Systemic canine adenoviral infection in a puppy
Dominique Comeau
Animal Health Laboratory, University of Guelph, Guelph, ON
AHL Newsletter 2025;29(3):24.
A six-week-old puppy was submitted to the Animal Health Laboratory for postmortem examination. The puppy presented to the primary care veterinarian for lethargy, anorexia, and wheezing. On presentation, he had prominent swelling of the face and enlarged submandibular lymph nodes. Treatment was initiated for presumed puppy strangles, however, the puppy passed shortly after.
On examination at the AHL, there was moderate subcutaneous edema along the mandibles and ventral neck, along with enlargement of the submandibular lymph nodes. The only other significant change was subjective enlargement of the liver and the mesenteric lymph nodes. Histologically, the most striking finding was multifocal random necrotizing hepatitis with large basophilic intranuclear inclusion bodies in affected hepatocytes (Fig. 1). Vascular endothelium was reactive in all levels of the brain, and the vessels were often surrounded by thin rims of macrophages and lymphocytes (Fig. 2). There was a mild interstitial pneumonia. The lesions in the skin of the jaw were not consistent with puppy strangles (a pyogranulomatous dermatitis would be expected), but instead showed a fibrinoid vasculitis and abundant edema.
Hepatitis with large intranuclear viral inclusions like those observed in this young puppy is typical of infectious canine hepatitis. Given the presence of cerebral and pulmonary inflammation, canine distemper virus was a key differential diagnosis in this case, and the possibility of multiple viral infections was also considered. This animal tested negative for canine distemper virus, but both the liver and the brain tested positive for canine adenovirus 1 (causative virus of infectious canine hepatitis). The Ct vales were between 17 and 23, indicating a moderate to high viral load. The presence of canine adenovirus was further confirmed in the liver using immunohistochemistry (Fig. 3).
Canine adenovirus 1 most often targets the liver leading to hepatitis and variably severe clinical disease. Vascular endothelial cells are also a common target for this virus, and injury to these cells can lead to rare systemic presentations of this disease, such as encephalopathy. In this case, cerebral vasculitis leading to perivascular inflammation and edema was diagnosed alongside the typical hepatic lesions associated with this virus. While neurologic disease due to vascular injury is rare in domestic dogs, it is the most common presentation of infection with canine adenovirus 1 in wild canids such as foxes.
The vascular changes in the submandibular tissues were different than those noted in the brain. Therefore, it is suspected, but not confirmed, that this vascular injury was virally induced. It is not certain if canine adenovirus 1 was the cause of the facial swelling in this animal.
Figure 1. Section of liver showing congestion, vacuolation, and single cell death indicating hepatic injury, as well as multiple large basophilic intranuclear viral inclusions (arrows). H&E stain.
Figure 2. Multiple vessels in the brainstem with large cuffs of lymphocytes, macrophages, and fewer neutrophils. H&E stain.
Figure 3: Section of liver showing numerous hepatocytes with strong positive immunoreactivity for adenovirus (brown pigment). DAB chromogen.
References
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2. Caudell D, et al. Diagnosis of infectious canine hepatitis virus (CAV-1) infection in puppies with encephalopathy. J Vet Diagn Invest 2005;17(1):58-61.
3. Green RG, el al. Epizootic fox encephalitis. IV. The intranuclear inclusions. American J of Epidemiology 1933;18(2):462.
4. Walker DE, el al. Infectious canine hepatitis in red foxes (Vulpes vulpes) in wildlife rescue centres in the UK. Vet Record 2016;178(17):421-426.