D. Murrell wrote:
> The first season on small
>cell without treatments, brings an increase in brood and in mites as the bee
>mite relationship develops. And significant colony loses are experienced
>between the first and second season. Her experience is right on track and to
>be expected.
But what is the effect of varroa invasion on hives that have been
using small cells all along, as in South Africa? In South Africa they
have always had small bees and use special small cell foundation. The
bees will not accept US sized foundation and their natural cell size
has a mean of 4.81 mm with a range of 4.37 to 5.59 for worker cells.
When varroa first arrived, they thrived in the colonies with small
cells, reaching levels of 50% or 30,000 mites in a large colony.
Hundreds of thousands of colonies died.
I have obtained a copy of "Beekeeping in South Africa" edited by M. F.
Johannsmeier (2001). In it he writes that it was hoped that "the short
post-capping period of African worker brood [would] disrupt the
reproductive biology of varroa mites" but " varroa mites are quite
capable of reproducing and increasing on worker brood of African
honeybees, the short post-capping period notwithstanding".
He says quite plainly:
"The smaller worker cells appear NOT to inhibit the mating of mites
during the post-capping period." He recommended AGAINST the use of
varroacides, however, because they will "artificially sustain the
susceptible honeybee population and prevent the development and spread
of naturally selected varroa-resistant population".
He recommended pesticide free areas where varroa resistant bees could
develop naturally, and "queens reared from these resistant colonies
can be used to re-stock other regions of the country".
* * *
According to Mike Allsop, this is exactly what happened in the
following years. He writes:
> In periods of initial exposure to the mite, the "front" of the spread of varroa, mite populations built up extremely rapidly in the honeybee colonies of South Africa, even dramatically. As many as 50 000 mites were found in commercial colonies, and average mite numbers of more than 10 000 per colony were found. This initial surge in mite population growth was accompanied by all the classic symptoms of varroa mite damage (scattered brood pattern; bees with vestigial wings; large amounts of chalkbrood; "disappearing" colonies), and it appeared that the pattern being followed was similar to that witnessed elsewhere. During this initial stage, colony decline and mortality was not unusual, and entire apiaries were lost to what was demonstrably varroa damage, to the extent that many commercial beekeepers quickly turned to varroacide treatments to protect their colonies.
> Data, from a wild Apis mellifera capensis population, illustrate the rapid development of mite tolerance, with mite numbers reduced to practically zero after not much more than three years of exposure.
> Notwithstanding the characteristics of African honeybee races that pre-adapt them to varroa tolerance, the lack of breeding and artificial selection in African honeybees is certain to be a critical factor in varroa mites not becoming a major problem in South Africa as it has almost throughout the world. Varroa tolerance requires constant selection pressure to maintain the tolerance, the selection pressure provided by free-mating and unmanaged colony survival. In contrast, a very large proportion of the commercial beekeeping industry in the USA depends on the purchase of commercially-produced queens with limited genetic variability, which are often poorly mated and infected with various pests and diseases (Camazine et al 1998).
> A similar situation exists in commercial beekeeping operations around the world. To compound it, beekeepers are forever introducing bees from across the globe in an effort to deal with local pests and diseases. All in all, the commercial bee population is generally not genetically diverse and not locally adapted. This is in complete contrast to the African honeybee population which is almost totally unselected, and probably as genetically diverse now as it was a thousand years ago. Bailey (1999) and Allsopp (1999) have argued that selective breeding for "quality" by and for beekeepers has decreased the resistance in honeybee populations to a wide range of pathogens. Highly intensive selection has decreased genetic variability and selected against critical "bee tolerance" factors such as swarming and defensiveness (Bailey 1999).
> A more sensible approach would be to: (a) Manage naturally occurring regional strains of honeybee, rather than importing strains from elsewhere. This is particularly important in Europe and Africa where Apis mellifera is indigenous and less so where it is an exotic species. (b) Practise "primitive" beekeeping as is the case in Africa by allowing natural selection processes to determine which are the most significant characteristics for selection and not the beekeepers or bee scientists, at least to some extent. It is also best to use an un-manipulated wild population, and for this population to be as large as possible.
* * *
If you got this far, the bottom line is:
* it has nothing to do with cell size and everything to do with not
treating for mites. By not treating for mites you get bees that don't
die from mites and/or mites that don't kill off colonies. IMHO this is
the most plausible explanation for the falling off of varroa
pb
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