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This paper gives a summary of our present-day knowledge concerning etiology, clinical aspects, diagnosis, pathology and pathogenesis of feline infectious peritonitis. Special emphasis is given to the participation of the immune system in the development of lesions. A therapy protocol is proposed and an extensive list of original literature for further study is given.
The antiviral activities of ribavirin (1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide; virazole), either alone or in combination with recombinant human leukocyte (alpha) interferon (rHuIFN-alpha), were evaluated against feline infectious peritonitis virus (FIPV) in feline kidney-cell cultures. The 50% inhibitory dose (ID50) of ribavirin for uninfected, rapidly dividing cells was approximately 17 micrograms ml-1 whereas the ID50 for FIPV was 2.5 micrograms ml-1. The therapeutic index (TI) of ribavirin (i.e. the ratio of the minimum cell-toxic dose to minimum virus-inhibitory dose) was 6.8. Although a dose-dependent inhibition of viral infectivity occurred at non-toxic doses, maximum antiviral effects (greater than or equal to 4 log10 reduction in FIPV) occurred at cytotoxic doses. When low or moderate doses of ribavirin were combined with either 10 or 100 U of rHuIFN-alpha ml-1, the resulting antiviral effects were significantly greater than the sum of the observed effects from either ribavirin or rHuIFN-alpha alone. Significant synergistic interactions with rHuIFN-alpha occurred at ribavirin doses of 1, 5, 12.5 and 25 micrograms ml-1. Synergistic combinations of rHuIFN-alpha and ribavirin produced up to an 80-fold or a 200-fold relative increase in FIPV antiviral activities compared with that produced by equivalent doses, respectively, of ribavirin or rHuIFN-alpha alone. In cell growth studies, the addition of either 10 or 100 U of rHuIFN-alpha ml-1 to test doses of ribavirin did not increase the anticellular effect observed with ribavirin alone; seemingly, the potentiation of ribavirin antiviral activity by rHuIFN-alpha was independent of any additive cytotoxic effects. Potentially, synergistic combinations of the two antiviral agents in vivo may decrease the therapeutic dose of ribavirin required for inhibition of FIPV and thus reduce drug toxicity.
Kittens vaccinated with an avirulent biotype of the Black strain of feline infectious peritonitis virus (FIPV; given oronasally) developed both indirect fluorescent and virus-neutralizing antibodies, but were not protected against oronasal challenge exposure with virulent virus. In fact, kittens vaccinated with avirulent virus were more readily infected than were nonvaccinated cats. A proportion of kittens could be immunized to FIPV by giving sublethal amounts of virulent virus. This technique, however, was too inconsistent and hazardous to have clinical relevance. The results of these studies indicated that humoral immunity was not protective in FIPV infection. There was no correlation between fluorescent and virus-neutralizing antibodies and either disease or immunity. Immune serum from FIPV-resistant cats failed to passively protect susceptible animals against virulent virus given intraperitoneally or oronasally, and as expected, actually sensitized them to infection. It was concluded that cell-mediated immunity was probably responsible for protection.
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A reverse transcriptase-polymerase chain reaction (RT-PCR) assay for the detection of the feline coronavirus (FCoV) genome and a co-cultivation method for the isolation of field strains of FCoV are described. Using the RT-PCR assay to assess blood samples from cats with feline infectious peritonitis (FIP) (n = 47) and healthy cats from households with endemic FCoV (n = 69) it was shown that approximately 80% of the cats were viraemic, irrespective of their health status. It was also shown that, over a 12-month period, a similar percentage of healthy cats remained viraemic, and that the presence of viraemia did not appear to predispose the cats to the development of FIP. The co-cultivation system proved to be a suitable method for the culture of field strains of FCoV from blood samples, so long as the cultures were maintained for at least 4 weeks. Using this system, followed by the RT-PCR, viraemia was detected as frequently as by RT-PCR on RNA extracted directly from peripheral blood mononuclear cells.
A simple technique demonstrating the presence of feline infectious peritonitis virus (FIPV) in cats is described. Smears from the third eyelid (membrana nictitans) were dried on microscope slides, fixed in aetone, and stained using an indirect immunofluorescence method with rabbit-anti-FIPV serum. By this method FIPV-antigen could be demonstrated in the cytoplasma of epithelial cells. The results obtained with this method (M3) were compared with serological and immunohistopathological methods for confirming FIPV-infection in cats. The results obtained by the M3 test were up to 85% in concordance with these other tests. Furthermore, the M3 test was easier and quicker to perform and should be well suited for clinical practice.
Using gut sections from pigs infected with porcine epidemic diarrhea virus (strain CV 777) and ascitic fluid from cats which had succumbed to feline infectious peritonitis (FIP), a weak cross reaction was found by immunofluorescence. Its specificity was confirmed when detergent-treated purified CV 777 showed a prominent reaction with FIPV antibodies in ELISA; no reaction was obtained with intact virions, which indicated common determinants on an internal component of the particle. Antigenic cross-reactions at the nucleocapsid level were found in Western blot ELISA performed both ways (CV 777/FIPV antibodies; FIPV/CV 777 antibodies). In immunoprecipitation using [35S]methionine labelled FIPV, anti-CV 777 sera recognized exclusively the nucleocapsid protein. The significance of these findings for the classification of coronaviruses is discussed.
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Between 1980 and 1987 about 10% of the cats which underwent a post mortem examination at the Institute of Veterinary Pathology of the Freie Universität Berlin were infected with feline infectious peritonitis (FIP). The exudative, granulomatous or mixed form of the FIP are all symptoms of the same disease whose clinical picture is dependent on the state of the cellular immunity. Statistically there is no significant relationship between the form of the FIP and the age of the cats. A breed or a sex disposition is also not apparent. 42 organs and/or tissue samples were taken from a total of 30 cats and were examined both histologically and immunohistochemically. The antigen is located, above all, in the mesothelium and the cells of the mononuclear phagocyte system, whereas the parenchymatous inflammation foci show little evidence of the FIP-virus-antigen. The antigen is, however, also found in the nerve cells. Within the framework of a second viraemia, occurring after infection of the mesothelium (polyserositis), a perivasculitis non purulenta generalisata occurs. Possible excretory organs of the antigen are the respiratory, digestive and urinary tract.
Seventy-four cats (52 treated and 22 untreated) were evaluated in efficacy studies of interferon (IFN), Propionibacterium acnes, or a combination of these drugs against experimentally induced feline infectious peritonitis (FIP). Cats were given doses of recombinant human leukocyte (alpha) IFN (rHuIFN-alpha), feline fibroblastic (beta) IFN (FIFN-beta) or P acnes at regular intervals before and after inoculation of virulent FIP virus (FIPV). Prophylactic and therapeutic administration of high doses (10(6) U/kg of body weight) or moderate doses (10(4) U/kg) of rHuIFN-alpha, FIFN-beta (10(3) u/kg), or P acnes (0.4 or 4 mg) did not significantly reduce mortality in treated vs untreated cats. However, the mean survival time in cats treated with 10(6) U of rHuIFN-alpha-/kg alone or combined with doses of P acnes was significantly (P = 0.03) increased after inoculation of highly lethal amounts (200 LD100) of FIPV vs survival time in untreated cats. Although P acnes alone was ineffective, there was some indication that a combination of P acnes and high doses of rHuIFN-alpha was more effective than rHuIFN-alpha alone. Seemingly, the efficacy of rHuIFn-alpha treatment was improved in cats challenge-exposed with less FIPV; in 1 trial, 4 of 5 cats (80%) treated with high doses of rHuIFN-alpha survived after inoculation of minimal lethal amounts (0.6 LD100) of FIPV, whereas only 2 of 5 untreated cats (40%) survived. Pretreatment of cats with 10(6) U of rHuIFN-alpha/kg resulted in detectable serum IFN activity 24 hours later; serum IFN activity was not detected in cats pretreated with P acnes, FIFN-beta, or 10(4) U of rHuIFn-alpha/kg.(ABSTRACT TRUNCATED AT 250 WORDS)
Two cats from the same household had posterior paresis and hypergammaglobulinemia. Histologic evaluation of the spinal cords revealed a pyogranulomatous reaction consistent with that reported for feline infectious peritonitis.
Infections of cats with feline peritonitis (FIP) virus are usually inapparent but may lead to fatal polyserositis. We have recently advanced the hypothesis that immune complexes play an essential role in the pathogenesis of the condition. To support this hypothesis, the role of the third component of complement in FIP was investigated. In the present paper, the isolation of C3 from normal cat serum and some of its physical and immunologic properties are described. The final protein had an apparent m.w. of 185,000 and was composed of 2 polypeptide chains with m.w. of 128,000 and 71,000, respectively. When tested against whole cat serum, an antiserum raised in rabbits against purified C3 recognized only 1 protein whose identity with C3 was established. With the aid of this antiserum, depositions of C3 in renal glomeruli of FIP-affected cats were demonstrated by immunofluorescence. Their localizaton coincided with that of deposited IgG, thereby supporting the concept of an immune complex pathogenesis of FIP.
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The amino acid sequence of the peplomer protein of transmissible gastroenteritis virus (TGEV) has been derived from the cloned cDNA sequence. The gene encodes a protein of 1447 amino acids with a molecular weight of 159 574. Comparison with the primary structure of the peplomer protein of feline infectious peritonitis virus (FIPV) (de Groot et al., 1987b) revealed one domain, from amino acids 1 to 274, in which the nucleotide homology was 39%, whereas in the second domain (from residues 275 to 1447) the homology was 93%.
Minimal-disease cats exposed to live human coronavirus 229E developed homologous antibody responses that suggested little or no replication of the virus in inoculated animals. Oronasal and subcutaneous inoculation of coronavirus 229E did not elicit an antibody response by heterologous (transmissible gastroenteritis virus, canine coronavirus) neutralization or by heterologous (transmissible gastroenteritis virus) kinetics-based enzyme-linked immunosorbent assay. No clinical signs attributable to coronavirus 229E were seen in inoculated cats. Although the number of animals in each of the five experimental groups was small (n = 2), antibodies produced in response to the virus did not appear to sensitize cats to subsequent feline infectious peritonitis virus challenge, but neither did they cross-protect cats against the challenge dose.
To gain insight into the genetic relationships among six canine coronavirus (CCV) strains, the variable region of the spike (S) protein gene was sequenced. The CCV strains were: two ATCC reference strains, the Insavc-1 vaccine strain, the National Veterinary Services Laboratories (Ames, IA) challenge strain, and two California field isolates (UCD-1 and UCD-2) from the 1970s. All six strains, downstream of the nucleocapsid (N) protein gene, had sufficient size for an ORF 7b, and thus, none were transmissible gastroenteritis virus (TGEV)-like since TGEV lacks ORF 7b. By sequence analysis of the variable domain at the 5' end of the S gene, five of the six CCV strains had a high degree of identity with feline infectious peritonitis virus (FIPV). However, one CCV field isolate (UCD-1) was different and had a high degree of identity with the 5' end of the TGEV S gene. This suggests that RNA recombination occurred at this site between antigenically related coronaviruses. The low passage field isolates, UCD-1 and UCD-2, varied in their initial infectivity for swine testicular cells suggesting that sequence differences in the variable domain of the S gene may account for biological variation among CCVs.