Canine herpesvirus infection in a 5-wk-old puppy
Maria Spinato, Margaret Stalker, Davor Ojkic, Murray Hazlett
A 5-wk-old male Springer Spaniel puppy was submitted to the AHL-Guelph laboratory for postmortem examination. One other animal had died from this litter of 9 pups the preceding week. Clinical signs included conjunctivitis, dyspnea, lethargy, and weight loss prior to death. The bitch was fully vaccinated and mastitis had been ruled out. Bacterial pneumonia was suspected.
The puppy was mildly dehydrated and in good body condition with adequate fat stores. Approximately 10 mL of clear fluid was present within the thoracic cavity. Lungs were rubbery, edematous, and mottled light/dark-pink with indistinct parenchymal petechiae. Liver was bronze and contained miliary dark-red depressed foci throughout the parenchyma (Fig. 1A). Scattered petechiae were also present overlying the adrenal glands and serosa of the small intestine. Kidneys were mottled dark-red/purple and contained coalescing cortical hemorrhages on cut section. Spleen was dark red and minimally swollen. Hepatic and mesenteric lymph nodes were mildly to moderately enlarged and a few were markedly congested. Scattered linear mucosal hemorrhages were present within the small intestines and terminal colon. A preliminary diagnosis of generalized visceral petechial hemorrhages due to a suspected systemic viral or bacterial infection was made. Tissue samples were collected for microscopic evaluation and pooled viscera were submitted for PCR testing for canine distemper virus, canine adenovirus, and canine herpesvirus (CHV).
Histologic examination of liver revealed random coalescing foci of hepatocellular necrosis and hemorrhage lightly infiltrated by karyorrhectic neutrophils (Fig. 1B). Occasional eosinophilic intranuclear inclusion bodies were situated within surrounding viable hepatocytes (Fig. 1C). A kidney section also contained coalescing renal cortical hemorrhages surrounding small clusters of tubules undergoing acute necrosis. Rare suspicious eosinophilic intranuclear inclusions were observed in adjacent epithelial cells. Similar punctate foci of necrosis and hemorrhage were present in the lung, adrenal gland, spleen, abdominal lymph nodes, small intestine, and colon. The PCR test for canid herpesvirus 1 was positive (Ct 16.8). PCR tests for canine adenovirus 2, canine parainfluenza virus, and canine distemper virus were negative. Bacterial culture was not pursued. Final diagnosis was multifocal hepatic, pulmonary, adrenal, renal, and intestinal necrosis caused by CHV.
This case is unusual given the older age of the puppy. A search of AHL pathology records from 2007 to present found 14 diagnosed cases of CHV in puppies. All of these animals were < 3-wk-old except for this case (5-wk-old) and one 8-wk-old puppy that had CHV isolated in cell culture prior to PCR testing becoming available.
Canid herpesvirus 1 is a ubiquitous virus that is relatively fragile in the environment. Therefore, the source is thought to be activation of latent carrier status during stressful events such as parturition. Transmission is via direct contact from respiratory or genital secretions. Puppies > 2-wk-old are generally resistant to clinical disease. Several factors may increase the susceptibility to disease at an older age, such as seronegative status of the dam and cooler environmental temperatures that promote the survival and replication of the virus. Infected dams should develop protective immunity and subsequently produce healthy litters. AHL
Figure 1. A. Foci of hemorrhage in intestine, liver (arrow), and lung. B. Focus of necrosis and hemorrhage (arrow) with some neutrophilic reaction in liver. C. Typical eosinophilic intranuclear inclusion body in hepatocyte (arrow).