**2.3. Histopathological picture**

From the previous clinical study, 73 biopsies were taken to characterize the histopathology of LCL caused by *L. (L.) mexicana*. The histopathological picture observed varied widely impairing classification into a meaningful pattern. Magalhães classification [13] identified a total of five histopathological patterns: type I) exudative-cellular reaction due to infiltration of histiocytes, lymphocytes and plasma cells, without granuloma; type II) exudative-necrotic reaction, characterized by cellular infiltration, necrosis and no granulomatous response; type III) exudative and necrotic-granulomatous reaction (unorganized granuloma) corresponding to pattern described as chronic granulomatous inflammation with necrosis; type IV) exudative granulomatous reaction (unorganized granuloma) without necrosis characterized by the presence of an unorganized granulomatous reaction; type V) exudative tuberculoid reaction in which a typical tuberculoid granuloma (organized) is formed. According to those histopathological patterns, 28.7% of type III and 43% of type IV were most commonly found. Parasite identification was positive in 68.5% of the biopsies. The size of the lesion was directly correlated with the time of evolution; however, an inverse correlation between the lesion size and abundancy of amastigotes was detected [14]. Therefore, the histopathology of LCL caused by *L. (L.) mexicana* as in other leishmaniasis is characterized by a chronic granulomatous inflam‐ matory response to this obligated intracellular protozoan infecting the macrophages.

#### **2.4. Treatment**

appearance of multiple lesions (**Figure 1D**–**F**). Those findings are suggestive of changes in

**Figure 1.** Clinical spectrum of the LCL in southeastern Mexico. (**A)** Acute ulcerated lesion on ear; (**B)** typical small, rounded, ulcerated lesion in forearm; (**C)** chronic lesion on ear; **(D and E)** nodular infiltrated lesions; (**F)** multiple ulcer-

From the previous clinical study, 73 biopsies were taken to characterize the histopathology of LCL caused by *L. (L.) mexicana*. The histopathological picture observed varied widely impairing classification into a meaningful pattern. Magalhães classification [13] identified a total of five histopathological patterns: type I) exudative-cellular reaction due to infiltration of histiocytes, lymphocytes and plasma cells, without granuloma; type II) exudative-necrotic reaction, characterized by cellular infiltration, necrosis and no granulomatous response; type III) exudative and necrotic-granulomatous reaction (unorganized granuloma) corresponding to pattern described as chronic granulomatous inflammation with necrosis; type IV) exudative granulomatous reaction (unorganized granuloma) without necrosis characterized by the presence of an unorganized granulomatous reaction; type V) exudative tuberculoid reaction in which a typical tuberculoid granuloma (organized) is formed. According to those histopathological patterns, 28.7% of type III and 43% of type IV were most commonly found. Parasite identification was positive in 68.5% of the biopsies. The size of the lesion was directly correlated with the time of evolution; however, an inverse correlation between the lesion size and abundancy of amastigotes was detected [14]. Therefore, the histopathology of LCL caused by

pathogenicity of the parasite that need to be studied.

140 The Epidemiology and Ecology of Leishmaniasis

ated lesions in forearm.

**2.3. Histopathological picture**

An investigation on the response of LCL to treatment with pentavalent antimonials (Sb5+ ) was carried out between January 1990 and December 1994 [15]. This study was not designed to be a controlled clinical trial, but rather to evaluate the response of the chiclero´s ulcer to treatment with meglumine antimoniate. Patient eligibility for the study included a confirmed diagnosis of acute LCL (time of evolution lesser than 12 months) based on both clinical diagnosis and parasite visualization by smear, biopsy and/or isolation‐culture, as well as no previous treatment with any antileishmanial drug, absence of any serious concomitant disease, and to be available for a 12‐month follow‐up. In all the 105 cases presented, at the end of the treatment, a complete re‐epithelialization of all lesions occurred without both residual erythema and relapse during a 1‐year monthly follow‐up. The mean number of injections required for complete re‐epithelialization of chiclero's ulcer was 25.1 (range = 5– 60), with a daily dose of one ampule. Since then LCL caused by *L. (L.) mexicana* in the Yucatan Peninsula has been successfully treated with a daily dose of meglumine antimoniate for 20 days, average 10 mg/kg/day. The dose seems lower dose compared to international recom‐ mendation of 20 mg/kg/day but it is effective. Moreover, the lack of report on resistance to the treatment is important to point out.
