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(Established in March 1996)

吳昭新 醫師 編著 (by Jau-Shin WU, M.D., Ph.D.)
(Posted Sep. 16, 1996; Updated May 14, 2009)



Leishmaniasis is a parasitic disease spread by the bite of infected sand flies, causing visceral, cutaneous, or mucocutaneous disease. Leishmaniasis is found in parts of about 88 countries. Approximately 350 million people live in these areas. Most of the affected countries are in the tropics and subtropics. The settings in which leishmaniasis is found range from rain forests in Central and South America to deserts in West Asia. More than 90 percent of the world's cases of visceral leishmaniasis are in India, Bangladesh, Nepal, Sudan, and Brazil.


Leishmaniasis is an infection with related species of genus Leishmania (protozoa). Leishmania is transmitted by tiny sandflies (Phlebotomus and Lutzomyia sp) and survives in the vertebrate host as intracellular amastigotes. Vector flies are infected by biting humans or animals; animal reservoirs include canines, rodents, sloths, and anteaters. Infection is spread rarely by blood transfusion, congenitally, or sexually.

Visceral Leishmaniasis (Kala-Azar; Dumdum Fever)

Visceral leishmaniasis is caused by parasites of the L. donovani complex (L. donomani, L. infantum, L. tropica, L.chagasi). The disease occurs in India, China, previous southern USSR, Africa, the Mediterranean basin, and several South and Central American countries. Children and young adults are particularly susceptible.

Symptoms and Signs

Patiens who suffer from visceral leishmaniasis usually have fever, weight loss, splenomegaly, hepatomegaly (usually the spleen is bigger than the liver), pancytopenia, and polyclonal hypergammaglobulinemia. In 5 to 10% of patients, twice-daily temperature spikes occur. Some patients have swollen glands. The manifestations of visceral leishmaniasis typically develop months, but sometimes years, after a person becomes infected. If untreated, symptomatic visceral leishmaniasis typically is fatal.

The primary lesion at the site of an infected sandfly bite is small and usually inapparent. Parasites disseminate from the skin via the bloodstream to the lymph nodes, spleen, liver, and bone marrow. Clinical signs develop gradually after 2 wk to 1 yr (generally 2 ~ 6 months). Emaciation and death occur within 1 to 2 yr in 80 to 90% of untreated symptomatic patients.

A subclinical variant with vague minor symptoms resolves spontaneously in 2/3 and progresses to full-blown visceral leishmaniasis in 1/3 of cases. Survivors are resistant to further attacks unless they develop depression of cell-mediated immunity (eg, AIDS). One to 2 yr after apparent cure, some patients develop nodular cutaneous lesions full of parasites, which can last for years.


A definite diagnosis is made by demonstrating parasites in Giemsa-stained smears or by culturing blood or aspirates from the spleen, liver, bone marrow, or lymph nodes. Use of PCR-based amplification and DNA probes increases sensitivity.

Specific serologic tests are now available. A recombinant antigen predicts which subclinical patients will develop full-blown visceral leishmaniasis if not treated. The leishmanin (Montenegro) skin test, which is negative during active infection, becomes positive a few weeks to 2 yr after cure and remains positive for life.

Prevention and Treatment

Mass treatment of cases, reduction of the vector population, and elimination of nonhuman reservoirs where appropriate and possible may be helpful. Insect repellents may provide individual protection, but the tiny flies may penetrate insect screens or bed nets in less than perfect condition.

The drugs of choice are pentamidine isethionate (2 to 4 mg/kg IM daily or every other day for up to 15 doses), amphotericin B (0.25 to 1 mg/kg by slow infusion every day or every other day for up to 8 wk), or pentavalent antimony compounds. Sodium stibogluconate (sodium antimony gluconate) is slowly injected IV or IM at the daily dose of 20 mg/kg for 20 to 28 days. If toxic effects (nausea, vomiting) appear, the drug should be given on alternate days, the dose reduced, or administration stopped. In general, the Indian and South American types of visceral leishmaniasis respond well to treatment; the African and Mediterranean-Asian types require high doses of drugs. Interferon- infusion or splenectomy may be required in resistant cases.

Supportive measures may be needed, such as bed rest, good oral hygiene, and adequate nutrition. Transfusions and antibiotics may be indicated.

Cutaneous Leishmaniasis

Cutaneous leishmaniasis is known under a variety of local names: the oriental or tropical sore, the Delhi or aleppo boil, the uta or chiclero ulcer, and forest yaws. The causative agents are L. major and L. tropica in southern Europe, Asia and Africa; the L. mexicana complex in Mexico and Central and South America; and the L. braziliensis complex in Central and South America. Outbreaks of cutaneous leishmaniasis have occurred among U.S. military personnel operating in the Middle East; isolated cases have been reported in casual travelers to endemic areas.

Symptoms and Signs

Patients who suffer from cutaneous leishmaniasis have one or more sores on their skin. A sharply demarcated skin lesion develops at the site of an infected sandfly bite after 1 to 4 wk. Multiple lesions may occur after multiple infective bites, accidental autoinoculation, or metastatic spread. The initial lesion is a papule that enlarges, ulcerates centrally, and often develops a raised, hyperpigmented border where the intracellular parasites are concentrated. The ulcers are painless and cause no systemic symptoms unless secondarily infected, a common event. The sores can change in size and appearance over time. They often end up looking somewhat like a volcano, with a raised edge and central crater. Some sores are covered by a scab. The sores can be painless or painful. Some people have swollen glands near the sores (for example, under the arm if the sores are on the arm or hand).

Cutaneous leishmaniasis is characterized by one or more skin sores (either painful or painless, with or without a scab) that develop weeks to months after a person is bitten by infected sand flies. If untreated, the sores can last from weeks to years and often eventually develop raised edges and a central crater.

The initial lesion is a papule that enlarges, ulcerates centrally, and often develops a raised, hyperpigmented border where the intracellular parasites are concentrated. The ulcers are painless and cause no systemic symptoms unless secondarily infected, a common event.

Skin ulcers generally heal spontaneously over several months and leave a depressed scar. The subsequent course depends on the strain of the infecting organism and the immune status of the infected host. In the Americas, skin lesions can be followed by metastatic mucocutaneous lesions if they are caused by some members of the L. braziliensis complex (see Mucocutaneous Leishmaniasis, below). Diffuse cutaneous leishmaniasis (DCL) is an uncommon form characterized by widespread nodular skin lesions resembling those of lepromatous leprosy. It is presumed to result from a specific defect of cell-mediated immunity to the leishmanial organism.


Diagnosis is made by demonstrating organism in Giemsa-stained smears or cultures of scrapings from the raised border of the lesion. Infected materials can be blotted onto filters or amplified by the PCR method and then tested for hybridization with specific DNA probes. Organisms causing simple cutaneous leishmaniasis can be differentiated from those causing mucocutaneous leishmaniasis with specific DNA probes or monoclonal antibodies, or by analysis of isoenzyme patterns of cultured parasites. The leishmanin skin test becomes positive early, but serologic tests usually remain negative until late in the infection.

Prevention and Treatment

Susceptible people may be inoculated in a covered part of the body with live amastigotes; this elicits immunity to the same parasite species and may prevent formation of a visible scar. Experimental vaccines are under evaluation.

Specific treatment is as for kala-azar. A new antifungal agent, itraconazole, may become the drug of choice. Experimental immunotherapy with dead promastigotes plus BCG is under evaluation. Applying heat or infiltrating the indurated edge and base of the ulcer with sodium antimony gluconate 3 to 4 times every other day may also be effective. DCL is very resistant to treatment.

Mucocutaneous Leishmaniasis (Espundia)

Mucocutaneous leishmaniasis is caused mainly by L. viannia braziliensis. A primary cutaneous ulcer appears after 2 to 3 months, lasts 6 to 15 months, and closely resembles lesions of simple cutaneous leishmaniasis. However, mucocutaneous leishmaniasis can metastasize to nasopharyngeal tissues, which usually occurs within 1 yr but occasionally years or even decades after the skin lesion has healed. Gross mutilations of the nose and palate may occur and require reconstructive surgery.

Diagnosis is as for simple cutaneous leishmaniasis, but parasites are difficult to isolate from mucosal lesions. The leishmanin skin test may be useful in late infections when parasites are scarce. Prevention consists mostly of using protective clothing and insect repellant. Treatment is as recommended above for other forms of leishmaniasis.

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(By Jau-Shin Wu, M.D.; Posted Sep. 16, 1996; Revised May 12, 2009)

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