Leishmaniasis (overview) B55.-

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 03.10.2022

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Leishmaniasis; Leishmaniosis; Oriental sore

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Granulomatous infectious disease caused by protozoa of the genus Leishmania.

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Commonly isolated pathogens of leishmaniasis (see under Leishmania):

Vectors: Leishmania is transmitted by sandflies, in the Old World by Phlebotomus spp. and in the New World by Lutzomyia species. Sandflies live in dark and damp places and can travel only 20-50 m from their breeding site in the biotope. New World sandflies do not fly very high and therefore usually bite their victim near the ground (e.g., lower leg). Because of their biological adaptability, they are common in tropics, subtropics, deserts, rainforests, and plateaus.

When uninfected sandflies bite an infectious host, the amastigotes are ingested during bloodsucking and transformed into promastigotes in the mosquito. Depending on the Leishmania species and host factor, local or disseminated distribution of the parasites may occur. Spontaneous healing is achieved by imprinting parasite-specific T cells, which migrate into the skin and activate macrophages by means of interferon gamma and other cytokines.

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Depending on the clinic and pathogen, a distinction is made between:

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About 10% of the world's population live in endemic areas and are at increased risk of disease.

Incidence: Approximately 1.6 million new cases/year worldwide; of these, 1.2 million are of the cutaneous forms. Leishmaniasis is the third most common vector-borne infectious disease after malaria and dengue fever.

Prevalence: worldwide (excluding Australia and Southeast Asia), approximately 12 million people are affected.

Increasingly, leishmaniasis occurs in tourists and HIV patients.

About 90% of the new cases occur in the Old World (Afghanistan, Algeria, Saudi Arabia, Iran, Iraq, Ethiopia, Middle East, Spanish Mediterranean islands). Pathogens here are predominantly: L. major, L. tropica, L. aethiopica, L. infantum.

About 10% of the new cases occur in the New World (Brazil, Mexico, Bolivia, Peru). The pathogens here are predominantly: L. mexicana, L. brasiliensis.

The co-infection of humans with HI virus and Leishmania parasites is seen as problematic. Protracted parasitemia occurring in HIV-infected individuals increases the likelihood of humans serving as reservoir hosts.

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Leishmania is transmitted by the bite of vectors (sand flies of the genera Phlebotoma, Lutzomyia, Psychodopygus). Visceral infections rarely occur through the use of infected needles in drug addiction, infected blood supplies or congenital.

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Occurrence is possible at any age.

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Mainly uncovered parts of the body (face, arms, lower legs) are attacked.

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Clinical findings (different clinic)

Detection of pathogens in smear, smear preparation (only for experienced examiners) or biopsy of a fresh lesion (biopsy from untreated lesion with pathogen detection is the option of 1st choice as primary examination).

Clearance preparation: In Giemsa and HE staining, amastigotes appear as light blue, oval-shaped corpuscles with a dark nucleolus and a small, punctate kinetoplast within the cytoplasm of the macrophages.

Antigen detection by PCR: highly sensitive method that can be performed on native material as well as from formalin-fixed material.

Culture: identification of the pathogen species (important for therapy and prognosis) from native preparations, e.g. non-fixed biopsies, in laboratories specialized for this purpose (e.g. Bernhard Nocht Institute for Tropical Medicine in Hamburg -www.bni-hamburg.de).

Serological detection methods: Leishmania-specific immunoglobulins can be detected (direct agglutination test (DAT), immunofluorescence antibody tests (IFAT), enzyme-linked immunosorbent assays (ELISA). They are of little use in uncomplicated Leishmaniasis infection (usually negative). In complicated cases, serological detection of antibodies may be diagnostically helpful.

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A wait-and-see attitude may be justified for solitary lesions of old world forms; the lesions usually heal spontaneously and lead to a permanent immunity (against the pathogen, not also against other Leishmania spp.)

Multiple lesions and lesions in cosmetically significant areas should be treated as early as possible.

Systemic therapy is usually more effective than topical therapy, but is also associated with significant side effects.

If an infection with L. brasiliensis is present, a systemic therapy is always indicated as this can prevent a transition to a mucocutaneous form.

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The prognosis depends crucially on the species of the pathogen and the immune status of the infected person. After healing has taken place, pathogen-specific immunity exists.

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The best prevention against theinfection is to avoid the sandfly bites.

People traveling to areas where the infection is common, or people living in such areas, can take the following measures:

  • Applying insect repellents containing DEET (diethyltoluamide) to exposed skin.
  • Using fly screens, mosquito nets and clothing impregnated with insecticides such as permethrin
  • Wearing long-sleeved shirts, long pants and socks
  • Avoiding outdoor activities between sunset and sunrise, when sandflies are most active

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Geographical distribution of leishmania and leishmaniasis (modified after Lainson)




Old World

L. tropica major

Africa, Asia

cutaneous leishmaniasis

L. tropica minor


L. donovani


Kala-azar (visceral leishmaniasis)

L. donovani infantum

Central, East, North Africa, Europe

Infantile Kala-Azar (visceral leishmaniasis)

L. archibaldi

Sudan, Kenya

Kala-azar and mucocutaneous leishmaniasis

New World

L. brasiliensis


Cutaneous and mucocutaneous leishmaniasis (Espundia)

L. mexicana - mexicana

Yucatan, Guatemala

Cutaneous leishmaniasis, more rarely diffuse cutaneous leishmaniasis

L. mexicana - pifanoi


Diffuse cutaneous leishmaniasis

cutaneous leishmaniasis

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Leishmaniasis is classified by the WGO as a neglected tropical disease (NTD). These are poverty-associated infectious diseases that occur mainly in the tropics (subtropics), are associated with high morbidity and mortality, and for which there are as yet no safe and long-lasting therapies.

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  1. Davies CR et al (2003) Leishmaniasis: new approaches to disease control. BMJ 326: 377-382
  2. del Giudice P et al (2002) Impact of highly active antiretroviral therapy on the incidence of visceral leishmaniasis in a French cohort of patients infected with human immunodeficiency virus. J Infect Dis 186: 1366-1370
  3. Dereure J et al (2003) Visceral leishmaniasis. Persistence of parasites in lymph nodes after clinical cure. J Infect 47: 77-81
  4. Donovan C (1903) The etiology of one of the heterogeneous fevers of India. BMJ 2: 1401
  5. Fernandez-Flores A et al (2015) Morphological and immunohistochemical clues for the diagnosis of cutaneous leishmaniasis and the interpretation of CD1a status. J Am Acad Dermatol doi: 10.1016/j.jaad.2015.09.038
  6. Handler MZ et al (2015) Cutaneous and mucocutaneous leishmaniasis: differential diagnosis, diagnosis, histopathology, and management.J Am Acad Dermatol. 2015 Dec;73(6):911-26; 927-8.
  7. Harms G et al (2003) Leishmaniasis in Germany. Emerg Infect Dis 9: 872-875.
  8. Leishman WB (1903) On the possibility of the ocurrence of trypanosomiasis in India. BMJ 2: 1376-1377
  9. Luz JGG et al. (2019) Where, when, and how the diagnosis of human visceral leishmaniasis is defined: answers from the Brazilian control program. Mem Inst Oswaldo Cruz 114:e190253.
  10. Parajuli N et al (2020) Case report: erysipeloid cutaneous leishmaniasis treated with oral miltefosine. Am J Trop Med Hyg 104:643-645.

  11. Zijlstra EE et al (2003) Post-kala-azar dermal leishmaniasis. Lancet Infect Dis 3: 87-98


Please ask your physician for a reliable diagnosis. This website is only meant as a reference.


Last updated on: 03.10.2022