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There are many agricultural pests which have become resistant to commonly used pesticides. This is Darwinian selection at work: the pesticide kills off 95%, leaving the resitant 5% to restart the population. Next time, the pesticide only kills 75%, unless you use more... and so on.
This could
be circumvented by using a fancy new pesticide, an old, weak pesticide and lab reared insects. Insects are grown in a lab and designed to be exquisitely vulnerable to an old, weak pesticide: the Achilles strain. This vulnerability could be attained via old fashioned breeding or via genetic engineering (eg: disable a key detoxifying enzyme).
A field is treated with the fancy new insecticide, killing 95% of the insects. The field is then treated with the Achilles insects, replacing about 5% of the population. These lab insects then breed with the remaining wild ones, and the gene for vulnerability spreads in the population. This is done every year. After several years, many of the insects in the field are immune to the fancy insecticide but nearly all carry the Achilles gene. When the field is treated with the older pesticide, it should be possible to attain nearly 100% kill.
In fact, the Achilles strain could be designed to be vulnerable to a very selective or otherwise weak pesticide - thus when it was time for the knockout blow, there would be little collateral kill on other harmless insects.
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Yeah, the original version has the A strain immune to the strong pesticide. But it seemed unnecessary if you used a strong pesticide which broke down quickly in the environment. |
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I like the logic of this. While you're at it (selectively breeding bugs for a susceptibility-to-a-particular-poison trait) maybe you could also foster the "Gigolo Gene" - find out what it is that makes females of a certain species of insect mate with particular males of that same species, and heighten those aspects in your captive Achilles bug army. (Avian example - hologrammatic tails for peacocks) - breed them to be freakishly extreme examples of what the females look for in a mate, so they would be more likely than their more-resistant wild brothers to have offspring, and thus literally sow the seeds of their own destruction. |
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An approach that is in effect very much like this (that is, it works on the same principle, but it's simpler to implement) is used to control parasitic mites on commercial honey bee colonies in the U.S. Drug A is fed to the bees (not during the time they're producing honey for human consumption) one year, and as the mites begin to develop a resistance to Drug A, the treatment is switched to Drug B. The way it works with these mites, at least, is that as they develop Drug B resistance, their resistance to Drug A is lost. So when the treatment regime switches back to Drug A again, you're not selecting for resistance to both drugs. |
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[Beauxeault] - I would like to know more about this. I did not realize there were multiple acaricides that bees could tolerate. Any links / drug names? |
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The mite to which I refer is the varroa mite. Drug A is a fluvalinate sold as "Apistan." Drug B may be formic acid vapor, or in recent years it could be coumaphos, sold by Bayer as "Bayer Bee Strips," in areas that have received FDA approval to use the treatment as an emergency measure against the small hive beetle (though the coumaphos also controls varroa mites). |
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To be a bit more accurate, what I've read is not precisely that mites lose their resistance to fluvalinate because they're developing resistance to another attack, but that they lose the resistance when the exposure to the fluvalinate is discontinued. So even some less aggressive measures, such as the manipulation of brood frames or switching to a queen bred for hygiene for one season can result in mites that are re-susceptiblized the following year. |
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cheesynachos: huh? Are you saying it would be better to spray crop fields with Formula 409? |
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I read somewhare, which I can't
seem to find at the moment, that
many organisms lose a resistance
after the agent that caused the
resistance is discontinued. I think
it's because the resistant
individuals are slightly
disadvangaged under non-
exposed conditions, so the
resistance trait tends to breed
itself away. |
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Yeah. "The Andromeda Strain". Great book. |
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/that many organisms lose a resistance after the agent that caused the resistance is discontinued/ - you would think that would be the case, since resistance costs energy, and energy savings = selective advantage. Yet Staph aureus seems to hang on to every antibiotic resistance trait it can acquire, and now multiresistant staph is common in the community, not just hospitals. Perhaps there is enough antibiotic usage going on that resistance retains a selective advantage. Or maybe if you can have a resistance gene, but only cue it up when you need it, it is not so costly to be resistant after all. |
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