As is usual, there is plenty of off List discussion on this topic. I
thought that i'd share with the List an elaboration of one such discussion.
The topic was why our bees appear to have quickly evolved resistance to
tracheal mite, but not to varroa.
Clearly, preadaptation for resistance to Tmite existed, but I don't know if
I can agree with the hypothesis that such preadaptation had anything to do
with prior exposure to Tmite. A population may contain traits that can be
co-opted to use against a novel parasite, despite that trait originally
having nothing to do with that parasite.
The above is a huge point, and Pete's recent post on the value of
behavioral changes is spot on.
The evolution of resistance to a novel parasite depends upon (1) the
available "tools" or behaviors for such resistance, or those that occur due
to mutation or hybridization, and (2) the degree of selection (the cost of *not
*having resistance, or the benefit of *exhibiting *resistance).
The above is complicated by the downside of some traits for resistance
(again, such as sickle cell anemia vs resistance to malaria). Realize that
evolution is all about random chance and simple math. The math is the
degree to which traits get passed to the next generation (if there is one;
sometimes a novel parasite simply extirpates a host).
So let's look at some previous invasions of parasites into the U.S. bee
population, as well as preadaptations and selective pressure.
When wax moth arrived, our bees apparently did not recognize it as an
invader, and it ran rampant through healthy colonies. But honey bees were
preadapted to bite and remove foreign invaders if they recognized them.
And they were preadapted to recognize invaders by odor. What much of the
bee population apparently lacked was a link between antennal sensors for
the cuticular hydrocarbon profile of wax moth larvae and the behavioral
response that such a cue indicated an invader.
Selective pressure was apparently high, judging from the reports of losses
due to wax moth (as opposed to such reports today, which are generally the
result of wax moth simply acting as a scavenger after a colony has weakened
due to other causes). Since the bee population already contained
predaptations for invader removal, all that evolution needed to select for
was for bees that linked the odor of wax moth larvae with a preexisting
behavior to remove them. And after a number of years, wax moth no longer
killed colonies--evolution happened rapidly in this case, without
particular help from beekeepers.
As I said tongue in cheek on this list some years ago when someone asked
whether any breeders were selecting for resistance to CCD, "As far as I
know, no breeder propagates stock from dead hives."
The invasion of SHB was similar--from my meager observations in Hawaii
(please email me with additional observations), naive bees ignored SHB--the
beetle could walk throughout the hive unmolested, and beetle eggs were not
necessarily removed. Within a few years, however, the surviving colonies
readily recognized the beetles and chased them. In this case again, bees
were generically preadapted; the only selective process necessary was to
eliminate those colonies that didn't recognize SHB as an invader.
Remember, that nature does not reward, it only penalizes. The penalty is
lack of ability to compete in the race to pass one's genes (and epigenes)
to the next generation. The ultimate penalty is death, whether to an
individual, a matriline, a race, or an entire species. History is written
by the winners--those who were able to pass their particular genetic
combinations to the next generation.
In the case of the invasion of chalkbrood fungus, things were different.
Bees didn't necessarily "recognize" the invader. I don't know all the
current resistance mechanisms employed, but one is to simply elevate the
temperature of the brood. Our bees were preadapted to regulate brood
temperature, so all that was necessary for resistance was for a link to be
established between the odor of chalkbrood and the behavior to raise the
brood temperature slightly. So resistance came fairly easily.
In the case of tracheal mite, selective pressure was strong. We lost about
70% of colonies in Calif. I again do not know all resistance mechanisms,
but a very simple one was to have a slightly different arrangement of the
setae (hairs) around the thoracic spiracles (breathing opening). There was
apparently preexisting variation that included such arrangement of the
setae. So the combination of strong selective pressure (leading to death
of the colony over winter), coupled with serendipitous preadaptation, led
to rapid evolution of resistance.
Note, that studies by Dr Jose Villa found Tmite to still be widespread in
the U.S. bee population as recently as 2008, with a large variability in
resistance between breeders, and even within a particular breeder's stock.
Apparently, there is not enough selective pressure to reduce the incidence
of Tmite to lower levels.
In the case of varroa, one should read Allsopp's analysis of what happened
in two different races of A. mellifera (scutellata and capensis) when
varroa invaded South Africa. The African races again serendipitously
possessed traits for resistance (as do our European stocks). Beekeepers in
that country did not intervene with miticides, and the bee populations came
to term with varroa in only a few generations.
This is apparently the key difference between the long-term agony that
American and European beekeepers are experiencing with varroa, compared to
its minimal impact in Africa.
Our bee population clearly possesses traits for varroa resistance, but most
breeders aren't selecting for them for a very simple reason--there is
little demand from consumers. So long as varroa can be cheaply and
relatively easily managed with miticides, why would there be a demand?
Especially if any varroa resistant lines had any negative attributes, such
as a trade off for lesser honey production or lack of manageability (in my
experience, such trade offs are not necessary).
Currently, U.S. beekeepers are losing about 30% of colonies each winter,
but only a fraction of those to varroa. And the better beekeepers lose
only a few percent at most to varroa most years. So there is little
selective pressure for our stocks to develop resistance. And there likely
won't be much selective pressure, nor demand from the consumer (those who
purchase queens), so long as we have effective miticides at our disposal.
On the other hand, the feral population does not have the benefit of
miticides, and was devastated by varroa. Dr Rob Page suggested that close
to 100% of the formerly abundant California feral population was lost to
varroa (honey bees only existed in California for less than 150 years prior
to varroa).
There is an additional problem for the development of resistance by the
U.S. ferals--the "domino effect." When one colony collapses from
varroa/virus, if there are other colonies within flight range, then
drifting and robbing can quickly overload the colonies that were previously
keeping varroa in check with a massive invasion of mites. The result is
that the normal evolutionary process is stymied.
It's all about host density. Without human intervention, the feral
population would be reduced to a low enough host density, that resistance
would have a chance to evolve. But we humans simply keep replacing fallen
colonies with new non-resistant colonies.
This is why "treatment free" beekeeping in Marin County wasn't working--the
number of surviving potentially resistant colonies was outnumbered by the
number of package colonies of domestic stock each spring. And as those
package colonies later collapsed, they'd flood the area with mites,
knocking off any partially-resistant ferals. (For several years now, I
I've been assisting Bonnie and Gary Bollinger in establishing a breeding
program in Marin to propagate local resistant stock, with what appears to
be some degree of success).
Back to the U.S. bee population in general, despite decimation of the feral
populations, not all were lost. Mitotyping confirms that many unbroken
matrilines have managed to survive through the invasions of all these novel
parasites. Those matrilines do not exist in the managed population (that
sold by queen producers), so constitute strong evidence that independent
feral populations exist sympatrically (living in the same geographical
area) with managed bee populations (as did distnct feral populations prior
to varroa).
The point is that those ferals (of many different matrilines) did not
disappear. They survived varroa and everything else. And they appear to
be slowly rebounding, despite the continual immigration of varroa from
nearby managed hives. So despite our worst efforts, evolution appears to
be ignoring us, and ticking along quite nicely.
At the time of the initial varroa invasion, had we not treated our hives,
two things would likely have happened: (1) the bee population would have
rapidly evolved resistance to varroa and its associated viruses, and (2)
nearly all beekeepers would have gone out of business. The latter was
unacceptable to most, so this didn't occur.
Another important note: as far as I'm aware, the only place on Earth that
honey bees have gone extinct due to varroa is on Santa Cruz Island (which
hosted an inbred population of only about 60 colonies). Thus, the
preponderance of evidence is that if humans don't meddle, bees are able to
fairly rapidly evolve resistance to varroa.
The above observations appear to me to put the lie to the claims that
there is no true feral population in the U.S. or that bees can't fairly
rapidly evolve resistance to varroa via natural selection. But the fact
remains that widespread development of resistant domestic stocks is
unlikely to occur until there is consumer demand to drive it, which is
unlikely to happen so long as chemical control of the mite is cheap and
effective.
In the interim, I'm personally trying to slowly wean my bees off of
chemical support. I ceased using synthetic miticides in the year 2000,
finding that I could adequately manage varroa via selective breeding,
biotechnical methods, and treatment when necessary with thymol and the
organic acids. I dream of the day when I can finally eliminate the
treatments. But it hasn't happened yet, likely due to a combination of my
selective breeding program not being rigorous enough, nor isolated enough
genetically.
But I'm not giving up, and I strongly encourage and support beekeepers
large and small to propagate any bee stocks that exhibit resistance to
varroa and viruses, yet maintain productivity and workability. Remember,
you can vote with your wallet--every time you purchase a queen or package
from a breeder who is not actively selecting for varroa resistance, you are
fighting the natural course of evolution (this is not a sales pitch--please
don't ask me for queens).
An exciting development is that a large California breeder (with isolated
breeding yards) is currently in discussion with me about seriously going in
this direction (a lot of us are simply getting tired of fighting varroa
each year). Cross your fingers!
--
Randy Oliver
Grass Valley, CA
www.ScientificBeekeeping.com
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