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 *********************************************** The BEE-L mailing list is powered by L-Soft's renowned LISTSERV(R) list management software. For more information, go to: http://www.lsoft.com/LISTSERV-powered.html