> >As such it deserves and new name, and in honor of where it first
> >appeared, I'll call it South American Foul Brood or SAFB for short.
>
> I suggest we call it bad AFB in honor and memory of Andy N. and his
> Bad and Sad bees.

Well, it crossed my mind, but what I see here is something that needs to be
recognized as a distinct new problem and the word 'bad' doesn't make it distinct
enough, just makes it seem a bit worse, not VERY DIFFERENT.

I'm *not* picking on South America here, anymore than anyone is picking on
Americans when speaking of ordinary old AFB or on Europeans when talking of EFB.
South America is where this new variety was first detected and therefore
deserves the honour IMO.  But even if we do not honour Andy in that way, I will
honour his spirit by pressing my  politically incorrect point past the point of
comfort for many, and by adhering to what some have perceived as my politically
incorrect appellation: SAFB.

> Hold on Allen.  There were reports of OTC resistance in Argentina at
> least as far back as 1989 well before that study was published.

Okay.  That was *one* instance AFAIK.  I maintain that we may well be still
talking about that one instance, but that it has spread.  Prove to me that the
new outbreaks are not just the same one spreading.

> In fact OTC resistance was found in the US for the first time within a
> year of the publication of that article when an inspector found some
> AFB that was responding to treatment and sent in a sample for testing.

Okay, but where did it come from?  Does anyone really know?  Why assume
spontaneous generation occurred when there is a simple and credible alternate
theory?  Opinions are not facts.  Enquiring minds need PROOF that the US and
Canadian samples are not descended from the Argentine AFB.

Although it is plausible that resistance could have occurred independently, we
know that the appearance of AFB resistance to oxytet had not been a common
occurrence prior to the South American find.  In fact the Argentine case was
*unique* for many years.  If one accepts Occam's razor there is no excuse for
ignoring and for not favouring the obvious simple theory that the subsequent
cases are just one and the same virulent strain of a very communicable disease,
spread around by international trade.

Now, maybe I am wrong and someone has PROVEN that the strains that are appearing
in the US and Canada are *not* at all closely related genetically to the strains
causing problems in the Argentine, but I have not heard of such proof.  That's
all it would take to change my understanding and my stance: PROOF.  I would have
thought that if there were any real proof, that someone would have taken the
pleasure of proving me wrong on this point by now.  But no one has.  I'm
beginning to believe that -- on this point, at this time -- no one can.

Until we get such proof, I must prefer the most simple and most obvious
explanation -- that the disease is imported and the outbreaks are related.  It
is very hard for me to believe  that after many, many uneventful years of use
and abuse of sulfa and oxytet, that suddenly, independently and spontaneously
AFB at *apparently* isolated locations all over the hemisphere is spontaneously
developing resistance.

Experience seems to have proven over many years that -- for some reason, and
surprisingly -- in consideration of how the drugs were used -- development of
oxytet and sulfa resistance in AFB organisms was a very improbable event.  At
least, that was true until a few years ago, when suddenly everything changed and
the improbable *appeared* to become somewhat common.

That makes me really suspicious.  Why?  Is there a change in the environment?
Is there somehow communication between distant populations of the bacterium?  Or
are they the same original colony of resistant micro organisms, spread by modern
transportation?  To me this last explanation has the most obvious merit, and the
first and most popularly accepted explanation is to me the least convincing.

It seems, however, that the most obvious explanation -- true or false -- happens
to be politically uncomfortable, and the least meritorious argument is the one
that makes the most people happy.  Why is it that everyone looks the other way
when the question of importation is raised, or takes offence; and why is it that
those who bother to argue against the suggestion do not offer any proof.
Instead they dismiss this possibility out of hand and dwell happily on the
politically acceptable alternatives.

I realize that people *have* been looking for a common factor between the
breakdowns of this new AFB disease, and have settled on extender patties as an
explanation: they see extender patties as something new in the administration of
drugs and assume that everything else is the same as ever.  It also conveniently
allows everyone to blame powerless beekeepers rather than well connected
international traders, the government scientists, the extension people and the
regulators.

But hold on there a minute.  There is something wrong with the extender patty
scenario.  Sulfathiozole apparently uses the same mechanism against AFB as
oxytet does.  Sulfathiazole is a very persistent compound which stays on and on
in hives, much like the oxytet in extender patties.  If continuous application
of such an antibiotic were going to cause widespread independent episodes of
resistance, why did this not happen when everyone was using sulfa?  Sulfa was
universally used and much preferred to oxytet, except where EFB might be a
problem.

And, I wonder how much serious thought has been given to the idea of
communication between the bacteria, either through ubiquitous barnyard or human
associated bacteria coming into contact with AFB.  It is no secret that there
has been widespread tolerance of antibiotics in such familiar and commonplace
bacteria and that the resistance to common antibiotic treatments has snowballed
recently in such organisms, organisms that are whisked around the world with
cattle, hogs and fowl...

> >That is not to say that all resistance necessarily originates in the
Argentine,
> >but we do know that AFB can be very contagious in the absence of resistant
bees
> >or drugs that are effective, and we do know that honey carries AFB spores
very
> >nicely.  We also know that honey is 1. discarded in open sites, 2. honey
drums
> >are re-used, sometimes without washing for feeding bees, 3. hobbyists (and
> >occasionally commercial beekeepers) sometimes purchase honey to feed their
bees.
> >You don't have to be a rocket surgeon to figure out the rest...

I stick with this.

> >What I learned watching TV last night was that micro organisms swap
> >DNA on a regular basis when they come into contact with one another and that
> >resistance in one bacterium can and will transfer into others that come into
> >contact.  This may explain why suddenly we are seeing resistance appear all
over
> >the place in types of bacteria that have previously been isolated and very
> >limited in their habitat such as those causing AFB; perhaps they are meeting
more
> >ubiquitous types of bacteria that are resistant and the resistance is
transferring.
>
> Again hold on there!  First horizontal gene transfer ( the process
> referred to above ) appears to not be that frequent of an event and
> requires close contact between the organisms involved.

True, perhaps, but it is just as reasonable -- if not more so -- an explanation
as the unsubstantiated party line being supplied to beekeepers by government
employees.

> Second the
> rise of antibiotic resistance does not require such transfer nor
> mutation.  Simply using an antibiotic will select for those organisms
> in the target population which have such resistance.  Each and every
> use of the antibiotic will select for resistance that is already in
> the population.

No argument here.  But why now, and all over the place, not years ago?  The
mechanisms of resistance may or may not involve mutation.  It depends whether
there are any individuals in the population that normally have resistance.  From
the zero incidence of resistance appearing over the first few decades of
antibiotic use against AFB, we must assume that the incidence of resistant
individuals in normal populations was a number very closely approaching zero,
and that mutation must have been necessary, or that the resistant members of
normal populations were not sufficiently fit to stand by themselves if selected.

> In fact here resistance appeared first in those
> beekeeper's outfits who were most diligent in their treatment program
> i.e. they subjected the population of AFB in their hives to the
> strongest selection for resistance.

I have no evidence of this -- other than anecdotal.  Where can I get an
authoritative account that I can subject to scrutiny?  Who has critiqued these
conclusions?  Who has analysed them for flaws and pursued alternate explanations
and commonalities?  And, why were they so diligent?  Were they finding that they
were unable to control AFB and therefore stepping up their treatment efforts?
One is not normally that diligent unless the problem is pretty bad.

> Another observation is that
> resistance appeared a few years after the widespread use of TM
> extender patties which hold the antibiotic in the hive for extended
> periods of time in an active form hence vastly increasing the
> selection for resistance.

See above comments re the probabilities and how my hives seldom were without
significant sulfa residues in the brood chambers.

> In short, we probably have imported some
> but we almost certainly also selected some of our own.

Okay, Thanks for conceding the point about probable importation.  That was my
guess too.

And, "almost certainly" is an interesting way of putting the possibility of our
having generated our own.

IF we have not generated our own and we HAVE INDEED imported some, who is
responsible?

> Now reread that stuff above on selection and use pesticide instead of
> antibiotic and you have a pretty good description of how varroa
> resistance to Apistan or other treatments develops.  The development
> of resistance in both cases involves very similar mechanisms.

Yup, same thing.  Give the beekeeper only one legal treatment, one that has a
certainty of failure in a finite time if used alone without rotation, let
resistance develop, then blame the beekeeper -- if some of the SAFB is "Made in
USA" (and Canada) -- which I *still* doubt.

One thing for sure is that fluvalinate resistance in mites is a lot faster
coming about and much more commonplace than the SAFB phenomenon was for many,
many, years.  Very different in my estimation.

> Good discussion and very relevant.

Agreed, and it's fun.  Thanks for the workout.  I look forward to your response.

allen
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