>
> >The explanation of this is that nosema is further advanced in the healthy
> colonies because they live longer, giving nosema a longer time to develop.
> As I have oft noted, ferreting out cause and effect is difficult, but not
> impossible. I think they are elucidating the concept that high levels of
> particular microorganisms should not be taken as an indicator of declining
> health and could be the exact opposite. Healthy colonies tolerate these
> levels better than colonies that are weakened by some other factor.


Pete, you hit the nail on the head!

I have been in correspondence with the authors since their previous paper,
pointing out that exact fact.

An inherent problem with their analyses (both studies) is that they only
analyzed either live bees from the broodnest, or dead bees caught in
entrance traps.  What they DIDN'T analyze were the majority of sick bees
that flew off via the normal process of altruistic self removal.

Of the 14,500 young bees that were marked, the researcher apparently only
recovered a few hundred (he is loathe to give me an exact figure).  It is
well known that when bees are individually sick from either viruses or
nosema that they fly out of the colony to die--this is a typical sign of
either virus- or nosema-caused colony collapse.

The problem with analysis of the surviving bees in the hive is that you
miss the sick ones!  This is why the cause of CCD is so difficult to
determine if you only study the handful of remaining bees.

Look at it this way:  The "symptom" of acute virus or nosema infection is
for a bee to disappear from the hive.  The symptom of smallpox in humans is
pox marks on the skin.

So let's imagine that we are studying two populations, one of bees, one of
humans, both with raging epidemics of those respective pathogens.

However, since any bees mortally sick from virus or nosema would be
"disappeared," then we could only study those without the typical symptom.

If we studied the human population that was suffering from a smallpox
epidemic in the same manner, then we would have to also omit any with the
typical symptom--meaning that we could not analyze any humans with pox
marks.

Obviously, in the human case, we would then likely have a hard time making
any correlation between mortality and smallpox.

So although the cited study is a great data set, and the varroa and DWV
data are of great use, I must question the ABPV and nosema conclusions.  I
have copied the authors, should they wish to respond.

-- 
Randy Oliver
Grass Valley, CA
www.ScientificBeekeeping.com

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