Cutaneous leishmaniasis (CL) is a parasitic disease characterized by single or multiple ulcerations. Secondary bacterial infections are one of the complications that can increase the tissue destruction and the resulting scar. To better determine the incidence of real secondary bacterial infections in CL, we designed the current study. This was a cross-sectional study performed in Skin Diseases and Leishmaniasis Research Centre, Isfahan, Iran. A total of 1,255 patients with confirmed CL enrolled in the study. Sterile swaps were achieved for ulcer exudates and scraping was used for non-ulcerated lesions. All samples were transferred to tryptic soy broth medium. After 24 hr of incubation at 37degrees C they were transferred to eosin methylene blue agar (EMB) and blood agar. Laboratory tests were used to determine the species of bacteria. Among 1,255 confirmed CL patients, 274 (21.8%) had positive cultures for secondary bacterial infections. The bacteria isolated from the lesions were Staphylococcus aureus in 190 cases (69.3%), coagulase negative Staphylococcus in 63 cases (23.0%), E. coli in 10 cases (3.6%), Proteus sp. in 6 cases (2.2%), and Klebsiella sp. in 5 cases (1.9%). The results show that the overall incidence of secondary bacterial infections in the lesions of CL was 21.8%, considerably high. The incidence of secondary bacterial infections was significantly higher in ulcerated lesions compared with non-ulcerated lesions.
Adolescent ; Adult ; Aged ; Aged, 80 and over ; Bacteria/classification/isolation & purification ; Bacterial Infections/*complications/microbiology ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Leishmaniasis, Cutaneous/*complications ; Male ; Middle Aged

INTRODUCTIONAntimonial compounds are regarded as the treatment of choice for cutaneous leishmaniasis (CL). Systemic administration of these drugs has some side effects including cardio toxicity and electrocardiogram (EKG) changes. The objective of our study was to evaluate EKG changes in the patients with CL treated with systemic glucantime.

MATERIALS AND METHODSOne hundred and thirty-one patients were enrolled in this prospective study. All of the selected patients had confirmed CL and were candidates for treatment with systemic glucantime. The patients were treated with systemic glucantime and EKG was performed before, during (weekly) and 1 month after cessation of the treatment. All of the collected data were analysed using SPSS software.

RESULTSThe most common change was prolonged QT interval that was seen in 19% of the patients. ST depression occurred in 6.1% of the patients. Minimal ST elevation occurred in 3% and inverted T was observed in 7.4% of the patients. Single premature atrial contraction (PAC) and single premature ventricular contraction (PVC) occurred in 0.7% and 2.29% of patients, respectively. Bradycardia was observed in 10.6% and left bundle branch block in 0.7% of the patients. All of these changes reversed after stopping the treatment except 1 case with left bundle branch block that lasted for 1 month after the treatment.

CONCLUSIONSOur results showed that treatment with glucantime can induce many ECG changes as QT prolongation have significant risk. We suggest that ECG monitoring should be performed in high-risk patients undergoing glucantime treatment with special attention to ECG changes mostly prolonged QT interval.

Administration, Oral ; Adult ; Animals ; Antimony ; Antiprotozoal Agents ; administration & dosage ; adverse effects ; Atrial Premature Complexes ; chemically induced ; physiopathology ; Bradycardia ; chemically induced ; physiopathology ; Bundle-Branch Block ; chemically induced ; physiopathology ; Dose-Response Relationship, Drug ; Electrocardiography ; drug effects ; Female ; Follow-Up Studies ; Humans ; Leishmaniasis, Cutaneous ; complications ; drug therapy ; physiopathology ; Male ; Meglumine ; administration & dosage ; adverse effects ; Organometallic Compounds ; administration & dosage ; adverse effects ; Prognosis ; Prospective Studies ; Ventricular Premature Complexes ; chemically induced ; physiopathology