Literature DB >> 27186576

Probable Buruli Ulcer Disease in Honduras.

Paul M Southern1.   

Abstract

Entities:  

Year:  2015        PMID: 27186576      PMCID: PMC4866575          DOI: 10.1093/ofid/ofv189

Source DB:  PubMed          Journal:  Open Forum Infect Dis        ISSN: 2328-8957            Impact factor:   3.835


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Buruli ulcer disease, caused by infection with Mycobacterium ulcerans, is prevalent in central and western Sub-Saharan Africa and in southeastern Australia, and it occurs sporadically in other tropical and subtropical locales [1-3]. This report addresses a case of possible Buruli ulcer disease in an adolescent girl in Honduras. The subject was a 16-year-old female living in a rural coastal village in Honduras (near La Ceiba). She developed 2 ulcerative lesions on her leg that grew from small pinpoint lesions, to abscesses, to large undermined ulcers over a period of several weeks (see Figure 1). The lesions were painless. Local topical remedies were ineffective. She had no systemic symptoms, and she did not develop other lesions. There was no history of trauma. Insect and mosquito bites are a part of everyday life in her village, and she had not traveled elsewhere. There were no contacts with similar lesions. She was discovered during a medical mission trip to Honduras. Scrapings and small biopsies were performed and transported in sealed, insulated sterile tubes (with a minuscule amount of sterile saline) for processing in the United States. Treatment with topical antifungals and oral itraconazole was of no benefit. She was later treated with oral rifampin and clarithromycin [4, 5]. When other members of the mission team returned to the area several months later, the young woman could not be found. After return to the United States, the scrapings and biopsies were processed in the clinical microbiology laboratory of Parkland Health and Hospital System in Dallas, Texas. They were cultured in the MGIT (Becton-Dickenson) system as well as on Lowenstein-Jensen medium. Both scrapings and tissue biopsies were stained with acid-fast stains. The stains revealed clumps of acid-fast bacilli, both intra- and extracellular in location. Cultures performed at 30°C, and held for 8 weeks, grew scantily and were presumptively identified as M ulcerans by phenotypic methods. There was growth at 30°C, but not at higher temperatures, nor at 25°C. Small colonies showed rough morphology on Lowenstein-Jensen medium, they were nonpigmented, and niacin and nitrate reduction tests were negative [6]. AccuProbes for Mycobacterium tuberculosis, Mycobacterium avium, Mycobacterium gordonae, and Mycobacterium kansasii complexes were negative. Funding limitations precluded molecular characterization. We believe that this represents a case of Buruli ulcer disease acquired in coastal Honduras. No reports of this condition in Honduras were found in the PubMed, MeSH, or Cochrane Reviews databases [7, 8]. Thus, this is the first known report of Buruli ulcer disease acquired in Honduras.
Figure 1.
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4.  Pharmacokinetics of rifampin and clarithromycin in patients treated for Mycobacterium ulcerans infection.

Authors:  J W C Alffenaar; W A Nienhuis; F de Velde; A T Zuur; A M A Wessels; D Almeida; J Grosset; O Adjei; D R A Uges; T S van der Werf
Journal:  Antimicrob Agents Chemother       Date:  2010-06-28       Impact factor: 5.191

5.  Oral treatment for Mycobacterium ulcerans infection: results from a pilot study in Benin.

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Journal:  Clin Infect Dis       Date:  2011-01-01       Impact factor: 9.079

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Authors:  Gene Khai Lin Huang; Paul D R Johnson
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Review 7.  Ecology and transmission of Buruli ulcer disease: a systematic review.

Authors:  Richard W Merritt; Edward D Walker; Pamela L C Small; John R Wallace; Paul D R Johnson; M Eric Benbow; Daniel A Boakye
Journal:  PLoS Negl Trop Dis       Date:  2010-12-14
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