>  One problem I now have with studies coming from the western US is, supposedly, AHB was released there earlier
>  than when it arrived naturally so any feral bees there are suspect. We know that AHB is compatible with Varroa
>  and is on small cell.

Interestingly, the AHB, was derived from A. m. scutellata, the
Savannah bee.  In South Africa, where it is native, it wasn't
originally mite tolerant.  It took 6-7 years of varroa pressure to
evolve such tolerance.

Similarly, in South America, the AHB performed well against the
nonvirulent Japan haplotype of mite, but collapsed as the Korean
haplotype (which we have in the US) replaced the Japan mite.  However,
the AHB again evolved tolerance.

Data from Peru suggest that African genes would be currently working
their way into the North American EHB genome, and that we will not see
any morphological change.

The AHB is a warm-climate bee, and therefore (likely due to
thermodynamics) a smaller bee.  Thus it will likely have a smaller
cell.  Allsopp's thesis (posted earlier by Peter Borst) does not
support the hypothesis of small cell being the prime factor in AHB
resistance to varroa.

I am not in the small cell nor large cell "camp."  I'm a data guy.
I've seen Dee's bees, and they appear to be very healthy, and free of
mites.  Whether Dee's explanation as to why that is is true, I don't
know.

There is a notable paucity of good controlled trials, and that is why
I undertook the HSC trial.  However, that trial was not a small cell
trial per se--it was a trial of HSC, which just happens to also be a
small cell size.  As I note in my discussion, the apparent effect
against the mite could have been due to other factors inherent in the
plastic HSC frames.

Now, for an update:
Yesterday, I went to the almonds to check the colonies.  Nearly all
the HSC colonies had collapsed.  There was not typical PMS
symptoms--the brood looked healthy, and no sign of DWV.  The one
sample that I tested had about a 15% mite infestation.  Brood that I
sampled had some mites, but they were not overwhelming.  There were no
nosema spores.

In addition, the two treatments (HSC and controls) had been in a
relatively isolated apiary, and cold, wet weather would have prevented
significant robbing from any collapsing colonies.  So I doubt that the
HSC colonies went down due to a "domino effect."

There certainly appear to be serious virus issues in some operations
in the West.  Colonies are collapsing without high mite levels, nor
the other usual suspects (including pesticides).  My guess, currently
unsubstantiated by data, is that the relatively high mite level in all
the colonies in the trial (remember, no colonies received any mite
treatments) allowed the virus(es) to get the upper hand.  I will be
sending in samples for confirmation.

Based upon my experience in other yards, a single fall treatment would
likely have saved at least the HSC colonies.  The bottom line is that
the HSC colonies appeared to significantly decrease mite buildup (by
whatever means), but that due to unforseen factors (perhaps viral),
the colonies collapsed in February, during cold, rainy weather (cold
appears to be a common factor with the collapses we're seeing).

Randy Oliver

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