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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