Cats of all ages can develop FPL, but kittens and young cats are most commonly affected. In kittens, the period of greatest susceptibility to infection is when maternal antibodies are waning and vaccine-induced immunity has not yet fully developed. Cases tend to cluster when there is a buildup of susceptible kittens, a function of the seasonal breeding in a given cat population.¹ FPL is associated with high morbidity and mortality, but infections can range from subclinical to severe depending on the immune status and age of a cat when it is infected. Infection in pregnant queens can result in fetal resorption, mummification, abortion, or stillbirth.⁶ Fetuses infected in utero that survive and kittens less than a few weeks of age that become infected can have cerebellar hypoplasia, retinal dysplasia, and optic neuropathy.⁷

Peracute enteritis is a manifestation of the disease most often seen in kittens less than 16 weeks of age. In these cases, there is severe intestinal damage, and death can occur within 24 hours because of a combination of secondary bacterial septicemia and endotoxemia in the face of profound leukopenia.⁶ Kittens more than 16 weeks of age tend to have less severe disease; in these cases, supportive treatment that addresses severe dehydration and intestinal bacterial invasion can be effective. While there is no question that FPL virus infects and kills dividing cells, some evidence suggests that secondary bacterial infections make an equal or greater contribution to the clinical signs and the intestinal damage in cats with FPL. This important component of the pathogenesis of FPL has been illustrated in studies in which specific pathogen-free cats infected with FPL virus developed mild or no intestinal lesions.^4,9 Adult cats are generally the least severely affected and may show mild signs or none at all.

The greatest fecal virus shedding corresponds with the peak of clinical disease, but keep in mind that the virus can be shed for up to six weeks after recovery⁷ and that subclinical animals can also shed virus. Lifelong immunity is thought to follow recovery from disease, and a carrier state of the disease has never been identified. So persistence of the disease in cat colonies is attributable to persistence of the virus in the environment and shedding from new infections, not chronic shedding.