Spinosad resistance in the housefly, Musca domestica, is due to a recessive factor on autosome 1
Introduction
Houseflies are the probable carriers of more than 65 human and animal intestinal diseases [1], [2], [3], including bacterial infections such as salmonellosis, shigellosis, and cholera; protozoan infections such as amebic dysentery; helminthic infections such as pinworms, roundworms, hookworms, and tapeworms; as well as viral and rickettsial infections. Recently houseflies were shown to spread a deadly strain of Escherichia coli in Japan [4]. Flies also transmit eye diseases such as trachoma and epidemic conjunctivitis, and infect wounds or skin with diseases such as cutaneous diphtheria, mycoses, yaws, and leprosy [2]. Considering houseflies are highly mobile, come into contact with excreta, carcasses, garbage, and other filthy matter and that they are intimately associated with humans, our food and utensils, it is not surprising that abatement of fly populations is essential for controlling many serious and widespread diseases [1], [2].
Spinosad is a new and highly promising insecticide, derived from the bacteria Saccharopolyspora spinosa, with efficacy against a wide range of insects, including houseflies [5], [6]. The mechanism of action of spinosad appears to be unique, with a primary site of attack being the nicotinic acetylcholine receptor and a secondary site of attack being GABA receptors [7], [8]. This unique mechanism(s) of action suggests that resistance due to changes in the target sites of other insecticides (i.e., kdr or Rdl) would not result in cross-resistance to spinosad.
With any new insecticide there are several questions to be addressed: how rapidly could resistance develop and to what level, how many genes are involved, is the resistance gene(s) dominant or recessive and is there cross-resistance to other insecticides? To investigate these questions we selected field collected houseflies for resistance to spinosad. We also examined the linkage, inheritance of, cross-resistance patterns of and effects of synergists at overcoming the resistance.
Section snippets
Chemicals
Spinosad was from DowAgroSciences. Methomyl, DPX-MPO62, and DCJW were from DuPont. Fipronil was from Rhone Poulenc. Dimethoate and chlorphenapyr were from American Cyanamid. Nicotine, dieldrin, piperonyl butoxide (PBO), and diethyl maleate (DEM) were from Aldrich. Tetrachlorvinphos and S,S,S-tributylphosphorotrithioate (DEF) were from Chem Service (West Chester, PA) and cyfluthrin was from Bayer.
Housefly strains
Two laboratory strains were used: CS, an insecticide susceptible (wild type) strain [9]; and aabys,
Results and discussion
Selection of the field collected houseflies (Table 1) produced a highly spinosad resistant strain of housefly within just 10 generations of selection. The selections resulted in a strain >150-fold resistant to spinosad (Table 1, Table 2). The NYSPINR strain showed cross-resistance to all insecticides tested, ranging from 1.5-fold for dieldrin to 43-fold for cyfluthrin. However, since the NYSPINR strain was established from multi-resistant field collected flies [10] it is not clear if these
Acknowledgements
We thank A. Paul for technical assistance, J. Bloomquist for valuable discussion, and K. Wing for the samples of DCJW and DPX-MP062. This work was supported by DowAgroSciences, Elanco Animal Health, and Hatch project 414.
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