For anyone who cares about this thread :
 
What I said :
>> > 3. I wonder why Varroa has variability for a character like
>> >fluvalenate resistance anyways ?  Why do alelles that confer
>> >fluvalenate resistance  exist in natural Varroa populations...?...
 
Allen Dick's response :
>> >What about mutation?  There are, I assume, billions upon billions of >mites
>> >under pressure from fluvalinate.  Any sucessful mutations would soon
>> >dominate.
 
P. Aras et M. Boily response to Allen :
 
>> Insect resistance to pesticides is not the results of mutation. If an
>> given specie of insect is poisened by a pesticide they will not transform
>> themselves (mutate) to be resistant to that substance. Pesticide
>> resistance of a specie is the result of a more or less small proportion
>> of the population: Of the billions of individuals that form a specie
>> there are always some that are slightly different as a result of errors
>> in the replication of their genetic code...
 
Well, what about mutation ?  One scientist that has done much work on the
genetics of resistance development in insects is Dr. Fred Gould at North
Carolina State Univ.  From a review he wrote for a book titled 'Evolution of
Insect Pests, Patterns of Variation' he writes :
 
'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 one of the 1000 eggs laid by a
female is a genetic mutant and, on average, only 2 of these 1,000 eggs
escape mortality factors before they reproduce, there is only 1 chance in
500 that the mutant will not be lost from the population in the first
generation... 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.  For example, let us consider two mutants, one with half the
fitness of average individuals in a population (mutant H) and the other with
twice the fitness of average individuals in a population (mutant T).  Each
is the offspring of a single female lays 1,000 eggs.  Mutant H has a (0.5) x
(1/500) or 1 in 1,000 chance of surviving to reproduce, wheras mutant T has
a (2.0) x (1/500) or 1 in 250 chance of surviving to reproduce in the first
generation'
 
 
Phew, that was a lot to copy out. Dr. Gould goes on to write that 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.
 
Now, adapt Dr. Gould's logic over to Varroa.  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.  The advantageous
mutation to this rare Varroa mite also likely will not confer 100 %
resistance to Apistan, but rather, some elevated level of resistance (say 25
% more resistant than the average resistance found in natural Varroa
populations).  For the sake of agruement 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.  The mutant needs only to
emerge from the cell healthy, locate a suitable cell for reproduction, have
offspring that develop normally and the resistance will have become
established (assuming the resistance is highly heritable). Not all Varroa
will survive development, not all will find a cell, not all will reproduce
when they find a cell, although I would guess the odds are much better than
in Dr. Gould's example.  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.  Hmmm.  How likely is all that to occur.  Let me list the events
that have to occur to get to our colony infested with resistant Varroa :
 
1 - rare mutation conveying improved resistance to Apistan occurs (mutation
has not negatively correlated with some other important gentic character
needed by Varroa)
 
2 - resistance is complete and apistan is unlikely to result in mutant
mortality or reduced fitness (e.g. reproductive capibilities remain totaly
intact)
 
3 - mite lives long enough to have offspring and offspring make it to adulthood.
 
4 - outbreeding with a huge population of Apistan suceptible mites does not
wash away the resistance (yet another reason to study the outbreeding
capacity of Varroa).
 
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.  Having said that, I still wonder how resitance 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.
 
 
***********************************
** Adony P. Melathopoulos *********
*** Center for Pest Management ****
**** Simon Fraser University ******
***** Burnaby, British Columbia ***
****** Canada, V5A-1S6 ************
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"The pursuit of agriculture promotes the strength of the mind
 as well as the body"
         - Rev. John L. Blake, 1853