458 Hansen's Bacillus leprae, 180 Hardness, total, of water, method of estimating, 654 permanent, of water, method of estimating, 654 temporary, of water, method of estimating, 654 Harris, ulcer of, section of intestine showing in case of amoebic dvsenterv, Hay fever, tropical (rhinitis plasties vasomotoria), 404 686 INDEX Hay fever, tropical, treatment, 404 Health, maintenance of, in Tropics, general rules for, 541 Heart failure cause of sudden death in Asiatic relapsing fever, 15 treatment of, in typhus, 380 Heat as means of disinfection, 593 exhaustion, 530 stroke (sunstroke), aetiology, 391 and heat syncope, differences between, 390 causation, theories as to, 391 definition, 391 diagnosis, 394 (direct), 391 ■ (indirect), 393 . mortality, 393 prophylaxis against, 392 results of, 392 • symptomatology, 392 treatment, 394 syncope, 389 aetiology, 390 definition, 390 • symptomatology, 390 treatment, 391 Heating in sterilization of water, ^58 Helminth ova in faeces, preservation of, 323. . . Helminthiasis, complication of African trypanosomiasis, 146 Helminths, diseases due to, 226 distribution, 228 factors controlling, 228 grouping of, 231 mode of infection by, 320 ■ nomenclature, 230 pathogenic action, variation of, 229 preservation and examination of. ^21-2 . toxic, 449 Herpetomonas, 5 Hindu water-carriers, vessels used by, 552 Hirsuties, 471 treatment, 471 Hirudiniasis, aetiology, 324 definition, 323 • symptomatologx', 324 treatment, 324 Histoplasma capsulatum, 6 date of discovery, 6 diseases caused by, 6 habitat, 6 Horny growth from cheek, 504 Horse, preparation of antitoxic sera from, 599 serum, immune in spirochtetosis icterohaemorrhagica, 19 Horsley, Sir Victor, death of, from heat stroke, 393 Hot-air sterilizer, 622 Hot climates, pathological effects on Europeans, 538 , physiological effects on Euro- peans, 537 House-fly (Musca domestica), enemies of, 225 habits, &c., of, 224 how man is infected by, 225 ways of suppression of, 225 Houses, disinfection of, fumigation as means of, 595 suitable, construction in tropical districts, 535, 536 Hughes, Basil, method of cleansing washing water, 560, 561 Humerus, chondrosarcoma of, 498 Hydatid disease, cystic form of, due to infection by Echinococcus granulosus, 267 multilocular form of, pro- duced by Echinococcus multilocularis, 268 Hydrocele, see Orchitis and hydrocele , filarial Hydrochloric acid in sprue, 360 Hydrochloride (emetine) in amoebic dys- entery, 42 Hydrophinae, 425 ■ genera of, 426 in Australia, 433 Hydrophine venom (snake bite), sym- ptoms, 442 Hydrophis coronatus, photograph of, 424 Hygiene, constitutional, 535 relation to tropical diseases, 539 Hymenolepis diminuta common to rats and mice, 263 nana, dwarf tapeworm of man, 263 ■ intestinal irritation and anaemia resulting from infection by, in children, 263 Hyperaesthesia, deep, in African trypano- somiasis, 142 in cerebral stage of African trypano- somiasis, 145 Hyperkeratosis, 495 Hyperpyrexial fever, high mortality in, 396 Hyphomycetes, divisions of, 630 ICHTHYOL in acrodermatitis vesiculosis tropica, 460 in climatic bubo, 411 in filarial lymphangitis, 281 ointment, application to Calabar swellings, 300 Ichthyosis glossae, 477 hystrix, 473 treatment, 473 simplex, 473 Immunity, acquired, definition, 598 active, 16:5 • natural, 165 definition, 598 passive, 165 theories of, 163 to diseases afforded by vaccines and sera, 601 Impetigo, 473 treatment, 473 Incubation of trypanosomiasis, African incubation, 139 India, bacterial standards for purity of drinking water in, 649 deaths from snake bite annually in, 419 diet of natives and Europeans con- trasted in relation to incidence of typhoid fever, 215 IXDEX 687 India, standard for bacteriological ex- amination of water in, 645, 646 waters of, faecal contamination ev- cessive, 6415 Infant feeding in Tropics, 580 table for, 580 foods, prepared, dangers of, 581 Infants, biliary cirrhosis in, 409 Infective diseases, common, some prophy- lactic measures for, 598 Infectivity theory in aetiology of pellagra, 331 Influenza, diagnosis of phlebotomus fever from, 361 Injections, local, in snake bite, 446 preservative, for preservation of meat, 575 Insecticides, ^94 Insects, eye diseases (local), due to, 510 how infected with animal parasites, 7 Intertrigo saccharoraycetica, 473 ■ treatment, 473 Intestinal disorders, dietetic causes of, symptoms and lesions of ascariasis. 3". Intestine, elimination of toxins b>', in yellow fever, 371 great, lesions of amcebic dysentery ^^' .3*^. irrigation of, in intestinal schisto- somiasis, 256 with sodium hypochloride or tannic acid in schistosomiasis, 256 sections from, in case of amoebic dysenterv, showing ulcer of Harris, 38 Intestines, post-mortem appearances of, in schistosomiasis infected with S. japonicum, 252, 253 Iodides in granuloma inguinale, 469 in sporotrichosis, 488 Iodine, tincture of, application in dif- ferent forms of tinea (ringworm), 490, 491, 493, 494 . Iodoform injections in lein'osy, 189 suppositories in oxyuriasis, 313 Ipecacuanha in ciliar dysentery (Balan- tidium coli), 46 in amoebic dysentery, 43 in hepatitis in liver abscess, 55 in sprue, 360 Irido-cyclitis in cerebral stage of African trypanosomiasis, 146 Iritis, complication of African trypano- somiasis, 146 Iron in afebrile splenomegaly, 417 in water, method of estimating, 655 water pipes, diminution in dia- meter, 552 Irrigation, regulations regarding, in the Soudan, 534 Ixodidse (tick), spirochsetes of, African tick fever transmitted by, 19 Jails, _ planning and construction, in tropical districts, 536 Japanese river fever, aetiology, 394 Japanese river fever and spotted fever of Rockv Mountains, similarity between, distribution, 394 — — ■ (Tsutsugamushi disease), definition, 394 mortality, 395 • symptomatology, 395 treatment, 395 Jaundice not due to increased formation of bile in spirochaetosis icterohaemor- rhagica, 18 Jaw, lower, cystic bone, sarcoma (mye- loid ?) of, 499 sarcoma of (? myeloid), 497 Jelly fish, sting from, symptoms, 449 venomous, 448 Jiggers, complication of African trypano- somiasis, 146 Kala-azar, aetiology, 56 and oriental sore, differentiation be- tween, 66-68 blood in, 60 • definition, ,6 diagnosis. 60 geographical distribution, 56 history, 56 incubation, 58 infantile, aetiology, 62 antimony, 63 — - complications, 62 definition, 61 ■ distribution, 61 symptomatology, 62 synonyms, 61 morbid anatomy, 60 prognosis, 60 symptoms, 59 termination, 59 transmission, mode of, 8 treatment, 61 prescription in, 61 see also Pseudo-kala-azar Kaposi's disease (Xerodermia pigmen- tosum), 474 Kcrandal's cure for African trypano- somiasis, 150 sign in African trypanosomiasis, 142 Keratoma plantare sulcatum, 474 ■ treatment, 474 Keratomalacia, 510 Keratosis pilaris, treatment, 473 (xerodermia), 473 Khartoum, bacteriological examination of river and well water in, 642, 643 Kidney, most venom excreted by, in snake bite, 445 Kidneys, elimination of toxins by, in yellow^ fever, 371 in blackwater fever, 386 Klcbs-Loffler bacillus. See Bacillus diphtheri(s Klein's protective inoculation prepared from organs of animals dead of plague, 177 advantages, 177 Knee, acute synovitis of, associated with filaria infection, 294 688 INDEX Koch's comma bacillus, 62 1 cause of cholera, 205 Kraurosis vulvic, 477 Krcotoxismus, 45 ^ treatment, 45s Laboratory, hints for work in, 603 Lacertilia, 423 Lactose fermenting organisms in water, test for, 643 Lake water, bacteriology of, 648 Lakes, purity of, 547 water supplies from, 547 Lamblia intestinalis, 5, 47 parasite of ciliar dysentery, 46 Lamus megistus as agent in spreading South American trypanosomiasis, 154 Lanoline, amplication in ichthyosis hystrix, 473 ointment in filarial lymphangitis, 281 Laryngitis, complication of African try- panosomiasis, 146 Latah, geographical distribution, 406 symptomatology, 406, 407 Lathyrismus, 453 causes of, 572 symptoms, 453, 454 treatment, 454 when endemic and when epidemic, 453 Latrines, Chinese, 587 European, 588 for troops in the field, chemical method, 588 in tropics, 1585 Indian, 588 native, 585 separation system in, 587, 588 river, practice of, insanitary, 586 Lead and opium lotion in filarial lym- phangitis, 281 in filarial orchitis and hydrocele, 281 dissolution from water pipes by peaty water, 5:52 — in water, method of estimating, 655 lotion, application in climatic bubo. 411 Leeches, land and water, in aetiology of Hirudiniasis, 324 Legs, elephantiasis of, 284-287, 293 Leishman-Donovan parasite of kala-azar, r 5.7 Leishmania, 6 Leishmaniases, 55 Leishmaniasis, canine, 68 acute and chronic, 69 dermal (oriental sore), 63 aetiology, 63 definition, 63 diagnosis, 65 points to be noted in, 65 distribution, 63 histopathology, 63 prognosis, 65 symptomatology, 64 treatment, 66 naso-oral and oro-pharyngeal, 68 symptoms, 68 treatment, 68 Leishman's stain, 604 for staining malarial parasite in blood, 608 Leproline in leprosy, i8g Leprosy, Eesthctic, macular in, 187 deformities in, 184 variety, 186 antitoxic serum in, 599 bacillus, 180 definition, 179 geographical distribution, 180 history, 179 how spread, 181 little influenced by climatic and tropical conditions, 540 — mixed variety, 188 — nodular, in Hindoo woman, 183 — pathology, 181 — post-mortem appearances, 182 — prognosis, 188 — symptomatology, 182-3 — treatment, 188 tubercular variety, 184, 186 Leptothrix, 471 treatment, 471 Leucocytes in lymphatic leukaemia, 606 percentage in normal blood count, 605 total, diseases during which diminished, 605 Leucocytosis in blackwater fever, 387 in verruga peruviana, 364 ' Leucocytozoida?, 5 Leucoderma, 474 treatment, 474 Leucolysins in snake venom, 441 Leucopenia in dengue, 3,77 in sprue, 357 . Leukaemia, lymphatic, leucocytes in, 606 spleno-meclullary, myelocytes in, 606 Leukoplakia of tongue, 477 varieties, 477 Lice, venom of, 451 Lichen convex, 474 treatment, 474 planus, 4715 treatment, 475 external, formula for, 475 ■ formula for, 475 Ligature in snake bite, 445 Lightning causing blindness, 510 Lime, chloride of, use in purification of water, 5 55 chlorinated, for purification of ^vater, 5 56 Limnatis in a!tiology of Hirudiniasis, .324 Li]5omatosis, nodular, 483 Licj[uor arsenicalis in pellagra, 336 plumbi a])plication to Calabar swellings, 300 Liver abscess, causation, 48 diagnosis, 52 high mortality, 53 in amoebic dysentery, 50 incidence, 48 — operation for, after-treatment. 54 method of, 53 pathology, 50 INDEX 689 Liver abscess, position, 48 spontaneous rupture of, 52 symptomatology, 51 termination, 52 ■ treatment, 53 — varieties, 48 abscesses of, multiple, ania^bic, 49 condition in yellow fever, 367 in blackwater fever, 386 microscopical appearance in African trypanosomiasis, 139 post-mortem appearances of, in schistosomiasis infected with S. japoni- cum, 252 tropical, 414 parasite of dermal leish- maniasis, 63 sym]5tomatology, 414 treatment, 55, 414 prescription for, 414 Lizards, venomous, 4^3 Loa loa, carrier of, 298 causative parasite of loasis, 296 habits, 298 • illustrations of, 296, 297, 298 life-history, 298 morphology, 296, 297, 298 Loasis, causative parasite, 296 definition, 295 geographical distribution, 295 symptomatology, 299 treatment, 299 Lolismus, 454 Loos hypothesis of schistosomiasis, con- clusions as to prevention and treatment based on, 249-250 theory of, relating to S. mansoni. Lotions, application to tropical ulcera- tions, 505 Low intermittent non-malarial fever, long course of, 396 symptomatology, 396 Lungs, microscopical appearance in African trypanosomiasis, 139 Lupus erythematosus, differentiation from lupus vulgaris, 475 treatment, 476 Lustig's and Galeotti's serum in prophy- laxis of plague, 176 Lymphangiectasis, filarial, definition, 281 symptomatology-, 281 treatment, 282 Lymphangiomata, 502 Lymphangitis, filarial, definition, 280 post-mortem findings, 280 symptomatology, 281 treatment, 281 Lymphatic glands, fibrosis, in filariasis. 279 142 in African trypanosomiasis, in cerebral stage of African trypanosomiasis, 145 microscopical appearance m African tryjianosomiasis, 139 varicose, 282 treatment, 2S2 — tissue, bacilli of typhoid chiefly invading, 216 fever Lymphocele, 284 Lymphoc\tes, diseases in which in- creased, 605 percentage in norma i blood count,, 605 Lymphoderma perniciosum, 502 Lymjihuria. See Chyluria and lyvi- -phnria Lysol as disinfectant, 594 Macgregor, Sir William, plan of pro- tected well suggested by, 550 Maculae in aesthetic leprosx", 187 Macular fever of Tunisia, definition, 397 symptomatology, 397 Mahommedan water-carriers, infection of water by, 551 Maiche automatic sterilizer, 558 Maignen's process for softening water. Maize theory in a?tiology of pellagra^ 330-1 Malaria, 69 aetiology, exciting causes, 71, 72 predisposing causes, ~o carriers of, 69 ■ complication of African trypano- somiasis, 146 cure of, possible future method, 74 definition, 69 diagnosis of phlebotomus fever from, 361 eradication of, l)y ciuinine in pre- vention of h?emoglobinuria fever, 384 • history of, 69, 70 parasites of, 69, 71, 72 behaviour in blood, 72, 73 ha;molytic action, 74 infection by, mode of, 8 intracorporeal or human cycle,. 74 life-cycle, 75 life-history, 72, 73 — pernicious manifestations of, in- brain and pancreas, 74 — preceding t\'phoid fever in the- tropics, 217 — prevalence of, conditions favouring,. 540 — recurrent attacks of, followed by blackwater fever, 387 subtertian and blackwater fever,. relation between, 384 diagnosis of yellow fever from,. 370 symptoms, general, 69 Malarial fever, factors necessary for an attack of, 72 large mononuclears increased during, 605 phases of related to phases of life-cycle of parasite, 72 ciuartan, parasite causing, "jz — '_ tertian, parasite causing, 73 infection, active, theory that ha2mo- globinuric fever is manifestation of, 381 previous theory that haemo- globinuric fever is condition brought about by, 383 — pigment, constituents of, 628 690 INDEX Malarial pigment, where it is and how to look for it, 628 pigments, manner of showing in laboratory work, 629 Male, adult, not engaged in hard work, average diet for, 564 fern in hymenolepis nana, 263 in intestinal schistosomiasis, 256 in schistosomiasis, 248, 256 in tapeworms, 269 Malignant connective tissue tumours, 502 Malta fever, diagnosis of phlebotomus fever from, 361 — — ■ see also Undulaiit fever Manchineel tree fruit, poisoning by, 454 Manchuria, pneumonic plague in, how started, 171 Mania in cerebral stage of African try- panosomiasis, 145 Manson, Sir Patrick, reasons for elephan- tiasis arabum being due to Filariaban- crofti, 287, 288 Massage in dengue, 379 in elephantiasis of legs, 286 of scrotum, 291 Mast cells, 605 staining of, 605 Mastigophora (flagellata), 4 Measles in tropical countries, 401 Meat, decomposed, results from con- sumption of, 572 diet in sprue, 359 extracts, limited use of, 567 stimulating but not nutritious, 566 frozen, means of testing, 573 inspection and high cooking in, pro- phylaxis against trichiniasis, 309 — preservation of, 574 methods, S/S native method, 575 preserved, means of testing, 573 Meats, examination of, 572 Medical ofticer, control of water by, 553 Memory, loss of, in tropical regions, 539 Men, women and children, food necessary for, compared, 564 Meningitis, cerebro-spinal, a complica- tion of African tryijanosomiasis, 146 sunstroke, a form of, 393 Meningococcus, diagnosis of, 620 Menstruation in cerebral stage of African trypanosomiasis, 145 Mercurial ointment in oxyuriasis, 313 Mercury, atoxylate of, in treatment of African trypanosomiasis, 148 solutions of, in treatment of African trypanosomiasis, 149 Metals, poisonous, in water, detection and estimation of, 655 Metchnikoff, jihagocytic theory of, 600 Methremoglobin, demonstration by spec- troscope, 613 Methylene blue in ciliar dysentery (Balan- tidium coli), 46 ^ — Loeffler's, use of, as stain, 604 Mucorinal, diagnosis, 630 Micrococcus melitensis, cause of undulant fever, 190-1 Micrococcus melitensis, diagnosis of, 620 Microfilaria demarquayi, film prepara- tion, 276 diagnosis of, points of value in, 277 infection of man, dangerous elements in, 276 loa, film preparation, 275 ■ nocturna, 274 habits in man, 274 habits in mosquito, 275 perstans, film preparation, 275 various species of, differentiation, 277 Microfilarije, examination of fresh blood for, 610 Micro-organisms, diagnosis of, 615 examination of, 613 staining of, 613 Microsporon audouini (ringworm), 631 A/Iicrosporons, 489 and trichopytons, tween, 489 Milk, adulteration of, rence in the tropics, buffaloes, 568 condensed, 568 decomposed, results from consump- tion of, 572 diet in si^ruc, 358 dried, 568 food value of, 567 goats', 568 — — heating of, 567 homogenized, 568 infected, results from consumption differences be- common 569 occur- of ) :>/■ manipulations of, skimmed, 568 ■ dried, 568 sour Bulgarian, D/^ use of, for thera- peutic purposes, 631 transmission of, cholera by, 206 of Mineral acidosis, theory in aetiology of pellagra, 332-3 or chemical constituents of water, ill-effects of, 553 • waters, 584 Molasses and botassa in milk, tests for, 569 Moles, epithelial, 49, Molluscs essential for transmission bilharzia, 543 Molluscum contagiosum, 495 Mongolian spots, 476 Alonilia vaccines in sprue, 360 Moniliasis, ocular, due to fungi. Monilethrix, 471 Mononuclears, large malarial fever, G05 l^ercentagc :ii increased normal in during l)lood count, C05 Monsoon weather, bacteriology of water and fasces during, 646 Montana, spotted fever of Rocky Moun- tains in, mortality and prophylaxis against, 376 Morphia for relief in griping in amoebic dysentery, 42 in sprue, 360 Morphine injector's septicaemia, 415, 416. See also ]Vhit]iiore's disease INDEX 691 }vlosquito destruction as prophylactic measure against yellow fever, 372 habits of, microfilaria in, 275 Mosquitoes, destruction of, 596 dissection of, 638 time of day at which biting, 71 venom of, 453 Muco-enteritis, from drinking water con- taining non-pathogenic bacteria, 553 Mucorinal, diagnosis of, 630 Mucous membrane, pathological skin conditions affecting, 476 Mucus in faeces, examination of, 632 Muraena (fish poisonous by bite), 447 Musca domestica, 224. See: also House--fly Muscles, calcification of Trichinella spiralis in, 308 Mussurana, enemy of venomous snakes, 447 Mycetoma (Madura foot), 478 aetiology and pathology, 470 478 fungi producing, 478 geographical distribution, symptomatology, 480 treatment, 482 varieties, 481 Mycosis fungoides, 502 Mydriatics and cycloplegics in c\e dis- eases, 52 Myelocene, inunctions in keratosis pilaris, 473 Myelocytes in spleno-medullary leu- kaemia, 606 Myiasis, 482, 483 kinds of flies causing, 482, 483 Alyocarditis considerable in typhoid fever in the tropics, 218 European, fatal complication of European relapsing fever, 11 Myocardium, section from cases of beri- beri, 33Q, 340, 341- Myomata, 502 Myotics in eye diseases, 528 Xaja, species of, in Africa, 431, 432 bungarus (king cobra), mortality caused by, 429 fasciatus, characteristics of, 428, 429 tripudians (cobra-di-capello), photo- graph of, 425 _ Xaphthalin suppositories in oxyuriasis, 313 Nasha fever, symptomatology, 396 treatment, 396 " Nastin " for leprosy, 188 Xecator americanus, 314-5 points of difference between the Ankylostome duodenale and, 320 Xeck, fibroma of, 496 pendulous fibroma of back of, 497 sarcoma of, 500 Negroes, immunity of, from sunstroke causes, 391 Nemathelmia (group of helminths), 231 Nematodes, morphology, 270 pathogenic to man, 270 preservation and examination of, 270, 321-2 X'^eosalvarsan in f ramboesia tropica ; in- jection, intramuscular, 27 intravenous, 26 in granuloma inguinale, 469 in treatment of African trypano- somiasis, 148 Neosporidia, 5, 6 Nerve symptoms in typhus, drugs in, 380 Nervous symptoms in South American trypanosomiasis, 157 — system, disturbances of, in tropics, 405 Neurasthenia, tropical, 405 Neuritis, peripheral, endemic, 406 Xeurofibrosis of Recklinghausen, 502 Neurotoxins, in snake venom, import- ance of, 440 Night blindness, 509 Nitrates in water, detection of, tests, 656, 657 estimation of, methods, 656,. 657, 658 — in milk. test for, 569 beri- Nitrogen, deficient, in aetiology of beri, 338-g estimation of, in faeces, process, 633 — -_ — ingestion of, 565 Nitrogenous foods, necessity for, 562, 563- Nocardiasis, ocular, due to fungi, 511 Nodes, juxta-articular, 473 Nomenclature, international rules of, 230 language, rule of, 230 rule of, appropriateness, 231 priority, 231 Nourishment, average, for man, 565 Nucleus of protozoa, 3 Nutrnegs poisonous in large doses, 454 Nutrient media, vessels used for, 621 Nutrition, 562 O2, absorption in sewage, rate of, after filtration, 662 Oatmeal jelly in infant feeding, 581 (Edema in cerebral stage of African try- panosomiasis, 146 localized, in African trypanoso- miasis, 142 Ointments, application in different forms of tinea (ringworm), 490-494 nourishing application in alopecia, 470 Oleate of iodine, hot fomentations on, for tropical fever, 55 Oleum chenopodii treatment of ankylo- stomiasis, 319-20 Onchocera (filaria) volvulus, life history, 300 morphology, 300 ^ pathogenicity, 300 Onyalai, aetiology, 417 definition, 416 geographical distribution, 417 symptomatology, 417 treatment, 417 Ophidia, 423 Ophthalmic irritation, 510 • resulting from exposure to wind and dust, 510 Opisthoglypha, 423 Opium contra-indicated in yellow fever, 37^ 69^ INDEX Opium, tincture of, in ama^bic dysentery, 43 Opsonic index, 164, 600 definition of, 164 Opsonin, 600 ■Orchitis and hydrocele, filarial, s\mpto- matology, 281 Oriental sore, 504 Ornithodorus moubata (tick) found throughout tro|)ical Africa, ig Orpimcnt in treatment of African tr\-- panosomiasis, 148 Ova, detection in fceces, 637 Ovary, carcinoma of, 502 Oxalate poisoning in aetiology of beri- beri, 337 Oxidation, water rendered potable by, 561 Oxidizable organic matter in water, method of estimating, 658 Oxyhsemoglobin, demonstration by spec- troscope, 612 Oxyuriasis, 312 parasite causing, 312 symptomatology, 313 treatment, 313 vermicularis, morphology and life- history, 312 ova of, 637 parasite causing, 31: Oysters, cholera and tyi^hoid fever re- sulting from eating, 572 Ozone, sterilization of water by, 556 Facet's disease of nipple, 495 Paints, application to mouth in sprue, 360 Pancreas, pernicious manifestation of malaria in, 74 Pancreatin in sprue, 360 Pancreatitis, chronic, diagnosis of sprue from, 358 Pandemic diseases, 543 Papalismus, 454 Papular fever, symptomatology, 403 treatment, 379 Paragonimiasis (endemic haemoptysis), definition, 240 diagnosis, 242 distribution, 240 morphology, 241 parasite of, 240 pathology, 241 symptomatology, 242 treatment, 209, 242 Paralysis, general, late manifestation of yaws, 25 Parasites, animal and vegetable, stain- ing for, 604 eye diseases, local, due to, 511 in aetiology of pellagra, 331 infection of insects with, how effected, 7 demonstration in laboratory work, 626 — in haemoglobinuric fever, ciuestion of, 382 — macroscopic examination of faeces for, 634 — malarial, benign tertian, 609 in blood, staining of, 607, 608 in brain, mounting and stain- Parasites, malarial, in brain, manner of showing in laboratory work, 627 living, demonstration of, 607 Ciuartan, 609 subtertian, aestivo-autumnal or malignant, 609 varieties of, 609 vegetable m £Etiology of pellagra, causes in aetiology of beriberi, ing section, 627 331 Parasitic 340 theory in aetiology of pellagra, 331 Paris Convention (1903), International regulations to prevent importation of cholera, plague and yellow fever, 596-98 Parotid timiour, mixed, 501 Parrots, epizootic fatal among, 189. See also Psittacosis Parthogenesis in protozoa, 4 Pasteur-Chamberland filter, 558 use in phlebotomus fever, 361 Peat, avoidance of, in catchment areas for water supplies, 547 in water, effect on leaden pipes, 552 Pediculosis, 483 pathology, 483 treatment, 484 Pellagra, jetiology, 329 deficiency disease, 572 definition, 329 diagnosis, 335 eruption of, predisposing factor, 540 geographical distribution, 329 • pathology, 333 prognosis, 335-6 ■ seasonal prevalence, 540 symptomatology, 333-5 treatment, 336 • dietetic, 336 Pemphigus contagiosus, 484 treatment, 484 Penicilliaceae, diagnosis of, 630 Penicilliosis, 485 Peptone waters, glucose and lactose, pre- paration of, 622 Perforation in typhoid fever in the tropics, signs of, 219 Peritonitis, fatal in ascariasis, 311 in severe trichiniasis, 308 Perleche, 478 Permanganate pills in cholera, 209, 210 Perspiration, importance of, in tropical climates, 537 Phagedaena (tropical sloughing), 485 treatment, 485 Phagocytes, 164 Phagocytic theory of protection formed by vaccines and sera, 600 Phagocytosis, 164 Phenacetin in yellow fever, 371 Phlebectasis, filarial, 282 Phlebotomus fever, setiology, 361 carrier of, 361, 362 definition, 360 diagnosis, 361 — dift'erential, 361 geogra))hical and seasonal dis- tribution, 360, 361 symptoms, 361 INDEX 693 Phlebotomus fever, treatment, 361 papatasii, carrier of phlebotomus fever, 362 characters, habits. 362 life-historv and Phosphorus, in food, deficient, in aetiology ■ of beriberi, ssg Photodynamic theory in aetiology of pel- lagra, 330-1 Pickles for preservation of meat, 575 Piedra, 471 treatment, 485 Pigmentary fever, 395 Pigmentation of viscera explained, 72 Pinguecula resulting from wind and dust, 510 Pinta (carate), 485 symptoms, 485 treatment, 486 Pits as latrines for natives, 585 deep, as latrines for Europeans, 5? for natives, 586 in malaria, how exposure to Pityriasis rubra ; see Dermatitis exfolia- tiva versicolor ; see Tinea versicolor Plague, 165 abortion in, 173 ambulatory, 174 antitoxic serum in, value, 599 bacillus causing, 168 blood changes in, 173 bubo, inguinal, external appearance, 173 of. bubonic, 167, 174 - transmission to man, mode '/ j where . 171 carrier of, 171 cause of death in, — historical memoranda, 166 — in rats, acute, i6g, 170 — chronic, i6g, 170 — incubation period, 172 — introduction into countries obliterated, 543 — mode of onset, 173 — mortality, 174 — or cholera on infected ships, quaran- tine measures respecting, 597 — pathology, 171, 172 — pneumonic, 167 in Manchuria, how started, 171 primary infection in, 172 primary and secondary, 174 transmission, mode of, 171 post-mortem appearances, 172 prodromal symptoms, 172 prophylaxis against, private, public, 175 176 — septicsemic, general features, 174 — ; species of rat principallv infected with, 170 resistant to, 171 — spread of, by ground squirrel, 171 by rats, 167 conditions favouring, 539 — symptomatology, 172, 173 — transmission from one species of rat to another, 170 — vaccine, effect on case mortality, 601 Plague, varieties of, general characteris- tics, 174 Plasmodium malariae, cause of quartan malarial fever, j^ vivax, cause of tertian malarial fever, 73 Platyhelmia (group of helminths), 231 Pneumonia a complication of African trypanosomiasis, 146 lobular and lobar, in pneumonic plague, 172 Podophyllin in treatment of tapeworms, 269 Poikiloxytosis, 606 Poison ordeals, 456 Poisons for animals, 457 for fish, 457 taken accidentally by man, 453 Polychromatic cells, (3o6 Polymori^honuclears, percentage in nor- mal blood count, 6ot when increased physiologically and when pathologically, 605 Polyneuritis, sciatic nerve of fowl suffer- ing from, 342 Ponos, limited to young children, 413 resemblance to biliary cirrhosis, 413 symptomatology, 414 Popliteal nerve in case of acute beri- beri, 342 Pork, inspection in proph\laxis against trichiniasis, 309 Porocephalosis, geographical distribution, 325 pathology, 325 symptomatology, 325 Porter-Clarke process for softening water, 555 I^otash, permanganate of, sterilization of water by, 557 Potassium iodides in blastomycosis, 462 in framboesia tropica, 27 salts, vegetable products rich in, 563 " Poudrette " method in disposal of ex- creta, 590 Precipitins, action of, 600 Prepuce and legs, elephantiasis of, 288 Preservatives, chemical, 576 external, for preservation of meat, 57S Prickly heat, 486 aetiology, theories as to, 486 treatment, 486, 487 Protargol in amoebic dysentery, 43 ointment for ulcerative lesions in framboesia tropica, 27 Protein deficiency theorv in cTetiology of pellagra, 331 foods, proprietarv, constituents of, 567 Proteolytic ferments, 441 probability of, in snake venom, 44, 441 Proteroglypha, 423 Protozoa as factors in causation of tropical diseases, 2 classification, 4 definition, 2 diseases due to, i life-history, 3 morphology, 3 694 INDEX Protozoa, of pathogenic significance in man, 5 origin of infection by, 2 reproduction asexual, 3 methods of, 3 transmission of, 2 Protozoal diseases, modes of transmis- sion, 7, 8 Protozoology, introduction to, 2 Pseudo-Banti's disease, 417. See also Splenoinegaly, afebrile Pseudo-kala-azar, definition, 69 geographical distribution, 6q prognosis, 69 symptoms, 69 Pseudo-myxoedematous symptoms in chronic stage of South American try- panosomiasis, 156 Pseudopelade, 471 Pseudoxanthoma or elastorrhexis, 502 Psittacosis, aetiology of, 189 definition, 189 pathology, 190 sypmtomatology, 190 treatment, 190 Psoriasis, 487 - treatment, 487 Pterygium, 510 resulting from exposure to wind and dust, 510 Pulex irritans, transmission of plague by, Pulse in typhoid fever m the tropics, Pus, spontaneous evacuation of, in liver abscess, positions of, dangers, 52 Pylorus, carcinoma of, 502 Pyosis Corletti (1915), 484 treatment, 485 palmaris, 487 Pyrethrum powder as protection against Ornithodorus moubata, 21 Pyrexia, charts of, in undulant fever, 192-3 Quarantine, 596 Quartz lamp in sterilization of water, 558 Quassia, rectal injections in oxyuriasis, Quinine bihydrochloride m chronic stages of amoebic dysentery, 43 in chyluria and lymphuria, 284 intestinal irrigation Avith, in ciliar dysentery (Balantidium coli), 46 poisoning, theory that haemoglobin- uric fever is result of, 381 Radiotherapy in granuloma inguinale, 469 Radium, in varicose, Ivmphatic glands, 282 Rainfall, 533 annual, estimation of, 546 as predisposing cause of malaria, 71 Rain-water, storage of, 54O collection of, 545 rejection of roof-washings, 546 Rash in typhoid fever in the tropics, 217 Rat-bite fever, aetiology, 398 definition, 398 geographical distribution, 398 Rat-bite fever, mortalit\- in, 398 symptomatology, 398 treatment, 398 Rats, destruction in prophylaxis of trichiniasis, 309 extermination of, 596 • plague in, 169, 170 species principally infected with plague, 170 resistant to i^lague, 171 — spread of plague by, 167 — transmission of plague from one species to another, 170 Trichinella spiralis parasitic in, 308 Recklinghausen, neurofibrosis of, 502 Rectitis, gangrenous epidemic, cause of death in, 409 ■ definition, 408 prevalence among chil- dren of natives and animals, 408 symptomatology, 408 . — treatment for animals m, 14 and children, 409 Refrigeration for preservation of meat, Refuse, collection, removal and disposal of, in tropics, 584 dry, disposal of, in tropics, 592 Relapsing fever, American, 13 Asiatic, 13 -, cause of sudden death in^ IS mortality, 15 • parasite causing, 13 percentage of relapses symptoms, 14 treatment, 15 cause of, 9 diagnosis, 12 diiTerential, 12 of yellow fever from, 37O" European, cause of. 10 — ■ ■ causes of death in, 12 — ■ ■ complications, 11 incubation, 10 infection, transmission- from mother to foetus, ic morbid anatomy, 13 parasite of, 10 prognosis, 12 prophylaxis, 13 relapse in, 11 symptomatology, 10, 11 treatment, 12 of symptoms, 12 geographical distribution, 9 ■ — — history of, 9 parasite of, carrier, 10 transmission, mode of, 8, 9 Reptiles, classification, 423 cranial skeletons of, 422 general features, 419 geographical distribution and iiecu- liarities, 427, 428 heads of, 420, 421 poisonous, manner of striking prey. 436 venom apparatus of, 435 vield of venom of various species, 436, 437, 438 INDEX C^95 Reservoirs, construction of, 552 points to be watched before, 55- . , , — — filtration of water in, mctliod, 559 pipe-supply of water froni, 552 Resorcin and salicylic acid, spirit lotion of, for removal of horny masses in elephantiasis of legs, 286 application in different forms of tinea (ringworm), 491, 492, 493, 494 ointment, ap]ilication in xanthoma areatum, 506 Respiration, effects of tropical climates on, 537 Rhinitis spastica vasomotoria. See Hay ft'7>er, tropical Rhino-pharyngitis mutilans. See G{i?i- Rhinosporidiosis, geographical distribu- tion, 7 treatment, 7 Rhinosporidium seebcri, habitat, 7 Rhizoplast in protozoa, 3 Rice, nutritive value of, 564, 565 Rickets, dietetic causes of, 571 Ringworm, diagnosis of, 630 fungi, families of, 489 (tinea), appearance of lesion, 489 varieties of, 490-494 lesions and regions of body attacked, 490-494 treatment, 494 See also Tinea River water in Khartoum, bacteriological examination, 642 River waters, classification for drinking purposes, 649, 650 tropical, purity of, 547 Rivers, shallow, avoidance for water supply, 547 Rocky Mountains, spotted fever of, 374 Rodent ulcer, 495 Rogers' method in treatment of para- gonimiasis, 209 09, in treatment of cholera, 2 210 Russell's viper, 431 fatality of bite of, 442 Saccharin, test for, 59 Saccharomyces cerevisiae, 631 pastorianus (wild yeast), 631 Salamanders, venomous, toxicity of, 448 Salicylic acid, application in ichthyosis hystrix, 473 as preservative, test for, 578 Saline purgatives in Nasha fever, 396 solution, intravenous injection in cholera, 210 • isotonic, 613 and hypertonic, compared results, 211 Salines in ciliar dysentery (Balantidium . coli), 46 in snake bite, 441; normal, in blackwater fever, 388 Salisbury cure, in sjMaie, 359 Salol in chyluria and hmphuria, 284 Salt solution, rectal injections in oxyu- riasis, 3n 44 Salt water, distillation of, to obtain drinking water, 544 Salts, uses of, in body, 563 Salvarsan in chappa, 413 in framboesia tropica, 26 in treatment of African trypano- somiasis, 148 Sambon, theor\- of, relating to .S". t/ian- so)ii, 254 Sand filters, mechanical, z,()u Sanitation in tropics, 584 Santonin in ascariasis, 311 in oxyuriasis, 313 in sprue, 359, 360 Saponin, dangers of, in mineral waters, 584 Sarcina?, arrangement, 162 Sarcocystis lindemanni, 6 muris, 6 tenellas buboli, habitat, 6 Sarcodina (Rhizopoda), 4, 5 Sarcoma (myeloid ?) of lower jaw, 497 of neck, 500 see also Bone sarcoma Sarcomatosis, multiple, 502 Sarcosporidiosis, 7 Sardines, dangers of, 572 Sausages, nutrition in, 567 Scabies, 487 treatment, 487 Seal]), elephantiasis of, 293 Scarlet fever, no spread of, in tropics, 401 Schistosoma haematobium, infection in schistosomiasis, incubation time of, 248, 249 symptomatolog\', 248 treatment, 248 life-history, 244 — mori3holog\- of male and female, 243 ova of, 243, 637 — ■ percentage of population of Egypt infected with, 242 — japonicum from dog, 251 infection in schistosomiasis, 251 diagnosis, 254 geographical distribution, 251 ova of, 637 pathology, 252 prognosis bad, 254 schistosomiasis spread by, 2^1 symptomatology, 254 treatment, 254 — mansoni, infection in schistoso- miasis, theory of Loos, 255 theorv of Sambon. 254 ova of, 637 Schistosomiasis, causative parasites, 242 geographical distribution, 242 infected with Schistosoma haemato- bium, low mortalit\- in, 249 Schistosoma japonicum, 251 post-mortem appearances, ^52, 253 _ intestinal, geographical distribu- tion, 255 pathology, 25!') prognosis, 256 — ^ treatment, 256 c^oo INDEX Schistosomiasis, pathology, 245 post-mortem appearances of bladder in, 245, 246 prevention, conclusions as to, based on Loos' hypothesis and on Bilharzia Mission (1915), contrasted, 249, 250 symptomatology, 256 treatment, 256 conclusions as to, based on Loos' hypothesis and Bilharzia Mission (1915), contrasted, 249, 250 Schiiffner's dots in benign tertian para- site, 609 Sciatic nerve of fowl suflfering from poly- neuritis, 342 Scorpions, venomous, mortality in chil- dren from, 449 stings from, mortality, 449 symptoms, 449 treatment, 450 290 of Scrotum, elephantiasis of, 289, Scurvy, dietetic causes of, 571 Seaports, large, recommendations Paris Convention regarding, 597 Sea serpents, 42^. See also Hydrophina Sebaceous glands, high development in natives of Tropics, 458 Seborrhoea, 488 treatment, 488 Sections, mounting of, on slides, 626 preparation of, 624 staining of, 613, 626 Septicaemia, development in plague, 172 morphine injections, 4, 15, 416. Sec also Whitviore^s disease Sera, antitoxic, 599 comparative value, in treat- ment of various diseases, 599 preparation from horse, 599 protection afforded by, hypotheses accounting for, 600 Serotherapy in typhoid fever in the Tropics, 222 Serum in prevention of snake-bite, 444 Lustig's and Galeotti's, in prophy- laxis of plague, 176 Yersin's, in prophylaxis of plague. 176 Sewage, disposal of, care of Chinese in, 587 ■ effluents, examination of, 662 examination of, 662 Sexual desire in cerebral stage of African trypanosomiasis, 141; " Shake '' cultures, 624 Shiga-Kruse type of dysenter\- bacil 619 Ships, health)^, quarantine measures specting, 597 infected, quarantine measures specting, 597 with yellow fever, distance lus. re- re- anchorage from shore, 372 — suspected, quarantine measures of re- specting, 597 Side-chain theory, tection afforded 601 Simaruba officinalis in nmnpbic dvsentery, prescriptions, 44 Ehrlich's, of protec- by sera and vaccines. Simpson, W. J., results of inoculation of living vaccines against cholera, 212 summary of cholera epidemics in Europe, 203-4 Simulidse in setiologx uf pellagra, 2>2>~ Siriasis, 539 Sistrurus catenatus (Prairie rattlesnake), 430 Sitotoxismus, 453 Skin, condition of, in cerebral stage of African trypanosomiasis, 145 diseases of, 458 elimination of toxins by, in yellow fever, 371 fibromatous condition of, curious example, 496 in typhoid fever in the Tro]:)ics, 217 pigments, 488 Sleeping sickness stage in African try- panosomiasis, 144-6 Slides, method of cleaning, 604 Smears, manner of staining, 613 Smegma bacillus, 616 Smoking, avoidance in sprue, 359 Snake-bite, antitoxic scrum in, value of, 599 deaths per annum due to, in India, 419. immunity from, acquired and natural, 444 maintenance of strength of patient in, 445 . prevention of secondary infection in, 445 prophylactic measures against, 446 symptomatic treatment in, 445 symptoms, 441 treatment, 443 Snake venom, aid in cxecretion of, in treatment of snake-bite, 445 apparatus of poisonous reptiles. 435 — characters of, 438 — manner of analysing, 440 varieties of, 438 Snakes, cranial skeletons of, 422 heads of, 420, 421 Soamin in treatment of African trypano- somiasis, 148 vSodium antimonyl, in kala-azar, 61 bicarbonate in onyalai, 417 bisulphate, tabloids of, in schisto- somiasis, 250 hyposulphite, for purification of water, 556 Soil, 533 disturbance of, iMedisposing cause of malaria, 71 permanent damjiness of, injurious to health, 533 Solids in suspension in sewage, method of estimating, 662 total, in water, method of estimat- ing, 653 . Solutions, cleansing and antiseptic, 526 Soya bean (glycine soja), nutritive value of, 564 Sparganum (human tapeworm), 261 producing acne-like eruption, 261 Sjiectroscopic examination of blood, 612 INDEX by) Spiders, vt-numuus, 449 effect of venuin, 4-,i stings from, mortalit\-, 450 symptoms, 450 treatment, 450 Spirillum cholerae asiaticae, diagnosis of, 621 I"" inkier-Prior, diff'erentiation Koch's comma bacillus, 621 (vibrio-proteus), 621 Spirit lotion, application to skin inickly heat, formula for, 487 Spirochaeta carteri cause of Asiatic lapsing fever, 13 duttoni, 10 recurrentis, 10 from m re- Spii^ochsetes causing relapsing fever, 9 field rat reservoir host for, 17 S|Mrocha;tosis icterohsemorrhagica (Weil's disease), ajtiology, 17 definition, 17 diagnosis, 18 geographical distribution, 17 history, 17 prognosis, 18 symptomatology, 17 treatment, 19 Spleen, enlargement in relapsing fever, 13 . . microscopical appearance in African trypanosomiasis, 139 Splenomegaly, afebrile, definition, 417 geographical distribution, 417 symptomatology, 417 treatment, 417 Sponge-fishers' asthenopsia, 509 Sporadic diseases, 542 Spore formation in protozoa, 4 Spores, method of staining, 61^ Si)orogenes test for bacteriological ex- amination of water, 643 Sporotrichosis, 488 ocular, due to fungi, 511 treatment, 488 Sporozoa, 4 S]50tted fever aetiology, 374 complications, 375 definition, 374 diagnosis, 375, 376 differential, 375, geographical distribution 376 and seasonal incidence, 374 in Montana, 37'- 37(> mortalit\', prophylaxis against, incubation period, 375 pathology, 374 prognosis, 376 symptomatolog\-, 375 treatment, 376 (conjunctivitis aestivalis), Spring catarrh 516 Spring water, 548 Springs, contamination of, 549 Sprue (psilosis), aetiology, 352-6 causes of death in, 357 condition of tongue in, 357 definition, 352 • diagnosis, 35S Sinuc, diagnosis, differential, 358 geographical distribution, 352 pathology, 3^,6 post-mortem examination, 356 -- — • state of blood in, 3^7 treatment by Cantlie's method, 350 by drugs, 360 ' by vaccines, 360 dietetic, 358, 359 local, 360 symptomatology, 357 yeast infection in, 357 •• Stab '' cultures, 624 Stains, choice of, 604 Staphylococci, arrangement, 162 Staphylococcus i^yogenes aureus, dia- gnosis of, 620 Starvation, death from, 564 Steam as means of disinfection, 593 ^ — pipes in sterilization of water, 558 Stegomyia calopus carrier of virus of yellow fever, 365, 366, 367 (fasciata), adult female, 373 eggs and larvae, 373 habits, 373 notes on, 373 transmission of dengue for preservation of in vellow fever. of Rocky Mountains, 271 hy, 37(} Sterilized enclosures meat, 575 Sternberg's treatment formula for, 371 Stomatitis, diagnosis of sprue from, 358 Stools in typhoid fever in the Tropics, 217 Storage tanks for rain water, ^4'^' " Streak "' cultures, 624 Streptobacilli, 162 Streptococci, arrangement, 162 in water, method of enumeration of, 652 Streptococcus pyogenes, diagnosis of, 620 Streptothfix madura, diagnosis of, 630 Strongyloides stercoralis, 270 - intestinal catarrh produced by, Sublimate, corrosive, as disinfectant, 594 Sullivan's diamond drill for producing bore well, 551 Sulphates in amoebic dysentery, 44 Sulphur anhydride and sulphurous acid gas as disinfectant for houses, 595 ointment, application in different forms of tinea (ringworm), 490, 493, 494 in trichomycosis, 495 in scabies, 487 in seborrha>a, 488 Sulphurous acids and sulphites as pre- servative, test for, 579 Sun, rays of, in Tropics, effect of on skin, 459 Sunlight, bacteria susceptible to, and re- sistant to eft'ects of, 645 direct, simple method of disinfec- tion, 592 pathological effects, 539 predisposing factor in eruption of pellagra, 540 Sunstroke, 539 see also Heai stroke Ocjb INDEX Surtaci' water, 547 catchment areas, site of, 547 Sweat, secretion of, in excess in natives of Tropics, 458 Synovitis, acute, of knee associated witli filaria infection, 294 Syphilis, 488 diagnosis bv \Va>-eiinann leaction, 610, 611 predisposing factor m ha>moglo- binuric fever, 384 Svjjhilitic ulcers, 504 Tabks^ late manifestations of \a\vs, 25 Tablet foods, concentrated, 582 Taenia saginata affecting muscles of tongue and of mastication of cattle, 26O largest human tapeworm, 265 solium, 264 Tannic acid in ama^bic d\senter\ , 43 intestinal irrigation with, in ciliar dysentery (Balantidium coli), 46 Tapeworms found in man, list of, 260 treatment, preliminary, 269 prescription for, 269 prophylactic, 270 thorough, 269 See also Cestoda i)athog.entc to iiuiii Tapioca, 564 elimination of poisonous elements from, 454 Tarabagan (Arctomys bola?), spread of lineumonic plague in Manchuria by, i/t Thresh's disinfecloi, 59^ Thvmol treatment of ank\lo.,tuniiasis, 318-9 Tick fever, African, mode of trans- mission, 8 Ticks, largest specimens of order of Acariaa, 19 manner of propagation, 19 venom of, infection by, symptoms. Tartar emetic m 469 in treatment of African try- panosomiasis, 148 method of administration in treatment of African trypanosomiasis, 149 Tattooing, 488 risks of, 488 treatment, 489 Tea, cold, w4iy a suitable drink for travellers, 555 qualities of, 582 Telangiectasis, multiple, 502 Telosporidia, 4, 6 Temperature of air in tropics, 531 Tetanus, antitoxic serum in, value, 599 bacillus, diagnosis of, 617 Telracocci, arrangement, 162 Tetramitus mesnili, 5 — parasite of ciliar d\ ,-,enter\-, 47 Tetrodin in poisonous fish, 448 Tetrodonic acid in poisonous fish, 448 Theft, propensity to, in cerebral stage of African trypanosomiasis, 14^ 'Thermal methods of sterilizing water, 558 'Thiosinamin injection in elephantiasis of legs, 286 'Thiosulphite for purihralion of water, Thoracic duct, blocking ot. in tilanasis, 279 Three-day fever. See Phleboiovuis fever Thresh, j. C, method of inuifxing water, 550 450, 451 treatment, 451 Tinea alba, 490 lesions and regions attacked. n-anuloma inguinale, 490 parasite, 490 regions attacked, 490 treatment, 490 - albigena, 490 parasite, 490 treatment, 490 - barbae (sycosis), 490 lesions and regions at- tacked, 490 liarasite, 490 treatment, 490 capitis (tonsurans), lesions and re- gions attacked, 490 -^ parasite, 491 treatment, 491 cincinata (ringworm of the bod.\), lesions and regions attacked, 491 parasite, 491 treatment, 491 cruris (eczema marginatum, dhobie itch), lesions and regions attacked, 491 parasite, 491 treatment, 491 decalvans, 492 flava, lesions and regions attacked. 492 parasite, 492 treatment, 492 — imbricata, lesions and regions of body attacked, 492 parasite, 492 treatment, 493 — intersecta, lesions and regions of body attacked, 493 parasite, 493 treatment, 493 nigra, 493 lesion and regions of l:)()dy attacked, 493 parasite, 493 nigro-cincinata, lesion and regions of body attacked, 493 l)arasite, 493 treatment, 493 nodosa, 471, 493 treatment, 471 ocular, due to fungi, 511 palpcbralis, 494 (ringworm), 489 Sabouraudi tropicalis, lesions and region attacked, 494 parasite, 494 treatment, 41)4 tonsurans, 489, 490 ungium, lesions, 494 parasite, 494 treatment, 494 INDEX 6(j9 Tinea versicolor (Pityriasis versicolor), lesions and regions attacked, 494 — ■ parasite, 494 treatment, 494 Tissue changes in sections, staining for, 604 Tissues, embedding of, in preparation of tissues, 625 • fixing of, in preparation of sections, 624 hardening of, in pre])aration of sec- tions, 625 Toads, venomous, slightlv toxic to man, ,448 1 ongue and mastication, muscles of, in cattle affected by taenia saginata, 266 condition of, in sprue, 357 denuded epithelium of, diseases in which seen, 358 leukoplakia of, 477 Townships, planning and construction in tropical districts, 536 Toxicity theory in aetiology of pellagra, Toxins, elimination in \ellow fever, 370, 371 . Trachoma, aetiology, 513 complications and seciuelse, 573 definition, 513 (granular conjunctivitis), 512 surgical remedies for, 515 symptomatology, 513 - treatment, 514 Trematoda pathogenic to man, classifica- tion, 232, 236 habitat, 235 life-history, 235 morphology, 234 pathogenic, varieties, 236 — treatment, 236 Trematodes, ova of, 637 preservation and examination of, 322 Trench fever, aetiology, 400 — ■ — definition, 400 distribution, 400 symptomatologv', 400 treatment, 401 Trenches, deep, unsatisfactory as latrines for natives, 586 prepared as latrines for natives, ^86 shallow, as latrines for natives, s8s Trenching and cultivation in disposal of excreta, 590-592 Treponema pertenuis, framboesia tropica (yaws) due to, 21 Trichinella spiralis, calcification in muscles, 308 cysts of, 306 larvae of, 306, 307 m.orphology, 306, 307 ■ iiarasite causing trichiniasis. 306 of rats, 30S Trichiniasis, definition, 306 geographical distribution, 306 parasite of, 306 prophylaxis against, 309 symptomatology, 308 treatment, 308 Trichocephalus dispar, ova of, 637 Trichocei^halus trichiuris (whipworm), morphology, 305 parasite causing tricho- cephaliasis, 305 pathogenicity, 306 Trichocephaliasis, definition, 305 parasite of, 305 treatment, 306 Trichomonas hominis, 5 intestinalis, characters, 5 parasite of ciliar dysentery, 47 vaginalis, 5 geographical distribution, 5 Trichomycetes, divisions of, C29 Trichomycosis, 494 capillitii, 472 treatment, 495 Trichonocardiasis (nodules on the hairs), 4gj Trichophyton megalosporon (ringworm), 631 Trichophytons, 489 and microsporons, dift'erence be- tween, 489 Trichorrhexis nodosa, 472 treatment, 472 Tropical diseases, protozoa as factors in causation of, 2 liver, Europeans attacked by, 55 internal medications in, 55 Trypanosoma brucei (rhodesiense), 127 animal susceptibility to, 130-1 carriers of, 131 — division of, 129 general features of, 127 geographical distribution of, 130 group of, 127 history of, 130 morphology of, 130 notes on, 157 reservoir of, 131 — caprae, 129, 137 — cruzi, agamony of, 155 cause of South American try- panosomiasis, 154 microscopical examination of, 156 post-mortem, 156 131 schizogony of, 154 sporogony of, 155 equiperdum, 128, 158 evansi, 128 gambiense, 125, 128 ■ animal susceptibility to, 132 carriers of, 133 conclusions as to, 134 cycle of development, 132 geographical distribution of, history of, 131 morphology of, 132 reservoir of, 134 pecorum, 128 carriers of, 135 development of, 128, 136 general features of, 128 group of, 128 morphology of, 135 pathogenicity of, 135 reservoir of, 136 700 INDEX Ti\ panosoma siiniae, 128, 136 uniforme, 129, 136 vivax, 120, 136 development of, 121; — — general features of, group of, 129 Trypanosome cazalboui, notes I2g on. 157, 159 dimorphun, notes on, 160 equinum, notes on, 158 evansi, notes on, 157 hippicum, notes on, 159 Soudanese, notes on, 159 Trypanosomes, classification of, 126-7 habitat of, 126 methods of searching for, 147 pathogenic, Central African, 127 groups of, general charac- ters, 127-137 Trypanosomiasis, African, aetiology of, 124-5 cases of, 143 complications, 146 definition of, 122 diagnosis of, 146-7 geographical distribution, 123-4 history of, 122 macroscopic appearances, post- mortem, 137 ■ microscopic appearances, post- mortem, 138 pathology of, 137 prognosis of, 147 prophylaxis against, 150 symptoms, summar.\- of, 140 symptomatology of, 139 treatment of, 147-8 — development, conditions favourable for, 540 — mammalian, pathological, notes on, 157 — parasite of, 125 — South American, aetiology of, 154 chronic, with acute and subacute exacerbations, 157 history of, 154 ])athology of, 155 prophylaxis against, 157 — — ■ symptomatology of, 156 treatment of, 157 transmission, mode of, 8 low water m tropics, Trypanosomid?e, 5 Tube well for sha .,551 1 ubercle bacillus, diagnosis of, 615 in milk, test for, 570 Tubercular ulcers, 504 Tuberculosis, antitoxic serum in, 599 in animals, recommendations of Royal Commission on Human and Animal Tuberculosis, 574 Tumour, leaking, discharging fluid giv- ing reaction of bile, 501 Tumours, 495 Turpentine, application in tinea flava. 492 — — oil, application in tinea capitis, 491 Typhoid bacilli, removal from water, chemical process for, 556 bacillus, destruction bv storage of water, 554 T\phoid bacillus, in water, dithculties of detection, 652 - method of detection of, 652 fever, carriers, fa;cal, 214 fly, 214 urinary, 214 case incidence and case mor- tality, affect of anti-typhoid vaccine on, 601 - diagnosis b\ \A'idal reaction. 611 spotted fever of Rocky Mountains from, 2,j^ epidemic following use of con- taminated shallow wells, 550 sources of, 215 house-flies, carriers of, 224 in tropics, 213 causes of death, 218 complications, 218 diagnosis, 219 - bacteriological. importance of, 219 liability of freshly arrived Europeans to, 215 pathology, 215 symptomatology, 217 treatment, 222 in special sym- ptoms, 223 sources of infection, 214 Typhus fever, aetiology, 213, 379 and spotted fever of Rocky Mountains, similarity between, 376 complications in, 380 definition, 379 distribution, 379 symptomatology, 379 treatment, 380 Ulcer, perforating, amputation for, in the foot of lepers, 185 Ulcerations, tropical, 502 causes of, 502 nomenclature of, 503, 504, 505 treatment, 505 Ulcers, blastomycotic, 503 cancerous, 503 diphtheroid, ^03 framboesial, 504 infantile, 504 interdigital, ,04 leprotic, 504 or elephantoid, ^503, ^04 septic, 504 ■ syphilitic, 504 tubercular, 504 varicose, 503, 505 Ultra-violet ravs in sterilization of water, .55,8 Undulant fever, aetiology of, 190 complications of, 195 definition of, 190 diagnostic features, 195 geographical distribution of. 190 modes of infection, 191 pathology of, 191 post-mortem appearances, 191 prophylaxis against, 195 JNl-fEX 701 Undulant fovcr, symptomatology of, iqi, 104-5 ■ transmission, modes of, 540 treatment of, 195 United States, mortalit\' from yello\v fever in, 370 Urinary carriers of typhoid fever, 214 Urine in blackwater fever, 387 in chyluria and lymphuria, 283 LTrobilin, increase of, in faeces, in haimolytic diseases, 634 Urotropine in chvluria and Ivmphuria, 284 Uterus, cervix, carcinoma, 502 \'accination, definition, 5q8 Vaccine, Haffkin(>'s, in prophylaxis of plague, 176 dosage, 176 inoculation against cholera, 212,213 Vaccines, autogenous, 598 in Archibald's fever, sgj in dermatitis cupoliformis, 465 in pyosis Corletti, 485 classification of, 590 compound, 602 imported, manner of preservation, 598 Verruga peruviana, ^vvvrc iy])C (Car- rion's fever), 364 — — symptomatolog\-, 364 treatment, 365 Vertigo, paralytic, endemic, 40O Vesicular fever, diagnosis, 403 Vibrio-proteus. See S-pirillum. F/iik/cr- Prior Villages, native, planning and construe tion in tropical districts, 536 Vipera russelii (daboia, or Russell's viper), 431 Viperidse, 426 Viperinse, 426, 430 in Africa, 432 Viperine venom (snake bite), post-mor- tem, 443 — symptoms, 442 ^'iruses, filterable, 561, 562 \'itamines, 569 A'oit's standard diet, 565 \^olvulosis, 300 geographical distribution, 300 \'omit of yellow fever, 368 Vomiting in ackee poisoning, 455 in blackwater fever, drugs in cure of, 388 in cholera, treatment, 210 living and devitalized, inoculation \'ulva, elephantiasis of, 292 against cholera, 213 — protection afforded by, hypotheses accounting for, 600 — sensitized, 599 — streptococcal in sprue, 360 table of, with doses, 599 Vacuoli in protozoa, 3 Vacuum apparatus (Elliott and Paton's) for steam disinfection, 595 Van Gieson's stain in staining sections, 627 • use of, 604 ^^ariola in India and Africa, 401 \'egetable matter in water, ill-eft"ccts of, products, rich in potassium salts, 563 Vegetables, deficient, in aetiology of beri- beri, 339 green, transmission of cholera by, 206 Vegetarianism, 580 A'cldt sore, 503, 505 Venom, absorption of, in snake bite, pre- vention of, 443 manner of neutralizing, 444 See also Snalie venom Venoms, diseases due to, 418, 419 Vcrrucae, 495 Verruga peruviana, retiology, 363 atypical, 365 blood condition in, 364 definition, 363 ■ — erythema of, 364 geographical and seasonal dis- tribution, 363 histopathology, 363 history, 363 mild type, 364 pathology, 363 prognosis, 365 -_ regional distribution, with various resulting lesions and symptoms, ^61; Wars, relation of cholera epidemics to, 204, 205 Warts, 495 Washing water, cleansing of, method described, 560, 561 Washington-Lyon apparatus for disin- fection by steam, 595 Wasps. See Bees \Vassermann reaction (Fleming's modi- fication), diagnosis of syphilis by, 610, 611 - substances required for, 610, 611 611 technique of,' 610, Water and faeces, bacteriology during monsoon weather, 646 amount required daily for personal and domestic use, 544 analysis of sample of, certificate, 662 as thirst quencher, 582 bacteria in, enumeration by British methods, 650, 651 boring for, 545 carriers, Hindu, vessels used by, 552 Mahommedan, infection of water by, 5 151 chemical examination of, 653 closets in tropics, 588 containing peat, effect on leaden water-pipes, 552 contamination, source of, methods of tracing, 553 control of, by medical officer, 553 distilled, aeration of, 545 examination, 639 bacteriological, 640, 64 1 - in India, standard for. 645, 646 tests for, 642, 643-646 702 INDEX Water examination, biological, 640 physical, 640 filtration of, 558 hard, not injurious to health, S'^2 pathology of, S'52, 553 I)urification, 554 by precipitation, 555 by storage, 554 ■ chemicals used for, 555 ■ rendering potable by oxidation, s*"'! soft, ill-effects of, 552 softening of , chemicals used for, 555 solvent uses of, in diet, 563 sources of, 544 sterilization aided by storage, 554 by electrical methods, 558 by thermal methods, 558 subterranean, 548 classification of, 548 transmission of cholera by, 205 transport of, 551 unfiltered, spread of schistosomiasis by, 250 \Vatercre5s, dangers of, 572 Water-pipes, iron, diminution in dia- meter, 552 Water supply pipes, dimensions of, method of ascertaining, 546 Weigert's inethod for staining micro- organisms, 614 WeiTs disease. See Spirochcetosis ictero- hcemorrhag'ica Well and spring waters, classification for drinking purposes, 650 protected, plan of, 550 — shallow, bacteriology of water from. 647 water in Khartoum, bacteriological examination, 643 Wells, deep, 551 shallow, 548 contaminated, use of, followed by t.vphoid fever epidemics, 550 contamination of, 549 Whey, 568 Whipworm. tirus White men, impossible. See Trichocephahis trichi- existence in tropics racial . 538 Whitmore's disease, aetiology, 415 common in drug-takers, 415 ■ definition, 415 pathology and symptomato- logy, 415, 416 Widal reactions in diagnosis of typhoid fever, 219, 611 method of performance, 611, 612 Wind and dust, exposure to, causing l)inguecula i)terygium and ophthalmic irritation, 510 Women, men and children, food neces- sary for, compared, 564 XANTHOM.A areatum, 506 treatment, 506 diabeticorum, 502 lilanum, 502 tuberosum, 502 Xenopsylla cheopis (rat-flea), transmis- sion of plague by, 171 Xerosis, 510 among debilitated children, 510 X-ray treatment of tropical ulcers, 505 Yaws. See Framhoesia tropica Yeast, infection in sprue, 357 Yeasts, staining of, 632 Yellow fever, blood condition in, 367 course, crisis and termination. 369, 370 370 definition, 365 diagnosis, 370 differential, 370 in early stage, imported, disinfectant measures against. ?>1^ ■ endemic centres of, 366 endemicity of, mean tempera- ture necessary for, 539 geographical distribution, 366 immunity to, 368 natural, in very young children, 368 importation of cases into re- gions free from Stegomyia callopus not dangerous, 543 incubation period, 369 mortality, 370 pathology, 367 post-mortem findings in bodily regions and organs, 368 prognosis, 370 prophylaxis against, 371, 372 Boyce's summary. 372 — spread of, dependent on pre- sence of mosquitoes, 539 factors necessary for, 371 symptomatology, 369 — transmission, mode of, 8 treatment, 370 bv alleviation of svm- 370, 371 ptoms, 371 b\- elimination of toxins, - dietetic, 371 indications for, 370 virus of, 366, 367 carrier, 365, 366, 367 vomit of, 368 Yersin's serum in proph\laxis of plague, T76 John Bale, Sons & Daniei.sson, I-Tn., 83-91, Great Titchfield Street, London, W.i, ^ / mijri: HI lltlMII iiiiiiiin:!..:. 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