> > I have come to think -- even more than
> > before -- that much of the discussion here on BEE-L about the mechanisms of
> > developing tolerance by 'abuse' of Apistan may be predicated on concepts
that
> > are questionable in view of what is now known about the resistance
> > mechanism.
>
> This comment really caught my attention. What, specifically, is it that we
> know about the resistance mechanism and how does it potentially change our
> understanding of how one abuses Apistan?

Well, I'm in the middle of Mark Winston's excellent book, "From Where I Sit", (I
wonder if there is a pun in there somewhere?) and since I am too lazy to write
all my own (mostly derivative) thoughts out, I'll quote some of what he says for
background, and claim the proof to be intuitive, and give some hints at the end.

"Varroa mites have changed the picture and are a clear example of the speed at
which resistance can develop. Studies in Italy in the early 1990s, and in France
in the mid-1990s, found that Varroa had become resistant to fluvalinate, the
pesticide in Apistan strips, after about ten years of use. We expect 95 to 99
percent of Vurroa to be killed by a proper application of Apistan, but the
Italians found only about 80 percent mortality, which left enough Varroa o
multiply and kill a colony within a few months. First the Italians, and then the
French, were forced to switch to more toxic substances that are not, and likely
never will be, licensed for use in North America.

"What is particularly frightening about this scenario is that no other
registered chemicals effective against Varroa are available in the United
States, so resistance to fluvalinate would quickly devastate the U.S. beekeeping
industry. Even more frightening is the fact that many commonly used management
practices are perfectly designed to select for resistant Varroa mites. If I
wanted to do an experiment to produce resistant mites, I would do nothing more
than what is being done illegally today by some North American beekeepers, and I
could virtually guarantee that within five years or less I would have mites
resistant to Apistan.

"The development of resistance to miticides is a fairly common and simple
phenomenon. Mites feed on a wide variety of plants and animals, which have
evolved numerous protective chemicals to defend themselves from the mites. In
most cases, the hungry mites then developed enzyme systems able to break down
these chemical defenses. This ability of mites to detoxify natural compounds
works on artificial compounds as well. Thus, when mites encounter a commercialy
produced miticide, a few of them will survive because they have the ability to
break down the novel chemical. The surviving mites reproduce, and their
offspring thrive because the more susceptible competing mites have been killed
off, leaving a wide-open field for the resistant mites to take over. Ironically,
our usual pest management response to these survivors is to throw ever-higher
doses of chemicals at them, which further selects for even more resistant mites.

"Apistan is the type of product that can induce resistance even if properly
used. Its active ingredient, fluvalinate, kills mites by disrupting their
nervous system, and is thought to be more deadly to Varroa than to bees simply
because the mites are so much smaller; a dose lethal to a mite won't kill a bee.
Current recommendations all across North America suggest two or even three
applications of Apistan each season, for forty-two to forty-five days at each
application. Spring and fall applications are recommended, both so the honey
won't be contaminated and because the mites are more exposed to the chemical
when they are out of brood cells and on adult bees. Two or three annual
treatments are necessary to keep mite levels down, and the consequences of less
frequent or no treatments are diminished honey production and high colony
mortality. These repeated applications of the same miticide within a single
season follow both label and extension agent recommendations. But even properly
applied treatments may select for resistant mites, since the mites that survive
the first exposure to Apistan and reproduce are likely to be the ones most able
to detoxify the fluvalinate."

---
Add to that the point that 1.) the specimens that exhibit fluvalinate resistance
tend to be less 'fit' and 2.) That it may be that fluvalinate resistance in
mites is a yes or no thing and that there may -- or may not -- be intermediate
stages of resistance, and the whole question becomes very murky to the point of
being unknowable.  I believe that *no one*, including the manufacturer and the
regulators, knows if the label directions are, in fact, optimal.

Many problems with a large number of unknowns have an array of equally valid
solutions.  I believe that it is reasonable, from examining this particular
problem (applying fluvalinate), that there are many possible equally valid
possibilities for applying the chemical, and that the label is only one.  Or
several, if we take into account that the directions vary from country to
country.

What is very clear, is, in Mark's words: "Apistan is the type of product that
can induce resistance even if properly used".

My main point is this: I submit that, if probabilities are properly assessed,
the likelihood of resistance being developed by a relatively small number of
off-label uses of Apistan(R) (not other fluvalinate concoctions) is not
significantly greater than the _certainty_ that resistance will develop in a
relatively short time in one of the vastly many more situations where the label
is followed -- as much as humanly possible -- to the letter.

I suggest it is less.

allen
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