This is a hot discussion to step into, but I'll throw in my observations:

In answer to Bob about N ceranae, there more I track progress of the
infection, compare infected colonies, and compare treatments, the less I
suspect it as a serious killer of its own right.  This observation may prove
to be in error, but that's what it looks like right now--I need to count a
lot of spores this week to publish some actual data.

It appears to me, and some others with nosema experience, that N apis may
only be an issue during times of nutritional stress, or it another pathogen
is concurrently affecting the colony (some viruses clearly are suspect).

If N ceranae is indeed a problem only with nutritionally stressed bees, that
might explain why colonies collapse from nosema in corn, alfalfa, sunflower,
or white box (Australia).  All of the above have incomplete amino acid
profiles in their pollen.

Re genetics and CCD, when some colonies survive a CCD wave through an
operation, the most reasonable hypothesis is that those colonies were
genetically resistant by some mechanism (I strongly suspect an siRNA
mechanism, which I will cover in an article soon).  Dr Ilan Sela brought the
resistance of some bees to IAPV to our attention, and Rothenbuhler, Gilliam,
the Danes, and others have detailed how it is possible to breed bees
resistant to hairless black syndrome, chalkbrood, and nosema, respectively.

If you can breed resistance to viruses and other pathogens, that is clearly
genetic.  So I'd say that genetics likely have something to do with the
problem, or at least with the solution!  I'll be writing more specifically
about this issue soon.

Randy Oliver

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