Cutaneous Leishmaniasis and the Strategies for Its Prevention and Control

Abstract

Volume 2 • Issue 2 • 1000e114 Trop Med Surg ISSN: 2329-9088 TPMS, an open access journal Despite zoonotic leishmaniasis is considered as a public health problem worldwide, it is one of the most neglected diseases [1,2]. This disease is identified by an annual incidence of about 2 million cases and a prevalence of 12 million cases globally [3]. Leishmaniasis is the third most important vector-borne disease after malaria and filariasis [4]. The disease is caused by the intracellular protozoa of the genus Leishmania, is common in tropical and subtropical regions of the world and transmitted by phlebotomine sand flies [5]. The numbers of the leishmaniasis cases are increasing throughout because of some factors such as the lack of vaccines, the increased parasites resistance to chemotherapy and inability to controlling vectors. Depending on the tropism, leishmaniasis can be divided into at least four forms namely cutaneous leishmaniasis (CL), muco-cutaneous leishmaniosis (MCL) or mucosal leishmaniasis (ML), visceral leishmaniosis (VL) also known as kala-azar, and post kala-azar dermal leishmaniasis (PKAL) [6,7]. Approximately three-quarters of incidence cases of leishmaniasis are related to CL [6]. Leishmaniasis can vary from a self-limiting cutaneous disease to a fatal visceral disease depending on the effecting species [8]. CL is characterized by the presence of one or more ulcers which may heal spontaneously or persist for period of some months [4]. Rarely, CL may be transformed into ML at the advanced stages, if untreated [9]. In the Old World, CL is caused by primarily Leishmania major, and then L. tropica, L. infantum, and L. aethiopica [1,10,11], while in the New World, it is caused by L. Mexicana, L. braziliensis, and L. guyanensis species [6,12]. The parasite Leishmania exists in the extracellular promastigote form, inside the midgut of the vector and culture media, and in the intracellular amastigote form, in the mammalian host [2,13]. Diagnosis of the disease is made based on demonstration of the parasite by methods such as fine-needle biopsy of lymph nodes, bone marrow aspiration, splenic puncture, skin scraping cytology and culture [3,10]. Cytology including touch smear and needle aspiration is cheap and performed with high sensitivity for the typical cases, but it may be unable to detect the atypical cases of leishmaniasis [14,15]. The serology tests are limited because of the probable cross reaction of antibodies with some diseases like toxoplasmosis and trypanosomiasis [15]. Other methodologies such as immunohistochemistry (ICH) and polymerase chain reaction (PCR) are preferably applied for supplementary diagnosis of the disease in particularly CL form [1,15-17]. Treatment of CL may be topical or systemic, on the basis of several factors such as Leishmania species, geographic regions and clinical manifestations [18]. For focal therapy, thermotherapy, cryotherapy, paromomycin ointment, local infiltration with antimonials may be promising options with less systemic toxicity. Systemic treatment is provided by using azole drugs, miltefosine, pentavalent antimonials, pentamidine and amphotericin B and its liposomal formulation [18,19].