Kpeli, G. S., & Yeboah-Manu, D. (2019). Secondary infection of Buruli ulcer lesions. Buruli Ulcer: Mycobacterium Ulcerans Disease, 227-239. https://link.springer.com/chapter/10.1007/978-3-030-11114-4_13
The introduction of antibiotics as first-line treatment of Buruli ulcer (BU) disease in 2004 resulted in improvement in the management of the disease, confirmed by several studies, including a randomised controlled clinical trial (Nienhuis et al., Lancet 375:664–672, 2010). Despite successful outcomes with this treatment regimen, the healing process is still characterized by long hospital stays as a result of delayed healing, in a significant proportion of cases. Clinical observations and subsequent research identified secondary infection of the BU lesions by other bacteria as a cause of wound healing delay, debunking the widely held belief that mycolactone, the macrolide toxin of Mycobacterium ulcerans, has antimicrobial activity and is preventing secondary infection of BU wounds. Secondary infection in BU disease is not well characterized, but the few studies, which described its occurrence identified Staphylococcus aureus and Pseudomonas aeruginosa as the dominant bacterial species responsible for wound infection and provided evidence that delayed wound closure may be associated in some patients with a high wound bioburden. Standard guidelines for managing secondarily infected BU lesions are currently not available, but a common recourse for many clinicians is to prescribe additional antibiotics. Studies describing the antibiogram of isolated secondarily infecting bacteria showed high levels of antibiotic resistance, indicating that antibiotic treatment may not be the best option to manage secondarily infected lesions. Preliminary studies showed that good wound care and good infection prevention and control practices will reduce time to healing and the long hospitalizations associated with post antibiotic management of the disease.