Case 1 - 170623-1

Domestic cat, approximately six months old.

This cat had a brief history of listlessness and diarrhea.

Gross lesions were not reported by the submitter.

This slide has two similarly affected sections of ileum. Peyers patches are severely depleted with central hyalinosis, abundant macrophages with loss of central lymphocytes and occasional lymphocytolysis. Crypts are frequently dilated and contain variable amounts of necrotic cellular debris. They are lined by cuboidal to flattened (attenuated) enterocytes with an increased number of mitotic figures and single cell to segmental necrosis. Cuboidal, basophilic (regenerative) crypt enterocytes have moderate anisokaryosis, frequently large nuclea and prominent, central nucleoli. Rare crypt epithelial cells have amphophilic intranuclear inclusions that fill the nucleus and marginalize the chromatin. The lamina propria is infiltrated by a moderate number of lymphocytes, plasma cells and macrophages, which also form a thin band that mildly elevate the crypts from the submucosa. There is marked goblet cell hyperplasia, particularly affecting the villi. The villous goblet cells are intermixed with hypereosinophilic, poorly preserved enterocytes. The intestinal lumen is filled by mucous which separates villi and often fills ectatic crypts.

No special stains.

Ileum: Severe, diffuse, crypt necrosis with marked goblet cell hyperplasia, lymphoid depletion, villous atrophy and rare intranuclear inclusions

Although the type of virus was not indicated, the lesions in this case were confirmed to be caused by feline panleukopenia virus (FPV). This is a feline parvovirus, that, like many parvoviruses is ubiquitous and stable in the environment. It is a non-enveloped, single-stranded DNA virus, which replicates in the nuclei of dividing cells. Feline panleukopenia virus is closely related to canine parvovirus (CPV), which is presumed to have originated from FPV. Large, basophilic or amphophilic, intranuclear inclusions may be seen early in the course of disease. However, many cases are presented after viral proliferation has waned, and inclusion bodies are often not evident in such cases. In general, inclusion bodies are thought to be less common in cats than in other species affected by enteric parvoviruses.

Feline parvovirus infects and replicates within rapidly dividing and mitotically active cells including lymphoid tissue, intestinal cryptal epithelium, bone marrow and cerebellar Purkinje cells. Clinical signs are a result of these target sites and include diarrhea, variable leukopenia, vomiting, intestinal hemorrhage, cerebellar ataxia, vision deficits from retinal dysplasia, and hypoproteinemia from intestinal loss with subsequent ascites. The tissue tropism may vary with the stage of development of the host. A wider variety of tissues (e.g. brain) are susceptible in fetuses or neonates, before the cell proliferation is drastically reduced. Other tissues, such as gastric mucosa and bone marrow, have continual cell turnover and are susceptible in all life stages.

Unlike CPV, FPV infection of kittens in utero is frequently associated with cerebellar hypoplasia. On the other hand, CPV may cause myocarditis in infected puppies, whereas FPV is not associated with myocarditis in kittens.

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