| dc.description.abstract | Aedes aegypti, the principle vector of yellow fever, is responsible for more than 30,000 deaths annually. Compounds like carbon dioxide, amino acids, fatty acids and other volatile organic compounds (VOCs) have been widely studied for their role in attracting Aedes aegypti. Many VOCs from humans are produced by skin microbiota, which consists of over 1000 species. Staphyloccocus epidermidis, although not the most abundant bacteria according to 16S ribosomal RNA research, commonly occurs on human skin. Quorum sensing (QS) by bacteria serves as a source for VOCs. This study determined if QS by bacteria serves as a mechanism regulating A. aegypti attraction to hosts.
Four pairwise tests examine the response of female A. aegypti to tryptic soy TSB (media for the bacteria) and S. epidermidis wildtype. And three replicates tests differential response between wildtype vs. agr- strains and agr- vs. TSB (the agr gene can express an accessory gene regulator for quorum sensing). Differential attractiveness by the wildtype and agr- was determined. The blood-feeder treated with wildtype S. epidermidis attracted about two times more A. aegypti than the agr- S. epidermidis (P ≤ 0.001). Also, wildtype strain was more attractive by 20% to A. aegypti than the TSB. Replicate effects were detected demonstrating that some replicates were significantly different from others in the same experiment, resulting in heterogeneity among replicates. Future work should focus on reducing this variability in the assay and determining which genes are responsible for the VOCs that interfere with the ability of A. aegypti to locate hosts, possibly by manipulating bacterial quorum sensing systems. | en |
