key: cord-290509-56pfww0l
authors: Fleet, Graham H; Heiskanen, Paul; Reid, Iona; Buckle, Ken A
title: Foodborne viral illness - status in Australia
date: 2000-07-25
journal: Int J Food Microbiol
DOI: 10.1016/s0168-1605(00)00249-x
sha: 
doc_id: 290509
cord_uid: 56pfww0l

Norwalk-like virus contamination of oysters and orange juice, and hepatitis A virus contamination of oysters have been responsible for large outbreaks of foodborne viral disease in Australia. Rotavirus, adenovirus, astrovirus, parvovirus and other enteroviruses also contribute to the incidence of gastroenteritis in this country but the role of foods and waters in transmitting these viruses is unclear. Protocols for the investigation, surveillance and reporting of foodborne viral illness require further development to enable a more accurate description of the problem. Few laboratories have the capability to analyse foods for viruses and specific training in this technology is needed. Management of food safety in Australia largely relies on the implementation of HACCP principles, but these need to be adapted to address the specific risks from viruses.

government regulatory sectors. To achieve this safety, both sectors closely follow recommendations of The food industry is one of the largest manufactur-the Codex Alimentarius Commission by implementing and service sectors in Australia. It employs about ing appropriate quality assurance, HACCP, and risk 750 000 individuals and has an annual turnover value management programs, and ensuring that products of approximately $US 50 billion (Anonymous, conform to appropriate microbiological specifications 1999a). Because it has a strong focus on export, it is and standards (Fleet, 1996; Jouve, 1998 ; Peters, intimately linked with international trade. The suc-1998 The suc- , 1999 Hathaway, 1999) . cess of the industry depends on production, mana-As a nation, Australia is comprised of six States gerial and regulatory practices that ensure high and two Territories. Food safety is regulated by quality, safe products. Microbiological safety com-legislation that is administered through each State mands high priority by both the industry and the and Territory, using a common policy that has been developed at the national level by The Australia New Zealand Food Authority (ANZFA) (Anonymous, *Corresponding author. food safety standards based on HACCP principles 0168-1605 / 00 / $ -see front matter © 2000 Elsevier Science B. V. All rights reserved. PII: S0168-1605( 00 )00249-X that will also be administered at the State and attempts to collate the data of these reports at the Territory level. Foods for export are regulated separ-national level, but these initiatives have been ad hoc ately by the Australian Quarantine Inspection Service and irregular (Murrell, 1986a,b; Crerar et al., 1996) . (AQIS) which is an agency of the national Govern-In 1991, the Australian Government established the ment but, in essence, follows the safety policies of National Notifiable Diseases Surveillance System ANZFA. Imported foods are also monitored by (NNDSS) to compile national statistics on com-AQIS which administers the Imported Food Inspec-municable diseases including foodborne diseases. It tion Program based on policies developed by receives data from the State and Territory notifica-ANZFA (Fleet, 1996; Oram-Miles, 1999) .

tion programs, as well as other voluntary reporting In addition to the general requirements for due schemes such as the recently established National diligence and good manufacturing practice, the mi-Enteric Pathogen Surveillance Scheme (NEPSS), the crobiological safety of foods in Australia is regulated Australian Paediatric Surveillance Unit (APSU), the through a series of microbiological standards that are Escherichia coli Reference Laboratory and the Virolpublished in the Australian Food Standards Code ogy and Serology Laboratory Reporting Scheme (Anonymous, 1997a). Currently, these standards are (LabVISE). The NEPSS collates reports on the based on bacteriological and fungal criteria. Virologi-isolation of pathogenic organisms from foods and cal criteria are not part of these standards, mainly other environmental sources and the APSU monitors because little information is known about the occur-disease outbreaks in children. LabVISE collates data rence of viruses in local foods and because of the on virus diseases as diagnosed in 21 sentinel labtechnical difficulties associated with analysis of oratories operating throughout Australia. One objecviruses in foods. Nevertheless, as will be discussed tive of the NNDSS is to provide information that will in the following sections, Australia has a significant assist in developing a uniform, national policy history of food and waterborne viral diseases. The towards management of food safety (Anonymous, incidence of these outbreaks appear to be on the 1997b, 1999a). Reports of the NNDSS are published increase which, combined with newer methods that in the Communicable Diseases Intelligence, through enable the analysis of foods for viruses, are increas-the Department of Health and Family Services of the ing demands for greater quality assurance and regu-Australian Government. lation of this problem. As a basis for developing According to data compiled by the NNDSS, future programs for prevention and management, this notification of foodborne microbial diseases in Ausarticle examines the past and current status of food tralia increased from approximately 17 000 cases in and waterborne viral diseases in Australia. 1991 to 23 000 cases in 1999. Hepatitis A, the only notifiable virus disease, represented about 10-13% of the cases over this period. However, it is generally 2. Surveillance systems and epidemiological accepted that these statistics are a substantial underestatistics stimation of the real incidence of foodborne disease, and highlight major limitations of the surveillance Each State and Territory within Australia has system (Crerar et al., 1996; Hellard and Findlay, public health legislation that requires official notifi-1997; Anonymous, 1999a) . Many cases of foodborne cation of communicable diseases. Notification simply illness remain unreported or not diagnosed and, means that clinical diagnosis of the disease or consequently, are not notified. Also, the notification isolation of the causative organism must be reported system does not include illness caused by many to the appropriate Department of Health or equiva-foodborne pathogens, such as Staphylococcus aulent. Communicable foodborne diseases that are reus, Bacillus cereus, Clostridium perfringens or listed for notification are campylobacteriosis, sal-viruses other than hepatitis A. For example, orange monellosis, shigellosis, yersiniosis, typhoid, lis-juice contaminated with Norwalk virus was responteriosis and hepatitis A. Annual reports of these sible for over 3000 cases of gastroenteritis in Ausnotifications are published by each State and Territ-tralia in 1991, but these data are not included in the ory and have been accessed for the purposes of this official notifiable statistics. Based on the data availcontribution. Over the years, there have been various able and the limitations inherent in the existing surveillance system, several groups have indepen-causing disease. Eyles (1978, 1989) and Grohmann dently estimated that the true incidence of foodborne (1997) have made passing references to outbreaks of microbial illness in Australia is about 4.0-5.0 mil-foodborne viral disease in Australia as part of more lion cases per year. About 30-40% of these cases are general discussions of viruses in foods. The followprobably attributable to viruses (Anonymous, 1997b, ing sections provide a more detailed discussion of 1999a). This proportion of foodborne viral illness, viruses associated with or thought to be associated relative to the total, is similar to that reported for the with outbreaks of foodborne disease in Australia. USA (Anonymous, 1999b) .

As in other countries, significant outbreaks of poliomyelitis occurred in Australia during the early 3. Rotavirus part of the twentieth century, and foods and waters were frequently suspected as being involved in Rotaviruses were first discovered in Australia in transmitting the disease (Eyles, 1978) . However, 1973, and were found in the faeces and duodenal genuine interest in food or waterborne viral diseases mucosal epithelial cells of children who had been did not develop in Australia until 1978 when oysters hospitalised with acute, non-bacterial gastroenteritis were found to be responsible for a very large (Bishop et al., 1974) . These viruses are now recogoutbreak of gastroenteritis caused by Norwalk-like nised as a major cause of gastroenteritis in children agents. Table 1 shows the range of viral diseases that throughout the world. Rotaviruses belong to the have the potential to be food or waterborne and are family of Reoviridae, and infect the epithelial cells now routinely monitored throughout the country by of the small intestine (Christensen, 1989; Dessel-LabVISE. The values in Table 1 do not represent the berger, 1998). Illness becomes evident after 1-2 true incidences of each of the viral diseases since days incubation and is characterised by the sudden they are compilations of reports from only 21 onset of acute, watery diarrhoea and vomiting, often sentinel laboratories. However, based on compari-accompanied by fever. The symptoms persist for sons with NNDSS data for hepatitis A virus, a fully several days or longer, leading to dehydration which, notifiable viral disease, the values in Table 1 proba-in severe cases, can cause death. High levels of bly represent an approximate five-fold underestima-infectious virus particles are excreted with the tion of the real incidence. Nevertheless, the data of faeces. Transmission of the disease from person to Table 1 are significant in showing annual trends and person occurs mostly via the faecal-oral route, the relative frequency of the different viruses in because the virus is highly infectious. However, , 1996) . A National Rotavirus Reference Centre survival rate in the environment (Christensen, 1989;  has recently been established to improve surveillance Hedberg and Osterholm, 1993; Bishop, 1994) . and management of the disease (Masendycz et al., In Australia, gastroenteritis caused by rotaviruses 1999). is responsible for the annual hospitalisation of about 12 000 children under the age of 5 years. This represents about 50% of all children hospitalised 4. Norwalk or Norwalk-like viruses with gastroenteritis and is estimated to cost the nation about $US 10 million annually (Bishop and

The Norwalk or Norwalk-like viruses belong to a Barnes, 1996; Carlin et al., 1998; group generally called the small round structured 1999). Outbreaks of the disease are mostly associ-viruses (SRSVs) because of their morphology. Their ated with child care centres, pre-schools and other genome consists of single stranded RNA, the sesituations where there are large numbers of children quence of which corresponds with their classification (Hanna, 1992; Hanna and Brookes, 1993; Ferson, in the family Caliciviridae (Appleton, 1994; De-1995) . However, outbreaks in adults, especially at sselberger, 1998; Anonymous, 1999a). They have nursing homes for the elderly, can occur (Bishop, been a major cause of food or waterborne gastroen-1994). While person to person contact is considered teritis in Australia (Eyles, 1989; Grohmann, 1997 ; to be the principal mode for spread of the virus in Marshall and Wright, 1999) . Characteristic sympthese situations, the involvement of faecally contami-toms of nausea, vomiting and diarrhoea generally nated water and foods is often suspected, but re-appear after 24-48 h of incubation and last about quires more specific investigation. Crerar et al. 48-72 h. (1996) refer to one outbreak, involving 55 indi-

The first evidence of a problem with these viruses viduals, where salad vegetables were considered to occurred in 1977, when oysters harvested from have transferred the virus. Diagnosis of the disease Georges River, Sydney, caused outbreaks of gasgenerally relies on the symptoms it causes and troenteritis in the UK. The oysters had been opened detection of the virus in faecal specimens by and frozen in the half shells before export. The serological and electron microscopic techniques.

frozen oysters conformed to Escherichia coli stan-The epidemiology of the illness has been exten-dards ( , 2.3 E. coli / g) as tested by exporting sively monitored over the last 25 years by serotyping authorities in Australia and importing authorities in and electrophoretic differentiation of the viral RNA the UK. No bacterial pathogens were detected in the (Rodger et al., 1981; Barnes et al., 1998 ; Diwarkala oysters at levels that would cause gastroenteritis. and . The incidence of outbreaks Subsequent investigations revealed that the implifollows a seasonal pattern, predominating in mid to cated oysters had been harvested from Georges River late winter months, but minor variations in this at a time during rainfall and that unfrozen batches of pattern occur across the country. In tropical regions, the oysters had exhibited counts exceeding the E. peak times of infection may occur in summer months coli standard. Evidently, freezing of the oysters (Bishop and Barnes, 1996) . Different states within killed the E. coli but not the suspected virus. The Australia also have different rotavirus notification same batch of frozen oysters caused gastroenteritis rates, ranging from 9.2 per 1000 to 49.8 per 1000 more than 6 months after storage (Fleet, unpublished children under the age of 5 years (Carlin et al., data) . Although oysters and specimens from victims 1998). Similar serotype patterns are observed in of the outbreaks were not examined for viruses, the different cities, emphasising the endemic nature of symptoms of gastroenteritis were characteristic of rotavirus infection in the population. The majority of Norwalk or Norwalk-like viruses. Moreover, oysters the outbreaks are caused by Group A rotavirus, harvested from the same location several months serotype G1 (about 80% of cases), but epidemics later in 1978 caused outbreaks of similar gastroencaused by serotypes G2, G3, G4, G6 and G8 have teritis in Australia affecting over 2000 consumers. occurred (Palombo and Bishop, 1995) . Substantial These outbreaks have been extensively studied, and heterogeneity occurs in the RNA electrophoretic Norwalk virus was detected by electron microscopy, profiles of the serotypes, and suggests the continual immunoelectron microscopy and reverse transcrip-tion (RT)-PCR in faeces of many of the affected faecal specimens from affected individuals by directconsumers (Murphy et al., 1979; and immuno-electron microscopy did not give con-1980; Linco and Moe et al., 1994) . clusive evidence of virus presence, but ELISA Unfortunately, Norwalk virus could not be detected testing of sera as well as epidemiological data in oysters implicated in these outbreaks, although suggested the occurrence of Norwalk-like agents. echovirus type 8 and reovirus were isolated, but not Private hospitals, hostels, parenting centres, and considered responsible for the gastroenteritis (Eyles nursing homes are often involved in outbreaks of et al., 1981). These outbreaks resulted in major Norwalk-like gastroenteritis (Oliver et al., 1985;  changes to the regulation of oyster production in the Selden et al., 1993; Taylor and Murphy, 1994 ; Wilby state of New South Wales (NSW) of Australia and, and Ferriera, 1995; ; Marshall subsequently, it became mandatory for all oysters to and Wright, 1999) . Transmission of the disease by be subjected to a process of depuration before sale mechanisms other than food or water seems to have (Souness and Fleet, 1991; Ayres, 1991) . While occurred in these outbreaks but, generally, the source depuration combined with quality assurance pro-of the virus and its mode of transfer were not grams have managed to prevent further major out-thoroughly investigated. breaks of oyster associated Norwalk virus, some Wright et al. (1998) have completed a major authors have questioned the efficacy of depuration in retrospective study of the incidence of Norwalk-like eliminating the virus (Eyles, 1980 (Eyles, , 1989 gastroenteritis in Australia, principally the state of et al., 1981; Grohmann, 1997) . Oysters harvested Victoria, by examining for the virus in faecal specifrom an estuary in northern NSW and supposedly mens that had been submitted for suspected viral depurated were suspected of causing an outbreak of gastroenteritis over the period 1980-1996. Faecal 97 cases of Norwalk virus gastroenteritis in 1996. samples were screened for presence of the virus by The virus could not be detected in faecal specimens electron microscopy. Positive samples were further but was detected in one sample of oysters by RT-examined by RT-PCR followed by partial sequenc-PCR (Stafford et al., 1997) . Further research is being ing of the amplified DNA. Of the 6226 samples conducted at the University of New South Wales to examined, about 3.5% were positive for presence of determine the kinetics of virus depuration from local Norwalk-like virus with the majority (82%) represhellfish, and to evaluate the use of bacteriophages as senting submissions from adults or elderly persons. potential indicators of estuary and shellfish contami-Of the positive samples, 36% were submissions from nation with human viruses such as the Norwalk or hospitals, 19% were from nursing homes, 13% were Norwalk-like viruses. associated with outbreaks related to a restaurant or The largest outbreak of Norwalk virus associated reception, 5% from camp, chalet or child-care setgastroenteritis involved over 3000 individuals who tings, and 26% were from family or uncertain had consumed orange juice that was largely served to origins. Outbreaks were more common in late winter passengers on domestic airline flights during August and early summer months. Based on DNA se-1991. Extensive surveying of passengers as to what quences, the viruses were classified into genogroups they had consumed, enabled identification of the 1 and 2, with most cases of gastroenteritis being causative food, in this case orange juice which was associated with genogroup 2. While the source of the traced to one manufacturer. Inspection of the pro-virus was not reported in this study, epidemiological duction facilities identified several areas where con-data suggested a significant involvement of foods or tamination of the juice could have occurred. The waters. A recent report has suggested that Norwalk virus was not detected in the juice but the outbreak and Norwalk-like viruses probably account for the terminated when the juice was withdrawn from the greatest incidence of foodborne disease in Australia market. Faecal specimens from affected individuals (Anonymous, 1999a) . showed the presence of characteristic Norwalk-like particles (Lester et al., 1991) .

Sewage contaminated drinking water was suspect-5. Hepatitis A ed to be the cause of an outbreak of Norwalk-like gastroenteritis in several hundred guests at a caravan Hepatitis A virus (HAV) is classified in the family park in NSW (McAnulty et al., 1993) . Analysis of Picornaviridae which also includes the poliovirus and enterovirus groups. Their genome consists of tected in the sera of affected individuals (Dienstag et single stranded RNA which, in the case of HAV, is al., 1976; Locarnini and Gust, 1978) . A dredge, highly conserved, giving only four genotypes and discharging untreated sewage into the water near one serotype (White and Fenner, 1994) . Spread of where the mussels were growing, was thought to be the virus occurs by the faecal-oral route, where the source of the virus. The largest outbreak of HAV contaminated foods and waters can be significant in Australia occurred over several months during vectors. After ingestion, the virus multiplies within 1996-1997 after consumption of oysters harvested the intestinal epithelium, passes into the blood from the Wallis Lakes region in northern NSW. stream and then attacks liver cells. Onset of the Almost 500 individuals were affected and one person disease occurs after an incubation period of 2-6 died as a result of the disease. Analysis of samples of weeks and is evidenced by symptoms of malaise, oysters collected from the region during the time of anorexia, nausea, lethargy, jaundice, pale faeces, the outbreak were positive for the presence of HAV dark urine and liver pain. Illness may last 4-6 as determined by a PCR method. The oysters also weeks, after which full recovery is usual. However, tested positive for the presence of adenoviruses and shedding of the virus in the faeces can extend for enteroviruses but not Norwalk viruses. However, 3-6 months and some individuals experience re-they conformed to bacteriological standards (less lapses of the disease. Death due to liver failure may than 2.3 E. coli / g) and, supposedly, had been subject occur, but is rare (White and Fenner, 1994; Anony- to depuration according to legislative requirements of mous, 1999b). the state government. A subsequent coronial enquiry Statistics on HAV infection in Australia have been into the outbreak revealed numerous sources by reviewed and discussed by several authors (Scott and which untreated sewage could contaminate the lake Sheridan, 1994; Selden et al., 1994; Ferson et al., and oyster cultivation areas (e.g. no reticulated 1998; Merritt et al., 1999; Amin et al., 1999) . As sewage systems in nearby villages, leaking public noted already, HAV infection is a notifiable disease toilets, caravan parks, and recreation water craft) in Australia. Data from the NNDSS indicate 1500- (Anonymous, 1997c; Grohmann, 1997 ; Wilcox, 3000 cases per year over the period 1991-1999. 1999 ). More stringent quality assurance programs for Notification statistics vary between States and Ter-oyster cultivation and processing have been imritories, and range from 1.9 to 51.7 cases / 100 000 plemented to avoid future problems of this nature individuals. Significant outbreaks of HAV infection (Wilcox, 1999) . However, the question as to whether have been reported in homosexual men (Ferson et HAV is effectively eliminated from oysters after al., 1998), individuals within institutions (Hanna and commercial depuration processes remains unresolved Brookes, 1994; Bell et al., 1994) , child care centres and requires research. Another concern arising from ( Ferson et al., 1994; Tallis et al., 1996) , in lower this outbreak was the failure of E. coli standards to socioeconomic communities or families (Dick et al., reliably indicate oyster contamination by viruses. 1994) and after consumption of foods (Dienstag et  Sporadic outbreaks of foodborne HAV occur al., 1976; Anonymous, 1997c,d) . Apart from the well throughout the country and generally involve foods described foodborne outbreaks, person to person served at restaurants. One such outbreak involved 23 contact is considered to be the main mode for spread cases and was traced to the consumption of imported of the virus. However, poor hygiene and faecal frozen, fresh water prawns. PCR testing of leftover contamination of foods and waters may be respon-prawns failed to detect HAV and blood samples taken sible for spread of the virus in institutional and child from restaurant staff all tested negative for recent care settings.

HAV infection (Anonymous, 1997d). The first documented foodborne outbreak of HAV in Australia was attributed to the consumption of incompletely cooked mussels that had been harvested 6. Astroviruses from faecally contaminated waters in the state of Victoria. Seven out of the 10 individuals who Astroviruses contain single-stranded RNA within a consumed the mussels developed symptoms of hepa-capsid that has a characteristic star-shaped appeartitis A. Antibodies to HAV were subsequently de-ance when visualised by electron microscopy. They cause gastroenteritis, especially in young children, serotype 40 (less than 20%). Seasonal patterns of the giving symptoms similar to those caused by rotavir-virus genotypes were evident, with type 41 being uses, but generally, are less severe. Transmission of prevalent in late autumn and type 40 remaining the virus occurs by the faecal-oral route (Lew et al., prevalent year-round. The source of the virus and its 1991; Appleton, 1994) . Very little has been reported mode of transmission were not examined in these about the occurrence of this virus in Australia. Using studies. a specific DNA probe, astrovirus was detected in 4.2% of faecal specimens from 378 children who were hospitalised with gastroenteritis in the state of 8. Human calicivirus or Sapporo-like viruses Victoria during 1995. Incidence of the virus was greatest during winter months and in infants of 6-12

Human caliciviruses (HCVs), also known as Sapmonths of age (Palombo and Bishop, 1996) . The poro-like viruses, are a subgroup of the Caliciviridae epidemiological significance of these findings was and cause gastroenteritis similar to that caused by not reported. Clearly, astrovirus-associated gastroen-Norwalk or Norwalk-like viruses. The first reported teritis does occur in Australia (Table 1 ) but the role outbreak in Australia attributed to HCV occurred in a of food or water in its transmission needs further day care centre in 1988. Fifty-three people were investigation. The specific role of shellfish in its affected, with HCV being found in 32% of faecal transmission would be worthy of more thorough samples from symptomatic adults and children, and investigation, because of their previous association in 8% of asymptomatic individuals. The outbreak, with outbreaks of HAV and Norwalk-like viruses in which affected young children more severely, lasted this country and overseas reports of shellfish-associ-more than 10 weeks due to the number of asymptoated outbreaks of astrovirus gastroenteritis (Ap-matic individuals and the prolonged excretion of pleton, 1994).

virus particles. The outbreak persisted despite taking many control measures such as closing the central kitchen, encouraging handwashing, and modifying 7. Adenovirus diaper changing practices (Grohmann et al., 1991) . Since 1988, the cases of HCV in Australia have Adenoviruses contain double stranded DNA with-remained sporadic and rare (Table 1) . A study of in an icosahedral capsid. Many of the 47 or more faecal samples from patients with gastroenteritis known adenovirus serotypes can multiply in the during 1980-1996 found that only 0.14% of cases small intestine, but only types 40 and 41 have been were due to HCV, compared with 3.5% of cases due associated with gastroenteritis (Grimwood et al., to Norwalk and Norwalk-like viruses (Wright et al., 1995) . The most common method of transmission is 1998). via the faecal-oral route, with food and water as possible vectors (Mickan and Kok, 1994) . Illness lasts slightly longer than rotavirus infections, but the 9. Other viruses symptoms of diarrhoea, vomiting and fever are milder (Christensen, 1989) .

Parvovirus-like particles were responsible for an Several studies covering the analysis of about outbreak of gastroenteritis involving 217 children 5000 faecal specimens during the period [1981] [1982] [1983] [1984] [1985] [1986] [1987] [1988] [1989] [1990] [1991] [1992] [1993] [1994] [1995] [1996] and teachers at a primary school in Sydney, NSW, in indicate that adenoviruses contribute 3-9% of the 1977, but the source of the virus was not determined gastroenteritis cases admitted to Australian hospitals (Christopher et al., 1978) . Although these viruses (Pitson et al., 1986; Mickan and Kok, 1994; Grim- contribute significantly to the sporadic incidence of wood Palombo and Bishop, 1996) .

gastroenteritis (Table 1) , their transmission in foods Diagnosis of the virus is generally based on its is not reported. Coronaviruses have been detected in detection in faecal samples by electron microscopy the faeces of adults in Australia (Marshall et al. , and enzyme immunoassay. The majority of the cases 1989), including aborigines where the excretion rates are associated with young children and involve were higher than those for non-aboriginals (Schnagl serotype 41 (40-80%) and to a lesser extent, et al., 1978) . While the standard of hygiene is thought to relate to the incidence of this virus, foods (Armon and Kott, 1996) . With the absence of evidence of a direct role of foods in its transmission analytical monitoring, management of foodborne is not clear (Caul, 1994) . Coxsackie, echo and other viral disease largely relies upon the proper imenteroviruses have been detected in oysters harvested plementation of HACCP principles. However, it is from NSW estuaries (Eyles et al., 1981; imperative that these be adapted to account for 1997) but not implicated in outbreaks of gastroen-specific viral hazards. teritis. Nevertheless, these viruses have been connected with numerous cases of gastroenteritis, the causes of which were not reported (Table 1) eration and action to improve the surveillance, Anonymous, 1999a. Food Safety Standards, Costs and Benefits. monitoring and control of viruses in foods. Com-Australia -New Zealand Food Authority, Commonwealth Government of Australia, Canberra, pared with bacteria, epidemiological investigation Anonymous, 1999b. Discussion paper on viruses in food. CX / FH and reporting of foodborne viral illnesses were

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