Insecticide resistance to permethrin and malathion and associated mechanisms in Aedes aegypti mosquitoes from St. Andrew Jamaica

Abstract

The emergence of novel diseases spread by the Aedes aegypti mosquito in Jamaica and the Caribbean, has prompted studies on insecticide resistance towards effective management of the vector. Though Jamaica has been using the organophosphate insecticide malathion in its vector control program for more than 30 years, resistance to the pesticide has not been tested in over a decade. We analyzed resistance to malathion and the pyrethroid insecticide, permethrin on mosquitoes collected across St. Andrew, Jamaica, and analyzed the molecular basis of resistance. The Center for Disease Control (CDC) bioassay revealed that Ae. aegypti mosquitoes from St. Andrew, Jamaica were resistant to permethrin (15 μg/bottle) with mortalities at 0–8% at 30 minute exposure time, while contact with malathion (50 μg/bottle) revealed ≤ 50% mortality at 15 minutes, which increased to 100% at 45 minutes. The standard susceptible New Orleans (NO) strain exhibited 100% mortality within15 minutes. The activities of multifunction oxidases and p-nitro phenyl-acetate esterases were significantly greater in most Jamaican populations in comparison to the NO strain, while activities of glutathione-S-transferase, acetylcholinesterase, α-esterase and ß-esterase activity were relatively equal, or lower than that of the control strain. The frequency of knockdown resistance mutations in the voltage dependent sodium channel gene were measured. All collections were fixed for Cys1,534 while 56% of mosquitoes were Ile1,016/Val1,016 heterozygotes, and 33% were Ile1,016 homozygotes. Aedes aegypti from St. Andrew Jamaica are resistant to permethrin with variations in the mode of mechanism, and possibly developing resistance to malathion. Continued monitoring of resistance is critically important to manage the spread of the vector in the country.

Association of age, sex, and pyrethroid resistance status on survival and cytochrome P450 gene expression in Aedes aegypti (L.)

“…Known mechanisms of resistance to multiple insecticide classes often involve increased activity of detoxification enzymes such as esterases, cytochrome P450s, and glutathione S-transferases (GSTs) (Lumjuan et al, 2005;Strode et al, 2008;Francis et al, 2017) and/or target site modifications, mainly in the sequence of acetylcholinesterase (Hemingway et al, 1989), the gamma-aminobutyric acid (GABA) receptor (Thompson et al, 1993), and the voltage-gated sodium channel (Brengues et al, 2003;Du et al, 2016). Although multiple nonsynonymous target site mutations were detected in strains of pyrethroidresistant A. aegypti from Puerto Rico, the Grand Cayman, Cuba, Thailand, French Guiana, Guadeloupe, New Caledonia, and Isla Mujeres (Mexico), these strains also exhibited high levels of cytochrome P450 gene expression (Strode et al, 2008;Bariami et al, 2012;Reid et al, 2014;Dusfour et al, 2015;Estep et al, 2017).…”

Activity of a selective insecticide (methoxyfenozide) against two mosquito species (Culex pipiensandCuliseta longiareolata): toxicological, biometrical and biochemical study

“…They are generally controlled by conventional insecticides such as organophosphate, carbamate and pyrethroid (Zaim et al ., ; Molyneux, ). However, these insecticides result in several environmental concerns worldwide, such as insecticide‐resistant strains (Francis et al ., ). To reduce the impact of these synthetic neurotoxins on the environment, more new selective chemicals have been tested, such as the insect growth disruptors (IGDs) (Rehimi & Soltani, ; Soltani‐Mazouni et al ., ; Bouaziz et al ., ), Juvenile hormone analogues (Hamaidia & Soltani, ), molting hormone agonists (Boudjelida et al ., ; Tine‐Djebbar & Soltani, ; Alouani et al ., ; Rehimi et al ., ; Hamaidia & Soltani, ), spiromesifen, which is an inhibitor of lipid synthesis (Bouabida et al ., ), and some plant extracts (Dris et al ., ).…”

The need to harmonize insecticide resistance testing: methodology, intensity concentrations and molecular mechanisms evaluated inAedes aegyptipopulations in Central America and Hispaniola

“…Prior to the implementation of the Zika AIRS Project, none of the five countries included in this study had functioning programs that monitored insecticide resistance in Zika vectors. Additionally, this study follows the path of only few previous studies that have explored the molecular mechanisms of insecticide resistance present in the region (51–53) and is the only study that raises technical issues regarding the dual internationally-accepted system of detecting and reporting insecticide resistance that might result in contrasting outcomes.…”