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Fall 1997 Newsletter

Bovine Respiratory
(Footrot) of Cattle
PCR for the
Detection of Lawsoniain-
tracellularis, Serpulinahyo-

and salmonellaspp.
from Porcine Intestinal Specimens
Enteric Canine
Parvovirus Infection
Plant Toxicities
Diseases of
Yew Poisoning
in Livestock
Serum Vitamin E Analysis


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Diagnostic Aspects of Enteric Canine Parvovirus Infection

Canine Parvovirus (CPV) infection most often occurs as a severe systemic and even life threatening illness in susceptible canine populations. It is caused by a single-stranded DNA virus which replicates only in cells that are rapidly proliferating and synthesizing DNA. The diagnosis of CPV infection is based on clinical findings, in-office test kits, other tests available at diagnostic labs, and gross and microscopic pathological lesions.

Clinical Signs - There is a wide variation in clinical response of dogs to infection with CPV, ranging from mild or inapparent infections in dogs more than 6 months of age to acute fatal disease in puppies less than 6 months of age.  The initial clinical signs of enteric CPV infection in most puppies include sudden onset of anorexia, depression, lethargy and fever, followed within 24 hours by vomiting and usually diarrhea. Diarrhea can be profuse and hemorrhagic. Death can occur in severe cases, and it is attributable to severe dehydration,   protein   loss,   electrolyte imbalances,  concomitant infection and systemic shock.

Clinical Pathology -Leukopeniadue to lymphopenia is the most consistent hemotologic finding associated with CPV infection. Total white blood cell count can decrease to less than 2000 cells/jJL. Severe neutropenia often occurs due to virus- induced myeloid degeneration of the bone marrow and the extensive loss of neutrophilsthrough the damaged intestinal wall. Serum chemistry analysis may be nonspecific and are usually related to changes associated with anorexia, vomiting, diarrhea and dehydration.

Diagnostic   Tests   -  Parvoviralenteritis must be differentiated from other causes of acute onset of vomiting, diarrhea, and leukopenia, such as salmonellosis, canine distemper, infectious canine hepatitis and small intestinal obstruction (e.g. foreign body,  intussusception).     A definitive diagnosis is made on detection of the viral antigen in feces or by demonstrating a rising titer   of  IgM   antibodies   to   CPV. Commercially available diagnostic test kits based on enzyme-linked immunosorbentassays (ELISAs) have enabled in-office testing, which allows rapid identification, isolation and treatment of animals infected with CPV. These tests are quite specific for CPV and relatively sensitive. False negative results may occur because of binding of test antigen with serum neutralizing antibodies in hemorrhagic diarrhea.

Feces from acutely infected animals can also be submitted to university and state diagnostic laboratories where different tests to detect CPV are available such as virus isolation, hemagglutination (HA), electron microscopy, ELISA and latex agglutination.

Necropsy Diagnosis - The gross intestinal lesions are nonspecific and variable. Ileum and jejunum are most often affected.   These affected parts may be flaccid and show serosal hemorrhages or congestion. The intestinal lumen is usually empty but may contain watery contents. The mesenteric lymph nodes are usually enlarged, with petechiae in the cortex. Characteristic microscopic changes seen in the rapidly proliferating cells of intestines, especially small intestines, include necrosis of crypt cells, resulting in dilated crypts that are filled with necrotic debris.  In severe cases, complete villus collapse occurs.

Post mortem (PM) diagnosis of CPV infection is strongly confirmed by detection of intranuclear inclusion bodies in the epithelial cells of the intestine. However, inclusions are not always present and the autolysis that occurs quickly in the intestinal epithelium often makes it difficult to confirm  the  presence  of inclusions. Examination of squamous cells of tongue may be helpful in confirmation of CPV infection because tongue epithelium is less affected by autolysis.  Moreover, exam­ination of tongue using immunofluorescencemay provide antemortem confirmation of CPV infection.

- byJatinderRana,ECFVG

- edited by LavunAnothayanontha.DVM




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