>    Re your described use of extender patties: are you aware of the
>    supposed link between long term (beyond what would have been applied
>    as dust) use of antibiotic extender patties especially in the presence
>    of AFB scale, and the development of resistant AFB strains?
 
Yes.  But if you use extender patties properly, where is the scale going
to come from?
 
>    AFB cultures to 1994 were no more tolerant of oxytetracycline, than
>    cultures from old scales (50 or so years old), but since 1996 cultures
>    from apiaries have been found in the U.S. that ARE less susceptible. I
>    think the link with extender patties is just a hypothesis, but it does
>    make sense (continuous selection pressure, a recent change in practice
>    that has become more frequent lately).
 
Well, when I think about this, I assume that there must be several modes
of AFB function for this to be credible, rather than the simple live and
kill the larva or die without offspring scenario I have always assumed.
 
I am quite ignorant here and am assuming (again) that that bacillus
larvae (or whatever it is called now) is specific to honeybee larvae and
has no other host.  My understanding is that in a case of larval infection
that either there are enough AFB germs to kill the larva and make spores,
or there aren't.
 
In the first case, there is a vast increase in the AFB organisms in the
cell.  In the second case, the sub-lethal one, what happens?  Do the
bacteria reproduce or do they die unreplicated?  If they reproduce, where
do they then live since the larva goes on to pupate?  In the pupa? In the
cell?  Are they communicated to other larvae?  Do they sporulate?  Or
remain vegetative and viable somewhere?  Or all the above?
 
I don't know.  I always just assumed that if specific AFB spores did not
kill the larva and sporulate and make scale, that was the end of those
particular individual germs and unless there was an occasional breakdown
and death of a larva in a hive, that the bacteria just became fewer and
fewer as they germinated and failed to gain a foothold.  That's why I
figured -- and continue to figure -- that after years of completely
suppressing AFB in a hive, that hive becomes increasingly unlikely to
break down with AFB.  We know that is true empiracly.  This is my
rationalization of that knowledge.
 
Am I wrong?  Is there another form of AFB infection besides the obvious
one with scale and dead larvae?  Is there one where the bacillus merry
goes on forever in the background without breakdown?  This seems to me to
be a necessary condition for the evolution of the resistance in the
presence of oxytet scenario you describe.  And if this is the case, then
resistance is almost inevitable unless another control is alternated
periodically.
 
>   In discussions of the issue at CAPA, I think the concensus was that
>    antibiotic patties are best used in a limited period (no longer than
>    dust would have been applied) and if patties are desired for their
>    tracheal mite benefit,  non-antibiotic patties be used.
 
Perhaps, but maybe that is all based strictly on conjecture?  Does anyone
there actually understand the whole AFB process in detail?  If so I am
really interested in hearing about it.  I have never come across anything
in my reading, which I must confess is somewhat limited in scope.
 
>    I can see it might be a tough call: the patties seem a good tool to
>    win the "battle" at an individual hive, and seem a benefit against
>    varroa, but it could be a risk in the longer term "war". One might
>    hope that resistant AFB would be eliminated by each beekeeper who
>    finds hives that don't respond to oxytet, and destroys the equipment,
>    but how little "leak" would that system need to allow enough survival
>    to lead to an established resistant strain?
 
Well, here we go again with only one registered chemical to control a
serious pest and we are talking hive destruction because we haven't
developed a second line of defence.  You would think we would have learned
but we don't.  FWIW, We are right in the middle of a developing disaster
in the US because of that kind of lack of forsight.  Apistan is the only
legal treatment for varroa and within a year it will not work reliably
anywhere in the US.  Sure they'll get formic registered soon, but I'll bet
real $ (US$) that they find what we have learned here in Canada -- and
that is that formic only sorta works and does not give the kind of
reliable and thorough results that Apistan did for years -- and the kind
of results that US commercial beekeeping needs to survive.
 
There is no good excuse for not having a second line ready and approved
for AFB, except inertia and good luck -- so far.  It is well known that
there are a number of known effective treatments for AFB, including the
best one I know of: sulfathiazole.
 
We lost sulfa due to lack of good guidance and poor mitigation of the
emergency caused by the discovery of residues.  At the time of the big
sulfa problem with amounts around one part per million showing up in
honey, I sat down and quickly figured out how much syulfa medicated feed
syrup would have to get into a 100 pound honey crop to give that 1ppm
level, and it came out at about one cup per hive as I recall.   Well,
considering how bees move honey around in a hive, I think we were dreaming
if we didn't think a cup of the honey in the brood chamber from the spring
could not wind up in a super come summer once in a while.  At any
rate, rather than get the abuse under control, the industry capitulated
and we lost one of our best AFB defenses
 
We know that we cannot tolerate any sulfa in honey.  No argment there.  I
can see why sulfa in syrup is a dumb idea, but why not okay it in pollen
patties or something that the bees consume?   What about sulfa in extender
or pollen patties?  There is zero risk of it getting into honey as far as
I can see.  After all, the bees *eat* or rub against it.  They don't
regurgitate it in its entirety and store such patties in a honey-like form
like they do with syrup.
 
There are other drugs too that should be considered for rotation with
oxytet.  IMO, anyhow, and now, not after the inevitable resistance
develops.
 
Back to the resistance scenario proposed: FWIW, If it matters, I think
there is much more likelihood of using oxytet in the presence of scale
using dust than by using patties if they are made properly, and I'd wager
that over 50% of the patties used are made with a vastly incorrect dosage.
 
And anyhow, I have yet to read any really convincing explanation of how
resistance develops.  I hear it is from overdosing and then I hear it
comes from underdosing, then I hear that it is inevitable regardless of
what we do.  I trust that all these explanations must be true, because
they all originate at some university or another.  Being just a dumb
farmer, it seems to me that the obvious solution is just to use
everything available in rotation and keep the pest pinned down in a
crossfire and guessing where the next assault will be coming from, not to
just licence one product and use it until the pest gets to like it.
 
>    I haven't heard recent news of the situation in Argentina, where
>    resistant AFB is also said to be a problem.
 
Thanks for bringing this up.  It is a good subject and I do worry about
it, but not enough to stop using patties.  As you can see by my rambling,
I really know nothing about these matters, except a few things that seem
to work.  There is a lot writtten and even more said, but not a lot of it
makes sense to me, so I go with the little I do know and that is they
worked for me last year.
 
FWIW, if I were to quit using patties or dust, it would not be because of
the spectre of resistant AFB, but would likely be due to the warnings
given by my old friend and former boss, Ulf.   But that is another matter
entirely, and concerns my own health and that of my workers.  On that
matter, I am much more impressed by the arguments...
 
Later
 
Allen