Difference between revisions of "Feline Panleucopenia"

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===Laboratory Tests===
 
===Laboratory Tests===
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On haemotology, a striking panleucopenia is the most consistent finding and neutrophils are particularly depleted. Leucocyte counts are usually between 500 and 3000 cells per decilitre. Routine biochemistry is not associated with any specific changes.
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Paired serum sampling should reveal a rising antibody titre to FPV during an acute infection. A CITE test can also be used to quickly detect FPV antigen in the faeces, although this is only truly licensed for use for canine parvovirus. Confirmation of diagnosis is by virus isolation or PCR of viral antigen using faeces, infected tissue, oropharyngeal swabs or post-mortem material.
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===Pathology===
 
===Pathology===
  

Revision as of 10:06, 10 August 2010



Also known as: Feline Infectious Enteritis
Feline Parvovirus

Description

Feline panleucopenia is a viral infection of cats caused by feline parvovirus (FPV). Feline parvovirus is a small, non-enveloped, single-stranded DNA virus of one serotype only, that is closely related to canine parvovirus type 2 (CPV-2). In order to replicate, FPV must infect dividing cells, and so tissues with a high mitotic rate undergo actue cytolysis. FPV is very stable in the environment and may survive for years on infected premises. It is also highly contagious.

Feline panleucopenia takes its name from the severe depletion of leucocytes thats results from FPV infection. As well as targeting immune cells, FPV destroys the cells of the intestinal crypts causing enteritis, villous atrophy and malabsorption. In utero infection of foetuses can occur, leading to foetal death, resorption, mummification, abortion or stillbirth. In neonatal kitten the retinal cells of the eye and the granular cells of the epithelium are rapidly dividing. Infection of these by FPV causes permanent retinal dysplasia and cerebellar hypoplasia.

Signalment

Although routine vaccination can give almost complete control of feline panleucopenia, the disease is seen worldwide in unvaccinated populations. All domestic and exotic felids may contract FPV, as well as some exotic canids. Mink are particularly susceptible, and infection may also be seen in racoons, pandas and coatimundi. Although there are no breed or sex predilections, the severity of disease varies with age. Once maternal immunity has waned, unvaccinated, previously unexposed cats can become infected at any age. However, severe infections are most likely in kittens of 2-6 months of age, and adults usually suffer on mild or subclinical disease.

Diagnosis

A presumptive diagnosis can be made on the basis of clincal signs, vaccinal status, age, exposure and the presence of a sever panleucopenia. Laboratory tests are available to confirm the diagnosis.

Clinical Signs

The clinical signs of feline panleucopenia can vary in severity, particularly between ages of cat. It is therefore important to remember that especially in adult animals, disease may be mild or even subclinical.

Certain elements of a patient's history may be suggestive of feline panleucopenia. For example, the animal may have recently been exposed to a potential source of infection, such as a cattery, or be a kitten obtained from a premisis with a history of feline panleucopenia. Lack of vaccination, or vaccination before the demise of maternally-derived antibodies, may also point to FPV infection. Owners usually report a sudden onset of illness including vomiting, diarrhoea, depression and complete anorexia, and cats are often said to hang their head over the food or water bowl but do not actually eat or drink.

On clinical examination, cats show varying degrees of depresssion and are often severely dehydrated. Vomiting and diarrhoea may be apparent and body temperature can be mildly to moderately elevated or depressed in the early stages of disease. When the cat becomes severely ill, a markedly subnormal temperature is seen. Animals are often painful on abdominal palpation, and the small intestine can be felt to be either abnormally flaccid or turgid due to fluid or gas filling. A typical "hunched up" posture is adopted by affected kittens. Damage to the enteric mucosal integrity can lead to secondary infections and sepsis and perforation of the gut can cause peritonitis.

Infection of the pregnant queen may result in in utero infection of kittens. When this occurs in early to mid gestation, foetal death, resorbtion, abortion or mummification can occur. Infection of kittens in late gestation or early in neonatal life may give cerebellar hypoplasia. This becomes apparent at around 10-14 days old. Affected kittens are ataxic with a wide-based stance, inco-ordination and tremors, and these signs persist for life. Apart from occasional retinal dysplasia, these cats are otherwise normal and healthy and are said to make good pets.

A per acute presentation of disease is possible, where kittens are found dead with little or no evidence of preceding enteritis.

Laboratory Tests

On haemotology, a striking panleucopenia is the most consistent finding and neutrophils are particularly depleted. Leucocyte counts are usually between 500 and 3000 cells per decilitre. Routine biochemistry is not associated with any specific changes.

Paired serum sampling should reveal a rising antibody titre to FPV during an acute infection. A CITE test can also be used to quickly detect FPV antigen in the faeces, although this is only truly licensed for use for canine parvovirus. Confirmation of diagnosis is by virus isolation or PCR of viral antigen using faeces, infected tissue, oropharyngeal swabs or post-mortem material.

Pathology

The virus targets crypt cells and lymphoid areas,causing villus atrophy. In the cat, the intestine becomes thickened, turgid and swollen, with a pale, dull and mottled appearance.

The contents appear rather dry, and this becomes increasingly evident lower down the gut.

Lower down in the gut, enteritis is apparent. In the cat this is fibrinous enteritis, and in the dog it is haemorrhagic.


The crypt lining cells undergo complete necrosis, but very little inflammation is seen. Fibrinous exudates may be seen on surface of the mucosa. However,the submucosa and lamina propria are often unaffected. Cyst-like structures are seen in the deepest parts of the glands of the intestinal mucosa after only a few days of infection. These cystic glands are lined with flattened epithelial cells.

Inclusion bodies may also be seen, but these are often very hard to find.

The Lymph nodes appear pale and oedematous, and almost aplastic. The Bone marrow appears pale and fatty looking and is depleted of cells.

Treatment

Modified live and inactivated virus vaccines are avaliable, with boosters every 1-2 years required. One should also try to prevent exposure to kittens with feline panleukopenia.

Prognosis

Links

References