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Peer-reviewed veterinary case report

Puppy with severe heart and brain damage from parvovirus infection

By Agungpriyono, D R et al.·Published in Veterinary pathology·1999·View original on PubMed

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Original publication title: Subacute massive necrotizing myocarditis by canine parvovirus type 2 infection with diffuse leukoencephalomalacia in a puppy.

Species:
dog

Plain-English summary

A 4-week-old mongrel puppy was found to have severe heart problems and brain damage due to a canine parvovirus type 2 (CPV-2) infection. The puppy showed signs of heart failure, which can include weakness and difficulty breathing, and the infection caused significant damage to the heart muscle. While the brain showed some damage, it was determined that this was likely due to the lack of oxygen from the heart issues rather than a direct effect of the virus. Unfortunately, the puppy's condition was severe, and it likely did not survive.

People also search for: puppy heart problems · canine parvovirus symptoms · puppy brain damage treatment

Abstract

Severe necrotizing myocarditis associated with canine parvovirus type 2 (CPV-2) infection and diffuse leukoencephalomalacia was recognized in a 4-week-old mongrel puppy. The cardiac lesions were characterized by severe diffuse myocardial degeneration and necrosis with occasional massive mineralization and distinct intranuclear inclusion bodies. Immunohistochemical examination revealed the presence of CPV-2 antigens in both the cytoplasm and nuclei of the myocytes. In the white matter of the cerebrum, moderate to severe diffuse necrosis with diffuse infiltration of gitter cells and occasional diffuse mineral deposits were recognized symmetrically and bilaterally. In the meningocortical area of the cerebellum, there was mild focal hemorrhage and accumulation of hemosiderin-laden histiocytes. In addition to the absence of viral antigen (as judged by immunohistochemistry), neither viral inclusions nor other vascular lesions were identified in examined sections of brain. These findings suggest that the brain lesions were not induced by direct CPV-2 infection but were related to severe myocardial lesions producing prolonged hypoxia and/or ischemia.

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Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/9921761/