Genetics in the Host‐Mycobacterium ulcerans interaction

Abstract

Buruli ulcer is an emerging infectious disease associated with high morbidity and unpredictable outbreaks. It is caused by Mycobacterium ulcerans, a slow-growing pathogen evolutionarily shaped by the acquisition of a plasmid involved in the production of a potent macrolide-like cytotoxin and by genome rearrangements and downsizing. These events culminated in an uncommon infection pattern, whereby M. ulcerans is both able to induce the initiation of the inflammatory cascade and the cell death of its proponents, as well as to survive within the phagosome and in the extracellular milieu.In such extreme conditions, the host is sentenced to rely on a highly orchestrated genetic landscape to be able to control the infection. We here revisit the dynamics of M. ulcerans infection, drawing parallels from other mycobacterioses and integrating the most recent knowledge on its evolution and pathogenicity in its interaction with the host immune response.

The buzz around the zoonotic infection, Buruli ulcer

“…Readers are referred to several excellent, recent reviews on the range of issues surrounding Buruli ulcer. 2,4,[8][9][10][11][12][13] The focus on this current article is a summary of efforts to address the 80-year mystery of how M. ulcerans is spreading from the environment to humans in south-eastern Australia; where a One Health perspective has become so critical to help understand why there are surging local case numbers in Victoria (and beyond) and why the pathogen is spreading.…”