PhD Thesis Demeter Zoltan

ecame an occasional finding, compared to its occurrence during the widespread
epizootic outbreaks of the late 1970’s in CPV naive dogs (McCaw & Hoskins, 2006).
CPV2 infections have also been associated with neurological diseases, but these
are more commonly secondary consequences of DIC, hypoglycemia, sepsis or acid-base
electrolyte disturbance and hypoxia (Agungpriyono et al., 1999). Cutaneous
manifestations, such as erythema multiforme have also been reported in case of a severe
necrotizing CPV2 infection, suggesting that viral pathogens should also be considered in
case of canine erythema multiforme in which a causative drug cannot be clearly
established (Favrot et al., 2000).
Secondary clinical complications of CPV2 infections are represented by
thrombosis due to hypercoagulability, asymptomatic bacterial urinary tract infections,
and intravenous catheter infection (McCaw & Hoskins, 2006).
3.3.4 Pathology
The most relevant pathological changes can be found in the small intestine,
myocardium, and lymphoid tissues. The most severely affected intestinal segment is the
distal duodenum and jejunum. These intestinal loops appear thickened and segmentally
discolored, with denudation of intestinal mucosa and the presence of dark, sometimes
bloody, watery material within the stomach and intestinal lumen (McCaw & Hoskins,
2006). The enlargement of the mesenteric lymph nodes is also considered to be a very
frequent finding. Histopathologically, the shortening and collapsus of the intestinal villi,
and the presence of necrotic debris in the dilated crypts, as well as the presence of large,
intranuclear inclusion bodies in the epithelial cells of the digestive tract are considered
to be highly suggestive of a CPV2 infection. The pathologic changes may range from
mild inflammation to diffuse, hemorrhagic enteritis (McCaw & Hoskins, 2006).
Necrosis and depletion of lymphoid tissues, such as Peyer’s patches, mesenteric lymph
nodes, thymus and spleen, are also present.
Viral myocarditis is characterized macroscopically as pale streaks in the
myocardium (McCaw & Hoskins, 2006). The lesions are usually represented by
nonsuppurative myocarditis, mild fibrosis, myocyte degeneration, microcalcification,
and the presence of intranuclear inclusion bodies (Agungpriyono et al., 1999). The
presence of CPV2 particles can be demonstrated by the means of EM, IFAT, IHC and
ISH (McCaw & Hoskins, 2006).
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