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Subject:
From:
Allen Dick <[log in to unmask]>
Reply To:
Informed Discussion of Beekeeping Issues and Bee Biology <[log in to unmask]>
Date:
Mon, 13 Dec 1999 12:48:23 -0700
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> I have been considering this for a couple of days to try to improve
> my reply.  So here goes.

Same here.  I think there is no need to rush to discuss these matters.  If I
have doubts about what I write, I let it sit a day or two, then edit or send (or
sometimes discard).  Sometimes these discussions go on over years.  from time to
time I find something in the archives when I am browsing and write a reply or a
sequel to it, even though years have passed.  In this case, couple of days in
the mountains on a snowboard have kept me occupied and cleared my mind.

(I hope others feel free to write comments or questions about things that are
not necessarily under current discussion.  New ideas, new comments and new
questions on old topics are what keeps things interesting.  Sometimes a
discussion gets hot and heavy, then dwindles off, and I wonder if latecomers
feel that the time for comment has passed.  It hasn't.  This list thrives on
good articles regardless of when the matter was last discussed).

> 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 brood comb if it is
> regular or bad AFB...

That's the point.  SAFB mimics the old variety, but there the similarity ends
for practical purposes.  I am assuming the worst and that SAFB is or becomes
totally unresponsive to oxytet in any dose that bees can tolerate and that there
is no replacement made available.

> >Okay, but where did it come from?  Does anyone really know?...

> Proof can be had if some researcher will do the DNA fingerprinting
> work but AFAIK that work has not been done yet.

It needs doing -- badly before we can proceed intelligently..

> 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.

Who is observing, what measurements are being used, and where can I find the
research?  Or this subjective?  FWIW, I have been reporting for over 15 years
that the dose recommended by North American government extension people is just
enough to prevent an immediate outbreak, but not enough to knock the disease
back to where it is unlikely to recur the moment medication stops.

I wonder if chronic undermedication is part of this resistance picture.

> When we first found resistance I figured that it was equally likely
> that it was accidentally 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.

*How*?

> 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...

Doesn't bother me a bit.  The facts -- no matter how seemingly nasty -- are our
friends.  What is really really uncomfortable -- and dangerous -- is proceeding
with incomplete information or making unsupported assumptions.

> 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.

Well, I think that we need proof, not just theories, to justify change and also
facts to determine exactly what change is in order.  We also need to know +HOW+
the resistance has arisen from within domestic AFB -- if it has.  Otherwise, we
will be acting superstitiously.

If the mutation was facilitated by exposure to other common bacteria that have
previously developed resistance, that means something completely different than
if the resistance developed in AFB in isolation.

* In the first case, the existence of other resistant bacteria in the
environment means that resistant AFB is likely to evolve *anywhere* these other
bacteria are and our current oxytet use for *any* AFB has a very limited life
expectancy.

* In the second case, it is possible, as postulated by many authorities, that
some relatively new beekeeper practices are causing the new AFB strains to arise
in an almost predictable manner, and that by *scientifically* identifying and
then desisting from these practices, oxytet's usefulness may be prolonged in
areas where the new AFB has not spread.

> 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.

Not really.  The imperative here is to understand the *real* cause of the
increasing frequent appearances of the new strain(s) and not to take the
politically easy way out.  Identifying who and what is responsible -- and why --
can help prevent and limit future episodes.  Witch hunts on the other hand are
counter-productive.

> 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.

What do you suggest as an alternative?

> 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.

Well, I really don't know for sure either.  I'm just repeating what I heard and
hoping to hear from someone who knows.  I hope *someone* does.

> 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.

Interesting.  I guess then, that we cannot culture AFB on agar or whatever?

> 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.

Sounds promising.  I can see the headlines now,"NEW ANIBIOTIC FROM SICK
HONEYBEES CURES HUMANS". <G>

> 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.

Well, the thing is that to get an AFB breakdown, a few resistant individual
spores cannot do the job; critical mass is required.  A number (30?) spores of
AFB have to be present at the right time and the right place.  The chances 30
resistant spores evolving at the same time and place is very low.  That presents
a kind of a hurdle.

I am sure that AFB has taken a run at that hurdle a countless times over the
years and fallen back.  One or two resistant specimens can't do it alone.  What
is necessary is for the number of specimens that are resistant to build to that
point before they can make a foothold.

> 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.

What is different about varroa is that it only takes a single gravid female with
resistance to start things going.  No such hurdle there.  Heritability of the
trait is the main wildcard here.  Now my math is a bit rusty, but I think the
probabilities of AFB resistance to oxytet and varroa resistance to fluvalinate
developing in a given timeframe are many orders of magnitude apart.  Relative
population numbers  may skew this and also add an interesting dimension to the
question of what is an appropriate dose and schedule for oxytet use.  Computer
models might be very interesting...

> 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...  Any use not
> just misuse leads to ( selects for ) resistance...

You're not the only one, and such bogus talk makes us tend to mistrust all those
who blame beekeepers for anything.

> 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.

And sharing a common environment.  This something that those who advocate
disinfecting frames, using foundation, abandoning medication and burning, don't
seem to be able to understand.  Without medication or something such as
resistant bees that makes it unnecessary, all of the combs in North America
would, with few exceptions need to be rendered and replaced.  Even if this were
done all at once, the reservoir of disease in the environment and the potential
for infection from discarded honey would make the effort a waste ultimately.

Moreover, if it were possible to start over, if all the comb were rendered at
once, the bees that year would be relatively pitiful and -- barring an
exceptional year weatherwise -- honey crops and pollinated crops would be very
much reduced.  It would be a disaster.

There really is no acceptable alternative to finding a replacement treatment for
oxytet or bees that are immune to ensure that the current equipment can continue
to be used until such time as bees no longer are vulnerable to the disease.

> >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.

The first step in finding a solution is finding the true cause(s).  Else, all
efforts may well be in vain.

> We are seeing the end of the
> usefulness of the most effective antibiotic treatment for AFB we are
> likely to ever see.

I beg to differ, Sulfathiozole was -- and still is -- the very best we have ever
used in all regards except the problem of residues.  Given a situation where EFB
was not a concern, sulfa was always first choice over oxytet.  FWIW, sulfa still
could safely be used in any situation where the hives are unlikely to produce
honey for human consumption or store much syrup, such as dedicated pollination
units, queen rearing hives, baby nucs, etc.  If you are right and sulfa does use
a different mechanism from oxytet, it could be part of the answer to the SAFB
problem.

> 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.

But we have no good facts, only guesses.

> 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.

I think that is a very fallacious and dangerous belief.  If it were that simple,
none of us would get colds or the flu, which are diseases that come from social
interaction.  Given a choice of health or being part of the society around us,
all of us must necessarily choose interaction.

The simple fact is that if most of us in North America do not interact with
other bees and beekeepers, our bees will do it for us.  We are all vulnerable to
what our neighbour does and we do not live in a fascist system.  Any solution
must take that into account, as well as the economic realities that face us.

allen
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