Profiling Mycobacterium Ulcerans: Sporulation, Survival Strategy and Response to Environmental Factors

Abstract

Mycobacterium ulcerans is the causative agent of Buruli ulcer – a necrotizing skin infection. As an environmental pathogen, it has developed stress response mechanisms for survival. Similar to endospore formation in M. marinum, it is likely that M. ulcerans employs sporulation mechanisms for its survival and transmission. In this review, we modeled possible transmission routes and patterns of M. ulcerans from the environment to its host. We provided insights into the evolution of M. ulcerans and its genomic profiles. We discuss reservoirs of M. ulcerans as an environmental pathogen and its environmental survival. We comprehensively discuss sporulation as a possible stress response mechanism and modelled endospore formation in M. ulcerans. At last, we highlighted sporulation associated markers, which upon expression trigger endospore formation.

Plain Language Summary

Buruli ulcer is an infectious disease characterized by extensive sores on the skin and soft body tissues. The disease is caused by a bacterium called Mycobacterium ulcerans and is mainly found in tropical countries. Over the years, several attempts to understand the means by which humans get into contact with this bug as well as how it thrives in its host remain futile. In this review, we describe a possible survival strategy, known as sporulation, that is adopted by the pathogen for dispersal and survival.

Keywords:

• Buruli ulcer
• environmental pathogen
• mycobacteria
• Mycobacteria ulcerans
• sporulation
• stress response mechanisms

Author contributions

A Isawumi and EA Ayerakwa conceived and prepared the first draft of the manuscript. A Isawumi and MK Abban revised the draft for important intellectual content. Mosi made substantial contributions to the draft, critically reviewed the manuscript and approved the final version for publication. All the authors approved the final draft of the manuscript for submission.

Acknowledgments

The authors appreciate Mosi Research Lab and AMR Research Group led by A Isawumi at the Department of Biochemistry, Cell and Molecular Biology and West African Centre for Cell Biology of Infectious Pathogens at the University of Ghana for support.

Financial & competing interests disclosure

EA Ayerakwa and MK Abban are supported by a WACCBIP-World Bank ACE PhD fellowship (ACE02-WACCBIP: Awandare) and a DELTAS Africa grant (DEL-15-007: Awandare). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.