cord-014527-nvzfpntu	2015	
cord-021452-9rukc80y	2009	Infectious inflammatory disease is the most common categorical differential diagnosis in cats with spinal cord dysfunction. 1 Common infectious inflammatory spinal cord diseases include FIP, cryptococcosis, FeLV infection, and toxoplasmosis. 6, 7 Polioencephalomyelitis, an inflammatory disease of unknown cause, is associated with 8 per cent of cases of feline spinal cord disease 1 and may present with clinical signs of paraparesis. FIP accounts for more than half of the infectious inflammatory causes of myelitis in cats, and 16 per cent of all spinal cord diseases reported in cats. In a case series of cats with spinal cord-related signs, more than 75 per cent were younger than 2 years of age. Overall the most consistent diagnostic findings in cats with the CNS form of FIP include a positive coronavirus IgG titer in CSF, a high serum total protein concentration, and abnormalities in brain imaging. 19 Clinical signs of spinal cord dysfunction, including paraspinal hyperesthesia and paresis, have been reported in at least one case series.
cord-022203-t2f0vr1w	2009	Clinical signs are often non-specific and include fever, anorexia and weight loss. Gastrointestinal signs are uncommon in cats compared to dogs, and include chronic diarrhea, mesenteric lymphadenopathy and anorexia. • Dysfunction of any organ system may result from granuloma formation within the tissue of that organ, e.g., liver, kidney, spleen, intestines, lungs, etc., however, organ failure producing clinical signs only rarely occurs, and most dysfunction is only detected on biochemical tests. Clinical signs in the acute, fatal form of extraintestinal disease are caused primarily by tissue damage from the rapidly dividing tachyzoites. • Young kittens are more likely to have gastrointestinal signs, although mild clinical disease has been reported in adult cats as well. Systemic signs, which are not present in all cats, include fever, anorexia, lethargy, vomiting, diarrhea and lymphadenopathy. Systemic signs such as fever, anorexia and depression are commonly reported (44% of cats) and can be seen with skin lesions.
cord-022555-a7ie82fs	2011	One study found that, of cats investigated for gastrointestinal disease, 9 of 33 cats (27%) had no pathology recognized proximal to the jejunum (i.e., the effective length of diagnostic endoscopes would have precluded diagnosis), and other organs were affected in 9 of 10 cats with inflammatory bowel diseases and 7 of 8 cats with intestinal small cell lymphoma. 60, 64 Quantification of serum cobalamin levels is recommended in cats with clinical signs of small bowel diarrhea, ones suspected to have an infiltrative disease of the small intestine (inflammatory bowel disease or gastrointestinal lymphoma), or ones with pancreatic dysfunction. Survey radiographs may be normal in cats with esophagitis and strictures, but are useful to rule out other causes for the clinical signs, such as a foreign body, or to detect related problems, such as aspiration pneumonia. 8, 29 Other non-neoplastic causes reported for gastric or gastroduodenal ulceration in cats include parasites (e.g., Ollulanus tricuspis, Toxocara cati, Aonchotheca putorii, Gnathostoma spp.), bacterial infections, toxins, inflammatory bowel disease, and foreign bodies.
cord-023034-j8zwcfys	2010	SUMMARY: Feline infectious peritonitis (FIP) virus multiplication was demonstrated in the brains of one‐day‐old laboratory mice using direct immunofluorescence tests. In order to determine the specificity of the observed fluorescence for FIP virus, indirect IFT were carried out in parallel on poslitive mouse brain sections (homologous reaction) and on porcine kidney cells infected with TGE virus (heterologous reaction). The conclusive experiment for establishing the FIP virus specificity of the immunofluorescence in mouse brain was performed by inoculating SPF kittens with fluorescence-positive material of the 6th mouse passage (isolation series A, Table 1 ). Feline infectious peritonitis (FIP) virus multiplication was demonstrated in the brains of one-day-old laboratory mice using direct immunofluorescence tests. Specificity was assessed by virus reisolation, indirect immunofluorescence and reproduction of FIP after inoculation of SPF kittens using brain material from the 6th mouse passage. Specificity was assessed by virus reisolation, indirect immunofluorescence and reproduction of FIP after inoculation of SPF kittens using brain material from the 6th mouse passage.
cord-023121-hewbl5yu	2008	Twenty‐one cases of feline infectious peritonitis (FIP) were diagnosed using a direct immunofluorescence test on cytocentrifuged pleural and peritoneal effusions from cats sampled in vivo (11 cases) and at necropsy (10 cases). In the remaining 2 1 cats, the clinical diagnosis of FIP was confirmed by pathological and histological findings and was also confirmed in 10 of these cases by a positive DIF test carried out on cryostatic sections of affected organs. A marked disagreement between the result from the DIF test on ascitic fluid and the final FIP diagnosis was found in only one case (case 11; Table 1) which at the age of four months showed clinical signs of thoracic effusions with fever. The cases where pathological entities different to FIP were identified and where the DIF test had never been positive on either the samples of the effusions or the cryostatic sections of affected organs were useful negative controls.
cord-253498-w6qfzpi4	2010	title: Electrophoretic fractionation of creatine kinase isoenzymes and macroenzymes in clinically healthy dogs and cats and preliminary evaluation in central neurologic disease Background: Information about the electrophoretic distribution of CK‐MM, CK‐MB, and CK‐BB, serum creatine kinase (CK) isoenzymes that are indicators of skeletal muscle, cardiac muscle, and brain lesions, respectively, and CK macroenzymes (macro‐CK1 and macro‐CK2) in dogs and cats with and without central neurologic disease is scant and equivocal. Objectives: The objectives of this study were to describe the electrophoretic distribution of CK isoenzymes and macroenzymes in healthy dogs and cats and to provide a preliminary assessment of the utility of CK enzymatic electrophoresis in dogs and cats with central neurologic disease. Conclusions: This study identified the electophoretic distribution of CK isoenzymes and macroenzymes of dogs and cats and provided encouraging data about the possible use of CK‐BB as a biomarker for canine neurologic disorders, but not for FIP.
cord-254375-otj044by	1998	Haematology, antibody titers and serum protein electrophoresis from 48 cats (34 effusive and 14 noneffusive forms) affected with feline infectious peritonitis (FIP) were studied and compared with those of 20 healthy cats. Even if antibody-enhanced infection has been recently questioned (Olsen et al., 1992 (Olsen et al., , 1993 Addie et al., 1995) , many experimental results demonstrate that anti-FCoV antibodies facilitate the uptake of the virus by the macrophages (Hayashi et al., 1983; Stoddart and Scott, 1989 ; Barlough and Stoddart, 1990; Hohdatsu et al., 1994; Pedersen, 1995a) , and that immunocomplexes lead to a type III hypersensitivity reaction with disseminated intravascular coagulation and fibrinoid necrosis of the vessel''s walls, responsible for the effusions (Hayashi et al., 1977 (Hayashi et al., , 1978 Pedersen and Boyle, 1980; Weiss et al., 1980; Jacobse-Geels et al., 1980; Weiss and Scott, 1981; Fenner, 1987; Pastoret and Bourtonboy, 1991; Pedersen, 1995a) . To further understand the pathogenesis of the disease, parameters indicative of the involvement of humoral immunity (total and fractioned proteins and antibody titers in serum and in effusions), and the distribution of viral antigen and immune cells in the lesions were studied in cats with spontaneous FIP.
cord-258374-qht98q0l	2009	title: Neutrophil survival factors (TNF-alpha, GM-CSF, and G-CSF) produced by macrophages in cats infected with feline infectious peritonitis virus contribute to the pathogenesis of granulomatous lesions Furthermore, it was investigated whether macrophages, one of the target cells of FIPV infection, produce neutrophil survival factors (TNF-alpha, GM-CSF, and G-CSF). The neutrophil survival rates were significantly increased in the presence of the culture supernatant of macrophages infected with the mixture of FIPV and MAb 6-4-2 compared to those in the presence of other supernatants (Fig. 5) . When SPF-cat-derived alveolar macrophages were infected with a mixture of FIPV and MAb 6-4-2, the intracellular TNF-alpha, GM-CSF, and G-CSF mRNA levels increased (Fig. 6 ). These cytokine mRNA levels were also elevated in macrophages infected with FIPV and MAb 6-4-2, clarifying the presence of neutrophil survival factors in the macrophage culture supernatant. It was suggested that: (1) FIPV-infected macrophages release TNF-alpha, GM-CSF, and G-CSF in response to virus replication, and (2) these cytokines act on neutrophils and prolong their survival.
cord-264315-3hum7rqm	2001	Abstract Blood was collected from 55 cats with feline infectious peritonitis (FIP) and from 50 control cats in order to define whether differences in pathological findings and in distribution of feline coronaviruses (FCoV) can be associated with changes in haemograms, serum protein electrophoresis, and antibody titres. Based on the pathological findings or on the immunohistochemical distribution of viral antigen, FIP-affected cats were divided in the following groups: subacute against acute lesions; low against strong intensity of positivity; intracellular against extracellular positivities; positive against negative lymph nodes. Lymphopenia was more evident in cats with acute forms, strong intensity of positivity, extracellular antigen and negative lymph nodes. The haematological and serum protein profiles of cats with feline infectious peritonitis (FIP) were in agreement with those reported in previous works (Sparkes et al 1991 , Pedersen 1995a , Paltrinieri et al 1998b .
cord-266155-hf3retap	2020	Although recombinant feline interferon omega (FeIFNω: Virbagen Omega, Virbac, France) was previously shown to reduce FCoV shedding, this is the first report to document an anti-viral that stopped the excretion of FCoV in the faeces of naturally infected cats. Results from five cats from Household E could not be included because the intervals between faecal tests left the possibility that the cats might have spontaneously stopped shedding virus, rather than Mutian X having stopped virus shedding: thus they were excluded from both treatment and control groups (Table 1) . Prior to the observational study we report here, the cattery owner (SC) discovered she could reduce coronavirus shedding in some cats using Mutian X tablets: we worked with her to optimise dose and duration of treatment for stopping virus shedding. Mutian X pills stopped faecal FCoV shedding in 29 naturally infected cats; however, four of the 29 cats required a second course of treatment before virus was eliminated.
cord-268492-0rbmqarx	2020	The RCPCH and CDC have published a case definition and scientists refer to this novel but still very rare severe clinical condition in children as "paediatric inflammatory multisystem syndrome temporally associated with SARS-CoV-2" (PIMS-TS). While reflecting on this syndrome and its characteristic features, some interesting similarities come to mind when comparing the clinical course of PIMS-TS cases and the specific features of a disease in cats called feline infectious peritonitis (FIP) caused by the feline coronavirus (FCoV), an alphacoronavirus [2] . On this note, it would be of great interest to see whether mutations in the viral genome, particularly in regions affecting the S-protein of SARS-CoV-2, could lead to a change in cell tropism enabling the virus to more effectively infect and replicate within human monocytes/macrophages subsequently leading to the clinical picture of PIMS-TS.
cord-270414-gh9agf4x	2011	title: Randomized, Placebo Controlled Study of the Effect of Propentofylline on Survival Time and Quality of Life of Cats with Feline Infectious Peritonitis Several case reports can be found in the online Veterinary Information Network (http://www.VIN.com) that describe a positive effect of the methylxanthine derivative pentoxifylline (PTX) (Trental a ) on the survival time in cats with FIP. ALT alanine aminotransferase AP alkaline phosphatase CI confidence interval FCoV feline coronavirus FeLV feline leukemia virus FIP feline infectious peritonitis FIPV feline infectious peritonitis virus FIV feline immundeficiency virus IFAT immunofluorescent antibody technique PPF propentofylline PTX pentoxifylline RBC red blood cells SPSS statistical package for the social sciences TNF-a tumor necrosis factor-alpha TP total protein WBC white blood cells which cause endothelial cell damage. The aim of this study was to evaluate the efficacy of PPF on the survival time and quality of life in cats with a confirmed diagnosis of FIP in a placebocontrolled double-blind trial.
cord-271078-zyy8gx25	2010	title: Descriptive distribution and phylogenetic analysis of feline infectious peritonitis virus isolates of Malaysia The descriptive distribution and phylogeny of feline coronaviruses (FCoVs) were studied in cats suspected of having feline infectious peritonitis (FIP) in Malaysia. Feline infectious peritonitis (FIP) is a highly fatal disease of cats caused by generalized infection with a feline coronavirus (FCoV). Two biotypes of FCoV are described in cats: feline infectious peritonitis virus (FIPV) and feline enteric coronavirus (FECV). In present study, a conserved region of 3''untranslated region (3''UTR) is used to detect FCoV and determine the descriptive distribution and phylogeny of local isolates in FIP-suspected cats. An enteric coronavirus infection of cats and its relationship to feline infectious peritonitis Phylogenetic analysis of feline coronavirus isolates from healthy cats in Malaysia Quasispecies composition and phylogenetic analysis of feline coronaviruses (FCoVs) in naturally infected cats Descriptive distribution and phylogenetic analysis of feline infectious peritonitis virus isolates of Malaysia
cord-273424-iz1vat9p	2004	In contrast, during FIP disease, fAGP underwent several modifications in the sialic acid content, including decreased expression of both α(2–6)-linked and α(2–3)-linked sialic acid (76 and 44%, respectively when compared to non-pathological feline AGP). The biological significance of AGP overexpression during FIP and its correlation with the Veterinary Immunology and Immunopathology 99 (2004) [229] [230] [231] [232] [233] [234] [235] [236] Abbreviations: FIP, feline infectious peritonitis; AGP, a1-acid glycoprotein; fAGP, feline a1-acid glycoprotein; FCoV, feline coronavirus; HP, haptoglobin; SleX, sialyl Lewis X; HPLC, high pressure liquid chromatography; SNAI, Sambucus nigra agglutinin; MAA, Maackia amurensis agglutinin; AAL, Aleuria aurantia lectin * Corresponding author. In the present study we used the lectin binding specificity for carbohydrates in order to gain insight into some major (branching) and minor (sialic acid content) glycan microheterogeneity of feline AGP (fAGP) purified from FIP affected cats.
cord-276617-chgjpg0v	2008	The present study shows that: (1) the ratio of peripheral blood sIg(+) CD21(−) B-cells was higher in cats with FIP than in SPF cats, (2) the albumin-to-globulin ratio has negative correlation with the ratio of peripheral blood sIg(+) CD21(−) B-cell, (3) cells strongly expressing mRNA of the plasma cell master gene, B-lymphocyte-induced maturation protein 1 (Blimp-1), were increased in peripheral blood in cats with FIP, (4) mRNA expression of B-cell differentiation/survival factors, IL-6, CD40 ligand, and B-cell-activating factor belonging to the tumor necrosis factor family (BAFF), was enhanced in macrophages in cats with FIP, and (5) mRNAs of these B-cell differentiation/survival factors were overexpressed in antibody-dependent enhancement (ADE)-induced macrophages. We also collected macrophages from FIP cats and measured the expression levels of the viral RNA and mRNA of B-cell differentiation/survival factors: IL-6, CD40 ligand (CD40L), and Bcell-activating factor belonging to the tumor necrosis factor family (BAFF).
cord-281179-k7630is6	2011	Feline infectious peritonitis (FIP) is a fatal, immune-augmented, and progressive viral disease of cats associated with feline coronavirus (FCoV). Feline infectious peritonitis (FIP) is a fatal, immune-augmented, and progressive viral disease of cats associated with feline coronavirus (FCoV). Mutational transition in viral pathogenesis has been shown in HIV infection, where specific amino acid changes in the envelope gene determine which coreceptor (CCR5 or CXCR4) is used and hence virus success in cell entry (Hartley et al., 2005) . However, more recent in vitro studies of cathepsin B and cathepsin L activity in different isolates of FCoV showed that FECV isolates were able to induce a specific cleavage event in the spike protein in contrast to FIPV isolates, suggesting that cathepsin activity on the spike gene may play a role in viral pathogenesis at the level of cell entry .
cord-283202-5fq1wxz8	2009	This article reviews the clinical signs, pathophysiology, diagnosis, treatment and prognosis of four important systemic diseases with neurological consequences: feline infectious peritonitis, toxoplasmosis, hypertension and hepatic encephalopathy. A presumptive diagnosis is based on a combination of clinical signs, evidence of recent or active infection (gained via serology for immunoglobulins or immune complexes, or PCR), exclusion of other disease processes, and response to therapy. Consequently, affected cats often demonstrate signs relating to renal disease or hyperthyroidism, given the high prevalence of hypertension with these disorders. Hepatic encephalopathy is the clinical syndrome of abnormal neurological function caused by portosystemic shunting, with or without intrinsic liver disease. Use of anti-coronavirus antibody testing of cerebrospinal fluid for diagnosis of feline infectious peritonitis involving the central nervous system in cats Non-invasive blood pressure measurements in cats: clinical significance of hypertension associated with chronic renal failure
cord-284963-p0y5rrpb	2006	The spleen, mesenteric lymph nodes and bone marrow from naturally FCoV-infected cats with and without FIP and specific pathogen-free (SPF) control cats were examined for the quantity and activation state of monocytes/macrophages both by immunohistology and by quantitative real time PCR for the transcription of interleukin (IL)-1β, IL-6, IL-10, IL-12 p40, tumour necrosis factor (TNF), granulocyte colony stimulating factor (G-CSF), macrophage-CSF (M-CSF) and GM-CSF. Feline infectious peritonitis (FIP) is a well-known and widely distributed coronavirus (FCoV)-induced systemic disease in cats, characterised by fibrinousgranulomatous serositis with protein-rich effusions into body cavities, granulomatous-necrotising phlebitis and periphlebitis and granulomatous inflammatory lesions in several organs (Hayashi et al., 1977; Weiss and Scott, 1981; Kipar et al., 1998 Kipar et al., , 2005 . Taken together, our results indicate that IL-10 is a key cytokine in FCoV infection, ensuring an effective specific immune response, but avoiding the inflammatory processes associated with the development of FIP (Kipar et al., 2005) , by inhibiting the virus-induced macrophage activation.
cord-285335-agm4zbcx	2001	A population of Persian cats experienced an epidemic of feline infectious peritonitis (FIP) over 2 years. Feline coronavirus (FCoV) genomic RNA was detected consistently in this study in biologic samples from adult cats, kittens suffering from FIP, and their siblings. Analysis of viral 7a/7b open reading frame (ORFs) were analyzed and revealed two distinct virus variants circulating in the population, one with an intact 7a ORF and one with two major deletions in the 7a ORF. Both virus variants were identified in one cat, the sire ''''Dan'''', as sequence analysis of clones from a single PCR from this animal revealed the presence of the 7a deletion mutant as well as the intact isolate (Dan 1 and 2 in Fig. 2 ). The sire of the majority of FIP kittens was dually infected with both virus variants as revealed by sequence analysis of cloned 7a/7b genes from this cat.
cord-287157-6rwevq39	2004	authors: Kiss, I.; Poland, A.M.; Pedersen, N.C. title: Disease outcome and cytokine responses in cats immunized with an avirulent feline infectious peritonitis virus (FIPV)-UCD1 and challenge-exposed with virulent FIPV-UCD8 Feline infectious peritonitis (FIP) is a highly fatal disease in Felidae caused by a coronavirus and usually affects cats between 6 months and 3 years of age (reviewed by Pedersen, 1995) . Three of eight vaccinated cats (nos 522, 616, 622) developed effusive FIP within 2 weeks of challengeexposure to FIPV-UCD8, typical of classical nonenhanced disease (Pedersen and Boyle, 1980) ( Table 1) . In this study, two of eight vaccinated cats (nos 524 and 625) appeared immune to challenge-exposure with virulent FIPV-UCD8 and two (nos 623 and 624) developed non-effusive FIP (indicative of partial immunity; Pedersen, 1995) . In the presented preliminary experiment, vaccination of cats with an attenuated live strain of FIPV-UCD1 appeared to induce a degree of protection, in that two of eight cats were immune and two more developed non-effusive FIP post challenge.
cord-295491-zlah6u5s	2018	The aim of this study was to test two commercially available reaction mixtures in a reverse transcription loop-mediated isothermal amplification (RT-LAMP) assay to detect feline Coronavirus (FCoV) in body cavity effusions of cats with and without FIP, in order to minimize the time from sampling to obtaining results. The aim of this study was to test specificity and sensitivity of two commercially available reaction mixtures in a reverse transcription LAMP (RT-LAMP) to detect FCoV in body cavity effusions of cats with and without FIP, and to minimize the time from sampling to obtaining results. The FIP group (n = 34) included cats with a definitive diagnosis of FIP by one or more methods: All effusions of cats with FIP tested positive for FCoV by RT-PCR by a commercial laboratory, and in 26/34 samples putative disease-causing mutations could be detected.
cord-302161-ytr7ds8i	2020	Feline Infectious Peritonitis (FIP)—the deadliest infectious disease of young cats in shelters or catteries—is induced by highly virulent feline coronaviruses (FCoVs) emerging in infected hosts after mutations of less virulent FCoVs. Previous studies have shown that some mutations in the open reading frames (ORF) 3c and 7b and the spike (S) gene have implications for the development of FIP, but mainly indirectly, likely also due to their association with systemic spread. Based on the hypothesis that certain mutations are essential for the capacity of FCoVs to spread systemically, the present study investigated a cohort of systemically infected healthy carrier cats at different time points post experimental infection for the presence of a range of mutations in the genes encoding for the S protein, NSP 3abc, and NSP 7b, which have been shown to have implications for the development of FIP.
cord-304616-k92fa15l	2020	title: Assay validation and determination of in vitro binding of mefloquine to plasma proteins from clinically normal and FIP-affected cats As cats with feline infectious peritonitis (FIP) demonstrate altered concentrations of plasma proteins, the proportion of mefloquine binding to plasma proteins in both clinically normal cats and FIP-affected cats was also investigated. Consequently, the aim of this study was two-fold: first, to develop and validate a high pressure liquid chromatography (HPLC) method to detect mefloquine in feline plasma, and second, to determine the in vitro plasma protein binding of mefloquine in both clinically normal and FIP-affected cats. Here, although a significant difference was found between the plasma protein binding of mefloquine in clinically normal and FIP-affected cats, due to the unknown biological variability of the assay, it is likely that this difference is equivocal. This study has validated an accurate and reliable assay to detect mefloquine in feline plasma and demonstrated that mefloquine is highly plasma protein bound in both clinically normal and FIP-affected cats.
cord-306829-88nihy7q	2010	Infection with FCoV can result in a diverse range of signs from clinically inapparent infections to a highly fatal disease called feline infectious peritonitis (FIP). The currently available serological tests have low specificity and sensitivity for detection of active infection and cross-react with FCoV strains of low pathogenicity, the feline enteric coronaviruses (FECV). Therefore, a quantitative real-time RT-PCR assay that could determine the amount of viral mRNA in blood may be able to better differentiate FCoV-positive healthy cats from FIP cases. Detection of feline coronaviruses by culture and reverse transcriptase-polymerase chain reaction of blood samples from healthy cats and cats with clinical feline infectious peritonitis Protein electrophoresis on effusions from cats as a diagnostic test for feline infectious peritonitis Detection of feline coronavirus RNA in feces, tissues, and body fluids of naturally infected cats by reverse transcriptase PCR Detection of feline coronavirus RNA in feces, tissues, and body fluids of naturally infected cats by reverse transcriptase PCR
cord-308537-i6um5iu2	1993	Cats are susceptible to natural infection with several strains of feline coronavirus that result in either effusive and noneffusive feline infectious peritonitis or enteritis. 33 Most asymptomatic cats with positive coronavirus-antibody titers have been previously infected by strains of feline enteric coronavirus or FIP coronavirus, which usually do not cause fatal disease by natural routes of infection. The susceptibility of cats to FIP disease may involve several predisposing factors, including age at time of exposure, genetic susceptibility, physical condition, stress, presence of concurrent disease (especially feline leukemia virus and feline immunodeficiency virus infections), challenge dose and strain of feline coronavirus, route of infection, previous sensitization with nonprotective corona virus antibodies, and cell-mediated immunocompetence. Cats are susceptible to natural infection with several strains of feline coronavirus that may result in either effusive and noneffusive FIP disease or in subclinical to severe enteritis.
cord-308557-mvu97jsu	2005	Although known that purebreed cats are more likely to develop feline infectious peritonitis (FIP), previous studies have not examined the prevalence of disease in individual breeds. Other factors that have been less commonly reported to be associated with an increased disease prevalence include season (more cases are typically diagnosed in winter), FeLV infection, an increase in factors associated with ''stress'', high coronavirus antibody titer, regular introduction of new cats to a cattery, and increased frequency of coronavirus shedding (Kass and Dent 1995 , McReynolds and Macy 1997 , Foley et al 1997a , Rohrbach et al 2001 . Although the increased prevalence of FIP in purebreed cats has been previously reported, this is the first time that a predisposition of specific breeds to the development of disease has been examined (Robison et al 1971 , Rohrbach et al 2001 .
cord-313439-cadyykks	2019	
cord-315094-pzixgqcy	2004	Investigations showed that a high percentage of cats without FIP symptoms from exposed environments were positive for FCoV infection: 39-85% were seropositive, 37-95% viremic and 73-81% excreted virus in their faeces (Addie and Jarrett, 1992b; Sparkes et al., 1992; Herrewegh et al., 1995; Foley et al., 1997a,b; Gunn-Moore et al., 1998) . The recently developed reverse transcriptase polymerase chain reaction (RT-PCR) assays, using primers targeted to highly conserved regions of the viral genome (3 -UTR (untranslated region) (Herrewegh et al., 1995; Fehr et al., 1996) , or S-protein gene (Li and Scott, 1994; Gamble et al., 1997) ), which are common to all FCoV strains, became a valuable tool for the detection of FCoV nucleic acid in blood, body cavity effusions, faeces and tissue samples of infected cats. With the retrospective study presented here we investigated the prevalence of the two types of FCoVs in cats with histopathologically verified FIP using nested and seminested RT-PCR assays, with primers targeted as well to the S-protein gene.
cord-317411-6lc0wpoo	2011	Clinical findings, serum protein electrophoresis (SPE), analysis of the effusions (AE), antifeline coronavirus serology, serum concentration of α1‐acid glycoprotein (AGP) and histopathology were classified as consistent, doubtful or non‐consistent with FIP. The purpose of this study was to retrospectively assess the results of tests recorded in vivo and at postmortem examination in doubtful cases where FIP was clinically suspected and definitely confirmed or excluded by IHC or based on complete recovery and to evaluate which test had the best sensitivity, specificity and concordance for FIP. In cats with FIP, the tests that were not consistent with or doubtful of FIP included clinical signs (3 of 8 cases), analysis of effusion (AE; 3 of 6), SPE (5 of 8), serology or PCR (4 of 5) and postmortem examination/histology (5 of 8).
cord-319685-dw0qsl4s	2014	Recent evidence suggests that a mutation in the spike protein gene of feline coronavirus (FCoV), which results in an amino acid change from methionine to leucine at position 1058, may be associated with feline infectious peritonitis (FIP). Tissue and faecal samples collected post mortem from cats diagnosed with or without FIP were subjected to RNA extraction and quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) to detect FCoV RNA. Data evaluating FCoV relative copy numbers in tissue and faecal samples from cats with and without FIP were analysed using a multilevel modelling approach (MLwiN v2.27) [25] , to account for the repeated measures within cats, and a non-parametric Mann-Whitney U test. Moreover, the majority (77%) of FCoV RNA sequences in faecal samples from cats with FIP had a methionine codon at position 1058 in the FCoV S protein gene, suggesting that these animals were shedding an enteric form of the virus.
cord-322317-wsagoy52	2020	Histology, IHC, and nested RT-PCR (RT-nPCR) for feline coronavirus (FCoV) were performed on spleen, liver, mesenteric lymph node, kidney, large and small intestine, and lung from 14 FIP and 12 non-FIP cats. In the FIP group, the tissues that most often showed typical FIP histological lesions (Table 2) were the lung, kidney, and mesenteric lymph node, followed by the liver and spleen, while the small and large intestine were the organs less frequently affected by lesions imputable to FIP. In particular, this occurred in the same 6 cases from the non FIP group and in 15/21 FIP tissues in which histology was classified as negative and RT-nPCR was positive (spleen of cats n • 1 and 3, liver of cat n • 14, lymph nodes of cats n • 1, 2, and 14, kidney of cats n • 5, 12, and 13, small intestine of cats n • 9 and 12, large intestine of cats n • 2, 9, and 12 and lung of cat n • 14), whose histological findings have been described above.
cord-323805-9n63ms3c	2014	The cats were from several studies conducted over the past 5 years, and as a result, some of them had prior exposure to feline enteric coronavirus (FECV) or avirulent FIPVs. The cats were housed under optimized conditions of nutrition, husbandry, and quarantine to eliminate most of the cofactors implicated in FIPV infection outcome and were uniformly challenge exposed to the same field strain of serotype 1 FIPV. The cats were from several studies conducted over the past 5 years, and as a result, some of them had prior exposure to feline enteric coronavirus (FECV) or avirulent FIPVs. The cats were housed under optimized conditions of nutrition, husbandry, and quarantine to eliminate most of the cofactors implicated in FIPV infection outcome and were uniformly challenge exposed to the same field strain of serotype 1 FIPV. Genome-wide association studies (GWAS) on 73 cats that died of FIP after one or more exposures (cases) and 34 cats that survived (controls) demonstrated four significant associations after 100k permutations.
cord-323932-l14sjufm	2004	A total of 12 clinically ill cats previously diagnosed as feline infectious peritonitis (FIP) were treated with a combination of recombinant feline interferon and glucocorticoid. Summary A total of 12 clinically ill cats previously diagnosed as feline infectious peritonitis (FIP) were treated with a combination of recombinant feline interferon and glucocorticoid. The criteria of the diagnosis included: antibiotics non-responsive chronic fever, low normal PCV values or mild non-regenerative anemia (PCV <32%; normal range 29-48%), hyperglobulinemia with electrophoretic evidence of polyclonal gammopathy, non-septic inflammatory ascites/pleural effusion (effusive) with characteristic findings, cytologic or pathologic evidence of pyogranuloma (dry-type), and FCoV serum antibody titer by an immunoperoxidase method using infected cell antigen. The maintenance therapy with the weekly doses of rFeIFN and prednisolone at 1 mg/kg PO every other day, the cat was healthy at 14 months from the diagnosis, when the treatment was terminated and the FCoV antibody was <1:100.
cord-324530-tac1unnp	2019	title: Distinct mutation in the feline coronavirus spike protein cleavage activation site in a cat with feline infectious peritonitis-associated meningoencephalomyelitis CASE SUMMARY: This report describes a cat with chronic, progressive, non-painful, non-lateralizing multifocal neurologic clinical signs associated with feline infectious peritonitis (FIP). Molecular analysis of the coronavirus spike protein within the tissues identified a specific, functionally relevant amino acid change (R793M), which was only identified in tissues associated with the central nervous system (ie, brain and spinal cord). RELEVANCE AND NOVEL INFORMATION: This case report describes an early presentation of a cat with primarily neurologic FIP, with molecular characterization of the virus within various tissues. 18 Molecular analysis of the viral spike protein within the tissues identified a specific, functionally relevant amino acid change (R793M), which was only identified in tissues associated with the CNS (ie, brain and spinal cord). This case report describes a young cat with neurologic FIP in which detailed clinical and molecular characterization of the associated FCoV infection was performed.
cord-327352-cbnjsrmt	1998	Diffuse alterations on serosal surfaces were represented either by activated mesothelial cells with single coronavirus antigen-bearing macrophages or by layers of precipitated exudate containing single to numerous granulomas with areas of necrosis. Single plasma-cells positive for coronavirus-specific antibodies were found around blood vessels distant from inflammatory alterations, within the lung parenchyma, as infiltrating cells in the mucosa of the small intestine, and in spleen and mesenteric lymph node. Based on immunohistological and histochemical characterization of inflammatory cells as well as the presence of coronavirus antigen and plasma-cells producing coronavirus-specific antibodies in the lesions of 23 cats with spontaneous FIP, this study describes the composition of alterations observed in FIP after natural infection. Viral antigen was moderately expressed in granulomas, in the periphery of which few plasma-cells producing coronavirus-specific antibodies were seen.
cord-329866-io9fvy58	2019	With the aim to contribute to fill this diagnostic gap, a total of 61 effusions from cats with suspected effusive FIP were collected intra-vitam for detection of feline coronavirus (FCoV) antibodies and RNA by means of indirect immunofluorescence (IIF) assay and real-time RT-PCR (qRT-PCR), respectively. Fifty-one (48 ascitic and 3 pleuric fluids) of the 61 tested samples had FCoV antibody (Table 2 and Fig. 1 ), although only 37 positive effusions contained antibody levels ≥ 1:1600, which are considered highly suggestive of FIP diagnosis (Hartmann et al., 2003) . A recent paper (Meli et al., 2013) has investigated the agreement between FCoV antibody titres and RNA detection in the effusions of 13 cats with confirmed FIP, showing a correlation between high amounts of virus and lower signals in IIF assay, likely due to the fact that antibodies bound to viral antigens of the effusions are not able to bind to the antigens of the FCoV-infected cells used in serological tests.
cord-331045-i33nr27j	2003	For diagnosis, clinicians use a panel of tests including FCoV serology, albumin to globulin ratio, haematology, cytology of effusion and measurement of acute phase proteins, especially a1-acid glycoprotein (AGP). Present belief is that for cats to develop FIP, a mutation (more accurately -a deletion) must occur in the viral genome of non-pathogenic FCoVs (so called enteric coronaviruses) which allows the virus to replicate in macrophages (Vennema et al., 1998) . I have followed one cat with FIP over the time of treatment until death and I found that AGP and globulin levels correlated well with response to treatment and improving or worsening clinical signs, whereas repeatedly measuring FCoV antibody titre was unhelpful. Changes in some acute phase protein and immunoglobulin concentrations in cats affected by feline infectious peritonitis (FIP) or exposed to feline coronavirus infection
cord-335434-lgvoethn	2005	title: Cutaneous lesions associated with coronavirus-induced vasculitis in a cat with feline infectious peritonitis and concurrent feline immunodeficiency virus infection This report describes a clinical case of feline infectious peritonitis (FIP) with multisystemic involvement, including multiple nodular cutaneous lesions, in a cat that was co-infected with feline coronavirus and feline immunodeficiency virus. Immunohistology for feline coronavirus (FCoV) antigen, using a mouse monoclonal antibody (FCV3-70, Custom Monoclonals International, West Sacramento, USA), was performed on renal and skin biopsies as previously described (Kipar et al 1998, in press ). The diagnosis was confirmed by the presence of numerous FCoV antigen-positive macrophages within the granulomatous lesions, a finding only seen in, and therefore pathognomonic for, FIP (Kipar et al 1998, in press) . Taken together, the clinical signs, clinical pathology, histological changes and immunohistological findings in this case confirm that the cat had a ''non-effusive form'' of FIP, with involvement of the kidneys, skin and most likely brain and eyes.
cord-336332-9d1h68mi	2003	Immunoblotting with a polyclonal antibody against fAGP and with a monoclonal antibody against hAGP was performed on serum from healthy cats, from cats exposed to feline coronavirus (FCoV) infection and from cats with purulent inflammations, such as feline infectious peritonitis (FIP), feline immunodeficiency virus (FIV) and feline leukemia virus (FeLV). fAGP did not react with the anti-hAGP antibody which, in contrast, detected in feline serum a low MW protein that we called fAGP-related protein (fAGPrP). In contrast, the anti-hAGP detected an AGP-related protein whose blood concentration and tissue distribution was not related to that of fAGP. In order to investigate the distribution of fAGP and of fAGPrP in different feline pathological conditions, immunoblotting was repeated on serum from cats with purulent inflammations, FIV, FeLV and FIP, and from Fig. 2 Immunoblotting of hAGP and fAGP using as primary antibody the anti hAGP monoclonal antibody (a) or the anti fAGP polyclonal antibody (b).
cord-336639-jaue41mv	2004	A reverse transcriptase polymerase chain reaction (RT-PCR) for the detection of feline coronavirus (FCoV) messenger RNA in peripheral blood mononuclear cells (PBMCs) is described. The reason for this discrepancy became clear when the biological and genetic properties of FECV and FIPV isolates had been studied (Addie and Jarrett, 1992; Hohdatsu et al., 1992; Horzinek and Osterhaus, 1979) : the avirulent FCoV strains causing inconspicuous infections are responsible for the high seroprevalence; in cats experiencing some immunosuppressive event, expansion of the quasispecies cloud and mutations in the FECV genome lead to virulent variants that induce FIP (Vennema et al., 1998) . Detection of feline coronaviruses by culture and reverse transcriptase-polymerase chain reaction of blood samples from healthy cats and cats with clinical feline infectious peritonitis
cord-336730-hqgwj8vs	1997	title: Placebo-controlled evaluation of a modified life virus vaccine against feline infectious peritonitis: safety and efficacy under field conditions Abstract A modified live virus vaccine against feline infectious peritonitis (FIP) was evaluated in a double blind, placebo-controlled field trial in two high-risk populations. The vaccine was found to be safe and efficacious in one population of cats that had low antibody titre against feline coronavirus (FCoV) at the time of vaccination. Feline infectious peritonitis (FIP) is a normally fatal disease of cats caused by infections with feline coronaviruses (FCoV) which are antigenically related to a respiratory coronavirus strain of man (HCV 229E), transmissible gastro-enteritis virus (TGEV) of swine and canine coronaviruses13''. The aim of this study was to evaluate the efficacy and safety of a modified live virus vaccine in a double-blind study under field conditions in two cat populations with higher risk for FIP.
cord-348746-yaf61cmx	2008	F eline infectious peritonitis (FIP) is a fatal, immune-mediated disease produced as a result of infection of macrophages by mutant feline coronavirus strains (FIPVs). In acute MHV-A59 infection in CD8Ï© T-cell deficient mice, periventricular encephalitis occurs with lymphocytic infiltration into the choroid plexus, ependyma, and subependymal brain tissue. Depending on mouse strain and immunological status, MHV-JHM produces meningeal inflammation associated with T-cells and macrophages and demyelination but relatively little disease in axons. If mice are pretreated with passive infusions of antibodies or T-cells or if they receive neuroattenuated MHV strains, they develop chronic, but not fatal, disease after MHV-JHM infection. 62, 63 Immunocompetent C57BL/6 mice clear MHV-JHM virus from the brain but develop severe immune-mediated demyelination and paralysis. Two related strains of feline infectious peritonitis virus isolated from immunocompromised cats infected with a feline enteric coronavirus
cord-351955-9l4786lb	2009	Complete structural (S, E, M, N) and accessory (3a-c and 7 a, b) gene sequences were obtained from diseased omentum of the four related cats that died of FIP and the isolates designated were FIPV-UCD11, 12, 13 and 14 ( Table 1 ). The coronavirus isolated from Lucy''s feces (designated FECV-UCD3) had an intact (i.e., wild type or non-deliterious) 3c and its sequence was otherwise 99% identical to the sequence of FIPV-UCD14 found in her diseased omentum. FECV-UCD4, was most closely related to the FIPV isolated from Lucy and was 99.7% related to the consensus nucleotide sequences of coronaviruses obtained from the four related FIP cats ( Figure 1 , Table 2 ). The 3c gene sequence of the fecal virus of cat 388406 was intact and ≥99% related to the FIPV found in diseased tissue ( Table 2 ).