Different colors of mosquitoes in this picture represent a single base pair change, which is one of the mechanisms that can cause variability in a population, that can cause the different genes to insecticide resistance that the individual might have. Linda’s lab at the CDC is studying this genetic diversity. For example, adults that have been found to be resistant (they test them by exposing them to standard amounts of insecticides) could have the kdr mutation, as well as multiple copies of two esterase genes. They extract that individual’s DNA and are interested in the differences in the DNA sequences of both known resistance genes such as kdr and esterases, as well as several other genes. They compare the genetic variation of resistant individuals to individuals that are susceptible to the insecticide. This co-variation in a set of genes in resistant vs. susceptible mosquitoes can give them a better picture of what genes are involved in resistance.
There’s naturally occurring genetic diversity in any population, resistance happens when an individual, or group has a small variation that helps them survive better. So, over tens to hundreds of generations, the result is a population better adapted to their environment. If the mosquitoes’ environment includes an insecticide, some part of that population will become resistant over time. There are many ways that these changes could occur, so there are multiple genes that affect insecticide resistance. Some genes and mechanisms are well-characterized, but because Culex pipiens complex mosquitoes prefer what they euphemistically call “organically-enriched” larval habitats (i.e. they love water with lots of animal waste or rotting vegetation) it is thought that genes associated with helping larvae cope with such conditions could help them adapt to the pressures of insecticides. Here are some examples of insecticide resistance in Culex pipiens: Something called kdr (“knock down resistance”) is an example of one mechanism of resistance called Target Site Mutations, and results from a single base pair change in the genetic code for one of the sodium channel genes. The mutation changes the shape of the receptor targeted by the toxin in pyrethroid insecticides, and they are rendered ineffective. The other major mechanism that causes resistance is known as metabolic resistance. Here, genes are either up-regulated or they exist in multiple copies. Either way, more gene product is made, which detoxifies or sequesters the toxin in the insecticide. Genes in the esterase family sometimes exist in multiple copies and are associated with metabolic resistance.
Mosquitoes are vectors of human and other animal diseases. For example, Culex pipiens mosquitoes can carry the West Nile virus. Humans and horses are what are called dead-end hosts, meaning the virus doesn’t amplify in them. Birds, especially corvids (crows, blue jays, magpies, etc.) are considered amplifying hosts and the disease is spread by mosquitoes taking blood meals from infected birds, then biting humans. Insecticides are used to reduce the number of mosquitoes in the environment, and thus control transmission of the disease. Larvicides, which are designed to affect the aquatic juvenile stage of the life cycle, are added to areas of standing water. Adulticides are sprayed to kill adults. Adulticides are applied at night, when most beneficial insects are not actively flying, and are often used in doses of as little as an ounce per acre (about the size of a football field). Mosquito control districts vary in how much insecticide application they engage in. Where Linda lives, for example, adulticiding doesn’t take place until there are West Nile virus-positive mosquitoes detected during surveillance (the regular trapping and testing of mosquitoes). Repellants (i.e. “bug spray”) are used to keep mosquitoes from landing on humans and attempting to feed.