Hi Allen,
I have been considering this for a couple of days to try to improve
my reply. So here goes.
>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.
Hmm not sure it is that different more like the old AFB all
beekeepers knew and feared before we had antibiotics to treat it. In
fact, the only way to know if it is antibiotic resistant is to send in
a sample for a lab test to see how it responds to oxytet so it really
doesn't sound that different to me. Now I do understand your point
that it needs to be dealt with differently since it does not respond
to our usual medication. I have no real objection to the SAFB label
but just am not sure it is really all that different. I do know that
one cannot tell in the field by looking at a broodcomb if it is
regular or bad AFB but if you know treatment history one can make an
educated guess.
> 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.
Proof can be had if some researcher will do the DNA fingerprinting
work but AFAIK that work has not been done yet. One observation from
the researchers is that what we are finding in NA is not nearly as
resistant as that found in SA could suggest no recent direct
connection. Again, not proof just observation.
>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.
When we first found resistance I figured that it was equally likely
that it was accidently imported or selected here by our usage of
oxytet. Until the DNA fingerprinting is done we will never be sure
which or if in fact both are involved. The important thing is that we
know it is here and must deal with it.
>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.
My point is simply that we may have selected for it here as well in
other words we may have done it to ourselves. Now that is not a
comfortable thought but from what we know about development of drug
resistance it makes sense. The idea that we imported it is somewhat
comfortable since it did not happen because of what we were doing so
there may not be reason to change. Again, we need to change the way
we approach brood disease control here in North America because of the
drug resistance which is now here but it is nice to be able to blame
the problem on someone else. Of course if we selected it here we can
also do something about it by changing our management practices and
avoid repeating the same thing again in a few years with another
antibiotic. Experience in medicine has shown that the development of
multiple drug resistance is much quicker than development of the first
case of resistance so to continue on the treatment treadmill seems
unwise to me.
>But hold on there a minute. There is something wrong with the
extender patty
>scenario. Sulfathiazole 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.
Now I am not sure of the mechanism of action of these two drugs but
tend to doubt that they work the exact same way. Sulfathiozole is not
an antibiotic at all and the tetracyclines are which leads me to
strongly suspect a different mechanism but I admit that I do not have
any references here to actually find out if there is a common mode of
action. Just the presence of a common mode of action does not mean
cross resistance but does increase the possibility.
>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...
I tend to doubt transfer from other organisms for a couple of
reasons. First such transfer occurs when both organisms grow together
in the same environment. This does not occur in this case as the
foulbrood bacteria grows only in honey bees while those other bacteria
grow in other animals. Second the foulbrood bacteria itself produces
one or more antibiotics which greatly reduce the growth of other
bacteria in its host and it often found in pure or nearly pure culture
in the infected larvae - a rather unusual case in nature. It seems
much more likely that beekeepers selected for this drug resistance by
their management practices i.e. exposure leads to resistance.
> 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.
Maybe we used up our time. We selected for resistance for quite a
while before it appeared and then it started to show up here there and
everywhere. Once the selection had been applied ( drug used ) for a
long enough time resistance showed up. This is really what seems to
have happened with fluvalinate and varroa mites - after 10 years of
use you have resistant mites starting to show up in more than one
location. Now a little word about this. I have been very upset with
those Apistan ads that blame misuse by beekeepers of fluvalinate on
the development of resistance by the varroa mites - it just is not
true any use selects for resistance not just misuse. After using
Apistan according to all the label instructions for 10 years with
nothing to rotate to you will have fluvalinate resistant varroa mites
showing up. Any use not just misuse leads to ( selects 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 analyzed 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.
Here I suspect there may be a major difference between beekeeping in
the US and Canada. Here south of the border there is so much exchange
of broodcomb through sale of nucs, buying and selling frames of brood,
exchange of combs between outfits, sale of used equipment, etc that
many probably most commercial migratory beekeepers here are using a
common pool of broodcombs. We have been able to do this since TM
worked so well all we had to do was be diligent in our treatments and
we did not have a disease problem. So there has been for years here a
very good reason to be careful in your antibiotic treatments and make
sure they were there in a timely fashion or you paid the price in
disease. I don't know for sure of course but suspect you are a little
more isolated north of the border and so don't have that incentive to
medicate that we do.
> 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?
Does it really matter? Fixing blame does not deal with the problem
at hand namely dealing with antibiotic resistant AFB. It might be
comforting but it is mostly a waste of time and effort when we must
deal with the problem at hand. We are seeing the end of the
usefulness of the most effective antibiotic treatment for AFB we are
likely to ever see. We need to change our management practices if we
are to survive in the current situation. Here in North America
oxytetracycline AFB will be showing up in your area sometime fairly
soon if it isn't there already and you must be ready and able to deal
with it. The good thing about AFB is that most of the spread of this
serious disease is due to movement of infected equipment by us
beekeepers therefore we can greatly reduce the spread by changing our
management practices. If we are doing it to ourselves, we can change
that ourselves.
blane
******************************************
Blane White
MN Dept of Agriculture
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