Clinical Presentation of Cutaneous Leishmaniasis caused by Leishmania major.

BACKGROUND/AIMS: The diagnosis of cutaneous leishmaniasis (CL) is based on the microscopic detection of amastigote, isolation of the parasite, or the detection of Leishmania DNA. Nevertheless, since these techniques are time consuming and not usually available in many endemic countries, the diagnosis remains clinical. Consequently, such disease may be overlooked because of its similarity to other skin diseases. The aim of this study is to describe the clinical polymorphism of CL caused by Leishmaniamajor. METHODS: A cross-sectional survey was carried out on 166 patients. Diagnoses were made by both microscopic examination of stained tissue-scraping smears and PCR. The Leishmania species was identified by restriction enzyme analysis of the ribosomal internal transcribed spacer 1 region. The clinical polymorphism was analyzed only for patients with a positive diagnosis for CL and L. major as the identified species. RESULTS AND CONCLUSION: Of the 166 patients, 75 patients fit the inclusion criteria. Twelve different types of CL caused by L. major were defined. The most common type was the ulcero-crusted form followed by the papulonodular form and the impetigenous form. The ulcerated, mucocutaneous, lupoid, and sporotricoid forms were less common. The eczematiform, erysipeloid, verrucous, psoriasiform, and pseudotumoral types were represented by a single case. Zoonotic CL caused by L. major can simulate many other skin diseases, which may lead to a significant spread of this disease and increases in morbidity and drug resistance. This large polymorphism may be the result of a complex association between the genetics of the parasite and the immune response of the host.

Unexpected co-detection of promastigote and amastigote Leishmania forms in a human cutaneous lesion: implications for leishmaniasis physiopathology and treatment.

Cutaneous leishmaniasis pathogenicity depends on the survival and replication of the parasitic protozoa in the form of non-motile amastigotes inside macrophages. Here, we report the unprecedented observation of both Leishmania major amastigote and promastigote forms (the latter is normally detected only in the mid gut of the insect vector or in vitro culture) in a cutaneous lesion of a 6-year-old boy. This finding suggests that modifications of the skin lesion environment, such as maceration and changes in pH or temperature, could promote the in situ transformation of Leishmania amastigotes into promastigotes. This observation raises questions about the physiopathology of cutaneous leishmaniasis and the influence of micro-environmental changes on the efficiency of topical treatments.