Academic literature on the topic 'Feline infectious peritoniti'
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Journal articles on the topic "Feline infectious peritoniti"
TZIVARA (Α. ΤΖΙΒΑΡΑ), A., and S. K. KRITAS (Σ.Κ. ΚΡΗΤΑΣ). "Feline Coronavirus infections and feline infectious peritonitis." Journal of the Hellenic Veterinary Medical Society 50, no. 3 (January 31, 2018): 199. http://dx.doi.org/10.12681/jhvms.15710.
Full textAvila, Vicente, and Daniel Rissi. "Ulcerative dermatitis due to feline infectious peritonitis virus infection in a cat." Brazilian Journal of Veterinary Pathology 13, no. 1 (March 31, 2020): 48–50. http://dx.doi.org/10.24070/bjvp.1983-0246.v13i1p48-50.
Full textKipar, A., and M. L. Meli. "Feline Infectious Peritonitis." Veterinary Pathology 51, no. 2 (February 25, 2014): 505–26. http://dx.doi.org/10.1177/0300985814522077.
Full textAndrew, Stacy E. "Feline Infectious Peritonitis." Veterinary Clinics of North America: Small Animal Practice 30, no. 5 (September 2000): 987–1000. http://dx.doi.org/10.1016/s0195-5616(00)05002-6.
Full textHartmann, Katrin. "Feline infectious peritonitis." Veterinary Clinics of North America: Small Animal Practice 35, no. 1 (January 2005): 39–79. http://dx.doi.org/10.1016/j.cvsm.2004.10.011.
Full textKennedy, Melissa A. "Feline Infectious Peritonitis." Veterinary Clinics of North America: Small Animal Practice 50, no. 5 (September 2020): 1001–11. http://dx.doi.org/10.1016/j.cvsm.2020.05.002.
Full textErmakov, Aleksey, Tatyana Lipilkina, Pavel Lipilkin, and Igor Popov. "Feline coronavirus infection." E3S Web of Conferences 273 (2021): 02025. http://dx.doi.org/10.1051/e3sconf/202127302025.
Full textSweet, Arjun N., Nicole M. André, Alison E. Stout, Beth N. Licitra, and Gary R. Whittaker. "Clinical and Molecular Relationships between COVID-19 and Feline Infectious Peritonitis (FIP)." Viruses 14, no. 3 (February 26, 2022): 481. http://dx.doi.org/10.3390/v14030481.
Full textNururrozi, Alfarisa, Agistanya Andimi, Yanuartono Yanuartono, and Soedarmanto Indarjulianto. "Studi Retrospektif Profil Hemogram Kasus Peritonitis Menular Tipe Efusif pada Kucing." Jurnal Veteriner 23, no. 1 (March 31, 2022): 112–20. http://dx.doi.org/10.19087/jveteriner.2022.23.1.112.
Full textHora, A. S., P. O. Tonietti, S. A. Taniwaki, K. M. Asano, P. Maiorka, L. J. Richtzenhain, and P. E. Brandão. "Feline Coronavirus 3c Protein: A Candidate for a Virulence Marker?" BioMed Research International 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/8560691.
Full textDissertations / Theses on the topic "Feline infectious peritoniti"
Hora, Aline Santana da. "Diversidade gênica do coronavírus felino em populações virais entéricas e sistêmicas intra e inter-hospedeiros." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/10/10134/tde-22072014-140450/.
Full textFeline coronavirus (FCoV) occurs as a large genic diversity of strains and is classified as two pathotypes: feline enteric coronavirus (FECoV) and feline infectious peritonitis virus (FIPV). The FIPV pathotype is highly virulent and responsible for the onset of a highly fatal disease named feline infectious peritonitis (FIP), while the FECoV pathotype is widely disseminated in feline populations leading mostly to asymptomatic infections. No genic marker is currently known to differentiate the FECoV and FIPV pathotypes. This study has been divided in two chapters. In the first chapter, the aim was to evaluate the molecular diversity of the membrane (M) gene in 190 samples from 5 cats without FIP (FIP-) and 10 cats with clinical and histopathological evidence of FIP (FIP+). The conclusion of this study is that both the in vivo mutation hypothesis in the FECoV-to-FIP direction and the hypothesis of FIPV transmission amongst cats are plausible. In the second chapter, aimed to evaluate the diversity of genes 3a-c, E and M, clones of amplicons for these genes were obtained and sequenced from samples from six FIP+ and 2 FIP- cats. Genes 3a-c, E and M show a genic diversity that results in a quasispecies constitution of FCoV that leads to the probability of the emergence of the highly virulent pathotype in a host-specific way. The conclusion of this second study is that FIPV lineages show a truncated form of the 3C protein, making the 3c gene the only pathotype marker for FCoV observed amongst the genes studied herein.
Almeida, Cláudia Maria Urmal. "Peritonite infeciosa felina : casuística e formas clínicas." Master's thesis, Universidade de Lisboa, Faculdade de Medicina Veterinária, 2020. http://hdl.handle.net/10400.5/20190.
Full textA peritonite infeciosa felina (PIF) é uma doença patogénica e fatal, causada pelo coronavírus felino (FCoV), capaz de induzir uma reação inflamatória sistémica. A PIF é associada a falhas no sistema imunitário, nomeadamente à inibição da resposta humoral e celular, havendo um conjunto de fatores genéticos, ambientais e do hospedeiro que predispõem para o seu aparecimento. Estudos recentes sugerem novos fármacos, promissores na cura da PIF. O GS-441524 revela-se muito promissor para todas as formas clínicas de PIF, relevando altas taxas de remissão. Contudo, não se encontra comercialmente disponível e são ainda necessários estudos para o licenciamento deste medicamento. O presente estudo teve como objetivo caracterizar gatos diagnosticados com PIF na Unidade de Isolamento de Doenças Infeciosas do Hospital Veterinário da Faculdade de Medicina Veterinária da Universidade de Lisboa, entre outubro de 2013 e novembro de 2019. Com o auxílio dos médicos responsáveis por este departamento foi possível a obtenção de dados, não só relativamente ao historial dos animais, como resultados de exames complementares. O diagnóstico foi realizado através de necropsia ou por deteção de coronavírus através de PCR em tempo real a partir de líquido de derrame torácico ou abdominal. A partir de janeiro de 2019 o diagnóstico foi otimizado recorrendo-se à deteção de mutações do coronavírus por PCR em tempo real em diferentes amostras (sangue, líquido de derrame, granulomas ou linfonodos). Analisando os dados disponíveis, foi possível identificar na presente população os seguintes fatores de risco: idade, fator raça, origem e a presença de pelo menos um fator de stress antes do aparecimento dos sinais clínicos. Perante os desafios económicos que esta doença carece desenvolveu-se um fluxograma para direcionar os recursos financeiros de forma a obter um diagnostico definitivo ante-mortem, PCR em tempo real para deteção de mutações, e quando não é possível, post-mortem.
ABSTRACT - Feline Infectious Peritonitis: casuistry and clinical forms - Feline infectious peritonitis (FIP) is a fatal and pathogenic disease caused by the feline coronavirus, which is responsible for inducing an inflammatory reaction. FIP is responsible for a number of faults in the immune system, namely the inhibition of humoral and cellular response. A set of genetic, environmental and host factors can predispose its appearance. Recent studies have shown promising new drugs in the treatment of FIP. GS-441524 has been reported as a very promising drug in the treatment of all clinical forms of FIP, with high rates of remission. However, it is not yet commercially available and studies are required to its licence. The present study aimed to study cats diagnosed with FIP, in the Infectious Diseases Isolation Unit of the Veterinary Hospital of the Faculty of Veterinary Medicine of the University of Lisbon, between October 2013 and November 2019. With the help of the doctors responsible for this department, it was possible to collect data regarding the animal’s history, complementary test results. The diagnosis of FIP was made through autopsy or real time PCR positive for feline coronavirus in thoracic or abdominal fluid. Since January of 2019, the diagnosis was improved by using the real time PCR detection of mutation of feline coronavirus in different samples (blood, effusion fluid and granuloma or lymph nodes). With the analysis of the available data, it was possible to identify in the present population the following risk factors: age, being of breed, origin and the presence of at least one stress factor before the appearance of clinical signs. Facing the economic challenges of FIP, a flowchart has been developed to direct the financial resources in order to obtain a definitive ante-mortem diagnosis, real time PCR with detection of mutations, and if not possible, post-mortem.
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Silva, Filipa de Melo Gago Vassalo e. "Avaliação da carga viral do Coronavírus felino e sua relação com o perfil de expressão de mediadores imunitários, em animais portadores e com Peritonite Infecciosa." Master's thesis, Universidade de Lisboa. Faculdade de Medicina Veterinária, 2013. http://hdl.handle.net/10400.5/6270.
Full textA infecção pelo coronavírus felino (FCoV) em gatos, não só leva à excreção do vírus após infecção intestinal mas também à infecção sistémica, podendo manter-se assintomática ou manifestar-se como Peritonite Infecciosa Felina (PIF), uma doença fatal. Estima-se que 80 a 90% da população felina esteja infectada por este vírus mas apenas 5 a 12% desenvolvem a doença. O FCoV divide-se em dois subtipos, o tipo I e o tipo II, sendo o primeiro o responsável pela maioria das infecções. A patogénese da doença é complexa e não é totalmente conhecida, não estando claramente identificado qual o papel do sistema imunitário no seu estabelecimento e manutenção. Considera-se que uma forte resposta imunitária celular pode prevenir a doença e, pelo contrário, que uma forte resposta imunitária humoral pode levar ao estabelecimento da doença, na sua forma exsudativa ou não exsudativa. De forma a conhecer o perfil imunitário de animais naturalmente infectados pelo FCoV foram determinados os níveis de transcrição do mRNA das citoquinas IL-10, IL-4, IL-12p35, TNF-α e IFN-γ em amostras de sangue dos animais em estudo, através de RTqPCR. Estes foram divididos em três grupos para comparação dos resultados: o primeiro sem sintomatologia associada a PIF (I); o segundo com sintomatologia gastrointestinal suspeita de PIF (II) e o terceiro com sintomatologia neurológica e ocular suspeita de PIF (III). Foi ainda realizada a subtipificação viral e determinada a carga viral em líquido de derrame e em zaragatoas rectais e/ou amostras de fezes, avaliando o nível de excreção viral destes animais na tentativa de associar ao perfil de citoquinas. Apesar da tentativa de realizar o estudo com grupos com a maior homogeneidade possível, observou-se muita variabilidade nos níveis de transcrição. A carga viral entre os três grupos revelou-se sem diferenças significativas pelo que fica por responder o seu efeito no desenvolvimento e manutenção da doença. Já nos perfis de citoquinas, o TNF-α revelou-se inesperadamente elevado em animais naturalmente infectados e assintomáticos e diminuído nos dois grupos naturalmente infectados mas com sintomatologia suspeita de PIF. Os perfis da expressão de citoquinas aparentemente demonstram uma resposta predominantemente celular nos grupos I e III e mista no grupo II, apesar de estatisticamente não se terem verificado diferenças entre os grupos.
ABSTRACT - Evaluation of feline coronavirus viral load and its relation with the expression profile of immune mediators on healthy carriers and on animals with Feline Infectious Peritonitis - Infection with feline coronavirus (FCoV) in cats, not only leads to virus elimination on faeces after intestinal infection but also to systemic infection that may remain asymptomatic or manifest as Feline Infectious Peritonitis (FIP), a fatal disease. It is estimated that 80 to 90% of the cat population is infected with this virus, but only 5 to 12% develop the disease, one of the most important viral diseases in cats. FCoV can be divided into two types, type I and type II, the former being responsible for the majority of infections. The pathogenesis of the disease is complex and the role of the immune system in the establishment and maintenance of disease remains unclear. It is considered that a strong cellular immune response can prevent the disease, and, conversely, that a strong humoral immune response may lead to the establishment of the disease whether on in its exudative or non-exudative form. In order to learn about the immune profile of naturally infected cats with FCoV, the mRNA transcription levels of IL-10, IL-4, IL-12p35, TNF-α and IFN-γ cytokines was measured by RTqPCR in blood samples. The animals were divided into three groups for comparison purposes: the first had no symptoms associated with PIF (I); the second had gastrointestinal symptoms suspected of FIP (II) and the third had ocular and neurologic symptoms suspected of FIP (III). Furthermore viral subtyping was performed and viral load was determined in effusions and in rectal swabs and/or faecal samples, assessing the level of viral shedding of these animals in an attempt to associate with the cytokine profile. Despite the attempts to arrange the study groups with the greatest possible homogeneity, there was significative variability on the transcription levels. The viral load between the three groups revealed no significant differences, leaving the effect of viral load in the development and maintenance of the disease unanswered. The TNF-α profile proved unexpectedly high in naturally infected and asymptomatic cats and decreased in both naturally infected with suspected symptoms of FIP groups. The expression profiles of cytokines apparently show a predominantly cellular response in groups I and III and mixed in group II, although there have been no statistically differences between groups.
McArdle, Francis. "Studies on feline infectious peritonitis." Thesis, University of Liverpool, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316969.
Full textSTRANIERI, ANGELICA. "INNOVATIVE APPROACHES FOR THE CLINICO-PATHOLOGICAL DIAGNOSIS OF FELINE INFECTIOUS PERITONITIS AND FELINE CORONAVIRUS INFECTION." Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/488776.
Full textFeline infectious peritonitis (FIP) is a deadly disease of felids with a viral and immune-mediated pathogenesis. The nature of the etiological agent – feline coronavirus, FCoV – and the non specific clinical presentation make this disease particularly challenging both from a pathogenetic and a diagnostic point of view. Many aspects still represent an issue, like not knowing the mutation(s) responsible for the development of FIP, the lack of a gold standard for the diagnosis of FIP in vivo and the absence of an effective treatment. This thesis was aimed to clarify some of these aspects, specifically: a novel test on effusions was developed (namely, Δ total nucleated cell count – ΔTNC – i.e. the ratio between the two white blood cell count provided by the Sysmex XT-2000iV analyzer) (studies I and II); the frequency of atypical serum protein electrophoresis (SPE) patterns in cats with FIP, anecdotally reported during our diagnostic activity (study III) was investigated, a comparison of clinico-pathological and molecular tests for the diagnosis of FIP (study IV) was performed, a loop isothermal amplification method (LAMP) for the detection of FCoV was developed(study V) and an investigation on the prevalence of two mutations of the spike (S) protein gene in a wide number of samples from FIP and non-FIP cats was carried out (this latter study developed during an externship at the University of Bristol in collaboration with Prof. Séverine Tasker and Dr. Emi Barker) (study VI). The results of studies I and II demonstrated that the ΔTNC is a reliable method to support the diagnosis of FIP either on fresh or on frozen effusions. Study III confirmed that SPE profiles consistent with FIP are less frequent in recent years than in the past, possibly due to changes in the pathogenic characteristics of the FCoVs. However, study IV demonstrated that: on blood molecular tests may support a clinical diagnosis of FIP but none of the test, except the measurement of a1 acid-glycoprotein (AGP) may rule out this disease; cytology should be preferred on effusions either to exclude or confirm the disease and, on tissues, S gene sequencing should be preferred when histology is highly consistent with FIP while 3’ UTR PCR when FIP is less likely; the LAMP method developed in study V may be used to confirm the presence of FCoVs in the samples but is poorly sensitive and cannot exclude the presence of FCoVs. Finally, pyrosequencing of FCoV performed in study VI demonstrated the presence of gene S mutations also in FCoVs from fecal samples. The analysis of sequences recorded in this latter study, however, is still ongoing and future results may provide new insights on the pathogenesis and diagnosis of FIP.
McDonagh, Phillip. "Novel antiviral strategies for feline coronavirus and feline calicivirus." Thesis, The University of Sydney, 2014. http://hdl.handle.net/2123/12331.
Full textLuz, Flávia Serena da. "Aspectos anatomopatológicos da medula óssea na peritonite infecciosa felina." Universidade Federal de Santa Maria, 2017. http://repositorio.ufsm.br/handle/1/11756.
Full textFeline infectious peritonitis (FIP) is a highly contagious, progressive and invariably fatal viral disease of cats, and occasionally of wild felids, which results from antibody-mediated hypersensitivity reactions (types III and IV) in individuals incapable to produce a cell-mediated immune response. Although the prevalence of FIP is high worldwide, recent anatomopathological studies about this disease are scarce. Furthermore, the microscopic characteristics of the bone marrow of FIP-affected cats do not exist in the available literature. Based on this, the purpose of this dissertation is to describe possible bone marrow lesions seen in spontaneous cases of FIP. Therefore, the bone marrow collected systematically from the femoral diaphysis of 16 cats necropsied in the LPV-UFSM (Santa Maria, RS, Brazil), between January 2000 and June 2017, with a definitive diagnosis of FIP, were evaluated phenotypically (histopathology [hematoxylin and eosin] and histochemistry [Perls reaction]) and immunophenotypically (immunohistochemistry using anti-myeloid [MAC387] and anti-lymphoid [CD79αcy and CD3] markers). The results showed, regardless of the clinicopathological form of the disease (“dry” [noneffusive] or “wet” [effusive]), myeloid hyperplasia; erythroid hipoplasia; megakaryocytic dysplasia (dismegakaryocytopoiesis); and medullary plasmacytosis. In cases of “dry FIP”, but not in those of “wet PIF”, there was bone marrow and hepatic hemosiderosis. These lesions allowed establishing that cats with FIP develop myelodysplasia, a myeloproliferative lesion very similar to that reported in HIV-infected humans. It is suggested that, based on the findings described here, myelodysplasia is considered to be the main cause of hematological abnormalities observed in FIP, especially for non-regenerative anemia and thrombocytopenia, frequently developed by patients.
Peritonite infecciosa felina (PIF) é uma doença marcadamente contagiosa, progressiva e invariavelmente fatal de gatos, ocasionalmente de felideos selvagens, que decorre de uma reação de hipersensibilidade (tipos III e IV) em um indivíduo incapaz de montar uma resposta imune celular adequada. Apesar da prevalência da peritonite infecciosa felina (PIF) ser alta em praticamente o mundo todo, estudos anatomopatológicos recentes acerca dessa doença são escassos. Não obstante, as características microscópicas da medula óssea de gatos com PIF inexistem na literatura consultada. Com base nisso, o objetivo deste estudo é descrever possíveis alterações medulares ósseas vistas em casos espontâneos de PIF. Para isso, as medulas ósseas colhidas sistematicamente da região diafisária dos fêmures de 16 gatos necropsiados no LPV-UFSM (Santa Maria, RS, Brasil), entre janeiro de 2000 e junho de 2017, e que tiveram diagnóstico definitivo de PIF, foram avaliadas fenotípica (histopatologia [hematoxilina e eosina] e histoquímica [reação de Perls]) e imunofenotipicamente (imuno-histoquímica utilizando marcadores anti-mieloide (MAC387) e anti-linfoide (CD79 αcy e CD3). Os resultados permitem afirmar que, independentemente da apresentação clinicopatológica da doença (seca ou úmida), ocorre: 1) hiperplasia mieloide; 2) hipoplasia eritroide, 3) displasia megacariocítica (dismegacariocitopoiese) e 4) plasmocitose medular. Nos casos de PIF seca, mas não naqueles de PIF úmida, há hemossiderose medular óssea e hepática. Essas alterações permitem estabelecer que gatos com PIF desenvolvem mielodisplasia, uma lesão mieloproliferativa muito semelhante àquela relatada em humanos infectados pelo HIV. Sugere-se que a partir dos achados aqui descritos, mielodisplasia seja considerada a principal responsável pelas alterações hematológicas observadas na PIF, especialmente pela anemia e trombocitopenia arregenerativas tão frequentemente desenvolvidas pelos pacientes com essa doença.
Gunn-Moore, Danielle Audry. "Molecualar characterisation of feline coronavirus infection." Thesis, University of Bristol, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390379.
Full textParreira, Maria Manuel Manteiga Carvalho Roma. "Diagnóstico laboratorial em animais de companhia." Master's thesis, Universidade de Évora, 2022. http://hdl.handle.net/10174/31366.
Full textMEAZZI, SARA. "THE INTERPLAY BETWEEN HOST DEFENSES AND SYSTEMIC PATHOGENS IN PROMOTING DISEASES OF COMPANION ANIMALS." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/709076.
Full textThe gut microbiota (consortium of all the microorganisms that inhabit the gastrointestinal tract) plays different roles in the host. Among these, its relationship with the immune system has been of great interest in the last few years. Indeed, several studies highlight the presence of dysbiosis not only in gastrointestinal diseases, but also during autoimmune or infectious diseases. Literature about this topic is scarce in veterinary medicine. Thus, in this project, the possible relationship between gut microbiota and two specific diseases (feline infectious peritonis -FIP- and canine leishmaniasis) was investigated. These diseases were chosen due to the pivotal role of the immune response in their pathogenesis. The aims of this projects were: the evaluation of gut microbiota of cats with and without FIP (study I). Since in vivo diagnosis of FIP is quite challenging, the potential role of paroxonase-1 (a negative acute phase protein strongly influenced by oxidation) as a biomarker of FIP was investigated (studies II-III). For the same reason, the diagnostic agreement among histopathology, immunohistochemistry and RT-PCR on different organs was evaluated (study IV). Finally, the gut microbiota composition in dogs infected or not by Leishmania spp. was investigated. The results were correlated with the leukocyte populations studied by flow cytometry (studies V-VI). Results obtained in this project provided preliminary data about gut microbiota composition in cats affected by FIP or only Coronavirus positive. This achievement needs to be further investigated on a bigger sample size (study I). Paraoxonase-1 reference interval and its good performance as a diagnostic biomarker of FIP were determined (studies II-III). Despite the immunohistochemistry is still the gold standard for FIP diagnosis, the good diagnostic agreement obtained in the study suggested that a possible association with RT-PCR could minimize diagnostic errors (study IV). Finally, the gut microbiota composition and leukocyte populations of leishmaniotic dogs highlighted some significant differences compared with both healthy and exposed asymptomatic dogs. These promising results could be a starting point for further researches (studies V-VI).
Books on the topic "Feline infectious peritoniti"
Nicholas, Kim Alan. Serum antibody responses in cats experimentally infected with feline infectious peritonitis virus. 1985.
Find full textThe Man in the Cat-Hair Suit: And other true stories. Chapel Hill, NC, USA: William R. Greene, 2011.
Find full textThe Man in the Cat-Hair Suit: And other true stories. Chapel Hill, NC, USA: William R. Greene, 2011.
Find full textThe Man in the Cat-Hair Suit: And other true stories. Chapel Hill, NC, USA: William R. Greene, 2011.
Find full textThe Man in the Cat-Hair Suit: And other true stories. Chapel Hill, NC, USA: William R. Greene, 2011.
Find full textBook chapters on the topic "Feline infectious peritoniti"
de Groot, Raoul J., and Marian C. Horzinek. "Feline Infectious Peritonitis." In The Coronaviridae, 293–315. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4899-1531-3_14.
Full textSchmeltzer, Linda E. "Feline Infectious Peritonitis." In Nursing the Feline Patient, 185–88. Ames, Iowa, USA: John Wiley & Sons, Inc, 2016. http://dx.doi.org/10.1002/9781119264910.ch25.
Full textIshida, Takuo, Kazushige Toriyabe, Jun Fukuoka, and Shigekatsu Motoyoshi. "Serodiagnosis of Feline Infectious Peritonitis." In Coronaviruses, 577–78. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-1280-2_73.
Full textGershwin, Laurel J. "Case 30: Feline Infectious Peritonitis." In Case Studies in Veterinary Immunology, 145–49. New York, NY : Garland Science, [2017]: Garland Science, 2017. http://dx.doi.org/10.4324/9781315165462-30.
Full textMehrbod, Parvaneh, Mohammad Syamsul Reza Harun, Ahmad Naqib Shuid, and Abdul Rahman Omar. "Transcriptome Analysis of Feline Infectious Peritonitis Virus Infection." In Coronaviruses, 241–50. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2438-7_20.
Full textPedersen, Niels C. "Virologic and Immunologic Aspects of Feline Infectious Peritonitis Virus Infection." In Coronaviruses, 529–50. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-1280-2_69.
Full textSoma, Takehisa. "Feline Coronavirus RT-PCR Assays for Feline Infectious Peritonitis Diagnosis." In Springer Protocols Handbooks, 161–70. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3414-0_15.
Full textMcArdle, F., M. Bennett, R. M. Gaskell, B. Tennant, D. F. Kelly, and C. J. Gaskell. "Canine Coronavirus Infection in Cats; A Possible Role in Feline Infectious Peritonitis." In Advances in Experimental Medicine and Biology, 475–79. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5823-7_66.
Full textGerber, J. D., N. E. Pfeiffer, J. D. Ingersoll, K. K. Christianson, R. M. Landon, N. L. Selzer, and W. H. Beckenhauer. "Characterization of an Attenuated Temperature Sensitive Feline Infectious Peritonitis Vaccine Virus." In Advances in Experimental Medicine and Biology, 481–89. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5823-7_67.
Full textVennema, Harry, Raoul J. de Groot, David A. Harbour, Mieke Dalderup, Tim Gruffydd-Jones, Marian C. Horzinek, and Willy J. M. Spaan. "Immunogenicity of Recombinant Feline Infectious Peritonitis Virus Spike Protein in Mice and Kittens." In Advances in Experimental Medicine and Biology, 217–22. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5823-7_30.
Full textConference papers on the topic "Feline infectious peritoniti"
Jähne, S., S. Felten, K. Matiasek, M. Bergmann, C. Leutenegger, and K. Hartmann. "Detection of mutated and non-mutated feline coronaviruses in cats without feline infectious peritonitis." In 29. Jahrestagung der FG „Innere Medizin und klinische Labordiagnostik“ der DVG (InnLab) – Teil 1: Vorträge. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0040-1722399.
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