1. D I R E 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

2. Also known as;
 feline infectious enteritis
 feline parvoviral enteritis
 feline distemper
 feline ataxia
 cat plague

3. Etiology
 Group: Group II (ssDNA)
 Family: Parvoviridae
 Subfamily: Parvovirinae
 Genus: Protoparvovirus
 Species: Feline panleukopenia virus
 Replicate in the nucleus, form intranuclear
inclusion bodies.

4. Epidemiology
 Most species of 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.

5. Clinical Signs
 bloody diarrhea.
 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.

6. Pathogenesis
 Ingestion or inhalation, 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

7. Pathogenesis
. Intranuclear inclusions are 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.

8. Diagnosis
 A white cell 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.

9. Treatment
 No specific treatment 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.

10. Control
 Vaccination is the 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.

11. THANKS FOR PATIENCE