Siobhan O’Sullivan
Animal Health Laboratory, University of Guelph, Guelph, ON.
AHL Newsletter 2022;26(2):24.
A two-year-old, German Shorthair Pointer presented with acute onset circling to the left, mild ataxia, salivation, moderate tachypnea and tachycardia. The vaccine history (DHPP and rabies) was up to date. The patient died after failing to respond to a short course of NSAIDs and antibiotics.
On gross postmortem examination, the lungs were mottled red, poorly aerated, and there was a focal depressed area of pleural fibrosis. The liver was enlarged, firm, and mottled red, with fine strands of capsular fibrin (passive congestion). When the heart was dissected, multiple, long thin white worms were present in the pulmonary artery and right ventricle. Moderate numbers of intestinal worms (ascarids) were also identified. The brain was grossly unremarkable.
Histopathology revealed pulmonary edema, hemorrhage and occasional pulmonary thrombosis. In the grossly fibrotic area of the lung, there was localized endarteritis with periarterial granulomatous inflammation compatible with heartworm, although no parasites were captured in section (Fig 1). There was acute centrolobular hepatic necrosis in the liver, compatible with acute passive congestion and attributed to pulmonary hypertension/right sided heart failure secondary to infection with heartworm. Neurologic signs were attributed to small multifocal areas of thrombosis and hemorrhage in the cerebral cortex and a focal granuloma in the midbrain, presumed secondary to aberrant visceral larval migrans of nematodes, either heartworms or ascarids (Fig 2).
Fewer than a dozen fatal cases of advanced canine heartworm infection have been submitted to the AHL between 2012-2022. All dogs were relatively young (8 months to 5 years), and often presented for workup following sudden death, with no provided history of heartworm preventative administration. Heartworm (Dirofilaria immitis) is transmitted by mosquitoes, which take up larval microfilariae from the blood of infected animals, and transmit them to new hosts. Microfilariae develop into adult heartworms in the pulmonary arteries, resulting in endarteritis. Dogs can appear asymptomatic, but advanced infections and high parasite burdens result in pulmonary hypertension, the presence of heartworms in the right ventricle, and signs of right-sided heart failure. There are also sporadic reports of aberrant migration of heartworms or ascarids into the brain and other organs, with resultant localized inflammation and thromboembolic complications.
While treatable, heartworm is potentially fatal, and prevention is the preferred approach to combating heartworm infection. Veterinary practitioners can provide appropriate protocols for preventative parasite medication and annual antigen detection testing. AHL
Figure 1. Pulmonary endarteritis, periarterial granulomatous inflammation secondary to infection with heartworm. H&E stain
Figure 2. Focal granuloma in the midbrain attributed to aberrant parasite migration. H&E stain.
References
1. Frank J, et al. Systemic arterial dirofilariasis in five dogs. J Vet Int Med 1997;11(3):189-194.
2. Atkins C. Heartworm infection in dogs, cats and ferrets [Internet]. The Merck Veterinary Manual. 2020. [cited 2022 May 10]. Available from: https://www.merckvetmanual.com/circulatory-system/heartworm-disease/heartworm-disease-in-dogs,-cats,-and-ferrets [1]