Thanks to all who responded with comments or citations regarding my query on
whether or not resistance to TM by AFB has been detected or is developing
(or is likely to develop).
 
My evolving understanding of the subject leads me to focus on points made
by Andy and Kerry Clark.
 
Andy wrote:
 
"One reason for this good news in bee medication could be that in the
US and many other places for the most part beekeepers take out the
individual hives that do not respond to treatment and treat them to the
fire pit so we are treating mostly healthy hives."
 
 
 
Kerry Clark wrote:
 
"For some reason, resistant strains didn't survive in the field >
(or maybe they were infrequent enough that beekeepers weeded them out >
after the hives died). > > There's been a recent change, though, that
makes the appearance of > oxytetracycline resistant AFB more likely:
widespread, nearly continuous > use of antibiotic extender patties. This
is the one ingredient that was > missing: a continuous selection pressure."
 
 
These points lead me to believe that what has happened is that
resistant strains may have developed (or be in existence) but that when a
hive in which they develop fails to respond to TM treatment, it is either
burned or otherwise drastically treated (e.g., fumigation,, lye bath,
irradiation... have I missed any?) so that the strain in question is
eradicated.  This seems reasonable enough to me, but then I have to
wonder that in such situations the spores aren't spread to other hives
via robbing before the beekeeper gets a chance to remove the hive from
the yard and burn/treat it.  In other words, quick drastic treatment
preventing spread of the spores and resulting in destruction of the
strain could be the reason we aren't seeing resistance.  BUT...
 
Is this really happening?  I.e., do such hives really get pulled out of
the yard and isolated from robbing before the strain is spread?
 
Assuming this is not the case (I know I don't always catch a dying hive
(whether from foulbrood or mites (happily not THIS year... sofar))
however, I have to wonder if something else is not also at play.
 
Kerry emphasizes that CONTINOUS application may be the
determining factor and that until recently, continuous application was
not typical.  This makes me call into question my own (fragmentary)
understanding of how resistance to antibiotics is acquired/developed by
microorganisms.  Assuming that one can't "kill" i.e., remove the AFB
infection but only "treat the symptoms," isn't it necessary to
continually treat infected colonies (with short breaks in treatment
during the honeyflow) and doesn't this constitute continuous treatment?
Certainly, there's a break in the treatment, but it seems to me that
 
*the issue is whether or not the infectious organism is actually killed off
and removed*
 
by one or more treatments.  My understanding is that it is
never the case that AFB is removed by TM, so continuous, vs. one-time
treatment should not make any difference in terms of producing a
resistant strain.  The only difference would be that the hive treated
only once would eventually succumb, while the continuously treated hive
would survive.  (Kerry, I'm assuming you know a lot more about this than
me, so I'm hoping you can explain why my reasoning is false.)
 
At this point then, it seems to me that the primary factor is the
destruction/drastic treatment of
hives with the non-responsive strains of AFB (or non-responsive bees!)
and that even with robbing, as long as this practice is carried out,
outbreaks of resistant AFB would eventually be confined.  (I.e., the
colonies of the robbers would also be burned as they weakened and
were destroyed by the now alerted beekeeper.)
 
Andy also wrote:
 
"There may be other things at work with AFB which some have called a
disease of the "hive bees" because it is seldom found in the escaped
populations. Again this could be because of the good old survival of the
fittest rule, but one would think after reading the popular science on
the subject that if one hive in the wild went without treatment they all
would soon have AFB disease or all would dead in a season or two."
 
 
THis is a very interesting point.  The one person I know who has done
literally *hundreds* of feral removals (A.M. Buzas 1/800-47-STING) swears
that he has never seen a feral colony with foulbrood.  At first thought
this makes sense: Who's going to call and pay you to remove a dying or
dead colony?  I.e., his data set is biased toward strong, unafflicted
colonies, rather than weak/dead colonies.  But when I've pressed him on this
point he emphasizes that he's never seen even *one*.  And it's true, I
spent two summers working with him (we had NO business last summer!) and
of the 30 or so I've removed with him, there was never any sign of ANY
brood disease...  You'd think that you'd get one or two once in a
while...  Unless the feral populations were (are) (there still are some
out there) already somewhat resistant to brood diseases in general
- which is as Andy says, what you'd expect from natural selection.
 
Final point, since I'm not really sure where this leaves the question and
hope that the group will continue to mull it over:  If you assume that the
feral colonies really did/do have some resistance to brood diseases, what
are some likely mechanisms?  The one difference that I noticed regularly
was the heavier use of propolis.  (You could argue that they may not
actually use more propolis - they just never get the inside cavities
scraped down - but I'll testify that the feral colonies that I have
installed in regular deeps do use quite a bit more propolis than those
descended from packages or breeder queens.) I seem to recall a post a
number of months ago from someone in Arizona who said they were using
propolis as an AFB preventative...  I tried e-mailing them, but never got
a response...  Also, some strains of bees are apparently more resistant to
some brood diseases than others.  This has been known since at least 1915.
(My 1915 edition of Philips' "Beekeeping" states that the Italian strain
is "vastly superior"  to the German black bee with respect to resistance
to EFB.)
 
Dave T.