Well, I thought of responding line by line to the articles preaching doom
(in very general terms) regarding resistance, but on reflection, it occurs
to me that there is not, so far, any fact to debate, and so far there are
only repetitions of opinions.  These dire warnings appear to me to be
merely generalisations based on a sketchy understanding of some specific
cases that are not necessarily applicable in any other situation --
including the present one.
 
Rather than to try to debate with opinion, I'll make my points and
challenge those who believe that they understand the development of
resistance to prove their case.  If we see that they in fact can provide a
specific consistent factual argument that applies to AFB and
oxytetracycline, I will accept their wisdom and it shall prevail (I'll
lick their boots).  Otherwise I will have to continue to regard these
rants as I do all urban myths: there things that people somehow want to
believe, and which are oft solemnly repeated as fact, but which are, alas,
totally unsupported by objective analysis.
 
The challenge: First I need to know about the specific pest is being
discussed and about the control to which it is expected to develop
resistance.  Then I need to know how the pest reproduces, whether sexually
or asexually or both and the existing genetic variation in the population
and the potential for interbreeding.  I need to know the mechanism by
which the control works on the pest.  Then I need to know the
evolutionary mechanism by which resistance is expected to occur in the
pest (my expectations being either mutation or selection from an existing
resistant sub-population.  Are there others?  ...Spontaneous generation of
resistant specimens?).  What is the exact mechanism by which the
resistance will increase.  How do the pest organisms live?  Is it a simple
live/die scenario?  Are there several scenarios?
 
These are only the tentative questions posed by a rather dim intellect
which has been subjected to over half a century of groping with existence
(and, more recently, several measures of good honey found in close
proximity to Saccaromyces Bayanus).  I am sure that younger and fresher
minds will subject this question to closer questioning.  I sure hope so!
 
There will be other factors, naturally, and any good model will include
allowance for initial levels of infestation, natural resistance by the
host, effect of a number of (possibly random) outside factors and more...
 
If we really understand what is going on in the development of a specific
resistance, the process should be able to be expressed mathematically.
Once we have done that, then, of course the amount of pressure from the
control -- as expressed as dose or timing -- will be found to be a factor.
 
HOWEVER,  in many possible models (*possibly* including this one)  that
factor may turn out to be minor or inconsequential in relation to some of
the other factors.  In some cases, it will turn out that high pressure may
be preferable, in others less pressure may be desirable and in others, it
may not have any direct effect on the theoretical time to resistance.
 
This is not the same as the varroa/Apistan case which, I submit, was
predictable from the start.  And not due to abuse of the controls.
 
Allen