02791nas a2200193 4500000000100000008004100001653001600042653001900058653001600077653001400093653002400107100001300131700001400144700001600158700001300174245007100187520232500258022001402583 2014 d10aPhilippines10aHistopathology10aSkin biopsy10adiagnosis10aMycobacteria leprae1 aFiallo P1 aCabiddu F1 aClapasson A1 aParodi A00aLichen scrofulosorum caused by Mycobacterium leprae: first report.3 a
BACKGROUND: Tuberculides are skin lesions caused by the hematogeneous dissemination of Mycobacterium tuberculosis. Bacilli are rapidly destroyed in the skin and are thus neither visible histologically nor identifiable by culture. Diagnosis depends on previous knowledge of systemic and/or cutaneous tuberculosis. Lichen scrofulosorum (LS), the most uncommon variant of tuberculid, is usually associated with M. tuberculosis infection of lymph nodes or bone but was also reported in association with other mycobacterioses.
OBJECTIVES: We report a case of LS in a patient with M. leprae infection.
METHODS: In 2008, a 51-year-old woman from the Philippines was diagnosed with tuberculoid leprosy and treated. In 2010 the leprosy was considered to have been cured, and treatment was stopped. In 2011 the patient presented with lesions on the trunk and legs. Biopsy specimens were obtained for histopathologic examination and DNA detection for polymerase chain reaction (PCR).
RESULTS: Histopathology in the biopsy from the trunk revealed the dermis to be diffusely occupied by granulomas with perineural and periadnexal disposition. Granulomas were composed of epithelioid cells and lymphocytes. Fite-Faraco staining revealed a few solid acid-fast bacilli within nerve fascicles. Reinfection or the re-reactivation of multibacillary borderline tuberculoid leprosy was diagnosed. Histopathology in the biopsy taken from the leg showed superficial, well-formed granulomas in the vicinity of hair follicles and sweat ducts. No acid-fast bacilli were seen. Analysis by PCR revealed M. leprae DNA in specimens from both the leg and trunk. The clinical features of the papular eruption and the histopathologic findings and concomitant mycobacterial infection with M. leprae led to a diagnosis of LS. Treatment was commenced with dapsone 100 mg/day, clofazimine 50 mg/day and 300 mg/month, and rifampicin 600 mg/day. The lichenoid eruption on the legs disappeared at one month of therapy, whereas the other skin lesions resolved in one year leaving residual hypochromic macules.
CONCLUSIONS: Infection with M. leprae may cause LS. The use of PCR in skin biopsies from granulomatous dermatitis of unknown origin can help to identify the responsible agents.
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