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American Canine Hepatozoonosis

Photo from article by Lucia Helena O’Dwyer: 2001.  Some aspects of hepato-zoonosis.  Clinica Veterinaria. 31: 34-40.


Hepatozoonosis is an emerging disease in the United States caused by the protozoan Hepatozoon. Hepatozoon species have been found to infect a wide range of carnivorous hosts including domestic dogs, jackals, coyotes, foxes, hyenas, domestic cats, bobcats, lions, leopards, and cheetahs.  The causative agent of hepatozoonosis in the United States is a newly recognized species, Hepatozoon americanum, whereas in other parts of the world, Hepatozoon canis is the primary agent.  The features of American hepatozoonosis greatly contrast non-American infections.  The clinical presentation of dogs with hepatozoonosis in the US is much more aggressive than that of infected dogs from other parts of the world, indicating that Hepatozoon americanum is more pathogenic.   Non-American infections are often subclinical and seem to be limited to the immunosuppressed.  Most cases of domestic canine hepatozoonosis in the United States are diagnosed in the region from Texas to Georgia.  H. americanum infection has also been identified in coyotes in Oklahoma.

  The exact life cycle and transmission for  H. americanumhas not been completely elucidated.  Most portrayals are based on extrapolations from that which is known of H. canis.  The tick vector is the definitive host.  The vector for H. canis appears to be primarily the brown dog tick, Rhipicephalus sanguineus.  Evidence suggests the Gulf Coast tick, Amblyomma maculatum, as the vector involved in transmission of H.americanum in the United States.   Although some reports have demonstrated the ability of dogs to become infected with H. americanum after ingesting an infected R. sanguineus transmission from an infected dog to the tick has not been documented.

  The tick becomes infected by ingesting a blood meal, containing monocytes or neutrophils laden with isogamonts from an infected vertebrate host.  Syngamy occurs in the gut of the tick, producing a zygote which penetrates the tick gut wall.  Sporogony occurs in the haemocoel where an oocyst is formed containing multiple sporozoites.  The intermediate vertebrate host must ingest the tick to become infected since the sporozoites apparently do not migrate to salivary tissue in the tick.  Sporozoites penetrate the intestinal wall of the intermediate host and undergo schizogony, forming schizonts, and then cysts within mononuclear phagocyte or endothelial cells of the spleen, bone marrow, lungs, liver, lymph node, or muscle.  When the schizonts rupture, an inflammatory reaction is initiated.  In completion of the life cycle, gamonts are produced that infect circulating leukocytes.  A paratenic prey host in which only cysts are formed has not been documented with H. americanum, and the feeding of encysted meat to carnivorous hosts has not produced infection; however, such paratenic hosts have been identified with otherHepatozoon species.

  Immunosuppression seems to be an important determinant of susceptibility for infection with Hepatozoon species.  Concurrent infection, debilitating disease, immunosuppressant drugs, and young age seem to influence clinical manifestation.  It is unclear if clinical hepatozoonosis occurs only in the immunosuppressed, or if infection elicits immunosuppression in the host, predisposing to concurrent infection.

  American hepatozoonosis typically presents as severe clinical disease.  A majority of the clinical syndrome is composed of clinical signs related to chronic inflammatory disease.  Many patients present with recurrent fever, lethargy, depression, and weight loss.  Muscular disease is also apparent on presentation.  Schizogony of the hepatozoon causes a marked pyogranulomatous polymyositis which results in stiffness, lameness, hyperesthesia, and muscle atrophy.  Clinical signs fail to resolve with antibiotics.  Bloody diarrhea, related to intestinal penetration by the sporozoites, may be documented soon after exposure.  A generalized lymphadenomegaly may also be present.

  Clinical pathological changes are often typified by a marked, mature neutrophilic leukocytosis.  A mild nonregenerative normocytic, normochromic anemia is often observed.  An eosinophilia or thrombocytosis may be evident.  Hypoglycemia, low urea nitrogen, hypoalbuminemia, and hyperglobulinemia are other common findings.

  Electromyography may indicate a generalized polymyopathy.  Radiography of the appendicular skeleton may reveal disseminated periosteal bone proliferation mostly involving the diaphysis of long bones.  Histopathological examination of the osseous lesions displays changes that closely resemble those of hypertrophic osteopathy.  New spicules of bone forming in the periosteum are oriented perpendicular to the cortex without producing cortical destruction.  The pathogenesis of such changes is not well understood.  Changes do not seem to be associated with the presence of parasites or inflammation in the adjacent skeletal muscle.

  Immune-complex hypersensitivity resulting in fatal vasculitis or glomerulonephritis is a potential sequela of infection.  A protein-losing nephropathy may be diagnosed in dogs with glomerulonephritis.

  Definitive diagnosis is made by microscopic observation of the organism.  Gamonts may be detected in neutrophils and monocytes on peripheral blood smears, although this finding is more typical of Hepatozoon canis infection.  Successful diagnosis is usually achieved via muscle biopsy where developing organisms are usually abundant.  Histopathological changes often consist of pyogranulomatous myositis, muscular necrosis, and muscular atrophy.  Hepatozoon cysts, or zoites contained within acute granulomas, may be identified interspersed between the muscle fibers.  Lesions similar to those found in skeletal muscle may also be found in cardiac muscle and smooth muscle of the intestine.  Lymph node aspirates often yield reactive lymphoid hyperplasia, but organisms are very rarely found.  Bone marrow aspirates may indicate granulocytic hyperplasia and erythroid hypoplasia, and also rarely yield organisms.  Pyogranulomas and H. amer-icanum cysts may also be found in pancreas, lymph nodes, kidney, spleen, and lung.

  Since Hepatozoon americanum causes a relatively low level of parasitemia in comparison to H. canis, antibody production rate may be lower than expected and therefore cause higher numbers of false negatives when tested serologically.  Studies have not been performed to identify the prevalence of uninfected or subclinically infected seropositive dogs.  Future studies are needed to evaluate the clinical efficacy of serological diagnosis.

-by Michelle Dennis, Class of 2002
-edited by Dr. Mika Tanabe, ADDL Instructor


Craig TM, Green CE: 1998.  Hepatozoonosis.  Infectious Diseases of the Dog and Cat, 2nd ed.: 458-465.

Kocan  AA, Cummings CA, Panciera RJ, Mathrew JS, Ewing, SA, Barker RW: 2000.  Naturally occurring and experimentally transmitted Hepatozoon americanum in coyotes from Oklahoma.  Journal of Wildlife Diseases 36(1): 149-153.

Macintire CK, Vincent-Johnson N, Dillon AR,  Blagburn B, Lindsay D, Whitley EM, Banfield C: 1997.  Hepatozoonosis in dogs: 22 cases (1989-1994).  JAVMA 210(7): 916-22.

Matthew JS, Ewing SA, Panciera RJ, Woods JP: 1998.  Experimental transmission of Hepatozoon americanum Vincent-Johnson et al, 1997 to dogs by the Gulf Coast tick,Amblyomma maculatum Koch. Veterinary Parasitology 80 (1) 1-14.

Panciera RJ, Mathew JS, Ewing SA, Cummings CA, Drost WT, Kocan AA: 2000.  Skeletal lesions of canine hepatozoonosis caused by Hepatozoon americanum. Veterinary Pathology 37(3):225-230.

Panciera RJ, Ewing SA, Mathew JS, Lehenbauer TW, Cummings CA, Woods JP: 1999. Canine hepatozoonosis: comparison of lesions and parasites in skeletal muscle of dogs experimentally or naturally infected with Hepatozoon americanum. Veterinary Parasitology 82(4): 261-272.

Vincent-Johnson NA, Macintire DK, Lindsay DS, Lenz SD, Baneth G, Shkap V, Blagburn BL: 1997.  A new Hepatozoon species from dogs: description of the causative agent of canine hepatozoonosis in North America.  Journal of Parasitology 83(6): 1165-1172.


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