Abstract

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.

Highlights

  • Proper wound care is increasingly becoming a very crucial component of the management of Buruli ulcer (BU)

  • The cytopathic activity of the main virulent factor of the causative pathogen, M. ulcerans, leads to the formation of extensive necrotic ulcerative lesions, which are a good medium for the growth of other bacteria

  • The WHO recommends that secondary infection in BU should be suspected when a wound develops cellulitis or becomes painful [11]

Read more

Summary

Background

Proper wound care is increasingly becoming a very crucial component of the management of Buruli ulcer (BU). The cytopathic activity of the main virulent factor of the causative pathogen, M. ulcerans, leads to the formation of extensive necrotic ulcerative lesions, which are a good medium for the growth of other bacteria. Wound healing is delayed in a proportion of affected patients, in particular in those reporting with large lesions [4, 8, 9]. After completion of antimycobacterial therapy good monitoring and wound care is important to avoid massive secondary bacterial infections [10], potentially affecting the healing potential of wounds and increasing the risk of more severe pathology and sepsis. It was speculated that mycolactone secreted by M. ulcerans during active disease may sterilize BU wounds and prevent secondary infection by other bacteria, since a number of macrolides have broad spectrum activity against many bacterial species including streptococci, pneumococci, staphylococci, enterococci, mycoplasma, mycobacteria, rickettsia, and chlamydia [17].

Yeboah-Manu (*) Noguchi Memorial Institute for Medical Research, Accra, Ghana
Species Diversity
Sources of Infection
Findings
64 Sa NOG-W86 Sa NOG-W87 Sa NOG-W01 Sa NOG-W63 Sa NOG-W11
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call