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Buruli Ulcer Successfully Treated With Negative-Pressure Wound Therapy

Chiaki Murase, MD1; Michihiro Kono, MD, PhD1; Kazue Nakanaga, PhD2; Norihisa Ishii, MD, PhD2; Masashi Akiyama, MD, PhD1
[+] Author Affiliations
1Department of Dermatology, Nagoya University Graduate School of Medicine, Aichi, Japan
2Leprosy Research Center, National Institute of Infectious Diseases, Tokyo, Japan
JAMA Dermatol. 2015;151(10):1137-1139. doi:10.1001/jamadermatol.2015.1567.
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This case report details successful use of negative-pressure wound therapy for treatment of an advanced Buruli ulcer and suggests that such treatment might be effective in similar future cases.

Buruli ulcer (BU) is a slowly progressive lesion with local necrosis caused by Mycobacterium ulcerans.1 It is mostly seen in tropical areas,2,3 and the lack of awareness of BU in nonendemic areas sometimes leads to diagnostic delay. Significant delay places patients at risk of more extensive disease. Negative-pressure wound therapy (NPWT) is considered to be a great alternative because it accelerates wound healing. Herein, we report an advanced case of BU successfully treated with NPWT.

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Figure 1.
Genetic Analysis by Polymerase Chain Reaction (PCR) Targeting IS2404 and Virulence Plasmid pMUM001

A, Under PCR analysis of IS2404, the biopsy specimen was found to be strongly positive for the 154-bp product, which raised the possibility of Mycobacterium ulcerans or M ulcerans subspecies shinshuense as the causative organism. Lane M represents a 100–base pair (bp) ladder marker; lane NC, a negative control; lane PC, a positive control; lane S1, a DNA sample extracted from paraffin-embedded skin (patient) before antibiotic use; lane S2, a DNA sample extracted from paraffin-embedded skin (patient) after antibiotic use. B, Under PCR analysis of virulence plasmid pMUM001, only lane 3 was found to be negative. These results clearly indicate the diagnosis of Buruli ulcer caused by M ulcerans subspecies shinshuense. Lane M represents a 100-bp ladder marker; lane 1, repA (413 bp); lane 2, parA (501 bp); lane 3, the serine/threonine protein kinase gene MUP011 (479 bp); lane 4, a loading domain of mls (560 bp); lane 5, an acyltransferase domain of mls (504 bp); lane 6, the rep type II thioesterase gene (500 bp); lane 7, the rep type III ketosynthase gene (496 bp); and lane 8, the repP450 hydroxylase gene (500 bp).

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Figure 2.
Time Series of the Clinical Features of Buruli Ulcer (BU)

A, Painful ulceration with necrotic tissue surrounded by erythema on the right ankle on day 1 of BU-specific antibiotic treatment. B, The ulcer after radical debridement on day 20. The Achilles tendon and the calcaneal bone are exposed, and the articular capsule of the ankle joint has been destroyed. C, After negative-pressure wound therapy treatment, red granulation tissue covers the ulcer bed on day 69. D, The well-preserved skin graft completely encloses the lesion on day 127.

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