Parvoviral myocarditis in littermate puppies and a review of AHL cases 2013-2023
Emily Brouwer, Dominique Comeau, Patricia Lechten
Animal Health Laboratory, University of Guelph, Guelph, ON (Brouwer, Comeau); Allandale Veterinary Hospital, Barrie, ON (Lechten)
AHL Newsletter 2023;27(2):25.
Two littermate golden retriever puppies were submitted to the Animal Health Laboratory for postmortem examination approximately three weeks apart. The puppies originated from an unregistered breeder, and were subsequently adopted by a rescue organization. Of the six puppies in the litter, three had died suddenly and one was euthanized due to acute respiratory distress.
The first puppy that was submitted for postmortem examination was nine weeks old at the time of death. He had a four day history of slightly laboured breathing followed by sudden collapse and cardiopulmonary arrest. The puppy received routine vaccinations approximately one week prior to death. There were no clinical abnormalities noted at the time of vaccination.
The second puppy was eleven weeks old at the time of death. He was euthanized following an episode of labored breathing starting two days prior. At the time of his hospitalization, the postmortem examination had been performed on his littermate. Based on his clinical signs and the diagnosis made in his sibling, it was presumed that he was in congestive heart failure.
Postmortem examination of the first puppy revealed relatively mild gross lesions of pulmonary edema, meningeal congestion and petechial to ecchymotic hemorrhages within the pancreas. Lesions were more dramatic in the second puppy which had diffuse pulmonary edema and mild pleural effusion. Gross cardiac lesions were limited to the second puppy and were characterized by diffuse myocardial pallor and mild biventricular dilation. On cut section, the myocardial pallor was most pronounced in the interventricular septum (Fig. 1). The heart weight ratios were within published reference ranges for this species.
On histologic examination, the first puppy had extensive multifocal loss of cardiomyocytes with replacement by thin bands of edematous collagen, lymphocytes and plasma cells. Cardiomyocytes in affected areas were often shrunken with angular cell outlines. Rarely, the cardiomyocyte nuclei contained irregular, poorly-defined basophilic material suspicious for viral inclusion bodies. The lesions in the second puppy were more chronic in nature, with extensive replacement of the myocardium by fibrous connective tissue interspersed with clusters of lymphocytes and plasma cells (Fig. 2). Pulmonary lesions in both dogs were compatible with acute congestive heart failure.
Both puppies were positive for canine parvovirus using real-time PCR with cycle thresholds of 25.52 and 32.07, performed on scrolls of heart and fresh tissue in puppies one and two, respectively. The antigen was also demonstrated within the myocardial lesions using immunohistochemistry. Positive immunoreactivity was detected in both animals, both within the inflammatory population as well as the cardiomyocytes. Testing of the first puppy for canine herpesvirus, another common cause of myocarditis in puppies, was negative. Following these ancillary test results, a diagnosis of parvoviral myocarditis was made in both puppies.
Figure 1. Heart of puppy number two with ventricular myocardial pallor (left). Cross section of ventricular myocardium (right).
Figure 2. Myocardium of puppy number two, H & E stain, 10X. Note extensive fibrosis, nonsuppurative inflammatory infiltrates, and loss of cardiomyocytes.
In the last ten years, only five cases of parvoviral myocarditis have been diagnosed at the Animal Health Laboratory (Table 1.). These puppies ranged in age from 5.5 weeks to 11 weeks of age. Two were mixed breeds, one was a French bulldog, and two were golden retrievers. All had similar lesions of cardiomyocyte necrosis and lymphoplasmacytic inflammation with varying degrees of fibrosis. The etiology in all cases was confirmed using real-time PCR, immunohistochemistry, or both ancillary test procedures.
Table 1. Parvoviral myocarditis cases submitted to the AHL between 2013 and 2023
While most are familiar with the common diarrheal illness attributed to canine parvovirus-2 infection, widespread vaccination efforts have greatly diminished the incidence of myocarditis in young puppies. Development of myocarditis occurs when there is perinatal infection of the puppies either within the first two weeks of life, or if the naïve dam is infected late in gestation and in utero transmission occurs. Infection of proliferating cardiomyocytes results in necrotizing myocarditis, and those that survive the initial infection typically go on to develop nonsuppurative inflammation and myocardial fibrosis which impacts myocardial function. The amount of virus detectable within the heart will decrease as the infected myocardiocytes are replaced by fibrosis, and may not be detectable in a long-surviving animal. In the subset of AHL cases from the last ten years, five animals with lesions of nonsuppurative myocarditis were positive for parvovirus on PCR, but of these five, one case was PCR positive and the virus was not detectable using immunohistochemistry, and one case was not confirmed with immunohistochemistry.
The two surviving littermates of the submitted golden retrievers were assessed by a cardiologist following the diagnosis of their siblings. Both surviving puppies had echocardiograms performed which identified mild left ventricular dysfunction with subtle left-sided dilation in one puppy, and mild systolic dysfunction in the other puppy. Neither required medical intervention, though continued monitoring, including baseline troponin, was recommended. AHL
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