Over the next five months, the owners reported that the dog had short, intermittent episodes of pain. We continued the decoquinate
but switched the patient to carprofen (2.6 to 5.3 mg/kg orally daily as needed) for pain.
Five months later, about one year after the initial presentation (Day 367), the patient was presented to our hospital for
evaluation of a recent history of episodes of pain and stiffness that were becoming more frequent. The owners gave the dog
carprofen (5.3 mg/kg) the night before presentation. Physical examination findings were normal at this time.
The results of a CBC showed a mild leukocytosis with a mature neutrophilia (Table 1). A serum chemistry profile revealed mildly elevated aspartate transaminase (90 U/L; reference range = 15 to 66 U/L) and
creatinine phosphokinase (987 U/L; reference range = 59 to 895 U/L) activities.
With the history and laboratory test results supportive of myositis secondary to parasitic reproduction, we increased the
dosage of decoquinate to 2.5 tsp twice a day. Optimally, an additional two-week course of trimethoprim-sulfadiazine or trimethoprim-sulfamethoxazole,
pyrimethamine, and clindamycin should be administered to kill the merozoites in the tissues, as decoquinate functions mainly
to arrest the developing zoites.1
Thirty-nine months after the initial diagnosis, the owners reported that the dog was stable, with minimal cyclic discomfort.
In the United States, hepatozoonosis is caused by Hepatozoon americanum, which is thought to be transmitted by the Gulf Coast tick Amblyomma maculatum,2 and infection results in a distinct clinical syndrome.3 In other parts of the world, Hepatozoon canis causes the disease, which is transmitted by the brown dog tick Rhipicephalus sanguineus, and the organism is much less virulent.3,4
Clinically, hepatozoonosis presents as a waxing, waning disease consisting of intermittent fever, chronic weight loss, mucopurulent
ocular discharge, pain, muscle atrophy, and gait abnormalities (e.g. generalized stiffness, weakness, unwillingness to walk). The intermittent fever can reach as high as 106 F (41.1 C) and does
not improve with antibiotic treatment. The pain is often intermittent and may be generalized, joint-associated, cervical,
paraspinal, or abdominal.
In dogs with hepatozoonosis, a CBC often reveals a pronounced leukocytosis that is predominantly a mature neutrophilia. A
mild nonregenerative anemia and elevated platelet counts may also be present. Thrombocytopenia is usually not evident unless
the dog has concurrent ehrlichiosis, babesiosis, or Rocky Mountain spotted fever.3 A serum chemistry profile often reveals hypoalbuminemia, mild hypoglycemia, and mildly increased serum alkaline phosphatase
Osteoproliferation is also associated with hepatozoonosis and is thought to be due to increased blood flow and fluid retention
in the limbs, followed by proliferation of vascular connective tissue and periosteum and subsequent bone deposition.5 On radiographic examination, this is most frequently and most severely evident in the diaphyses of long bones and, to a
lesser extent, in flat and irregular bones5 such as vertebrae or the pelvis.2,3 These lesions are proliferative, can be subtle or obvious, and may consist of smooth lamellar periosteal thickening or irregular
proliferative exostoses.3 Pronounced neutrophilia in combination with periosteal proliferation may be highly indicative of American canine hepatozoonosis.2,3 However, in this case, the initial radiographs of the caudal thoracic, abdominal, and cranial pelvic areas obtained on presentation
did not show evidence of these lesions.
Follow-up pelvic and hindlimb long bone radiographs taken 19 months after initial presentation showed subtle evidence of periosteal
proliferation on the pelvis, which became more pronounced over the following two months.