Hepatozoonosis in dogs: 22 cases (1989-1994)

Abstract

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 microscopic examination of skeletal muscle. Procedure— We reviewed medical records of all dogs with a definitive diagnosis of hepatozoonosis that were referred to the Auburn University Small Animal Clinic between 1989 and 1994. Results— Diagnoses were confirmed by microscopic identification of H canis schizont or merozoite stages in skeletal muscle. The gametocyte stage was not detected in smears of blood obtained from a peripheral vein, buffy-coat smears, or bone marrow evaluation. Common clinical signs included fever, cachexia, ocular discharge, pain, stiffness, and paresis. Laboratory abnormalities included marked leukocytosis, hypoglycemia, hypoalbuminemia, mild anemia, hyperphosphatemia, and high alkaline phosphatase activity. Periosteal bone proliferation was evident radiographically in 18 of 22 dogs. Renal lesions included amyloidosis (1 dog), interstitial nephritis (3), and mesangioproliferative glomerulonephritis (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 months, with a mean time of remission before recurrence of clinical signs of 6 months. Clinical Implications— H canis infection in dogs can be associated with a distinct clinical syndrome that involves chronic myositis, debilitation, and death. The dogs of this report represent the first substantial number of domestic dogs naturally infected with H canis in the United States outside of the Texas Gulf Coast. Hepatozoon canis appears to be a serious pathogen in the United States that is becoming more widespread geographically. (J Am Vet Med Assoc 1997;210:916–922)