Feline panleukopenia by Dr Nadir Khosa

Feline panleukopenia by Dr Nadir Khosa

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  D I RE C T E D B Y : D R . N A D I R K H O S A D V M , U V A S , L A H O R E Feline Panleukopenia
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  Also known as; feline infectious enteritis  feline parvoviral enteritis  feline distemper  feline ataxia  cat plague
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  Etiology  Group: GroupII (ssDNA)  Family: Parvoviridae  Subfamily: Parvovirinae  Genus: Protoparvovirus  Species: Feline panleukopenia virus  Replicate in the nucleus, form intranuclear inclusion bodies.
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  Epidemiology  Most speciesof Felids are highly susceptible to infection which is generally endemic in unvaccinated cats.  Cats of all ages are susceptible to infection.  Disease occurs in young recently-weaned kittens, as maternally-derived antibody levels wane. High rates of virus excretion occur during the acute stages of the disease, mainly in feces but also in saliva, urine, vomitus and blood.  Cool,moist,dark environment is most susceptible for this disease.  fleas and humans act as mechanical vector for this disease.
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  Clinical Signs  bloodydiarrhea.  severe dehydration.  malnutrition.  Anemia.  often death is occurred  It causes a decrease in the cat's white blood cells.  Depression, lethargy, loss of appetite, fever, vomiting, loss of skin elasticity due to dehydration, and self-biting in the tail, lower back and back legs can be seen.
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  Pathogenesis  Ingestion orinhalation, then replication of virus occurs in mitotically active lymphoid tissues of oropharynx and associated lymph nodes. Viraemia develops within 24 hours, producing infection of mitotically active cells in other tissues, particularly the cells of the intestinal crypts and the lymphopoietic cells of the bone marrow, thymus, lymph nodes and spleen. Destruction of these target tissues results in panleukopenia and villous atrophy. The crypts of Lieberkiihn are dilated and contain necrotic epithelial cells
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  Pathogenesis . Intranuclear inclusionsare sometimes evident in crypt cells. Intestinal villi become blunted and may fuse. The effects of transplacental infection on foetuses generally relate to the stage of gestation at the time of viral invasion and range from cerebellar hypoplasia and retinal dysplasia to foetal death.
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  Diagnosis  A whitecell count of less than 7 x 109/L in acutely affected animals.  Neutropenia is more common than lymphopenia  virus isolations from oropharyngeal swabs, faeces, spleen, mesenteric lymph nodes and ileum.  A rising antibody titre may be detected in serum  samples by (HAI) or (VN)  Commercially available canine parvovirus kit can b used.  ELISA and PCR techniques can be used.
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  Treatment  No specifictreatment is available.  Intensive supportive therapy is usually necessary appropriate fluid therapy for dehydration should be given.  Whole blood or plasma from immune donors may be beneficial in cats with anaemia or hypoproteinaemia.  Parenterally administered broad-spectrum antibiotics can be used to combat secondary bacterial infections.  Affected animals should be housed in a clean, warm environment and maintained on an optimal diet supple- mented with B complex vitamins.
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  Control  Vaccination isthe principal control measures.  Modified live and inactivated vaccines are commercially available.  modified live vaccines can be used to immunize  kittens at 8 to 10 weeks of age, with a booster dose  at 12 to 14 weeks of age. Annual booster vaccinations are recommended by vaccine manufacturers.  These vaccines should not be used in pregnant felids.
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  THANKS FOR PATIENCE