Distribution and dynamics of Bemisia tabaci invasive biotypes in central China.

The tobacco whitefly, Bemisia tabaci (Gennadius), causes severe crop losses in many agricultural systems. The worst of these losses are often associated with the invasion and establishment of specific whitefly biotypes. In a comprehensive survey of biotypes present in central China between 2005 and 2007, we obtained 191 samples of B. tabaci from 19 districts in Hubei province and its surrounds. Biotypes were identified by RAPD-PCR and by sequencing the mitochondrial cytochrome oxidase I gene (mtCO1). We determined that these central Chinese haplotypes included the world's two most invasive B. tabaci biotypes (B and Q) and two indigenous biotypes (ZHJ1 and ZHJ3). The B biotype shared >99.7% identity with other Chinese B biotypes and the Q biotype shared >99.5% of its identity with Q samples from the Mediterranean, USA, Africa and East Asia. By 2007, the Q biotype was dominant over much of Hubei province and appeared to be supplanting all other biotypes, although both the invasive and indigenous biotypes existed in sympatry in some regions. The invasion and rapid establishment of the Q biotype in China mirrors events elsewhere in the world, and we suggest that this is a consequence of its reproductive isolation, its polyphagous nature and its broad-spectrum resistance to insecticides. Its dominance has severe implications for the sustainability of some insecticide groups and for the production of a number of crops.

The involvement of microsomal oxidases in pyrethroid resistance in Helicoverpa armigera from Asia.

Five contemporary strains of the bollworm Helicoverpa armigera Hübner from China, Pakistan and India, all with high resistance to pyrethroids, were compared with a standard susceptible strain that originated from the Cote D'Ivoire in the 1970s ('SCD'). Two of the Chinese strains ('YGF' and 'YGFP') were derived by laboratory selection from a third, field collected strain ('YG'). The strain 'YG' exhibited 7-, 14- and 21-fold resistance to fenvalerate, cypermethrin and deltamethrin, respectively. After selection with fenvalerate for 14 generations ('YGF'), this increased to 1690-, 540- and 73-fold. Selection with a mixture of fenvalerate and piperonyl butoxide (PBO) for 14 generations ('YGFP') resulted in resistance ratios of 2510, 2920 and 286. The synergistic ratios to fenvalerate that resulted from pre-treatment of PBO were 5-, 462- and 12-fold in YG, YGF and YGFP strains, respectively. Resistance ratios for a Pakistani strain (PAK) were 2320-, 4100- and 223-fold to fenvalerate, cypermethrin and deltamethrin, respectively. The synergistic ratio of PBO to these pyrethroids was 450-, 950- and 11-fold. The strong synergism of pyrethroids by PBO implied that an oxidative metabolism could be involved in pyrethroid resistance in these resistant strains. The activities of cytochrome P450 monooxygenases from midguts of final instar larvae to p-nitroanisole (PNOD), ethoxycoumarin (ECOD), methoxyresorufin (MROD) significantly increased in all the resistant strains when compared with the susceptible strain. This further implies that cytochrome P450 monooxygenases are involved in pyrethroid resistance in Asian H. armigera. Comparative in vitro studies of the metabolism of 14C-deltamethrin by midgut microsomes of the resistant PAK and susceptible SCD strains showed that the resistant strain had a much greater capacity than the susceptible strain for the metabolic degradation of deltamethrin. This enhanced metabolic degradation occurred in the presence of NADPH which suggested an oxidative detoxification. In the resistant strains, minor increases in glutathione S-transferase activity (to the substrates CDNB and DCNB), and esterase activity (to the substrate alpha-naphthyl acetate) further suggested that, of the putative metabolic mechanisms, oxidases are the most important. This study provides the first evidence that cytochrome P450 monooxygenases are a major metabolic mechanism responsible for pyrethroid resistance in H. armigera from Asia.

Analogous pleiotropic effects of insecticide resistance genotypes in peach-potato aphids and houseflies.

We show that single-point mutations conferring target-site resistance (kdr) to pyrethroids and DDT in aphids and houseflies, and gene amplification conferring metabolic resistance (carboxylesterase) to organophosphates and carbamates in aphids, can have deleterious pleiotropic effects on fitness. Behavioural studies on peach-potato aphids showed that a reduced response to alarm pheromone was associated with both gene amplification and the kdr target-site mutation. In this species, gene amplification was also associated with a decreased propensity to move from senescing leaves to fresh leaves at low temperature. Housefly genotypes possessing the identical kdr mutation were also shown to exhibit behavioural differences in comparison with susceptible insects. In this species, resistant individuals showed no positional preference along a temperature gradient while susceptible genotypes exhibited a strong preference for warmer temperatures.

METI-acaricide resistance in Tetranychus urticae does not confer resistance to the naphthoquinones.

The naphthoquinones and the METI group of compounds act on sites associated with mitochondrial respiration, but METI-resistant strains of two-spotted spider mite from Japan and the UK exhibited no cross-resistance to the naphthoquinones. The potential for developing commercial naphthoquinones therefore remains high.

Incidence and inheritance of resistance to METI-acaricides in European strains of the two-spotted spider mite (Tetranychus urticae) (Acari: Tetranychidae).

A strain of Tetranychus urticae (Koch; Acari: Tetranychidae), collected from hops (Humulus humuli L; Cannabaceae) in England with a short history of tebufenpyrad use, exhibited resistance to four METI (mitochondrial electron transport inhibitor)-acaricides; tebufenpyrad, pyridaben, fenazaquin and fenpyroximate. Resistance factors for these compounds in a microimmersion assay were 46, 346, 168 and 77 respectively, and corresponded to those exhibited by a Japanese METI-acaricide-resistant reference strain. Levels of resistance remained stable without further selection, and selection with tebufenpyrad did not increase them. The UK strain was also resistant (c 6-fold) to bifenthrin. Crosses of homozygous, diploid females with hemizygous, haploid males showed that, in the UK strain, METI-acaricide resistance was paternally and maternally inherited, and was an incompletely dominant trait. Another tebufenpyrad-resistant strain from the UK, originating from a chrysanthemum nursery (Chrysanthemum foeniculaceum Giseke; Asteraceae) was collected eight months later at a site c 210 km distant from the first. These are the first published incidences of METI-acaricide resistance in Europe and implications for the future use of these compounds are discussed.