1. Introduction

Leishmaniasis is a group of clinical entities present in 79 countries at a rate of 400,000 cases per year. The World Health Organization estimates a worldwide prevalence of approximately 12 million cases with population at risk of approximately 350 million. It is caused by a parasitic

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Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and eproduction in any medium, provided the original work is properly cited.

protozoan, which belongs to the Leishmania genus that is transmitted to human beings and animal reservoirs by phlebotomine sand flies [1].

Cutaneous leishmaniasis (CL) is the most widespread form, causing primary localized skin lesions from which parasites can disseminate to the nasopharyngeal mucosa and cause mucocutaneous leishmaniasis (MCL) or disseminate to the entire body as nodular lesions in diffused cutaneous leishmaniasis (DCL). Visceral leishmaniasis (VL) is the most severe form of the disease; according to the WHO in areas endemic for VL, many people have asymptomatic infection and a concomitant HIV infection increases the risk of developing active VL by between 100 and 2320 times [1].

VL is characterized by irregular fever, weight loss, swelling of the liver and spleen, and anemia. After recovery, patients sometime develop chronic DCL [2, 3].

American cutaneous leishmaniasis is characterized by a spectrum of clinical presentations caused by Leishmania species grouped in complexes; these include LCL caused by Leishmania (L.) mexicana; DCL caused by Leishmania amazonensis, Leishmania venezuelensis, and Leishmania pifanoi, all of them belonging to the L. mexicana complex; and MCL caused by members of the L. braziliensis complex. VL is caused by L. (L.) chagasi belonging to the L. donovani complex. Symptomatic diagnosis confuses CL with unrelated disorders such as tropical ulcers, sporotrichosis, leprosy, and skin cancer, among others [4].

In Mexico, Seidelin first recorded LCL caused by L. (L.) mexicana in 1912, who called it "chiclero's ulcer," because he found the disease in rubber workers. CL is distributed in three main endemic areas: Gulf of Mexico, Pacific of Mexico, and Central Mexico. In these regions, multiple species of Leishmania may coexist and several species can cause both LCL and MCL [5–7]. Several methods of detection of Leishmania based on deoxyribonucleic acid (DNA) have been described. The polymerase chain reaction (PCR) has been employed for selective amplification of Leishmania DNA. Several molecular targets for a diagnostic PCR have been evaluated including the minicircle kinetoplast DNA (kDNA), the miniexon (spliced leader RNA) gene, and the internal transcribed spacer (ITS) [8–10], among others.
