Leishmaniasis refers to a group of infections caused by the flagellate protozoa of the genus Leishmania. About half a million new cases are reported each year, and it is estimated that 12 million people are currently infected with this parasite. There are three clinical types of leishmaniasis: cutaneous, mucocutaneous, and visceral. The various infective organisms are indistinguishable morphologically but can be differentiated biochemically. Two subgenera are recognized (Leishmania leishmania and Leishmania viannia), each with several species. Any species has the potential to cause one of three clinical manifestations. The natural reservoir of the parasite varies with geography and species but is usually wild rodents, dogs, and humans. Transmission to humans is by the bite of the female sandfly of the genus Phlebotomus or Lutzomyia. The life cycle of Leishmania is shown in Figure 1.

fig1. Life cycle of Leishmania.

1. Cutaneous leishmaniasis (local name, “oriental sore”):

This disease is caused by Leishmania tropica in North and West Africa, Iran, and Iraq. The cutaneous form of the disease is characterized by ulcerating single or multiple skin sores (Figure 2). Most cases spontaneously heal, but the ulcers leave unsightly scars. In Mexico and Guatemala, the cutaneous form is due to Leishmania mexicana , which produces single lesions that rapidly heal.

fig2. Skin ulcer due to leishmaniasis, on the hand of a Central American adult.

 2. Mucocutaneous leishmaniasis (local name, espundia):

This disease is caused by Leishmania viannia brasiliensis in Central and South America, especially the Amazon regions. In this form of the disease, the parasite attacks tissue at the mucosal-dermal junctions of the nose and mouth, producing multiple lesions. Extensive spreading into mucosal tissue can obliterate the nasal septum and the buccal cavity, ending in death from secondary infection.

 3. Visceral leishmaniasis (local name, kala-azar):

This disease is caused by Leishmania donovani in India, East Africa, and China. In the visceral disease, the parasite initially infects macrophages, which, in turn, migrate to the spleen, liver, and bone marrow, where the parasite rapidly multiplies. Symptoms include intermittent fevers and weight loss. The spleen and liver enlarge, and jaundice may develop. Mortality is nearly 100% within 2 years if the disease is untreated. In some cases, complications resulting from secondary infection and emaciation result in death.

 4. Diagnosis and treatment :

Diagnosis is made by examination of Giemsa-stained tissue and fluid samples for the nonflagellated form (amastigote), which is the only form of the organism that occurs in humans and other mammals. Cutaneous and mucocutaneous disease can be diagnosed from tissue samples taken from the edges of lesions or lymph node aspirates. Visceral disease is more difficult to diagnose, requiring liver, spleen, or bone marrow biopsy. Serologic tests (for example, indirect fluorescent antibody, and complement fixation) are used by the Centers for Disease Control and Prevention. The treatment of leishmaniasis is difficult because the available drugs have considerable toxicity and high failure rates. Pentavalent antimonials, such as sodium stibogluconate, are the conventional therapy, with pentamidine and amphotericin B as second-line agents.