Abstract
Filariasis and virus diseases that are transmitted by Culex quinquefasciatus are still a global health problem. Control of mosquito vectors with synthetic insecticides causes resistance to these mosquitoes to insecticides so that detection of susceptibility of the mosquito larval stage to insecticides is important for evaluating mosquito control programs. The aim of this study was to evaluate the susceptibility of wild-caught Cx. quinquefasciatus larvae in Jakarta, Indonesia, following exposure to temephos, malathion, cypermethrin, and deltamethrin; this was done by examining the detoxifying enzyme activities and histological damage to the larval midgut. Cx. quinquefasciatus larvae were collected from five fields in Jakarta and exposed for 24 h to temephos (1.25, 6.25, 31.25, and 156.25 ppm), malathion (0.5 ppm), cypermethrin (0.25 ppm), and deltamethrin (0.35 ppm). The larvae were then examined for acetylcholinesterase (AChE), glutathione S-transferase (GST), and oxidase activities using biochemical methods. Histological damage to the larval midgut was examined using routine histopathological methods and transmission electron microscopy (TEM). After 24 h, temephos and deltamethrin led to 100% mortality in the Cx. quinquefasciatus larvae. Temephos and malathion significantly inhibited the activity of AChE, while cypermethrin and deltamethrin significantly inhibited oxidase activity. Histologically, all insecticides damaged the larval midgut, as indicated by irregularities in the epithelial cell (ECs), microvilli (Mv), food boluses (FBs), peritrophic membranes (PMs), and cracked epithelial layers (Ep). The TEM findings confirmed that temephos and cypermethrin damage to the midgut ECs included damage to the cell membrane, nucleus, nucleoli, mitochondria, and other cell organelles. Overall, Cx. quinquefasciatus larvae in Jakarta were completely susceptible to temephos and deltamethrin. Synthetic insecticides may kill Cx. quinquefasciatus larvae through their actions on the metabolic enzyme activities and histopathological midgut.