Feline infectious peritonitis was diagnosed in two captive servals (Felis serval) according to clinical, pathological, and immunohistochemical findings. They died 9 days apart, although the second serval, with effusive disease, was euthanatized during the acute phase of infection owing to a poor prognosis. Clinical signs consisted of abnormal behavior (1/2) and anorexia, depression, abdominal distension, and leukocytosis (1/2). The two other servals in the colony remained asymptomatic. The main pathologic findings were severe fibrinopurulent to pyogranulomatous meningitis and ventriculitis in the serval with abnormal behavior and ascites, fibrinonecrotizing to pyogranulomatous peritonitis, and fibrinous perisplenitis in the serval with effusive disease. Feline infectious peritonitis virus antigen (spike protein) was detected in the affected tissues of both servals by immunohistochemistry using monoclonal antibodies.
Feline infectious peritonitis (FIP) has been documented both in domestic and exotic cats.2 In captive exotic felines, FIP had been sporadically documented1 until a severe outbreak of FIP and other coronavirus-associated diseases caused death in 18 out of 35 cheetahs (Acinonyx jubatus) in a wildlife preserve in the early 1980s.1,3 Recently, FIP has been recognized as the cause of death in five of eight captive adult European wildcats (Felis silvestris) during a 10-year period.6 To our knowledge, this is the second report on FIP in exotic felines diagnosed by immunohistochemistry.
A group of four servals (Felis serval) was housed in a wire-fenced, outdoor enclosure at the Barcelona Zoo (Spain); stray cats did not have direct access to the enclosure. Indoor sleeping quarters were also available to the animals. In early 1993, a 2-year-old male serval (no. 1) stopped entering the indoor part of the enclosure 3 days prior to death—what was considered an abnormal behavior. Five days later, an 8-year-old serval (no. 2) began to show anorexia, depression, and a moderate abdominal distension. Hematology revealed leukocytosis and moderate anemia. This animal had been implanted with melengestrol acetate for contraception purposes. A differential diagnosis of pyometra and FIP was made. Exploratory laparotomy was performed, and effusive FIP-like lesions were seen. Due to a poor prognosis, serval no. 2 was euthanatized 9 days after the death of its cagemate. The two other servals remained asymptomatic; one of these animals had a pre-epizootic, negative feline coronavirus IFI antibody titer (1:25).
At necropsy, no gross lesions were seen in serval no. 1. Serval no. 2 had approximately 100 ml of a yellow-opaque fluid in the abdominal cavity and multiple, firm, 1–3-mm, white-yellowish nodules scattered throughout the abdominal serosal surfaces. There was a marked fibrinous perisplenitis. Microscopically, serval no. 1 had a fibrinopurulent ventriculitis in the brain with associated mononuclear perivascular cuffing, severe pyogranulomatous leptomeningitis, and focal pyogranulomatous nephritis. Serval no. 2 had fibrinonecrotizing to pyogranulomatous lesions in the mesentery and serosa of the liver and gall bladder, as well as fibrinous perisplenitis with focal pyogranulomatous-necrotizing splenitis.
Paraffin-embedded tissue sections from both servals were screened for the presence of FIP virus antigen by the avidin-biotin-peroxidase complex method using monoclonal antibodies to the spike protein of FIP virus.4 Positive staining was found in scattered macrophages within the aforementioned lesions of both servals.
On the basis of specific immunohistochemical studies, FIP was diagnosed in two servals. Clinical signs were similar to those commonly found in cats with FIP, but a presumptive diagnosis of FIP could only be obtained in serval no. 1 by histopathology, and in serval no. 2 at the exploratory laparotomy. In the domestic cat, clinical signs and results of hematology, biochemistry, analysis of effusions, and coronavirus serology seem to have a poor sensitivity and specificity for the antemortem diagnosis of FIP.5 Previous to this report, immunohistochemical diagnosis of FIP had been reported in European wildcats (Felis silvestris).6
The degree of susceptibility of different feline species to feline coronaviruses is poorly understood. The explosive nature of the cited outbreak of FIP in cheetahs could be related to the extreme genetic monomorphism observed in this species, especially at the major histocompatibility complex.3 Servals (Felis serval), along with other felines, are included in a group of species with a moderate to high genetic diversity.3
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2. Barlough, J.E., and C.A. Stoddart. 1990. Feline coronaviral infections. In: Greene, C.E. (ed.). Infectious Diseases of the Dog and Cat. W.B. Saunders Co., Philadelphia, PA. Pp. 300–312.
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4. Olsen, C.W., W.V. Corapi, C.K. Ngichabe, J.D. Baines, and F.W. Scott. 1992. Monoclonal antibodies to the spike protein of feline infectious peritonitis virus mediate antibody-dependent enhancement of infection of feline macrophages. J. Virol. 66: 956–965.
5. Sparkes, A.H., T.J. Gruffydd-Jones, and D.A. Harbour. 1991. Feline infectious peritonitis: a review of clinicopathological changes in 65 cases, and a critical assessment of their diagnostic value. Vet. Rec. 129: 209–212.
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