Abstract
Infection with Mycobacterium ulcerans causes Buruli Ulcer, a neglected tropical disease. Mosquito vectors are suspected to participate in the transmission and environmental maintenance of the bacterium. However, mechanisms and consequences of mosquito contamination by M. ulcerans are not well understood. We evaluated the metabolome of the Anopheles gambiae mosquito to profile the metabolic changes associated with bacterial colonization. Contamination of mosquitoes with live M. ulcerans bacilli results in disruptions to lipid metabolic pathways of the mosquito, specifically the utilization of glycerolipid molecules, an affect that was not observed in mosquitoes exposed to dead M. ulcerans. These results are consistent with aberrations of lipid metabolism described in other mycobacterial infections, implying global host-pathogen interactions shared across diverse saprophytic and pathogenic mycobacterial species. This study implicates features of the bacterium, such as the putative M. ulcerans encoded phospholipase enzyme, which promote virulence, survival, and active adaptation in concert with mosquito development, and provides significant groundwork for enhanced studies of the vector-pathogen interactions using metabolomics profiling. Lastly, metabolic and survival data suggest an interaction which is unlikely to contribute to transmission of M. ulcerans by A. gambiae and more likely to contribute to persistence of M. ulcerans in waters cohabitated by both organisms.
Highlights
Correspondence and requests for materials should be addressed to Control and Prevention, Bacterial Diseases Branch, Fort Collins, CO 80521
Metabolic and survival data suggest an interaction which is unlikely to contribute to transmission of M. ulcerans by A. gambiae and more likely to contribute to persistence of M. ulcerans in waters cohabitated by both organisms
This study suggested that the mechanism of exposure to most likely result www.nature.com/scientificreports in classical Buruli Ulcer disease was via direct injection of the bacteria into the skin, further implicating vector-borne transmission
Summary
Correspondence and requests for materials should be addressed to Control and Prevention, Bacterial Diseases Branch, Fort Collins, CO 80521. Before vector-borne transmission was suspected by investigators, it was widely believed that the acidfast bacilli (AFB) could be introduced into a previously existing cut or abrasion and subsequently result in Buruli Ulcer disease[12]. This mode of exposure was deemed unlikely in a study by Williamson (2014), which demonstrated a lack of pathology associated with M. ulcerans infection when abraded guinea pig skin was contaminated with a suspension of M. ulcerans[13]. This study suggested that the mechanism of exposure to most likely result www.nature.com/scientificreports in classical Buruli Ulcer disease was via direct injection of the bacteria into the skin, further implicating vector-borne transmission. Expression of mycolactone is not required for colonization in some invertebrate models[17]
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