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Housefly pyrethroid resistance

The issue of pyrethroid resistance in houseflies and mosquitoes and the countermeasures are described below. [Pg.17]

CYP6D1 of the housefly (Musca domestica) has been found to hydroxylate cyper-methrin and thereby provide a resistance mechanism to this compound and other pyrethroids in this species (Scott et al. 1998 see also Chapter 12). Also, this insect P450 can metabolize plant toxins such as the linear furanocoumarins xanthotoxin and bergapten (Ma et al. 1994). This metabolic capability has been found in the lepi-dopteran Papilio polyxenes (black swallowtail), a species that feeds almost exclusively on plants containing furanocoumarins. [Pg.32]

Mechanism of action can be an important factor determining selectivity. In the extreme case, one group of organisms has a site of action that is not present in another group. Thus, most of the insecticides that are neurotoxic have very little phytotoxicity indeed, some of them (e.g., the OPs dimethoate, disyston, and demeton-5 -methyl) are good systemic insecticides. Most herbicides that act upon photosynthesis (e.g., triaz-ines and substituted ureas) have very low toxicity to animals (Table 2.7). The resistance of certain strains of insects to insecticides is due to their possessing a mutant form of the site of action, which is insensitive to the pesticide. Examples include certain strains of housefly with knockdown resistance (mutant form of Na+ channel that is insensitive to DDT and pyrethroids) and strains of several species of insects that are resistant to OPs because they have mutant forms of acetylcholinesterase. These... [Pg.59]

Cross-resistance refers to a situation in which a strain that becomes resistant to one insecticide automatically develops resistance to other insecticides to which it has not been exposed. For example, selection of a strain of Spodoptera littoralis with fenvalerate resulted in a 33-fold increase in tolerance to fenvalerate. The resistant strain also showed resistance to other pyrethroids (11- to 36-fold) and DDT (lower than for the pyrethroids). Exposure of Cidex qninquefasciatus to fenitrothion resulted in the development of resistance to the carbamate insecticide propoxur. Similarly, selection of a housefly strain with permethrin resulted in a 600-fold increase in resistance to permethrin. The resistant strain also showed resistance to methomyl, DDT, dichlorvos, and naled (Hassall, 1990). [Pg.215]

Famham, A.W. (1973). Genetics of resistance of pyrethroid-selected houseflies. Musca domestieti L. Bestir. Sci. 4, 513-520. [Pg.196]

Fore recently a comparable enhanced inhibition in resistant strains has been observed with aryloxadiazolone anticholinesterases (38). A second promising example is the discovery that some natural and synthetic isobutylamides are selectively toxic against houseflies that carry the super-kdr resistance trait (39). This gene causes an alteration in the sensitivity of the site of action for DDT and pyrethroids and is a major threat to the continued efficacy of synthetic pyrethroids in many of their applications. [Pg.62]

Results used here to illustrate this approach refer to two insecticides widely used for housefly control, the pyrethroid permethrin and the OP trichlorphon (Figure 1), and to two mechanisms implicated in resistance to these compounds, kdr and AChE-R respectively. [Pg.95]

Houseflies on Danish farms have become resistant to almost every new insecticide introduced for their control since the 1950 s (M.). In the mid 1970 s, scientists showed that resistance to DDT and the new pyrethroid insecticides is due to a common resistance factor (the kdr and super-kdr genes), and they predicted that rapid resistance development to the more persistent SP compounds would rapidly evolve in the field. In 1978-79, surveys for SP resistance indicated that resistance to long-residual compounds was beginning to develop in the field. Overall, the survey data indicated that resistance would soon be widespread. Several steps were immediately taken to evaluate the resistance potential of... [Pg.157]

Characteristically, DDT resistance in flies does not extend to prolan however, strains that are resistant due to receptor-site modification are also resistant to prolan and pyrethroids. This was observed early in houseflies and stable flies (Busvine, 1953 Stenersen, 1966). The DDT resistance in stable flies did not depend on metabolism (Stenersen, 1965). [Pg.202]

The target biomolecules for DDT and the pyrethroids are the sodium channels in the axon. One very common type of resistance is the so-called knockdown resistance, or kdr resistance. In this case one or more amino acids have been changed due to point mutation so that DDT or pyrethroids do not bind. Whereas houseflies that are resistant due to the presence of the DDT dehydrochlorinase type of glutathione transferase will be paralyzed by DDT, it is found that when DDT has been detoxicated, the flies wake up and... [Pg.202]


See other pages where Housefly pyrethroid resistance is mentioned: [Pg.212]    [Pg.172]    [Pg.173]    [Pg.199]    [Pg.93]    [Pg.464]    [Pg.300]    [Pg.301]    [Pg.95]    [Pg.296]    [Pg.303]    [Pg.300]    [Pg.301]    [Pg.31]    [Pg.208]    [Pg.211]    [Pg.211]    [Pg.172]    [Pg.200]    [Pg.202]    [Pg.202]    [Pg.204]    [Pg.93]    [Pg.119]    [Pg.149]    [Pg.250]    [Pg.242]   
See also in sourсe #XX -- [ Pg.238 ]




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