BLOOD-MEAL PREFERENCE OF AEDES AGEYPTI (DIPTERA: CULICIDAE) TO RESOURCES TREATED WITH THE TOXIN PRODUCED BY MYCOBACTERIUM ULCERANS

Mycolactone is a unique toxin produced by Mycobacterium ulcerans (MU), the causative agent of Buruli ulcer. The primary vector for Buruli ulcer (BU) is still unknown; however, some hypothesize mosquitoes, such as Aedes aegypti, could be the culprit due to their high vector competence with other pathogens and association with environments endemic to BU. Through a simple attraction test, supplemented with Evans Blue dye in blood to distinguish blood meal sites, the affinity for A. aegypti to take a blood meal successfully from a mycolactone saturated area was evaluated and these results show that there is a higher attraction for the control blood meal site in the lowest and highest dose, 0.05 μg/mL and 1.0 μg/mL respectively, and a higher attraction for the treatment blood meal site in the mid-level dose of 0.5 μg/mL. These results thus explore the possibility of interkingdom communication between mycolactone and A. aegypti. Additionally, this research will test the possibility that A. aegypti could help in spreading Buruli ulcer or causing secondary infection in people infected with BU with another disease in which they are the primary vector

BLOOD-MEAL PREFERENCE OF AEDES AGEYPTI (DIPTERA: CULICIDAE) TO RESOURCES TREATED WITH THE TOXIN PRODUCED BY MYCOBACTERIUM ULCERANS

Mycolactone is a unique toxin produced by Mycobacterium ulcerans (MU), the causative agent of Buruli ulcer. The primary vector for Buruli ulcer (BU) is still unknown; however, some hypothesize mosquitoes, such as Aedes aegypti, could be the culprit due to their high vector competence with other pathogens and association with environments endemic to BU. Through a simple attraction test, supplemented with Evans Blue dye in blood to distinguish blood meal sites, the affinity for A. aegypti to take a blood meal successfully from a mycolactone saturated area was evaluated and these results show that there is a higher attraction for the control blood meal site in the lowest and highest dose, 0.05 μg/mL and 1.0 μg/mL respectively, and a higher attraction for the treatment blood meal site in the mid-level dose of 0.5 μg/mL. These results thus explore the possibility of interkingdom communication between mycolactone and A. aegypti. Additionally, this research will test the possibility that A. aegypti could help in spreading Buruli ulcer or causing secondary infection in people infected with BU with another disease in which they are the primary vector