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Mycobacterium ulcerans  is the causative agent of Buruli ulcer, a neglected tropical skin disease that is most commonly found in children from West and Central Africa. Despite the severity of the infection, therapeutic options are limited to antibiotics with severe side effects. Here, we show that  M. ulcerans  is susceptible to the anti-tubercular drug Q203 and related compounds targeting the respiratory cytochrome  bc   1   :aa   3  . While the cytochrome  bc   1   :aa   3   is the primary terminal oxidase in  Mycobacterium tuberculosis , the presence of an alternate bd-type terminal oxidase limits the bactericidal and sterilizing potency of Q203 against this bacterium.  M. ulcerans  strains found in Buruli ulcer patients from Africa and Australia lost all alternate terminal electron acceptors and rely exclusively on the cytochrome  bc   1   :aa   3   to respire. As a result, Q203 is bactericidal at low dose against  M. ulcerans  replicating in vitro and in mice, making the drug a promising candidate for Buruli ulcer treatment.

Targeting the Mycobacterium ulcerans cytochrome bc1:aa3 for the treatment of Buruli ulcer