NDLI: Microbiological, Histological, Immunological, and Toxin Response to Antibiotic Treatment in the Mouse Model of Mycobacterium ulcerans Disease

Content Provider	PubMed Central
Author	Sarfo, Fred Stephen Converse, Paul J. Almeida, Deepak V. Zhang, Jihui Robinson, Clive Mark, Wansbrough-jones Grosset, Jacques H.
Editor	Small, Pamela L. C.
Copyright Year	2013
Abstract	Mycobacterium ulcerans infection causes a neglected tropical disease known as Buruli ulcer that is now found in poor rural areas of West Africa in numbers that sometimes exceed those reported for another significant mycobacterial disease, leprosy, caused by M. leprae. Unique among mycobacterial diseases, M. ulcerans produces a plasmid-encoded toxin called mycolactone (ML), which is the principal virulence factor and destroys fat cells in subcutaneous tissue. Disease is typically first manifested by the appearance of a nodule that eventually ulcerates and the lesions may continue to spread over limbs or occasionally the trunk. The current standard treatment is 8 weeks of daily rifampin and injections of streptomycin (RS). The treatment kills bacilli and wounds gradually heal. Whether RS treatment actually stops mycolactone production before killing bacilli has been suggested by histopathological analyses of patient lesions. Using a mouse footpad model of M. ulcerans infection where the time of infection and development of lesions can be followed in a controlled manner before and after antibiotic treatment, we have evaluated the progress of infection by assessing bacterial numbers, mycolactone production, the immune response, and lesion histopathology at regular intervals after infection and after antibiotic therapy. We found that RS treatment rapidly reduced gross lesions, bacterial numbers, and ML production as assessed by cytotoxicity assays and mass spectrometric analysis. Histopathological analysis revealed that RS treatment maintained the association of the bacilli with (or within) host cells where they were destroyed whereas lack of treatment resulted in extracellular infection, destruction of host cells, and ultimately lesion ulceration. We propose that RS treatment promotes healing in the host by blocking mycolactone production, which favors the survival of host cells, and by killing M. ulcerans bacilli.
Related Links	http://dx.doi.org/10.1371/journal.pntd.0002101
Starting Page	2101
File Format	PDF
ISSN	19352735
e-ISSN	19352735
Journal	PLoS Neglected Tropical Diseases
Issue Number	3
Volume Number	7
Language	English
Publisher	Public Library of Science
Publisher Date	2013-03-01
Access Restriction	Open
Rights Holder	Public Library of Science
Subject Keyword	Pharmacology, Toxicology and Pharmaceutics(all) Public Health, Environmental and Occupational Health Infectious Diseases Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Infectious Diseases Public Health, Environmental and Occupational Health Pharmacology, Toxicology and Pharmaceutics

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