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Skeletal Lesions of Canine Hepatozoonosis Caused by Hepatozoon americanum

Departments of Veterinary Anatomy, Pathology and Pharmacology (RJP, CAC), Infectious Diseases and Physiology (JSM, SAE, AAK), and Veterinary Clinical Sciences (WTD), College of Veterinary Medicine, Oklahoma State University, Stillwater, OK

Canine hepatozoonosis, caused by Hepatozoon americanum, is an emerging tick-borne disease of dogs in North America. In addition to the skeletal and cardiac myositis that are prominent features of the disease, there is disseminated periosteal bone proliferation in most dogs that manifest clinical disease. Each of six experimentally infected animals (four dogs and two coyotes) and seven of eight naturally infected dogs had gross or histopathologic osteoproliferative lesions. Experimental animals were 6–9 months of age when exposed. Naturally infected dogs were 8 months to 11 years old when subjected to necropsy. Lesions occurred primarily on the diaphysis of the more proximal long bones of the limbs; however, flat and irregular bones were frequently involved. Lesions involving metacarpals, metatarsals, and digits were infrequent. The earliest observed periosteal lesions were in an experimentally infected dog 32 days after exposure to sporulated oocysts of H. americanum. There were hypertrophy and hyperplasia of osteoprogenitor cells, and osteoblasts appeared in the cellular zone of the periosteum. Spicules of woven bone oriented perpendicularly to bone cortex followed. Later yet, periosteal new bone was remodeled and tended to become oriented parallel to the cortical bone. Horizontally oriented zones of remodeled, condensed bone sometimes occurred in multiple layers on the original cortex, forming "pseudocortices." The osseous lesions of American canine hepatozoonosis, with few variations, are remarkably similar to those of hypertrophic osteopathy in domestic dogs and other mammalian species, including humans.

Key words: American canine hepatozoonosis; bone, hypertrophic osteopathy.

Request reprints from Dr. R. J. Panciera, Department of Anatomy, Pathology and Pharmacology, College of Veterinary Medicine, Room 250 Veterinary Medicine, Oklahoma State University, Stillwater, OK 74078 (USA).

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