Canine hepatozoonosis, caused by Hepatozoon americanum, is an emerging tick
-borne disease of dogs in North America. Ln addition to the skeletal and ca
rdiac myositis that are prominent features of the disease, there is dissemi
nated periosteal bone proliferation in most dogs that manifest clinical dis
ease. Each of six experimentally infected animals (four dogs and two coyote
s) and seven of eight naturally infected dogs had gross or histopathologic
osteoproliferative lesions. Experimental animals were 6-9 months of age whe
n exposed. Naturally infected dogs were 8 months to 11 years old when subje
cted to necropsy. Lesions occurred primarily on the diaphysis of the more p
roximal long bones of the limbs: however, flat and irregular bones were fre
quently involved. Lesions involving metacarpals, metatarsals, and digits we
re infrequent. The earliest observed periosteal lesions were in an experime
ntally infected dog 32 days after exposure to sporulated oocysts of H. amer
icanum. There were hypertrophy and hyperplasia of osteoprogenitor cells, an
d osteoblasts appeared in the cellular zone of the periosteum. Spicules of
woven bone oriented perpendicularly to bone cortex followed. Later yet, per
iosteal new bone was remodeled and tended to become oriented parallel to th
e cortical bone. Horizontally oriented zones of remodeled, condensed bone s
ometimes occurred in multiple layers on the original cortex, forming "pseud
ocortices." 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.