Jim, Zachary, Lloyd, Allen and All
> But how does this finding correlate with the "dual-resistance"
> to BOTH fluvalinate and coumaphos experienced by beekeepers who
> used coumaphos, and only coumaphos for a few seasons?
>
> From what you say, it follows that fluvalinate resistance cannot be
> "the same as" coumaphos resistance, and neither can be the same as
> "dual resistance". This seems to imply that there is more than one
> way to be "fluvalinate resistant".
In a way, yes, there could be a link. Zachary's paper focuses only on the
alteration of the sodium channel protein as a resistance mechanism. He
prefers to discount the possibility that there are other mechanisms also at
work in US resistant mites. It is quite conceivable that the full
resistance seen to fluvalinate in some strains of Varroa is due to a
combination of mechanisms: alteration of the sodium channel protein as well
as boosting the fluvalinate-degrading mechanisms.
Possible fluvalinate-degrading mechanisms include monooxygenases (see the
first two abstracts below) which are also implicated in resistance to
organophosphates (the third abstract, for example). So yes, it is
conceivable that as the mite adapts to coumaphos, or indeed to fluvalinate,
it becomes prepared to some degree for the challenge of the other class of
compound. So there *is* a theoretical reason why some cross-resistance, or
at least a degree of preparedness, exists in mites for these two classes of
compound. It may not be the full story, but may be a part of it.
all the best
Gavin.
Title: First data on resistance mechanisms of Varroa jacobsoni (Oud.)
against tau-fluvalinate.
Author: Hillesheim, Elke, Ritter, Wolfgang, Bassand, Denis.
Author Address: [a] Sandoz Agro Ltd., Biological Res. Station, 4108
Witterswil, Switzerland
Source: Experimental & Applied Acarology 20 (5) 1996. 283-296.
Abstract: In 1991, the first losses of efficacy of tau-fluvalinate against
the honeybee ectoparasite Varroa jacobsoni Oud. were recorded in Sicily.
Since then, diminished efficacy with available pyrethroid treatments has
been encountered in many regions of Italy. The aim of this study was to
investigate the type of resistance in V. jacobsoni to the pyrethroid
tau-fluvalinate by focusing on metabolic resistance mechanisms
(detoxication). After developing a suitable application method, two
synergists were used: piperonyl butoxide (PBO), as an inhibitor of the
microsomal monooxygenases of the cytochrome P450 complex and
S,S,S-tributylphosphorotrithioate (DEF), which blocks esterases. A
significant decrease in the LC-50 values of the susceptible and of the
resistant mite strains after the application of PBO was observed. A slight
decrease of the LC-50 values was also observed after the application of DER
However, this decrease was not significant. These results indicate that the
resistance of Varroa mites to tau-fluvalinate can partly be explained by an
increased detoxication due to the monooxygenases in the P450 system, which
is blocked by PBO. Esterases seems to play a negligible role. Whether
glutathione-S-transferases are involved, is still unknown, but other
mechanisms, such as the modification of the binding sites and/or reduced
uptake might be involved as well.
Title: First detection in Israel of fluvalinate resistance in the varroa
mite using bioassay and biochemical methods.
Author: Mozes-Koch, R., Slabezki, Y., Efrat, H., Kalev, H., Kamer, Y.,
Yakobson, B. A., Dag, A.
Author Address: [a] Inq.: U. Gerson, Faculty of Agriculture, Food and
Environment, Department of Entomology, Hebrew University of Jerusalem,
Rehovot, 76100, Israel
Source: Experimental and Applied Acarology 24 (1) Jan., 2000. 35-43.
Abstract: The aim of this study was to explore the extent of varroa mite
resistance to fluvalinate in Israel and to determine the underlying
biochemical mechanism. Assays at different apiaries indicated varroa mite
resistance at three of the five sites tested. Dose response assays conducted
with tau-fluvalinate on mites obtained from different sites indicated uneven
resistance. A monooxygenase assay revealed an increased rate (approximately
20-fold) of activity in mites that were not controlled by the pesticide, as
compared to activity in mites from untreated colonies. A minor, 1.5-2.5
fold, increase of esterase activity was also noted in the resistant mites.
This first demonstration of a fluvalinate-resistance mechanism in varroa
mites points to the need for more vigorous resistance management practices
to control the pest.
Title: The role of gene splicing, gene amplification and regulation in
mosquito insecticide resistance.
Author: Hemingway, Janet, Hawkes, Nicola, Prapanthadara, La-Aied,
Jayawardenal, K. G. Indrananda, Ranson, Hilary.
Author Address: [a] Sch. Pure Applied Biol., Univ. Wales Cardiff, P.O. Box
913, Cardiff CF1 3TL, UK
Source: Philosophical Transactions of the Royal Society of London B
Biological Sciences 353 (1376) Oct. 29, 1998. 1695-1699.
Abstract: The primary routes of insecticide resistance in all insects are
alterations in the insecticide target sites or changes in the rate at which
the insecticide is detoxified. Three enzyme systems, glutathione
S-transferases, esterases and monooxygenases, are involved in the
detoxification of the four major insecticide classes. These enzymes act by
rapidly metabolizing the insecticide to non-toxic products, or by rapidly
binding and very slowly turning over the insecticide (sequestration). In
Culex mosquitoes, the most common organophosphate insecticide resistance
mechanism is caused by co-amplification of two esterases. The amplified
esterases are differentially regulated, with three times more Estbeta21
being produced than Estalpha21. Cis-acting regulatory sequences associated
with these esterases are under investigation. All the amplified esterases in
different Culex species act through sequestration. The rates at which they
bind with insecticides are more rapid than those for their non-amplified
counterparts in the insecticide-susceptible insects. In contrast,
esterase-based organophosphate resistance in Anopheles is invariably based
on changes in substrate specificities and increased turnover rates of a
small subset of insecticides. The up-regulation of both glutathione
S-transferases and monooxygenases in resistant mosquitoes is due to the
effects of a single major gene in each case. The products of these major
genes upregulate a broad range of enzymes. The diversity of glutathione
S-transferases produced by Anopheles mosquitoes is increased by the splicing
of different 5' ends of genes, with a single 3' end, within one class of
this enzyme family. The trans-acting regulatory factors responsible for the
up-regulation of both the monooxygenase and glutathione S-transferases still
need to be identified, but the recent development of molecular tools for
positional cloning in Anopheles gambiae now makes this possible.
::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::
-- Visit www.honeybeeworld.com/BEE-L for rules, FAQ and other info ---
::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::
|
