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 .
• 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 .
• 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 infantum. L. 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  in the vertebrate host and in the promastigote form  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  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  laden macrophages → promastigotes form  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

Treatment

Prevention

Outcomes