ISSN 2398-2969      

Leishmaniosis

icanis
Contributor(s):

Gad Baneth

Susan E Shaw

Synonym(s): Leishmaniasis, CanL; Kala-azar (in its visceral form in humans


Introduction

  • Serious zoonotic protozoal infection of man and animals.
  • Cause: intracellular protozoan parasites of the genus Leishmania Leishmania infantum.
  • Transmission is predominantly by sand-fly bites Phlebotomine sandfly.
  • Signs: include alopecia, exfoliative dermatitis, nodular skin lesions, generalized lymphadenopathy, progressive weight loss, muscle atrophy, exercise intolerance, lethargy, decreased appetite, polyuria, polydipsia, ocular lesions.
  • Diagnosis: demonstration of the parasite in macrophages in lymph node or bone marrow aspirates Cytology: lymph node aspirate Bone marrow aspiration and serology or PCR Leishmania infantum: blood smear.
  • Prognosis: relapses usually occur.
    Print off the owner factsheet on Leishmaniosis Leishmaniosis to give to your client.

Pathogenesis

Etiology

  • The main species infecting dogs is Leishmania infantum Leishmania infantumL. chagasi is a synonym for the same organism occurring in Central America. L. infantum has been found in dogs infected in the US.
  • Other species causing clinical disease in dogs are:
    • L. tropica causes cutaneous/mucocutaneous leishmaniosis (with cutaneous nodules and ulcers) in dogs in the Mediterranean area, Middle East and central Asia.
    • L. braziliensis causes cutaneous form in dogs in South America.
  • Dogs can be infected with other species of Leishmania but clinical disease does not occur.

Predisposing factors

General

  • Exposure to sandfly challenge.
  • High prevalence of infected animals.
  • Virulence of parasite strain.
  • Immunocompromised host.
  • Infected blood transfusions, needle contamination.

Pathophysiology

  • The parasite occurs in the amastigote form Leishmania infantum: amastigotes in the vertebrate host and in the promastigote form Leishmania infantum: promastigote in the sandfly vector and on culture.
  • The promastigotes inoculated by the sandfly vector enter macrophages where they transform into amastigotes before multiplying.
  • Infection and multiplication in cells of the monocyte/macrophage line leads to generalized lymphadenopathy and splenomegaly.
  • Immune complex formation contributes to the pathological changes.
  • Visceral leishmaniosis is a chronic wasting disease in the dog.
  • While dogs can be infected in any area where leishmaniosis occurs, they appear to act as a reservoir host principally in the Mediterranean area, Central Asia, parts of China, Sudan and South America.
  • Sandflies of the genus Phlebotomus Phlebotomine sandfly are the principal vectors in Europe; Lutzomyia species are the principal vectors in South and Central America.
    Sandfly species have very specific bio-climatic requirements. They are not restricted to the coastal fringes but are prevalent in rural wooded areas. In South America, sandfly species have adapted to peri-urban environments.
  • Culicoides species have been suggested as possible vectors.
  • Female sandflies feeding on an infected dog ingest amastigote Leishmania infantum: amastigotes laden macrophages → promastigotes form Leishmania infantum: promastigote in the insect's gut and migrate to the proboscis.
  • Promastigotes (flagellated forms) are inoculated into the host, enter macrophages and transform into amastigotes.
  • They multiply in and disrupt the macrophages with the released parasite infecting other cells → lymphoreticular hyperplasia with generalized lymphadenopathy and splenomegaly.
  • Visceral leishmaniosis is associated with dissemination of the amastigotes throughout the reticuloendothelial system - particularly the spleen, bone marrow, lymph nodes, liver and small intestine.
  • The parasite has been detected in all organs and tissues.
  • Infection induces a cytokine response which results in over-exuberant antibody production. Excessive immune-complex formation results in the development of lesions in the kidneys, joints, eye and blood vessel walls. Auto-antibody production may result in Coombs positive hemolytic anemia Direct Coombs' test Anemia: immune mediated hemolytic and positive antinulclear antibody testing. A moderate to severe glomerulonephritis Glomerulonephritis with massive protein loss Protein-losing enteropathy is commonly present and renal failure is often the cause of death Kidney: chronic kidney disease (CKD). Immune complex desposition in joints produces a polyarthritis. Increased gammaglobulin levels may be associated with a monoclonal or biclonal spike Serum protein electrophoresis.
  • Local proliferation of the parasite in macrophages causes granulomatous lesions in many organ systems including the skin, joints and gastrointestinal system. Granulomatous dermatits in associated with scaling, alopecia Skin: alopecia - overview , ulceration and nodule formation.
  • Co-infection particularly with other arthropod borne infections such as Ehrlichia canis Ehrlichia canis may complicate the pathogenesis.
  • Direct transmission of amastigotes through blood transfusions/needle contamination.

Timecourse

  • Incubation period: 3 months-several years.
  • Clinical signs could appear in animals imported from endemic areas after leaving quarantine.

Epidemiology

  • The sandfly vectors are most active at dawn and dusk.
  • Sandflies have a limited flight range.
  • Transmission can occur by blood transfusion.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • McKenna M, Attipa C, Tasker S & Augusto M (2019) Leishmaniosis in a dog with no travel history outside of the UK. Vet Rec 184(14), 441 PubMed.
  • Wright I, Baker S (2019) Leishmaniosis in a dog with no history of travel outside the UK. Vet Rec 184(12), 387-388 PubMed.
  • Toepp A,  Larson M,  Wilson G et al (2018) Randomized, controlled, double-blinded field trial to assess Leishmania vaccine effectiveness as immunotherapy for canine leishmaniosis. 
    Vaccine 36 (43), 6433-6441 PubMed.
  • Fernández Cotrina J, Iniesta V, Monroy I et al (2018) A large-scale field randomized trial demonstrates safety and efficacy of the vaccine LetiFend® against canine leishmaniosis. Vaccine 36(15), 1972-1982 PubMed.
  • Solano-Gallego L et al (2009) Directions for the diagnosis, clinical staging, treatment and prevention of canine leishmaniosis. Vet Parasitol 165, 1-18 PubMed.
  • Pennisi M G, De Majo M, Masucci M, Britti D, Vitale F & Del Maso R (2005) Efficacy of the treatment of dogs with leishmaniosis with a combination of metronidazole and spiramycin. Vet Rec 156 (11), 346-349 PubMed.
  • Roze M (2005) Canine leishmaniosis. A spreading disease. Diagnosis and treatment. EJCAP 15 (1), 39-52 VetMedResource.
  • Franch J et al (2004) Management of leishmanial osteolytic lesions in a hypothyroid dog by partial tarsal arthrodesisVet Rec 155 (18), 559-562 PubMed.
  • Lamonthe J (2001) Activity of amphotericin B in lipid emulsion in the inital treatment of canine leishmaniasis. JSAP 42 (4), 170-175 PubMed.
  • Owens S D, Oakley D A, Marryott K et al (2001) Transmission of visceral leishmaniasis through blood transfusions from infected English Foxhounds to anemic dogs. JAVMA 219 (8), 1076-1083 PubMed.
  • Orndorff G R (2000) Canine visceral leishmaniasis in Sicily. Mil Med 165 (1), 29-32 PubMed.
  • Cavaliero T, Arnold P et al (1999) Clinical, serologic and parasitologic follow-up after long-term allopurinol therapy of dogs naturally infected with Leishmania infantum. JVIM 13 (4), 330-334 PubMed.
  • Denerolle P & Bourdoiseau G (1999) Combination allopurinol and antimony treatment vs antimony alone and allopurinol alone in the treatment of canine leishmaniasis (96 cases). JVIM 13 (5), 413-415 PubMed.
  • Bravo L, Franks L A & Brenneman K A (1993) Canine Leishmaniasis in the United States. Comp Cont Educ Pract Vet 15 (5), 699-708 VetMedResource.
  • Kontos V J (1993) Old World Canine Leishmaniasis. Comp Cont Educ Pract Vet 15 (7), 949-960 VetMedResource.

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