Synonym(s)
DefinitionThis section has been translated automatically.
Granulomatous infectious disease caused by protozoa of the genus Leishmania.
PathogenThis section has been translated automatically.
Frequently isolated pathogens of leishmaniasis (see Leishmania):
- Leishmania donovani (see below visceral leishmaniasis).
- Leishmania brasiliensis (see also South American leishmaniasis).
- Leishmania mexicana, L. braziliensis, L. amazonensis, L. peruvia, L. panamensis, Chiclero ulcer (solitary cutaneous leishmaniasis; see below South American leishmaniasis with the different clinical variants).
- Leishmania tropica (Oriental ulcer; see below cutaneous leishmaniasis).
- Leishmania major, L. infantum, L. aethiopicum (Oriental bubonic; see below solitary cutaneous leishmaniasis).
Vectors: Leishmania are transmitted by sand flies, in the Old World by Phlebotomus spp. and in the New World by Lutzomyia species. Sand flies live in dark and damp places and can only move 20-50 m away from their breeding site in the biotope. New World sandflies do not fly very high and therefore usually bite their victims close to the ground (e.g. lower legs). Due to their biological adaptability, they are widespread in tropics, subtropics, deserts, rainforests and plateaus.
If uninfected sand flies bite an infectious host, the amastigotes are ingested during bloodsucking and transformed into a flagellated promastigote in the mosquito. After division, this enters the proboscis of the insect. If the mosquito bites again, the pathogen enters the new organism. There, the promastigote pathogen is again taken up by phagocytizing cells, in which the transformation (metamorphosis) into the amastigote form takes place. After intracellular replication, the Leishmania are released with rupture of the host cells (Fischer T et al. 2024).
Depending on the Leishmania species and the host factor, local or disseminated distribution of the parasites may occur. The organism achieves spontaneous healing by imprinting parasite-specific T cells, which migrate into the skin and activate macrophages there by means of interferon gamma and other cytokines.
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ClassificationThis section has been translated automatically.
Depending on the clinic and pathogen, a distinction is made between:
- Old World Leishmaniasis
- Old World cutaneous leishmaniasis
- Solitary Old World cutaneous leishmaniasis (classic Oriental bump).
- Erysipelas-like cutaneous Old Worldleishmaniasis (rare variant)
- other rarer variants such as: paronychial, chankriform, annular, palmoplantar, zosteriform or even eczematoid cutaneous leishmaniasis.
Old World Recurrent Cutaneous Leishmaniasis (Leishmaniasis recidivans - lupoid leishmaniasis).
- Diffuse (anergic) cutaneous leishmaniasis of the Old World
- Old World mucocutaneous leishmaniasis
- Old World cutaneous leishmaniasis
- New World Leishmaniasis
- New World cutaneous leishmaniasis (South) American leishmaniasis
- Solitary cutaneous leishmaniasis of the New World (classical form, analogous to Oriental bump)
- Recurrent cutaneous New World leishmaniasis
- Diffuse (anergic) cutaneous New World leishmaniasis
- New World mucocutaneous leishmaniasis
- New World cutaneous leishmaniasis (South) American leishmaniasis
- Visceral le ishmaniasis
Occurrence/EpidemiologyThis section has been translated automatically.
Around 350 million people live in endemic areas and are at increased risk of contracting the disease.
About 90% of new cases occur in the Old World (Afghanistan, Algeria, Saudi Arabia, Iran, Iraq, Ethiopia, the Middle East, Spanish Mediterranean islands). The main pathogens here are: L. major, L. tropica, L. aethiopica, L. infantum.
About 10% of new cases occur in the New World (Brazil, Mexico, Bolivia, Peru). The pathogens here are predominantly: L. mexicana, L. brasiliensis.
Incidence: Approx. 1.6 million new cases/year worldwide; of these, 1.2 million are cutaneous forms. Leishmaniasis is the third most common vector-borne infectious disease after malaria and dengue fever.
Prevalence: worldwide (excluding Australia and South-East Asia) around 12 million people are currently infected.
Leishmaniasis is increasingly occurring in tourists and HIV patients. The co-infection of people with HIV and Leishmania parasites is seen as problematic. Protracted parasitemia occurring in HIV-infected persons increases the probability that humans will serve as reservoir hosts. A primarily zoonotic infection (original reservoir is mammals such as dogs or rodents) has now become anthropozoonosis.
EtiopathogenesisThis section has been translated automatically.
ManifestationThis section has been translated automatically.
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DiagnosisThis section has been translated automatically.
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.
TherapyThis section has been translated automatically.
See the individual clinical pictures below.
Progression/forecastThis section has been translated automatically.
ProphylaxisThis section has been translated automatically.
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
TablesThis section has been translated automatically.
Geographical distribution of leishmania and leishmaniasis (modified after Lainson)
Species |
Region |
Clinic |
|
Old World |
L. tropica major |
Africa, Asia |
cutaneous leishmaniasis |
L. tropica minor |
Europe |
||
L. donovani |
India |
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 |
Brazil |
Cutaneous and mucocutaneous leishmaniasis (Espundia) |
L. mexicana - mexicana |
Yucatan, Guatemala |
Cutaneous leishmaniasis, more rarely diffuse cutaneous leishmaniasis |
|
L. mexicana - pifanoi |
Venezuela |
Diffuse cutaneous leishmaniasis |
|
cutaneous leishmaniasis |
Note(s)This section has been translated automatically.
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.
LiteratureThis section has been translated automatically.
- Davies CR et al. (2003) Leishmaniasis: new approaches to disease control. BMJ 326: 377-382
- 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
- Dereure J et al (2003) Visceral leishmaniasis. Persistence of parasites in lymph nodes after clinical cure. J Infect 47: 77-81
- Donovan C (1903) The etiology of one of the heterogeneous fevers of India. BMJ 2: 1401
- 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
- Fischer T et al. (2024)Treatment of mucocutaneous leishmaniasis- a systematic review. JDDG 22:763-774
- 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.
- Harms G et al. (2003) Leishmaniasis in Germany. Emerg Infect Dis 9: 872-875
- Leishman WB (1903) On the possibility of the ocurrence of trypanosomiasis in India. BMJ 2: 1376-1377
- 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.
Parajuli N et al. (2020) Case Report: Erysipeloid Cutaneous Leishmaniasis Treated with Oral Miltefosine. Am J Trop Med Hyg 104:643-645
- Zijlstra EE et al (2003) Post-kala-azar dermal leishmaniasis. Lancet Infect Dis 3: 87-98
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