Feline Panleucopenia

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Also known as: Feline Infectious Enteritis — Feline Parvovirus — FPV — Panleukopenia

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). CPV-2 is also responsible itself for some cases of feline panleucopenia. In order to replicate, FPV must infect dividing cells, and so tissues with a high mitotic rate undergo acute 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 that 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 from mild or subclinical disease.

Diagnosis

A presumptive diagnosis can be made on the basis of clinical signs, vaccination status, age, exposure and the presence of a severe 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 premises 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 depression 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, in-coordination 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.

There are several differential diagnoses for feline panleucopenia. These include feline lymphoma virus, Salmonellosis and acute poisoning. Many other diseases cause vague signs which are similar to mild feline panleucopenia infection. The fact that white blood cell count is always low even in mild cases of feline panleucopenia can be used to differentiate this condition from others.

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

Macroscopically, the hair coat is seen to be rough, body condition is poor and there is evidence of severe dehydration. Faecal staining may be suggestive of diarrhoea during life. The intestine itself is oedematous and petechial or ecchymotic haemorrhages may be seen on the serosal or mucosal surfaces of the jejunum and ileum. Thymic atrophy is apparent, lymph nodes are pale and oedematous and the bone marrow is gelatinous or liquid in texture. Animals infected in utero or neonatally nay show gross hypoplasia of the cerebellum.

Histologically, the cells lining the intestinal crypts undergo complete necrosis and sloughing, but little inflammation is seen. The villi are shortened and blunted (villous atrophy) and fibrinous exudates may be seen on surface of the mucosa. There is an absence of lymphocytic infiltrates in all tissues and lymphoid depletion of lymph nodes, Peyer's patches and the spleen. Eosinophilic intranuclear inclusion bodies are formed during the early stages of infection, but these are usually not possible to observe on routine examination of sections. In neonatal and foetal infections, the granular and Purkinje cells of the cerebellum may be depleted.

Treatment

Treatment relies on supportive care. The aims of this are to rehydrate the animal, to re-establish electrolyte balances and to support the animal until the immune system produces antibodies to neutralise FPV. Intensive intra-venous fluid therapy is therefore essential, and fluids can be spiked with electrolytes to restore the animals balance. A blood transfusion may also be necessary if the total leucocyte count falls below 2000 cells per decilitre. The kitten should be maintained within a warm clean environment, and food withheld until the gastroenteritis is controlled, when a simple, moist diet should be gradually reintroduced. Drug therapy should involve broad-spectrum antibiosis to control secondary bacteraemias, gastric protectants, anti-emetics and B-vitamin supplements. Feline interferon omega can be helpful but is often cost-preclusive. Barrier nursing and effective cleaning and disinfection of the environment with household bleach is of paramount importance.

Feline panleucopenia is completely preventable by routine vaccination of kittens. Modified live vaccines are most commonly used, and should be given once at 8-12 weeks of age, and a second time 3-4 weeks later. It has also been advised to give a third dose once the kitten is over 16 weeks of age, to ensure that maternally transferred immunity does not interfere with the vaccine. Cats older than 16 weeks at the beginning of the course need two injections only. Boosting is required at one year, and then every one to three years after the first year.

Prognosis

Most acute cases last around 5-7 days. Although prognosis is guarded during acute disease, recovery is generally rapid if death does not result. It may, however, take several weeks for the animal to regain the body condition lost during the illness.

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References

  1. Tilley, L.P. and Smith, F.W.K.(2004)The 5-minute Veterinary Consult (Third edition) Lippincott, Williams & Wilkins.
  2. Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition) Merial




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