Cutaneous Leishmaniasis with Long Duration and Bleeding Ulcer Marco Manfredi 1,2* , Silvia Iuliano 1 , Barbara Bizzarri 2 , Alessandro Fugazza 2 , Pierpacifico Gismondi 1 and Gian Luigi de’Angelis 1,2 1 Department of Pediatrics, Azienda Ospedaliero-Universitaria di Parma, University Hospital-Parma-Italy 2 Gastroenterology and Endoscopy Unit, Azienda Ospedaliero-Universitaria di Parma, University Hospital-Parma-Italy * Corresponding author: Marco Manfredi, Department of Pediatrics, Azienda Ospedaliero-Universitaria di Parma, University Hospital-Parma-Italy, Tel: +393472822003; Fax: +39-521-702647; E-mail: marco.manfredi8@gmail.com Received date: October 16, 2015; Accepted date: January 07, 2016; Published date: January 14, 2016 Copyright: © 2016 Manfredi M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Leishmaniasis may cause visceral, cutaneous and/or mucocutaneous diseases. Cutaneous and mucocutaneous forms are caused by a single celled parasite transmitted by sand fly bites. Although the cutaneous form of the disease is often self-limiting, it results in significant scarring and can spread to more invasive, mucocutaneous disease. Therefore, treatment may be considered to prevent these complications. We describe a case report of cutaneous leishmaniasis contracted in a healthy man in Italy (Emilian Apennines). This cutaneous ulcer healed only with intralesional injection of meglumine antimoniate. After about 18 and 30 months a scar area is still present and no satellite lesion appeared. We have had no side effects or complications due to therapy. Introduction Leishmaniasis comprises a number of diseases of the viscera, skin and/or mucous membranes. Tis disease is transmitted by several genera and species of sand fies. Tree major clinical forms of leishmaniasis are recognized: a systemic leishmaniasis caused by L. donovani, the old world cutaneous leishmaniasis caused by L. major, L. tropica and L. aethiopica and the new world or american leishmaniasis caused by L. mexicana and L. braziliensis. Leishmania is an obligate intracellular parasite that in vertebrate hosts, exists only in the amastigote stage [1]. Te transmission occurs by contamination from the site of sand fies injection. Many of the promastigotes inoculated do not survive for direct cytolytic action by the tissues of mammals. Some promastigotes are phagocytized by histiocytes-macrophages, become amastigotes and thus begin replicating. Te main areas at risk of infection are the Mediterranean, the Middle East and parts of Asia. Leishmania tropica causes self-limiting skin ulcers in which the parasites are found within macrophages at the edge of the lesion. Dogs and rodents are ofen the natural reservoir of infection. Tere are two types of old world leishmaniasis: the wet and dry type. Te wet type is predominantly rural and is caused by L. major; it has a short incubation time, few parasites into the lesion and a fast recovery [2]. On the contrary, the dry type is a rather urban anthropo-zoonoses caused by L. tropica. It has a long incubation period, a long duration of infection and many parasites within the dermis of the lesion. In the early phase, there is a layer of corneal hypertrophy and hyperplasia of the dermal papillae resulting in necrosis of the central area due to obstruction papillary. Te ulcer becomes depressed with hardened and thickened edges and friable granulation tissue at the base. At this time it can be confused with carcinoma, tuberculous lesion, and syphilitic nodule. Cutaneous leishmaniasis (CL) may be limited to a single part of the skin or may produce multiple lesions [1]. Histologically there are lymphocytes, plasma cells, epithelioid cells and large giant cells. Afer the phlebotomus bite, an itchy red papulovesicular lesion appears; afer some weeks or months, the surface of the papule dries, the crust is formed and then it falls and gives rise to the deep ulcer. Although the cutaneous form of the disease is ofen self-limiting, it does result in signifcant scarring and can spread to more invasive, mucocutaneous disease. Terefore, treatment may be considered to prevent these complications [3,4]. Topical therapies to treat CL include both pharmacologic and non- drug modalities. Non-drug therapies including cauterization, surgical excision, cryotherapy, but the simplest of these treatments seems to be the local application of heat [3]. Te WHO recommends intralesional or systemic antimonials for the treatment of CL [1,2,5]. Intralesional infltration with pentavalent antimony produces the maximum concentration in the lesion and has few systemic side efects, but does not reach the metastatic injuries [3]. Manfredi et al., Clin Microbiol 2016, 5:1 DOI: 10.4172/2327-5073.1000229 Case Report Open Access Clin Microbiol ISSN:2327-5073 CMO, an open access journal Volume 5 • Issue 1 • 1000229 Clinical Microbiology: Open Access C l i n i c a l M i c r o b i o l o g y : O p e n A c c es s ISSN: 2327-5073