Canine Leishmaniasis

  • Current Advice on Parasite Control:

    Vector-Borne Diseases - Canine Leishmaniasis

    Last reviewed and edited Oct 2011

  • Species

    Leishmania infantum/chagasi

  • Overview of Life Cycle

    • Leishmania spp. are protozoan parasites (order Kinetoplastida) whose life cycles involve two hosts—a vertebrate (including rodents, canids, or humans) and an insect (sand fly). Canine visceral leishmaniasis is the result of infection with L. infantum in the Old World and L. chagasi in the New World; the two are considered sibling species.
    • In regions where these infections are endemic, phlebotomine sand flies (genus Lutzomyia in the New World and Phlebotomus in the Old World) are the vectors for transmission.
    • Although phlebotomid insect species (possibly competent as vectors of L. infantum/chagasi) occur in eastern North America, there is no evidence of ongoing vector-borne transmission of this infection.
    • Dogs are considered the primary reservoir hosts of L. infantum/chagasi.
    • Infection of dogs with L. infantum/chagasi involves cells of the lymphatic series resulting in visceralization of infection.
    • The infection is endemic among foxhounds in North America among which it is transmitted by direct, dog-to-dog mechanisms (e.g., blood and secretions).
  • Stages

    • In mammalian hosts, Leishmania spp. occur as amastigotes (2 to 3 μm in diameter) solely within mononuclear phagocytes in the skin, bone marrow, and visceral organs.
    • Leishmania spp. occur as flagellated, extracellular promastigotes in the gut of sand fly vectors.
  • Disease

    • Following acquisition of infection, dogs can remain asymptomatic for variable periods or never develop clinical manifestations.
    • Clinical manifestations can include chronic wasting, conjunctivitis, ocular signs (anterior uveitis, retinitis), facial alopecia, severe muscle atrophy, lymphadenopathy, polyarthritis, and protein-losing nephropathy, which may lead to renal failure.
    • Infection may result in severe systemic disease with hair loss, skin lesions, epistaxis, anemia, wasting, swollen limbs and joints, lameness, renal failure, lymphadenopathy, ocular lesions, and diarrhea.
    • Anemia, thrombocytopenia, lymphocytosis, hypoalbuminemia, hyperglobulinemia, hyperamylasemia, and azotemia are the most frequently detected laboratory abnormalities.
  • Prevalence and Geographic Distribution in Dogs

    • Leishmania infantum/chagasi is endemic in much of the Mediterranean basin (e.g., Italy, Spain and Portugal), the Balkans, central and southwest Asia, north and northwest China, north and sub-Saharan Africa, and parts of Central and South America.
    • Visceral leishmaniasis is occasionally diagnosed in the United States in dogs of any breed imported from southern Europe or South America where the infection is endemic.
    • Since the 1980s, locally acquired infection has been reported in kenneled foxhounds, and infection is now recognized in foxhounds from many eastern U.S. states and Canadian provinces.
    • Isolates obtained from foxhounds in North America indicate that the agent is L. infantum MON-1, which is the predominant zymodeme found in infected dogs and humans in southern Europe.
  • Host Associations and Transmission Between Hosts

    • In endemic regions, phlebotomine sand flies (genus Lutzomyia in the New World and Phlebotomus in the Old World) are the primary insect vectors for transmission; the protozoal life cycle begins with injection of the infective form, the promastigote, into the skin of the vertebrate host by the sand fly.
    • Once in the host, the promastigote is transformed into a nonflagellated form, the amastigote. Amastigote multiplication in macrophages occurs by binary fission either locally or systemically throughout the reticuloendothelial system.
    • Dogs are considered the primary reservoir host of L. infantum in endemic countries.
    • Leishmania infantum can also be transmitted directly from dog to dog by direct contamination with blood and secretions as well as transplacentally from an infected bitch to her pups.
    • Current evidence suggests that transmission in North America is limited to direct dog-to-dog mechanisms.
    • Owners of pet dogs have reported behavioral changes, including an increased tendency to be aggressive, as the first manifestation of leishmaniasis.
  • Prepatent Period and Environmental Factors

    • Infected dogs may remain asymptomatic for variable periods or never develop clinical manifestations.
  • Diagnosis

    • Diagnosis of visceral leishmaniasis in dogs is based on positive specific antibody assay with confirmation by demonstration of the parasites (amastigote forms) on touch prep stained (Wright-Giemsa) slides or in cultures of tissue aspirates or biopsy specimens of the spleen, liver, bone marrow, or lymph nodes.
    • Diagnostic antibody tests include the indirect fluorescent antibody assay (IFA), direct agglutination assay, and enzyme immunoassay (EIA). These tests vary in sensitivity and specificity, and although they verify presence of antibody, they do not prove or rule out active infection. Most of these assays give false-positive reactions with sera of dogs infected by Trypanosoma cruzi, another protozoan that sometimes infects dogs in North America.
    • The rK39 dipstick immunoassay (Kalazar Detect Rapid Test, InBios International Ltd., Seattle, WA) does not cross-react with T. cruzi or Babesia.
    • Polymerase chain reaction (PCR) assays (investigational) are available at some academic veterinary centers (e.g., North Carolina State University).
  • Treatment

    • Leishmaniasis in dogs is more resistant to treatment than this infection is in humans. Anti-leishmanial drugs used in dogs include pentavalent antimonials and allopurinol; to date, no drug has proven to be consistently curative for visceral leishmaniasis in dogs.
    • Antimonial compounds can suppress and sometimes cure the infection; such compounds include meglumine antimonate (Glucantime) in Europe and sodium stibogluconate (Pentostam) in the United States. Although clinical improvement may occur in response to chemotherapy, relapses are common, and chemotherapeutic elimination of L. infantum/chagasi has not been consistently achieved with any drug tested to date.
    • Maintenance therapy with allopurinol (10 mg/kg) decreases parasitemia, maintains infected dogs in an asymptomatic state, and decreases the likelihood of direct or vector transmission.
  • Control and Prevention

    • In leishmaniasis-endemic areas where vector transmission is the primary mode of transmission, vector control and elimination of stray dogs limit transmission; use of insecticide-treated dog collars helps protect dogs from contact with potential vectors.
    • In regions where the infection is not endemic, euthanasia of infected dogs has been promoted to prevent leishmaniasis from becoming endemic.
    • Some foxhound kennels in North America have adopted a test and elimination approach in an effort to remove infected dogs from the environment.
  • Public Health Considerations

    • In areas where L. infantum/chagasi is endemic and transmitted by insect vectors, it is an important agent of human disease and dogs are considered the primary reservoir host.
    • If sand flies in North America are able to transmit visceral leishmaniasis from infected to susceptible dogs, then vector transmission from infected dogs to humans is possible.
    • To date, no autochthonous human cases of visceral leishmaniasis have been reported from the United States, and there are no data to suggest vector transmission is occurring among dogs in North America.