ISSN 2398-2942      

Hepatozoon canis





  • Phylum: Apicomplexa.
  • Class: Sporozoea.
  • Subclass: Coccidia.
  • Order: Euccidiidae.
  • Family: Haemogregarinidae.
  • Genus & species: Hepatozooncanis.


  • Originally reported by James (1905) in India.

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Clinical Effects



  • The dog is the principal mammalian reservoir for H canis infection. Wild canids including foxes and jackals may act as natural reservoirs for domestic dog infection.
  • Ticks are the final hosts of canine hepatozoonosis.
    o The brown dog tick, Rhipicephalus sanguineus Rhipicephalus sanguineus is the main vector for H canis.
    o The Gulf Coast tick, Amblyomma maculatum Amblyomma maculatum serves as host to the other species of Hepatozoon infecting dogs, H americanum Hepatozoon americanum.
    o It is likely that other tick species also transmit H canisHepatozoon oocysts have been found in Haemaphysalis spp. in Japan that fed on naturally infected dogs.
  • The distribution of H canis and H americanum appear to be associated closely with the distribution of their tick hosts.
  • The global distribution of R sanguineus is wide and it is present in tropical, sub-tropical and temperate habitats worldwide. Therefore H canis infection can be found in a variety of geographical locations and continents.
  • A maculatum, the host of H americanum, appears to restricted to the southeastern USA and central America. The geographical distribution of this tick species is expanding.


  • Unlike most other tick-borne parasites of dogs which are transmitted in the tick's saliva through tick bites, Hepatozoon species are transmitted by oral ingestion of the tick by a dog.
  • Infected ticks containing mature Hepatozoon oocysts or parts of the tick are ingested while grooming or eating prey infested with ticks.
  • The oocyst membrane tears easily and releases sporocysts containing the infective sporozoites.


  • Sporozoites are released in the dog's intestinal tract and penetrate the gut wall.
  • They are carried via blood or lymph and reach target tissues such as liver, spleen and bone marrow, where the formation of meronts (merogony) takes place.


  • When meronts mature, they release slender elongated merozoites, which may penetrate more host tissue cells to form secondary meronts or parasitize leukocytes (mainly neutrophils and monocytes).
  • Merozoites develop in peripheral blood leukocytes into gamonts (gamontogony) Hepatozoon canis - blood smear.


  • Gamonts circulating in blood leukocytes are ingested by a tick.
  • Inside the tick's gut, gamonts are released, associate in syzygy and transform into male and female gametes Hepatozoon canis - gamonts in a tick.
  • Fertilization is followed by the formation of a zygote.


  • The zygote divides to form early oocysts.
  • The maturing oocysts are found in the tick's hemocoel.
  • Inside the large oocysts, sporocysts are formed.
  • 12-24 infective sporozoites develop in the sporocysts.
  • Ingestion of tick oocysts causes the infection in the dog.


  • Essentially by ingestion of infected ticks.
  • Trans-stadial transmission from the nymph to the adults stages of R sanguineus ticks has been demonstrated experimentally.
  • Transovarial transmission is unknown.
  • Vertical transmission (trans-placental) from infected dams to their offspring has been demonstrated.
  • Transmission by predation (ingestion of infected animal tissues) is suspected.

Pathological effects

  • H canis infection is often asymptomatic in:
    • The presence of hereditary or acquired immunodeficient states (corticosteroid administration, concurrent disease).
    • Young dogs.
    • Heavy tick infestation.
  • Concurrent diseases - especially other parasitic diseases eg canine ehrlichiosis Ehrlichiosis and leishmaniasis Canine leishmaniosis are frequently diagnosed. It is likely that Hepatozoon spp infection also induces a primary immunodeficient state.
  • Immune-mediated mechanisms are involved in pathogenesis of the disease in some cases when immune mediated anemia or glomerulonephritis are present.
  • Clinical signs range from mild, usually in dogs with a low parasitemia (1-5% of leukocytes parasitized), to severe in dogs with a high leukocytosis and parasitemia (up to more than 90% of leukocytes).
  • Main clinical signs are lethargy, weight loss Weight loss: overview and hyperthermia Hyperthermia Hepatozoon canis - infected dog.
  • Laboratory findings include a moderate to extreme leukocytosis with neutrophilia and a moderate to severe anemia Anemia: overview. Anemia is non-regenerative in most cases.

Other Host Effects

  • Dogs with H canis infection may be asymptomatic, have a mild disease or suffer from a severe infection with anemia Anemia: overview , lethargy and cachexia.


Control via chemotherapies

  • Imidocarb dipropionate Imidocarb: 5-6 mg/kg SC, IM, every 2 weeks, until gamonts are no longer found in blood smears.
  • Doxycycline Doxycycline : 10 mg/kg/day per os for 3 weeks may be combined with imidocarb dipropionate.
  • The anti-coccidial drug, toltrazuril: 5-10 mg/kg per os, 5 to 10 days, is effective in the improvement of clinical signs and in clearing gamonts from blood. Toltazuril is not approved in some countries.
    The clearing of gamonts is slow. Disappearance of gamonts from the blood may take several weeks following the initiation of imidocarb diproprionate or toltazuril therapy.

Control via environment

  • Based on good tick control using acaricidals both for the environment and dogs.
  • The ingestion of ticks or prey that may be infested with infected ticks must be prevented.

Public Health Significance

  • No record of infection with H canis.
  • A single case of infection of a human with an Hepatozoon spp has been reported from the Philippines.


  • No vaccination is currently available for canine hepatozoonosis.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Attipa C, Maguire D, Solano-Gallego L et al (2018) Hepatazoon canis in three imported dogs: a new tickborne disease reaching the United Kingdom. Vet Rec 183 (23), 716 PubMed.
  • Macintire D K, Vincent-Johnson N A, Kane C W et al (2001) Treatment of dogs infected with Hepatozoon americanum: 53 cases (1989-1998). J Am Vet Med Assoc 218 (1), 77-82 PubMed.
  • Baneth G, Barta J R, Shkap V et al (2000) Genetic and antigenic evidence supports the separation of Hepatozoon canis and Hepatozoon americanum at the species level. J Clin Microbiol 38 (3), 1298-1301 PubMed.
  • Baneth G & Weigler B (1997) Retrospective case-control study of hepatozoonosis in dogs in Israel. J Vet Intern Med 11 (6), 365-370 PubMed.
  • Vincent-Johnson N, Macintire D K & Baneth G (1997) Canine hepatozoonosis: pathophysiology, diagnosis, and treatment. Comp Contin Educ Pract Vet 19 (1), 51-65 VetMedResource.
  • Vincent-Johnson N A, Macintire D K, Lindsay D S et al (1997) A new Hepatozoon species from dogs : description of the causative agent of canine hepatozoonosis in North America. J Parasitol 83 (6), 1165-1172 PubMed.
  • Beaufils J P, Martin-Granel J & Jumelle P (1996) Hepatozoonosis in dogs and foxes: epidemiology, clinical findings and treatment. Prat Méd Chir Anim Comp 31 (3), 243-253 VetMedResource.

Other sources of information

  • Baneth G (2002) Hepatozoonosis. In: Proc 45th annual congress BSAVA. Birmingham UK. pp 187-190.
  • Macintire D K (1999) Canine hepatozoonosis. Proc 17th ACVIM. Chicago, IL, USA. pp 623-624.

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