Objective-To document hepatozoonosis in dogs from Alabama and Georgia
and to report associated clinical signs, method of diagnosis, response
to treatment, and course of disease. Design-Retrospective case series
. Animals-22 dogs in which Hepatozoon canis was identified by microsco
pic examination of skeletal muscle. Procedure-We reviewed medical reco
rds of all dogs with a definitive diagnosis of hepatozoonosis that wer
e referred to the Auburn University Small Animal Clinic between 1989 a
nd 1994. Results-Diagnoses were confirmed by microscopic identificatio
n of H canis schizont or merozoite stages in skeletal muscle. The game
tocyte stage was not detected in smears of blood obtained from a perip
heral vein, buffy-coat smears, or bone marrow evaluation. Common clini
cal signs included fever, cachexia, ocular discharge, pain, stiffness,
and paresis. Laboratory abnormalities included marked leukocytosis, h
ypoglycemia, hypoalbuminemia, mild anemia, hyperphosphatemia, and high
alkaline phosphatase activity. Periosteal bone proliferation was evid
ent radiographically in 18 of 22 dogs. Renal lesions included amyloido
sis (1 dog), interstitial nephritis (3), and mesangioproliferative glo
merulonephritis (4). Treatment with the anticoccidial drug toltrazuril
, despite an initial favorable response, failed to prevent relapse in
all but 3 of 21 treated dogs. Mean survival time was 12.6 +/- 2.2 mont
hs, with a mean time of remission before recurrence of clinical signs
of 6 months. Clinical Implications-H canis infection in dogs can be as
sociated with a distinct clinical syndrome that involves chronic myosi
tis, debilitation, and death. The dogs of this report represent the fi
rst substantial number of domestic dogs naturally infected with H cani
s in the United Stares outside of the Texas Gulf Coast. Hepatozoon can
is appears to be a serious pathogen in the United States that is becom
ing more widespread geographically.