Feline Leukemia Virus

FELINE PANLEUKOPENIA VIRUS

Virus Classification:

Order: Mononegavirales

Family: Parvoviridae

Subfamily: Parvovirinae

Genus: Parvovirus

Species: Feline panleukopenia virus

Also called feline infectious eneritis, feline "distemper", and feline ataxia or incoordination. Examples of other viruses belonging to the same genus as Feline panleukopenia virus include Canine parvovirus type 2, Porcine parvovirus, Mink enteritis virus, and Raccoon enteritis virus.

Virus Structure:

Feline panleukopenia virus (FPV) is a small (20 nm) autonomous , non -enveloped, icosahedral, single-stranded DNA virus that is approximately 5,120 nucleotides in legnth. The genome encodes for two genes which each form two proteins by alternative mRNA splicing. The non-enveloped capsid is assembled from 60 copies of a combination of the overlapping capsid proteins VP1 and VP2. The virus contains three capsid proteins. The capsids normally enter cells by clathrin-mediated endocytosis. Replication of the virus in the host occurs in cells that are rapidly dividing. FPV can survive in pH ranging from 3 to 9. The virus is highly resistant to most disinfectants (ether, chloroform, acid, alcohol, and heat), but is susceptible to Clorox bleach.

History and Natural Biology of Feline Panleukopenia Virus:

Feline panleukopenia is endemic to cats worldwide. The virus has been identified since the early 20th century. The virus is so severe that it was referred to as "cat plague" in earlier times when infections worldwide nearly wiped out cat populations in certain geographic areas. Now FPV rarely occurs in domestic populations in which vaccination is routinely practiced. There is a seasonality to the occurrence of FPV that usually coincides with the production of new populations of susceptible kittens. This seasonal effect may vary according to geographic location. In the northeastern United States, most cases of FPV are seen in the summer and early fall. However, outbreaks of FPV may occur at any time of the year. It is thought that feral domestic cat populations are a natural resevior for Feline panleukopenia virus.

Clinical Features and Viral Pathogenesis:

All members of the cat family (Felidae) are susceptible to infection with feline panleukopenia virus (FPV), as are raccoons, and minks, in the family Procyoniclae. Three major body sytems are affected by FPV. FPV specifically depresses the white blood cells and thus the immune system of the host, it attacks the rapidly reproducing cells lining the gut, and FPV affects the reproducing cells of the cerebellum and the retina of the eye when they are in their developing stage. The system it chooses depends on the age of the cat at the time of infection. The severity of the clinical signs exhibited also depends on the cat's age, and varies tremendously from case to case. Many cats show no signs of infection at all; the only method of diagnosis is the detection of FPV antibody in the blood. Mild clinical infections can be seen as a borderline drop in white blood cell count, mild temperature elevation, and slight inappetence. In a "typical" case of FPV, the clinical signs develop suddenly. Vomiting and severe diarrhea may develop within twenty-four hours of infection. During this time the cat's temperature may elevate to 104oF or greater. Severe dehydration and electrolyte imbalances occur as a result of ongoing vomiting and diarrhea. The hair coat becomes dull and there is a loss of elasticity of the skin due to severe dehydration. The lymph nodes in the abdomen become enlarged, and the digestive tract contains excessive amounts of gas and liquid. By this time the cat's abdomen is painful, and touching it will elicit a pain response. The mortality rate in an outbreak of FPV may vary from 25 to 80 percent. Death commonly occurs within the first five days of illness, but can occur later by subsequent complications by other problems. Signs in kittens infected in utero, often go unnoticed before sudden death. Ataxia, or incoordination, will sometimes occur within two weeks of birth due to the viruses tropism for the rapidly dividing cells of the cerebellum and retina. There is no treatment for ataxia, the damage has been done at this point. When a susceptible host is exposed to an infected animal, or with the feces or urine of an infected animal, FPV enters the oropharynx and replicates in regional lymphoid tissue and intestine.