Hepatozoonosis is caused by Hepatozoon canis. The host range include dogs and other carnivores including fox and wolf. The disease is transmitted by brown dog tick called Rhipicephalus sanguineus. The ticks become infected by ingestion of gametocytes in monocytes and neutrophils during taking of blood meal from infected carnivore. The organism replicates in tick and develop into sporocytes in the hemocele. The sporozoites do not migrate to salivary gland or mouth parts. Transmission from infected ticks does not occur by bite of ticks. Natural infection in dogs occur by ingestion of infected ticks. After ingestion, sporozoites of H.canis are released from ticks then penetrate intestinal wall of the host and are carried by blood or lymph to mononuclear phagocytes or endothelial cells of the spleen, bone marrow, lungs where schizogony results in development of macroschizonts and subsequent release of macromerozoites. The macromerozoites penetrate the cells of myocardium, skeletal muscles, lungs,spleen, lymphnodes and liver where further cycles of schizogony results in development of microscizonts. The microschizonts may persist in cells as cyst-like structures for varying periods without inciting inflammatory response. Eventually, micromerozoites are released from the microschizonts at which time,the granulomatous inflammatory process occur with neutrophils in skeletal muscles. Neutrophils and monocytes become infected by phagocytosis or direct penetration of micromerozoites which now develop into gametocytes. This is a form of H.canis found in the leucocytes of infected dogs.
DISTRIBUTION
The disease is found in southeast Asia , Arica, Middle east, Europe,Brazil and Golf coast region of texas in USA.
CLINICAL SIGNS
The only dogs that develop clinical signs of Hepatozoonosis are those that are concurrently infected with some other disease and are immunodepressed or those that have genetically defective neutrophil function or younger than 4 months of age. The most common clinical signs are intermittent or persistent fever, emaciation even though dogs appetite remain normal until terminal stages before death. Other signs are muscular hyperesthesia(excessive sensitivity),lumbar pain and reluctance to move, depression, bloody diarrhea, mucopurulent ocular and nasal discharge, leucocytosis, regenerative anaemia and cachexia. Anorexia can come terminally.
DIAGNOSIS
Definitive diagnosis is by finding the organism in neutrophils or monocytes in freshly prepared blood smears or biopsy of skeletal muscles. Blood smears should be prepared immediately after blood collection and should be stained with giemsa and leishman stain. Gametocytes in cytoplasms of neutrophils or monocytes stain uniformly light ice blue and may be present in one or two cells per 1000 leucocytes. Cyst with a central nucleus or developing microschzonts are found in biopsy of skeletal muscles.
TREATMENT
Imidocarb dipropionate clears the parasite from blood although results with this drug has been inconsistent both with and without other agents. The dose of this drug is 5mg/kg IM/SC once. A combination of tetracycline and imidocarb causes clinical remission and clearance of parasitemia. In chronic cases, palliative treatment with non steroidal antiinflammatory agent are recommended. Aspirin is given at 10-25mg/kg per os 3x daily. Phenylbutazone is given at 2-20mg/kg per os daily for 3-4 days. Flunixin is given at dose of 1mg/kg per os/sc once daily for up to 5 days. They relieve discomfort associated with the disease.
PREVENTION
Environmental hygiene
Control of ticks by routine dipping of dogs
Regular and routine spraying of kennel
Environmental vector control
Keeping the animal free from ticks
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