gms | German Medical Science

10. Kongress für Infektionskrankheiten und Tropenmedizin (KIT 2010)

Deutsche Gesellschaft für Infektiologie,
Deutsche AIDS-Gesellschaft,
Deutsche Gesellschaft für Tropenmedizin und Internationale Gesundheit,
Paul-Ehrlich-Gesellschaft für Chemotherapie

23.06. - 26.06.2010, Köln

Advances in diagnosis and treatment of Buruli Ulcer Disease

Diagnostik und Therapie des Buruli Ulkus – aktueller Stand

Meeting Abstract

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  • G. Bretzel - Klinikum der Universität München, Abteilung für Infektions- und Tropenmedizin, München, Germany

10. Kongress für Infektionskrankheiten und Tropenmedizin (KIT 2010). Köln, 23.-26.06.2010. Düsseldorf: German Medical Science GMS Publishing House; 2010. DocTRO 04-3

DOI: 10.3205/10kit053, URN: urn:nbn:de:0183-10kit0531

Published: June 2, 2010

© 2010 Bretzel.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Outline

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Buruli Ulcer Disease (BUD), caused by Mycobacterium ulcerans, has become the third most common mycobacterial disease after tuberculosis and leprosy. Cases have been reported from more than 30 countries worldwide with a focus in West Africa. The disease mainly affects impoverished inhabitants of remote rural areas with a preference for children under the age of 15. BUD involves the skin and the subcutaneous adipose tissue. The disease starts as painless papule, plaque, or nodule that evolves into large painless ulcerations with characteristically undermined edges, eventually accompanied by edema of the surrounding skin. Large ulcers may affect subjacent bones resulting in osteomyelitis. Self-healing processes may lead to scarring and contractures. Though mortality is low, morbidity and subsequent functional disability are severe. Whereas previously BUD was treated by wide surgical excision followed by skin grafting, since 2004 antimycobacterial treatment with Rifampicin (RMP) and Streptomycin (SM) for eight weeks (eventually followed by surgical intervention) has been considered the treatment of choice. In order to minimize the use of injectable drugs, oral drug regimens are under investigation. A recent clinical trial proved the efficacy of a switch to oral therapy (RMP/clarithromycin) after four weeks RMP/SM. In a recently published case series the application of local heat therapy also proved recurrence-free healing of lesions. With the introduction of antimycobacterial treatment laboratory confirmation of clinically suspected BUD cases as well as monitoring of treatment success became crucial for the clinical management of BUD. Currently available laboratory tests include microscopy, culture and IS2404 PCR of swab and tissue specimens (i.e. punch biopsies, fine needle aspiration, surgically excised tissue), as well as histopathology. WHO recommends that endemic countries should ensure that at least 50% of all cases are confirmed by PCR. Several IS2404 PCR assays were successfully applied for case confirmation in endemic countries, and IS2404 PCR is considered the most sensitive method for the laboratory confirmation of BUD. Due to the extended presence of mycobacterial DNA under antimycobacterial treatment however, PCR is not suitable for monitoring of treatment success. Currently cultures are considered the only valid confirmatory test for the detection of viable bacilli.