Caucasian bees are notorious for propolis production. The trait is likely an additive one, and can be relatively promoted and repressed in mixed stocks.
Caucasian bees are notorious for propolis production. The trait is likely an additive one, and can be relatively promoted and repressed in mixed stocks.
Let's go back and look at exactly what I said was the only way for IT to happen.
Well, I'm sorry I put ellipsis in your quote. I do not see how I miscast your position however. You are claiming "bees will figure out the traits they need" (which I assume you mean they will breed a new genotype) and your sole mechanism is Bond Testing.
I am trying to add some nuance and depth to your rather primitive understanding of population genetics.
Please read this article, THREE AMERICAN TRAGEDIES: CHESTNUT BLIGHT, BUTTERNUT
CANKER, AND DUTCH ELM DISEASE
for perspective on a wide-scale multi-generational "bond testing" in the face of exotic disease and insects.
Look, Solomon, I don't mind if you keep your hives underwater or at the top of pine trees, with pixie dust, or in solid silver frames. I am trying to add some glimmer of understanding about genetics, so your response to any question doesn't involve your constant chest-thumping about your "system". That's probably intemperate of me, but I also have a depth of experience you would find useful to learn from. I seen young bucks with all the answers before.
Chesnut, let me start out by admitting that I have only read the abstract due to time constraints.
But let me state the following as it relates to honeybees. As mentioned in some study quoted in another thread earlier, honeybees are uniquely capable of adaptation against their parasite. Typically it is the parasite that has the advantage, but not so with the honeybee. The honeybee has demonstrated itself capable of adapting to this parasite in a relatively short period of time. It is up to us now to align our methods thereto to benefit all parties involved. So totally unlike all the "you wouldn't let your children or your favorite dog die" comparisons, honeybees need to be evaluated on their own merits.
Let me also clarify that there is no specific genotype involved. This comes from the idea (prevalent in VSH discussions) that there is some purebred bee, some exact combination, some alignment of genes which allows certain hives to survive without treatment, therefore the Bond Test which kills all unfit colonies is responsible for destruction of traits, whole matrilineal lines, and inbreeding. This is demonstrably not the case. It is simply a matter of the balance of a population having a favorable mixture of traits which allows them to survive. As we've seen, these bees are of any race, of many mixtures of traits, and of widely varying rates of specific traits like VSH. It is a favorable mixture of traits, reordering of priorities in the process of finding a balance with the parasite.
Your mechanism is a testable hypothesis.
I understand you saying that fitness is selected for a the whole-apiary level. An apiary of some optimum size would have higher relative variation, and the variation would translate into individual colonies with enhanced variation due to wild out-crossing. Colonies with higher variation (more diverse fathers represented) would have better performance.
A hypothesis test would collect mitoDNA (female lineage) and compare survival (or honey production or disease risk) amongst apiaries with different levels of variation. MitoDNA primers and characterization has become quasi-automatic and inexpensive. Your hypothesis could be tested.
You are describing the process of reversion to mean which is, of course, the central core of the position I am trying to communicate.
I am describing a model that fits the observations. Most I hear do not. I can only speak from my experience.
Error in post.
Last edited by julysun; 08-16-2013 at 08:02 PM.
Julysun elevation 23 feet. 4 Hives, 2 years.
I'm puzzling over a couple of questions.
I'm not good at putting thoughts on paper and I don't have the skills to say things in a scholarly way so please excuse the basic language.
A hive is made of one queen (I know there's more than one queen in a hive alot of times but for the sake of this question it's irrelevant) with offspring from many different drones. I'm wondering how it can work that a hive can survive treatment free with so many different paternal lines of bees in the hive is it luck of the draw that all or most the drones the queen has mated with are mite tolerant or is it enough that only the queen shows those traits?
Another thought is how can a colony adjust/adapt to mites when the individual bees themselves live for such a short period.
And lastly is it feasable that you could keep your bees without treatments up until they started to show symptoms of mite problems and then treat and repeat meaning you leave your bees to deal with mites until they are over run but rather than letting them be over run and die you stop the mite the bees recover and as the mites build up again the bees are left to deal with them etc etc thereby giving the bees longterm exposure to mites but maybe building up some sort of defence against them.
A bit like a flu vaccine
Without covering a lot of the ground that has been spoken about, I would say... Why would you go through the time and expense of treatments on a genetic line that needs improvement?
People who are seriously breeding bees with the intention of developing mite resistance have isolated mating yards. They introduce the drone stock they need. It is not enough that only the queens display this behavior, their daughters can have any variability of that. However, a drone will posses ONLY the genetics of the queen mother has, and is actually a more direct conduit of resistance. I should also add that if you happen to live somewhere that there is a population of feral bees, those drones show much higher competition over managed colony drones.
In your hypothetical hive, if it is a critical mite load on non-treatment, VSH - you are looking at your 2nd or probably 3rd year before collapse. So, you have probably already made splits from this hive, maybe multiple times. Or if you are judicious breeder, you are only making nucs/grafting out of 3rd year plus queens anyway. You are either going to re-queen this hive with a brood break (or I am sure others will have something else to say), or cull it at the end of the year. Extract all the honey and use the equipment for the next nuc. So in my book, that's not a loss...
You can't help the individual bees in a hive build resistance through medicating. Or any bees, anywhere. I also, don't get a flu vaccine
It's taken me a while to figure it out, but the cause of a lot of these arguments / disagreements or whatever you want to call them, is simply because peoples experience has been different, but they then think that their experience should apply to everyone else. But it doesn't. So Bernhard for example (Germany), said his untreated bees typically lasted 4 years. But bees would never last that long here, yet at the other extreme there are people saying he must have missed something because 4 years is not long enough.
In the US there has been mites for a long time, and treatments started to become ineffective a long time ago also, so losses were big, 30% annual average or so. Coincide all this with the arrival of African genetics, and you have the recipe for whittling away at less resistant bees, whether in a commercial setting or otherwise, and the slow incorporation from African bees of mite resistant traits.
So Mike Bispham, is yet another example. No African genetics in his country via the same heritage as the US ones, but there are some selected African genetics, via Brother Adam, and possibly other sources. But they may be different to the US ones. So Mike Bisphams chances of success will be less than an average US hobbyist, as you guys have proven mite resistant bees, and the ones that have been properly DNA tested show Africanised genes. Mike does not have that. But he has some chance of success, because there are some African genetics in his country, although of unproven worth against mites. But his chances of success, while less than yours, would be greater then mine here, with no African genetics.
So I believe this is what is being lost, the importance of location. Everybody is telling everybody else what they should be doing and what should be happening, based on their own experience, in their own location, with their own bees. Forgetting the situation elsewhere can be, and is, totally different. In addition to people talking from just their own experience, is people talking from no experience at all.
Once these factors are understood, I believe 90% of the destructive argument that has occurred on this topic over the years, can be eradicated.
Very good point and very well said.
Also, I am not sure about the African genetics being the reason for mite resistance in the US. Varroa arrived long before Africanized bees migrated into the US from South America. I always assumed resistance in the US was much the same as the Pimorsky bees, which probably did not have any African genetic influence either, and were able to somehow survive.
Thanks Heaflaw, I take your point, it can never be proved there are NO feral survivors. What I can say, is despite time, money, and the resources of a government funded project to find "feral survivors", none have been found or documented. Had 5% of our ferals survived, we would have them everywhere. I have in the past, had a number of people on Beesource argue vehemently with me about this, saying it's wrong, there must be feral survivors. That, again, is them applying their experience, to a different place.
I too, have read that in the US around 5% of ferals survived the initial varroa onslaught. I've also read that they didn't. Seems like it is an open question.
Re the African genetics thing, it is just a theory I am putting up, although there is good evidence that is consistent with it. But first re the primorsky bees, you are quite right they have some mite resist mechanisms, I am not saying it is completely impossible for other bee strains to achieve resistance in fact I very much hope that it is possible, even for Italians. Primorsky's did it without human help so as a result some of their mechanisms, such as say, excessive swarming, need work, from a standpoint of their usefulness to humans.
But back to Africans, the arguably two best known commercial treatment free US beekeepers would be Beeweaver, and Dee Lusby. Bees from both of those have tested positive for African genetics. There are other treatment free commercial beekeepers, it would be interesting to DNA test their bees. It has been documented around the world, that where there are African or Africanised bees, once varroa arrive there is an initial die off but the bees quickly adapt, so fast, they are generally regarded as resistant.
Varroa did arrive in the US before African bees, but not much. For example for Beeweaver, both arrived at the same time. Which MIGHT have been a fortunate coincidence for them.
The bees we have in New Zealand are a much more limited range genetically than what you have in the US. Bees have not been imported for many years because we don't want the diseases that other countries have. The first bees here were AMM's from England, and they persisted and made up most of the approx. 4 million feral hives, until varroa arrived and exterminated them, you don't see an AMM now. The other breed was Italian, recognised internationally as a poor performer against varroa, and in the last few years some carniolan semen was imported. It has been noticed here that the carniolans tend to do better against varroa than Italians, but none are fully resistant.
There are several - perhaps many - behaviours that confer a measure of resistance. Its likely that the behaviour that was referred to above was uncapping, but any combination of useful behaviours within a colony will contribute toward an overal ability to manage mites successfully.
Of any gene combination confering a specific behaviour: If the queen has two copies and any drone (sperm - which I think has two copies of the same gene throughout) the same, there will be a 100% certainty of the gene coming down. If the queen has one copy, and the drone 2, a 75% chance. If the queen has none... and so on. I'm not clear about this stuff, because it isn't important to my approach - but there is info here if you want to get stuck in: http://www.glenn-apiaries.com/genetics.html
If you want learn about genetic transmission of heritable traits a short history of the work of the chap who uncovered it all is probably a good place to start: http://anthro.palomar.edu/mendel/mendel_1.htm
It isn't relevant in part because the qualities of the queen you get will depend on so many things that all you can really do is press the right sort of drones toward her mother as best you can, and take her mother from a thriving hive - and that's the best you can do. Yes, luck of the draw is very much how it all works, but you can seriously load the cards in your favour.
 Some people postulate an 'epigenetic effect' which seems quite scientifically reasonable. Some people will insist quite vigoursly that it happens on the basis of their own experience. But to my knowledge there is no published scientific work showing this happening in the case of mite resistance in honeybees. So it is a theory without scientific demonstration.
Last edited by mike bispham; 08-17-2013 at 02:54 AM.
If you search for 'mite resistance' and 'patrilines' you'll probably be able to turn something up fairly quickly. I expect you can evaluate the relevance and trustworthyness of the sources yourself.
Already searched. Nothing to back your claim.
Since you said you have committed them to memory I thought it would not be a hard thing for you so I asked.
These references would mean you could be taken seriously.
(We are talking in rounded out terms here - leaving out all the complications about patrilines and different sorts of resistance, and co-evolution of mites... - but that's fine for our purposes)
When exposure to varroa occurs, that 95% will die. The popluation will rebuild from the survivors, preserving in each generation the genes that confer the necessary behaviours. (This is thought to take between 10 and 20 years in nature). Now the population may be 80, or 90 or 95% resistant.
European bees now have some 25 years of exposure, and there are increasing reports of thriving feral honeybees. I know - solidly - of some myself. US bees have shorter exposure, but again there are increasing reports of feral resistance. In the US humal selection by small beekeepers and research bodies and some breeders has also helped. But in both countries massive producton of treatment-addicted queens has prevented, and continues to prevent, fuller adaptation.
As far as I'm aware (I know nothing) NZ bees have a shorter exposure to varroa, and few or no efforts have been made toward allowing or facilitating adaptation. If that's so, yes, you will be starting with a harder task than people working with US or European bees.
Note: It isn't the race that is resistant - people talk about Russians being resistant - its just that the population source of that race has had some exposure, and levels of resistance are accordingly high.
In case anyone is interested, one of the most powerful knowledge seeking tools in history was invented in the 5th C. BC, in Ancient Greece. It goes by the name 'Socratic dialogue'. Its nothing more than the process of earnest question and response undertaken by honest truth-seeking 'interlocutors' (participants). Its the foundation of all modern scientific enquiry, and most of our day to day exchanges. I highly recommend it. (BTW the idea of universal, eternal _principles_ was also invented at about the same time)
With regards to your former request that I do a search put context on your claim that "only a few mite resistant patrilines are needed to make a hive mite resistant", I did actually get a result, it was this, but hardly authoritative.