Adony carefully examines the logic of two theories for the recent
appearance of fluvalinate/flumethrin resistant varroa: 1.  It existed all
along and 2. It arose recently due to mutation
 
In either case,  lack of competition and lack of dilution from 'normal'
varroa (perhaps due to excessive doses of fluvalinate or constant
exposure) would allow them to emerge as a dominant type, even if
they are otherwise less fit:
 
> 'Most genetic mutants are thought to be less fit than common genotypes
> and should usually be removed from a population by natural selection.
 
> ...Even if a mutant is equal in fitness to common genotypes, it is likely to
> be lost from the population due to random mortality...
 
>  ...If the mutant is more fit than other individuals, its chance of
> surviving is somewhat greater, but it is still likely to be lost from
> the population...
 
> ... the only way rare mutants can get going in a population is if the
> population is quite small and experiences little gene flow with
> surrounding outside populations...
 
> ...Let's say a mutation occurs in an infested colony that confers a
> selective advantage to Varroa in the presence of Apistan strips.  These
> mutations are likely to occur very rarely, as mutations are rare events
> to begin with and most of them result in gibbled offspring that don't
> survive very long...
 
>  ...For the sake of argument lets say the mutant is
> 100 % resistant to Apistan, and the Apistan doesn't result in any
> sublethal effects to that mutant.  Suppose every mite in the colony, the
> mutant excluded, dies following application with Apistan...
 
>  Once that mutant Varroa's offspring get going and begin recolonizing
> the freshly Apistaned colony, the high amount of inbreeding (? -
> unresolved, sort of, from an old post) would likely make loss of the
> trait though outbreeding with Apistan suseptible stains of mite
> unlikely...
 
> I think there may be something to this scenario.  Nonetheless Allen, you
> must agree, the more established a resistance character in a population
> the more likely it is to surface.
 
Yes, you have very clearly outlined my thinking on this.  As far as I can
see, either mechanism (elimination of virtually all individuals except
those with a previously existing trait, or recent mutation) is a
reasonable explanation.  As far as which is more likely, I really don't
know.  And of course the question is which actually occured here.
In effect, one in a million chance is as good as a 100% chance if the
number comes up.  I doubt we will ever know which happened.
 
An aside: Of interest is that their host (our honeybee is also -- fairly
uniquely among cold blooded critters -- fluvalinate resistant) and I will
introduce a third -- and some will say preposterous -- suggestion, and
that is that the mite got it's fluvalinate resistance from the bee.  I
remember reading in Discover magazine some time back that DNA had been
proven to have been carried from on host to another by a common parasite
and that somehow, a characteristic from the first host had been
'transplanted' by the parasite and subsequently became established in the
second host.
 
Anyhow, what we do know is that there are many different subvarieties of
varroa, and the varroa one person has may not be the same as the varroa
that is found a few states -- or a few miles -- away.  This has not been
the case with other bee pests that we are used to, like AFB,  EFB and
chalkbrood as far as we know (excepting of course, the known
recent emergence of Tetracycline resistant AFB in South America).
 
With the other diseases, we could assume AFB is AFB, and not worry if we
got an exotic variety, because as far as we could tell there weren't any.
 
With varroa, each time we bring in new varroa to an outfit, we are bring
in a new population.  The results of mixing their population with our
own may be unpredictable, since each has a distinct genetic experience to
contribute to a new blend. Varroa may be fast 'learners'.
 
>  Having said that, I still wonder how resistance gets going in this
> strangely unique pest system beekeepers face (a possibly highly inbred
> pest which is seemingly adapted to nothing else but living off honey
> bees).  I suspect some long held truths established by scientists in
> other agriculural pest systems would be challenged if someone spent time
> on this problem.  I hope someone out there is interested in talking
> about this problem a little more.
 
I think we are just starting to get an idea of where this can go.  Unless
we can get a mechanism that they cannot *ever* adapt to (like
suscepibility to oil), we are doomed to find that controls expire in
effectiveness without warning and often.
 
Although oils are promising, I have some reservations since  current
application methods require complete disassembly of hives more often than
I even drive by some of my yards.  At present, the cure costs more than
any commercial outfit can pay in labour and disruption.
 
As I mentioned before, I heard of an oil fogging machine being used to
introduce an aerosol of an oil into beehives back when the tracheal mites
were first becoming a problem in North America.  I don't know what
happened to the idea. I have been unable to obtain details.
 
Allen