House flies are important vectors of a number of animal and human pathogens, thus controlling them is of great importance. Commercial insecticide control of house flies is limited to a few chemicals, and the development of resistance to these chemicals is an ongoing concern. Therefore, finding new effective insecticides is critical.
Spinosad is a relatively new promising insecticide that was released in 2005 for house fly control. It is derived from the bacterium Saccharopolyspora spinosa. It is highly effective against pest species and is thought to have a unique mode of action. A resistant laboratory house fly strain was developed and studies indicate the resistance mechanism is unique, recessive, and located on autosome 1.
Although house fly resistance to spinosad has been developed in the laboratory, resistance in field populations has not been characterized. In this study I monitored spinosad resistance at several dairy, hog and poultry farms over the summers of 2004 and 2005. Results showed that there was a variation in baseline susceptibility between different field sites, but no development of resistance was observed. Due to limitations of insecticide bioassays, developing a more sensitive resistance detection method and identifying the gene responsible for resistance will be important for future monitoring programs. As part of an important step in determining the gene for resistance, I linked a number of nicotinic acetylcholine receptor (nAChR) subunits to a particular house fly autosome. Spinosad toxicity is due to interactions with nAChRs and is associated with autosome 1. Of the four genes analyzed, two (Md?5 and Md?6) were associated with autosome 1, one (Md?2) was associated with autosome 2, and one gene association (Md?3) was not determined.
Lastly, I assessed the fitness effects of spinosad resistance on mating competition. I found that a laboratory susceptible strain had a mating advantage over a laboratory spinosad resistant strain.