A 1-year-old castrated male domestic shorthaired cat was presented for evaluation of a 10-day history of lethargy, anorexia,
decreased water consumption, and apparent discomfort. A complete blood count and serum chemistry profile revealed hypoalbuminemia,
leukocytosis, and neutrophilia. The results of a combined ELISA test for feline leukemia virus and feline immunodeficiency
virus were negative.
On presentation, the cat was quiet, alert, and responsive, and it had pale mucous membranes. It also had a distended abdomen
and a fluid wave. Abdominocentesis yielded a yellow viscous fluid with a total protein concentration of 4.6 g/dl and a nucleated
cell count of 2,500/μl with 90% segmented neutrophils. Given the effusion's characteristically high protein concentration
and relatively mild inflammatory reaction, feline infectious peritonitis (FIP) was tentatively diagnosed, and a poor prognosis
was given. The owners elected euthanasia and gave their consent for a postmortem examination.
Figure 1. The peritoneal cavity of a 1-year-old cat suspected of having FIP. Note the pale-yellow and tan strands of fibrin
The peritoneal cavity contained about 500 ml of a viscous, straw-colored fluid with pale-yellow to tan strands of fibrin (Figure 1). There were numerous fibrous and fibrinous adhesions between various organs as well as adhesions between organs and the
body wall (Figure 2). The spleen and liver were covered with a thick, yellow-tan fibrinous coating, and numerous smooth, raised, 1- to 2-mm,
circular, coalescing, white plaques were noted on the serosal surfaces of the intestines and parietal peritoneum (Figure 2).
Figure 2. The cat's abdominal cavity showing fibrous and fibrinous adhesions between the organs and the body wall (arrows).
Also note the fibrinous covering on the liver's surface. The black serosal plaques on the colon are normal Peyer's patches.
Histologic examination of the abdominal organs demonstrated that the serosal plaques were composed of large amounts of fibrin
and inflammatory cells consisting of lymphocytes, plasma cells, and macrophages with occasional clusters of degenerate neutrophils
with pyknotic nuclei (Figure 3). The clinical history, gross findings (fibrinous peritonitis), and histologic findings were most consistent with FIP.
Figure 3. A photomicrograph of a serosal plaque from the cat's jejunum showing large amounts of fibrin and inflammatory cells
(inset). Occasionally, this inflammation could be seen surrounding blood vessels and within the walls of small arterioles
(arrowhead) (hematoxylin-eosin, 20X).
FIP is an immune complex-mediated disease caused by pathogenic feline coronavirus. After pathogenic feline coronavirus infection,
the disease progresses quickly. Since systemic antibodies are not protective, development of cell-mediated immunity is the
most crucial factor in determining the outcome of this viral infection. Cats that produce humoral antibodies but fail to generate
an effective cell-mediated immune response develop effusive FIP. In this effusive form, immune complexes aggregate in the
vasculature and attract complement, causing a vasculitis and subsequent transudate.
The classic wet, effusive form, as seen in this case, is characterized by abdominal effusion with strands and mats of fibrin
with multifocal serosal pyogranulomas. The dry, noneffusive form is thought to result from a partially protective cell-mediated
immune response that is unable to wall off and contain the virus. This dry form is characterized by multiple granulomas or
pyogranulomas in various organs including the lungs, liver, kidneys, intestines, and central nervous system. Affected cats
often have a combination of both the effusive and noneffusive forms, with one form predominating.