Surgery for Buruli ulcer in the antibiotic era

The histopathology of early Buruli lesions reveals large numbers of clumped mycobacterial cells surrounded by fat cell ghosts with minimal local inflammatory response.1,2 This pattern is explained by the key virulence determinant of M ulcerans, mycolactone,3 a plasmid-encoded polyketide toxin4 that diffuses beyond the invading mycobacterial cells to cause necrosis, apoptosis, and inhibition of the cell-mediated immune response in a concentration-dependent manner.5 The appearance of the characteristic ulcer allows natural discharge and drainage of necrotic cells and bacteria but does not reliably clear the infection without medical or surgical intervention. In The Lancet Infectious Diseases, Akpeedje Wadagni and colleagues report the results of a prospective randomised controlled trial at a single centre in Benin that compared antibiotics plus surgery (if required) assessed at 8 weeks (standard-care group) with antibiotics plus surgery (if required) assessed at 14 weeks (delayed-decision group). [...]patients in the delayed-decision group had a lower overall need for surgery than did those in the standard-care group, without experiencing delay in healing or increase in disability at 12 months.