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Coevolution of Honey Bees and Varroa Mites: A New Paper

74K views 225 replies 24 participants last post by  souficoufi 
#1 ·
Here's a beautiful new paper. Look at this statement:

"Coevolution by natural selection in this system has been hindered for European honey bee hosts since apicultural practices remove the mite and consequently the selective pressures required for such a process."

More sound backing for the understanding: treatments ('apicultural practices') prevent the rise of resistance which otherwise occurs rapidly.

Mike

Host adaptations reduce the reproductive success of Varroa
destructor in two distinct European honey bee populations
Barbara Locke, Yves Le Conte, Didier Crauser & Ingemar Fries

Ecology and Evolution 2012; 2(6):
1144–1150
http://onlinelibrary.wiley.com/doi/10.1002/ece3.248/pdf

Abstract
Honey bee societies (Apis mellifera), the ectoparasitic mite Varroa destructor, and honey bee viruses that are vectored by the mite, form a complex system of host–parasite interactions. Coevolution by natural selection in this system has been hindered for European honey bee hosts since apicultural practices remove the mite and consequently the selective pressures required for such a process. An increasing mite population means increasing transmission opportunities for viruses that can quickly develop into severe infections, killing a bee colony. Remarkably, a few subpopulations in Europe have survived mite infestation for extended periods of
over 10 years without management by beekeepers and offer the possibility to study their natural host–parasite coevolution. Our study shows that two of these "natural" honey bee populations, in Avignon, France and Gotland, Sweden, have in fact evolved resistant traits that reduce the fitness of the mite (measured as the reproductive success), thereby reducing the parasitic load within the colony to evade the development of overt viral infections. Mite reproductive success was reduced by about 30% in both populations. Detailed examinations of mite reproductive parameters suggest these geographically and genetically distinct populations favor different mechanisms of resistance, even though they have experienced similar selection pressures of mite infestation. Compared to unrelated control colonies in the same location, mites in the Avignon population had high levels of infertility while in Gotland there was a higher proportions of mites that delayed initiation of egg-laying. Possible explanations for the observed rapid coevolution are discussed.
 
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#151 · (Edited)
Adam:

Here is a quote from a poster board presentation by Wayne Hunter et al.:

"Traditional PCR along with gel electrophoresis for each of these bee viruses showed that DWV and KBV have integrated into a segment of the A. mellifera genome."

http://flaentsoc.org/09festufts_hunter_integrate.pdf

Let me explain that the whole field of research involving retrotransposition into the Honeybee genome went 'dark' around this time.

I have found active retrotransposon activity in the R2 region of the 28s rDNA of A. mellifera however.

It's going to take some time for this field to open up again though.
 
#154 · (Edited)
...
"Traditional PCR along with gel electrophoresis for each of these bee viruses showed that DWV and KBV have integrated into a segment of the A. mellifera genome."...Let me explain that the whole field of research involving retrotransposition into the Honeybee genome went 'dark' around this time...
So they realized the honeybee is naturally transgenic, so it seems likley that it wouldn't be too hard to make artificial genetic modifications which would make bees that are immune to certain viruses. Which is where Beeologics became very interested. You could make "namebrand" bees.

You go on to say "I have found active retrotransposon activity in the R2 region of the 28s rDNA of A. mellifera however." I have no idea what this means.

It's like you're sharing and not sharing at the same time. I'm glad to have what you offer, but one can easily get the sense - and perhaps it is your intention to communicate - that you have much more information than you're actually sharing.

It's a bit frustrating, but as i say, I'm thankful for what what you do contribute.

Adam
 
#155 ·
Adam:

It simply means that there's an active jumping gene in our Honeybees.

It's also very well characterized in other insects.

I think that it's always better to look for jumping genes in a place (the R2 site) that has a great deal of research behind it.

I also think that Beeologics blundered badly when it tried to market their technology to beekeepers.

It's a mistake that shouldn't be repeated.

But, it's a viable 'natural' option for treatment-free beekeepers.

Those genes jump during splitting, etc. .
 
#159 · (Edited)
WLC says: "It's a modern genetics interpretation of how resistance can occur 'instantly' in Honeybees. You heard it from me first."

Adam says: Holy crap. And would that 30% translate roughly to the general population?

You say "during reproduction" with bees, that can be a variety of places. If I split an infected colony, and introduce a queen, does this kill the process? Do I have to let the split produce its own queen to get the potential benefit? I'm having trouble locating where the 'jump occurs' and how I work to assist it as a beekeeper.

You say "split into an infected colony" - what does "split into" mean? I can split, but then there is a portion with a queen and one without. The one without has to raise a new one using eggs from the old one, and then gets the genetic input from a random drone. OR I can introduce a mated queen from another source. Where does the jumping gene come into play? Is it simply the pressure that causes it to jump?

And consider this article "Published honey bee genome shows paucity of “jumping genes” "

A couple of quotes:

"Compared to other sequenced insect genomes, the sequence also clearly reveals that the honey bee genome has evolved more slowly and lacks major transposon or “jumping gene” families... "The honey bee genome is unusual in the sense that it appears to have very few transposons or retrotransposons in the assembled sequence, almost all of which are members of one family known as the mariner family.”... Transposons and retrotransposons in the honey bee constitute only about 1% of the assembled genome... it is unclear what the significance of this low incidence of mobile genetic elements in the honey bee genome may mean. It may reflect some evolutionary pressure to prevent detrimental damage to the organism’s genetic make-up over many generations."

This seems to suggest that the honeybee has far fewer "jumping genes" than a lot of other organisms.
 
#160 · (Edited)
Hi JB (Does that work?)

I obviously can't respond to a post of that length on a point by point basis, so I've just selected parts that might allow me to address some of the most important issues.

[Previously]

jbeshearse: In reality, treatments are an effective way to insure overall populations do not severely decline before the species rebounds on it's own.

Mike Bispham: There is absolutely no evidence that this is the case, and it flies in the face of fundamental evolutionary biology. It directly contradicts the clear statements, made by the authors. Bees have a natural defence mechanism - shared by all living things: die-back to resistant strains: rebuild from resistant strains. This process carries no cost in terms of diversity. Treatments frustrate that process entirely, and on an ongoing basis. Treating corrodes diversity by preventing the re-emergence of feral bees around apiaries.

jbeshearse (reply): What clear statements are you referring to? Please elaborate. Also tell me how this “flies in the face of fundamental biology.


I will elaborate. I'm going over familiar aground again, but I'm doing so to try to make a couple of points as clearly as I can. The first is about the nature and forcefulness of the principle of natural selection. The second is about the way that principle unifies many different explanations.

Here is the clear statement from the abstract:

"Coevolution by natural selection in this system has been hindered for European honey bee hosts since apicultural practices remove the mite and consequently the selective pressures required for such a process."

To those familiar with evolutionary biology or breeding sciences that statement needs no elaboration. Its a straightforward consequence of the general principle of natural selection for the fittests strains.

This is very very simple, but a clear understanding is essential!

Nature tends to breed more from the stongest individuals than from the weak. Since qualities are inherited, this passes more of the better qualities to the next generation than the less-good qualities.

There are many different mechanisms that press toward this outcome, perhaps the most obvious being that the weakest (most unfit) die before they are able to mate. The strongest reproduce the most, the weakest reproduce not at all, the middling ones reproduce in middling numbers.

Another powerful mechanism; the strongest males tend to win mating competitons. Again this contributes to each new generation tending to be made from genes supplied by the strongest parents. In these and other ways, generation after generation, weakness and vulnerabilities are winnowed out, on an ongoing basis.

Can you see how neat that is? If not, read it again, and think about it some more. When you feel some kind of shock at the sheer elegance of what goes on, a billion times a day, always, and how that is able to maintain life itself, please, hold on to that and don't let go! Come back to it whenever you feel wobbly! That is the underlying, fundamental principle of the organic sciences! Nothing less. You cannot argue with it, or twist it. It is simply a (rough) description of a fundamental reality.

In animal husbandry this process is copied. Now, instead of natural selection, artificial selection is used. The husbandryman chooses those parents that s/he thinks will make the best offspring, and uses those, and only those, as breeding pairs. ('Pairs' is misleading since often one male will sire many females - but they're all 'pairs')

The art of raising good breeding pairs is fundamental to the success or failure of the husbandry. Allowing weakly, slow-growing, or disease-prone stock to enter the breeding pool carries the probablity that those weakness will be reproduced in the offspring. And so any animal showing any deficiency is quickly removed as a contender for future breeding stock. Only the very best are allowed through.

Do you see how nature has been copied? How animal husbandry and natural selection are using the very same means to maintain health and vitality, and quickly take out weakness?

This is the golden rule of husbandry. Both nature and husbandry work with the fact that traits are heritable, that mother and father pass down parts of their make-up to their children. It isn't precise nor predictable in individual cases - but as things average out, it works.

Now lets marry to the above the following:

"Breeding is by no means a human invention. Nature, which in millions of years
has bought forth this immense diversity of wonderfully adapted creatures, is the
greatest breeder. It is from her that the present day breeder learnt how it must
be done, excessive production and then ruthless selection, permitting only the
most suitable to survive and eliminating the inferior." Friedrich Ruttner,
Breeding Techniques and Selection for Breeding of the Honeybee, pg 45

Now: Can you see how what Ruttner, one of the all-time great bee breeders, says is in complete agreement with my outline? Can you point to any strains or contradictions between what I've said and what he's saying?

I've sketched the evolutionary biology that underpins the statement made by the authors, and outlined the most basic animal-raising principle, and shown how Ruttner works from the same understanding. And there is complete concordance between them all. Complete agreement between scientists, animal husbandry principles, beekeeper. That concordance is that all are united by an understanding of this most basic principle of organic life - Natural Selection for the Fittest Strains.

There is complete concordance too between this web of interrelated understanding and the medieval dictum 'Put Best to Best.'

Can you see this? Can you see: this is the music of animal science, the tune that life dances to?

Stay with this. This is Golden.

Now: This process is - essential - to the maintainance of health. There is, we've heard, a sort of constant 'arms race' between every host and their many predators. The predators are constantly seeking to gain more food (for that's what its all about - everything needs food to live at all), the hosts must equally constantly seek to prevent that. The two populations therefore are locked in a sort of race, each seeking the upper hand. Constantly. And each uses the same tool, adaptation, evolution by natural selection.

And so... if you stop evolution in the host, you allow the predator to gain an advantage. In each generation.

Selection, by nature or by husbandryman, is then essential to prevent the predators gaining advantage.

Selection, by nature or husbandryman, is what allows - or creates - the necessary adaptation

So (last part): by logic: what happens when we prevent - or seriously inhibit - adaptation in the host by frustrating selection?

Something - anything - is essential. We remove it. What happens?

What does treatment do? It removes the natural selection that would otherwise occur. What happens when we stop the selection processes?

I can't do more than this. You have to be able to understand the dance, to hear the music, apply the understanding with simple logic. Then it all makes perfect sense, and you breath a sigh of relief, and sit in wonder at the magnificent elegance of nature's wonderful basic health-maintenance mechanism.

And the questions you ask me answer themselves, easily and naturally.

I've said far too much: the thing is beautifully simple and elegant. And what you have to do, as a husbandryman, is obey the dictum. Put Best to Best. Only.

Is that so hard?

If you keep looking until that is all properly clear and firm, you will be able to see that your next statement simply is not in accordance with the web of understanding that flows from the simple fact of inherited traits. I'll show you why:

jbeshearse (reply): We are not treating the bees for varroa, we are poisoning varroa and to a degree bees. This in no way removes the effects of fundamental evolutionary biology. Frustrate it yes, prevent it, no. As humans we interfere in the process, but we cannot overcome it. A die off is the last line of defense. Fundamental evolution demands that defenses that do not result in death will be favored over those that do result in death.

First, 'a die off' is not the last line of defence - the death of the weakest (without reproducing) is an important part of the _first_ line of defence!

Second: back to the paper: "Coevolution by natural selection in this system has been hindered for European honey bee hosts since apicultural practices remove the mite and consequently the selective pressures required for such a process."

Don't misread that 'hindered' - it doesn't signal a time issue as you think. Note the second part; the selective pressure is removed. Without selective pressure there will be no adaptation. Ever. Without sdelective 'pressure' on a population there is nothing to drive any change, nothing to adapt to.

jbeshearse (reply): It is never easy to make a convincing case to entrenched positions. I never said that evolutionary biology is going wrong. I don’t even know where that came from. What I did say was that treatments are only a stopgap measure until natural selection takes over.

The 'entrenched position' is the inarguable fundamental principle at the root of evolutionary biology. And what that tells us is: your 'stopgap measure' prevents natural selection from occurring. Natural selection, where it is given free rein works just fine. Where treatments are made it cannot work - and there is no adaptation. And that is the crux of the problem. That's why treatments are described as 'addictive'. The more you treat the more you need to treat. (Actually its worse that that: treating only a bit creates a downward spiral as resistance is progressively lost). Where treatments are removed, and husbandry is done properly, things work fine.

Can you see now how all the evidence fits together, and is united with the great web of understanding that is founded upon the recognition of inherited traits, and natural selection of the fittest?

Again: find that music. Dead animals don't reproduce; the strongest reproduce most, health is passed on down.... this _process_ is essential to life. Understanding it essential to successful husbandry.

You cannot treat and expect any adaptation to occur. Indeed, if you start treating adapted bees they will, over the course of a few generations, adapt to the new environment, and lose their resistance.

Best wishes,

Mike
 
#163 ·
Adam:

I've already read through the paper from the Honeybee Genome Consortium.
I've also read Gillespie's paper on rDNA, and more.

Unfortunately, key players involved in Honeybee Genome project also involved themselves with Beeologics' attempt to feed jumping genes to Honeybees.

For example, Gene Robinson, who was on Beeologics' advisory board, went on to work for Monsanto. He was also a key player in sequencing the Honeybee Genome.

There were other scientists (and beekeepers) who entangled themselves in a web of 'conflict of interest' as well. I've also identified examples of the delberate suppression of important findings/information/technology.

My own conclusion is that the entire Honeybee Genome needs to be re-sequenced independently, and they need to pay special attention to transposable elements.

You can't serve two masters, Science and Monsanto, at the same time.

All that being said, I did use Gillespie's results to target the R2 site in Honeybees.

PS-you split into a challenge to raise new queens.
 
#165 ·
Brain: WLC's (slightly used).
Literature research: Google Scholar.
Primers: (my design) from IDT.
iTaq: Biorad.
Thermal cycler: Biorad.
Gel electrophoresis: Biorad.
Sequencing: Genewiz.
Sequence editing: Muscle/Jailview.
etc., etc...

Mark:

You don't need to go 'molecular' to take advantage of what Honeybees do naturally.

What infuriates me is that those who made the initial discoveries could have informed beekeepers about how they could take advantage of it rather than 'clamming up' and trying to market it.

I think that you may be curious about beekeepers doing something similar themselves.

As a proponent of 'democratic science', I'd say it's possible.

Beekeepers have always been 'self sufficient' anyhow.

WLC.
 
#166 ·
What infuriates me is someone who is a proponent of "democratic science" being so cryptic and oddly evasive. I've respectfully asked a number of questions about how exactly a beekeeper can utilize the supposed benefits that you are referring to. I've sent pm's. But so far, all we have are breadcrumbs that leave us basically where we already are - we breed from the best of the stock we have. The only difference is that you seem to be suggesting that to make splits of stock which is under pressure is a good thing. To me that's pretty much unavoidable.

Beyond that - no details. 9 pages of scratching, a bunch of web searching to supplement your 'tidbits', as you seem bent on making what information you do share as difficult to understand as possible, and in the end I've got "you split into a challenge to raise a new queen".

Do you know anything about beekeeping? If you do, then maybe you could talk in beekeeping terms. Then maybe you wouldn't feel like you're speaking a language that no one can hope to understand - and you can quit speaking that language and speak in the one we're all familiar with. But maybe you don't speak that language. I have never heard anyone talk about "splitting into" anything. I can split and introduce a queen; I can split and let the bees raise a queen.

As I've said repeatedly. I am happy to have you at the table here, and I'm just about as open and interested as anyone. But I'm beginning to feel toyed with, and that's annoying.

Share or don't share. But don't go on suggesting you've got information of pivotal importance but refuse to break it down in such a way as to make it truly useful to the people your speaking to.

That's just weird.

Adam
 
#168 ·
Adam:

Beekeepers normally split from their best and healthiest hives.

That's basic selective breeding.

Once beekeepers understand that there's another mechanism at play that can allow them to 'instantly evolve' their own resistance genes from their own 'sick' bees, it creates a new paradigm.

More importantly, 'transgenesis resistance' is validated proof that treatment free beekeeping can produce resistant stock.

Hygienic behavior is the only other solid evidence for treatment-free resistance that I'm aware of.

I'm not convinved that the swedes were able to show anything beyond attenuated pests/pathogens in bottlenecked bees.

WLC.

PS-watch the personal stuff folks.
 
#169 ·
Once beekeepers understand that there's another mechanism at play that can allow them to 'instantly evolve' their own resistance genes from their own 'sick' bees, it creates a new paradigm.
We keep asking you to help us understand this new method. So far it seems to amount to:

"Beekeepers normally split from their best and healthiest hives. That's basic selective breeding."

'Don't do that, split from 'pressured' hives instead.' ('Pressured' here means 'sick')

So you're asking us to abandon the deeply empirically tested and deeply theoretically supported method we know, and ... just make splits from anything instead. And somehow, magically, our bees will gain resistance.

Have I got that right?

It seems we must also understand; the mechanism by which that happens is too complicated to explain.

Will you do us all a favour and just supply straight and fulsome answers to these exact and straightforward questions?

If you can do that perhaps you'll gain respect for your theories. Without that you almost certainly won't, and people will continue to express exasperation one way or another. Participate in a discussion properly and people won't be short. Otherwise you're in the way, and people will let you know how they feel about that.

'Bill':
"I'm not convinved that the swedes were able to show anything beyond attenuated pests/pathogens in bottlenecked bees."

I've learned in several years of this discussion that some folks won't be convinced that mite resistant bees are a possibility no matter what evidence is put in front of them. And they won't tire either of telling everyone about it. I'd hoped the non-treatment forum would allow us to discuss these things without the constant interruptions and distractions of nay-sayers. Maybe we could have a special nay-sayers forum?

Mike
 
#170 ·
Mike,

JB is fine.

You have elaborated needlessly for the most part. I have a well-founded understanding of fundamental evolutionary principal and animal husbandry. I can respond point by point to your post, but that will get tedious quickly. Your points are well taken and spot on. They work well in the lab, or petri dish or in completely controlled populations. Our bees are none of the above. Your bees and my bees will mate with feral and transient populations that we have no husbandry control over whatsoever. You can propogate horses that are virus resistant within your own stable and insure that you do not breed from non-resistant stock. You do not have to allow your non-resistant horses to die, you just don't breed from them. Eventually your horses will be in demand (assuming you have not breed out other disirable traits) because of the resistance. But that is a confined and isolated population. Bees are none of the above.

We agree on much but disagree on a few important points. Really only disagree on only one important and basic point. That revolves around your words of “prevent “, “never” and “stop”. Once again you read “hinder” as prevent and I read it as impede. Once again you ignore the time part. I’ll also quote from the article (I usually don’t for copyright issues) From the article:

“The coevolutionary process required for establishing a coexisting relationship between this parasite and its new host is lacking, both in time and in selective pressures because the selective disadvantage of being virulent is removed by apicultural practices aiming to control this damaging new mite pest.”

It appears that you disagree with the time element as much as I disagree with the “selective pressure is removed” aspect. Selective pressure is impeded, not removed and there is a difference, removal dictates 100% success of treatments which is not the case.

You also are ignoring the real world application as it applies to the bee population. Husbandry works very well indeed when you control all breeding. It works well in a domesticated stock as you can select and choose what is allowed to reproduce. That is just not the case in populations with wild/feral subpopulations that cross breed with your selections. It is even more difficult when there are large mobile populations of managed livestock that are allowed to free range and mate with your selections. Also history has shown husbandry is capable of making the wrong selections and breeding out a characteristic that was later determined to be important and desirable.

It is quite a large presumption to state that human interaction in a non-domesticated species will stop that species’ evolution. It just won’t happen. Evolution will march right on with or without human muddling. And it will likely march to a tune of it’s choosing not ours.

Your stance, if accurate will doom any of your results to fail as soon as exposed to the “treated” populations. By your stance, the superior genetics you are breeding to, will fail. So where does that superiority go and what does it achieve? How does that flow into fundamental evolution?
Sorry, but you are wrong. Superior genetics will win out, treatments or not. When an inferior genetic line is allowed to reproduce it produces inferior genetics. AGREED? When an inferior line is allowed to cross breed with superior genetics, the superior genetics have a better chance at survival with or without treatments/intervention. The only caveat is when the superior genetics are purposefully killed or prevented from reproduction and that is not the case in this instance.

But everything above aside, I am going to ask a series of questions, I will provide my answers and you (or anyone else) can provide your/their answers, and then maybe a more focused conversation can follow. I am sure you will get a feel of where I am headed from the questions.

What is the currently accepted average time from introduction of mites to colony collapse if untreated and nonresistant?
JB: 3 years

Are treatments 100% effective at removal of varroa?
JB: No

Do 100% of the treated non-resistant hives survive?
JB: No

Which has the better chance of survival, a treated resistant colony or a treated nonresistant colony?
JB: Resistant colony.

Which has the better chance of survival, a non-treated resistant colony or a non-treated nonresistant colony?
JB: Resistant colony.

Which has the better chance of reproduction whether treatments are present or not, Superior or inferior genetics?
JB: Superior genetics.

Are there less tracheal mite treatments applied in US apiaries today than 5 years ago?
JB: yes, tracheal mite treatments are almost never applied.

Are there less Varroa treatments applied in US apiaries today than 5 years ago?
JB:yes; less people treat and treat less often than 5 years ago.

Are feral populations rebounding at all?
JB: Yes, the feral populations are slowly returning.
 
#197 ·
Mike,

JB is fine.

You have elaborated needlessly for the most part. I have a well-founded understanding of fundamental evolutionary principal and animal husbandry.
Hi JB,

I will continue to contend: no you don’t. I often had people say to me that they understand natural selection. But ‘understand’ is a broad word. It often means they’ve heard of it, and have a rough idea of what its about – but little more. I think your comprehension is quite good. But you’ve a little further to go.

Specifically, you are not factoring in the ‘arm’s race’ aspect, nor appreciating to extent of the effect of allowing non-resistant genes to go through wholesale to the next generation.

Let’s try a thought experiment to bring the main issues into focus. We can imagine two apiaries of identical bees, both middle resistant, and both with middle-fecund varroa. For the sake of this thought experiment we’ll ignore any changes in the mite population. We’ll also assume any external input is identical, and similarly both sets of bees are middling in terms of resistance.

Apiary A) will be managed by close selection of the most resistant bees. Their genes will replace the weakest by queen rearing and re-queening.

Apiary B) will be managed by a systematic treatment regime. There will be no attempt to breed through selection.

This represents my way and yours respectively.

In my apiary any non-resistant strains will be swiftly terminated, leaving each new generation to be made from resistant parents. Genetics/the law of inherited traits will ensure the new generations are similarly resistant, and so within a few generations all non-resistant strains will be extinguished except those that have come in from outside. This will throw up non-resistant offspring, but less often that will be happening in your as my own drones will tend to reinforce resistance. My apiary will be made resistant, and kept resistant by systematic selection.

In your apiary both resistant and non-result equally contribute to each new generation. Each new generation, made of the same mix, will result in similar levels of resistance to the previous. This is exactly what the passage we’re interested in means: acaricide use inhibits the rise of resistance. Non-resistance doesn’t result in death – you stop that by treating. It doesn’t – even though it doesn’t work 100% - result in any progress, since many that would have failed go through.

The cost of hygienic behaviours
I can see your point: if the treatments don’t work 100% then you might think there will remain a small pressure toward growing resistance. But actually it doesn’t work like that: for this reason. The hygienic behaviours carry a small penalty – they carry a cost. Bees fussing about over-cleaning the place are not bees fetching pollen and nectar. For that reason the evolved mechanisms are, in nature, dropped as soon as possible. As mites become less of a problem those hives with a lower proportion of resistant patrilines gain an advantage over those with what is now too many. And this dropping of resistance is rapid. What this means is that the slightest easing in pressure to become resistant results in fast abandonment of resistance. And that is exactly the scenario in lightly, or incompletely treated apiaries.

So while my bees, and any feral bees far enough away from treaters to enjoy the benefits of natural selection will rapidly gain resistance due to the ruthless extinction of vulnerable strains, yours will make no progress whatsoever.

Now, separately, we can look at three possible further objections. I’ve mentioned drone input, and we can do that first. Then we’ll look at the possibility of inbreeding and loss of genetic diversity.

Both our apiaries, as you’ve pointed out, will be affected by external drones. In my case any benefits will be enjoyed, and disbenefits rapidly negated by my system. If the inputs contribute to health they’ll be incorporated; if they don’t, they won’t. Neat huh?

In your case the opposite will occur – any benefits will be lost as you press unfit strains forward in your mix, while any unfit drone input will just decrease any nascent resistance still further.

As to the fact of open breeding: yes, we cannot control mating, and so we cannot work with the sort of (probabilistic) precision that closed husbandry enjoys. But we can get ¾ of the way there, by adopting different strategies.

First, we can have total control over the queen side genetics. That’s 50% of the input, and is sufficient alone to start swinging things our way.

Second, we can increase our share of the male side input by two means: 1) by keeping large drone producing hives in and around our apiaries (standard bee farmers practice) and b) by the fact that our modus operandi encourages feral bees to establish and thrive around them – so we get the benefit of their (naturally selected) drones. Note; your management severely represses the local feral population, and so you get none of that resistant input.

Inbreeding.
The fact of open mating, the contact local ferals will have with bees from the wider area, and the possibility of deliberate input of selected resistant strains now and then add up to no danger of inbreeding.

(Possible loss of genetic diversity is covered below)

Your points are well taken and spot on. They work well in the lab, or petri dish or in completely controlled populations. Our bees are none of the above. Your bees and my bees will mate with feral and transient populations that we have no husbandry control over whatsoever.
First, I’m grateful for your appreciation, and I’d like to return it.

To real-world application. First, many people have been keeping bees treatment free for many years by using these techniques. The empirical evidence is there. The explanations for why it works are also there.

I’ve already addressed external input above, will add: the systematic nature of the selective propagation program is easily capable of dealing with input from neighbouring (treating) apiaries and transients – as long as they are not overwhelming. So its sensible to be at some distance from larger operations, and to make your own operation as large as possible so as to dominate the drone space. As to ferals – well as indicated above – their input is highly desirable.

In the real world, the evidence fits my way of thinking perfectly.

We agree on much but disagree on a few important points. Really only disagree on only one important and basic point. That revolves around your words of “prevent “, “never” and “stop”. Once again you read “hinder” as prevent and I read it as impede. Once again you ignore the time part. I’ll also quote from the article (I usually don’t for copyright issues) From the article:

“The coevolutionary process required for establishing a coexisting relationship between this parasite and its new host is lacking, both in time and in selective pressures because the selective disadvantage of being virulent is removed by apicultural practices aiming to control this damaging new mite pest.”
I agree, the paper does speak of a time factor. I will maintain that under strong treatment regimes, with no compensating feral or non-treater or deliberate resistant breeding to ameliorate, development of resistance cannot occur. I’ve covered that under ‘the cost of hygienic behaviours’.

It appears that you disagree with the time element as much as I disagree with the “selective pressure is removed” aspect. Selective pressure is impeded, not removed and there is a difference, removal dictates 100% success of treatments which is not the case.
Well, lets imagine you are right about this. Can you state the factors, the parameters under which resistance will rise, and give us a time frame? I’m not asking for guesses – I can give you a time frame for doing things my way – and prove that it works. Can you make a substantial claim that your slow development of resistance will outpace any compensating evolution in the mites? What is your evidence?

At least can we agree: my way clearly works; your way might do, but we know, and we can’t know when either?

Also history has shown husbandry is capable of making the wrong selections and breeding out a characteristic that was later determined to be important and desirable.
(Possible loss of genetic material or valuable traits)
I’m sure this is true (though I’d appreciate some examples with references). However, as far as I’m aware there is no comparable danger in what I’m advocating. In fact its exactly the point made by Marla Spivak: to have lots of beekeepers all maintaining their local populations by breeding on a local basis is the best possible protection for genetic diversity.

I’m no expert here, but my understanding is that there is little to no cost in diversity in allowing nature to play out in this sort of situation – which the bees have faced countless times before – nor in the kind of husbandry that mimics natural selection. The ‘winners’ carry through pretty much all the diversity in the prior population. Very very small populations may be at risk of ‘bottlenecks’ But we’re talking here about a handful of individuals – not the millions at large in the US or the UK.

A single isolated apiary that is overbred might suffer such a problem. But a bit of new (preferably resistant) blood will sort it out.

Evolution will march right on with or without human muddling. And it will likely march to a tune of it’s choosing not ours.
If you consider domesticated animal have marched very much to our tunes – and then think how much influence we have over bees wherever the great majority are in apiary hands – you’ll see that we can and are influencing them strongly. And … that is what the paper tells us is happening. Its not the first scientific study to make the point:
Survival of mite infested (Varroa destructor) honey bee
(Apis mellifera) colonies in a Nordic climate (2006)
Ingemar Fries, Anton Imdorf, Peter Rosenkranz
"Our results allow us to conclude that the problems facing the apicultural industry with mite infestations is probably linked to the apicultural system, where beekeepers remove the selective pressure induced from the parasitism by removing mites through control efforts."
http://www.apidologie.org/index.php...129&url=/articles/apido/pdf/2006/05/m6039.pdf
This is the part most beekeepers – and, it seems regulators and the advisors don’t understand: giving medical aid to an openly mating species has a horrific effect. The species simply adapts to the new situation, and doesn’t bother raising any defences against what it perceives to be non-problem. The pathogens, meanwhile, continue adapting – resulting in their growing resistance to the treatments.

Genetic care is an art. Go wrong and the results can quickly be catastrophic. As you yourself point out, bees are not closed mating populations, and the usual rules do not apply. Treating openly mating animals as you can closed populations is very much taking a wrong turn. The predictable – and now deeply demonstrated - result is a kind of ‘addiction’. The more you treat, the more the bees will adapt to your lifting their burden – and so it goes on.
Your stance, if accurate will doom any of your results to fail as soon as exposed to the “treated” populations. By your stance, the superior genetics you are breeding to, will fail. So where does that superiority go and what does it achieve? How does that flow into fundamental evolution?
Not where the sorts of precautions I’ve outlined, if needed, are taken. The point is to raise the number of resistant patrilines to a sufficient level (and variety of required behaviours) not to seek complete dominance. And then to keep them at a suitable level through ongoing selective propagation. That’s what nature does, and we can improve and lose most of the weakest. The trick is: build the selective _process_ into your management. Genetic management is part of the art of beekeeping – just as in closed populations.

Sorry, but you are wrong. Superior genetics will win out, treatments or not.
This is not substantiated, either by reference to theory or by any evidence. Its an article of faith. The well-established theory says: treatments supply an environment in which the pressure for change is removed. No change.

When an inferior genetic line is allowed to reproduce it produces inferior genetics. AGREED?
Two weak lines will most often produce a weak offspring. Agreed.

When an inferior line is allowed to cross breed with superior genetics, the superior genetics have a better chance at survival with or without treatments/intervention.
More or less, yes.

But everything above aside, I am going to ask a series of questions, I will provide my answers and you (or anyone else) can provide your/their answers, and then maybe a more focused conversation can follow. I am sure you will get a feel of where I am headed from the questions.

What is the currently accepted average time from introduction of mites to colony collapse if untreated and nonresistant?
JB: 3 years
MB Depend on level of resistance in bees and voracity of mites. I’m not sure, given that, that an average really indicates mush that is of use to us. What we want to know is: you much resistance do _these_ bees have.

Are treatments 100% effective at removal of varroa?
JB: No
MB I don’t know. Some might be some of the time.

Do 100% of the treated non-resistant hives survive?
JB: No
MB I doubt it. 100% of any hives anywhere anytime is unlikely given a reasonably large sample.

Which has the better chance of survival, a treated resistant colony or a treated nonresistant colony?
JB: Resistant colony.
MB Close to equal (dependent on effectiveness of treatment), but I’ll grant you the point.

Which has the better chance of survival, a non-treated resistant colony or a non-treated nonresistant colony?
JB: Resistant colony.
MB Resistant colony

Which has the better chance of reproduction whether treatments are present or not, Superior or inferior genetics?
JB: Superior genetics.
MB I’m not sure that speaking in terms of ‘superior’ and ‘inferior’ is useful. Resistance is supplied by specific genes that confer specific behaviours. In the natural context possession of those behaviours confers superiority. Only when all colonies have those protective behaviours can other considerations come into play. Same in the non-treated apiary.

However, in the context of a treating apiary, all sorts of other factors come into play that make resistance irrelevant. So the ‘superior’ bee (i.e. good producer) may have no resistance, but be a outstanding layer.

Are there less tracheal mite treatments applied in US apiaries today than 5 years ago?
JB: yes, tracheal mite treatments are almost never applied.
MB No idea – I’ll take your word for it. But how widely were tracheal mite treatments applied? I’m not sure a simple parallel can be made.

Are there less Varroa treatments applied in US apiaries today than 5 years ago?
JB:yes; less people treat and treat less often than 5 years ago.
MB Again, I’ll have to take your word for that. Can you supply proper support for the claim? How much have treatments been fine-tuned – just as effective though applied less often? How much have alternative systems of mite management been substituted? Don’t forget, they have exactly the same effect in breeding terms.

Are feral populations rebounding at all?
JB: Yes, the feral populations are slowly returning.
MB: Yes. And, its noteworthy that, as Joe Waggle predicted, this is happening first in those remote places where apiaries are few and far between. Treatments suppress feral populations by supplying incoming genetic material that undermines self sufficiency.
 
#171 ·
It's not a new mechanism for producing resistance in treatment-free beekeeping.

Your bees have been doing this all along. However, they've done this, on their own, very slowly.

If you want to speed things up, make sure that there's a pest/pathogen present (the source of the resistance 'gene').

Then you can make new queens [so that non-LTR, retrotransposon (the 'resistance gene')bearing RNPs (the package), can translocate from nurse cells to oocytes (the germ-line mechanism)].

Finally, after a few months, you can select from your resulting/surviving nucs for resistance.


Entomologists have studied this field for decades.

It's only a mystery to those who use terms like 'evolution' and 'natural selection' as if they understood their meaning.
 
#172 ·
Mike: The only solution to people who won't cooperate is to stop feeding them. He's not providing you with what you ask, so cut him loose.

JB: I mostly agree with your answers except the last one. In my experience, feral bees have been at normal population for a number of years now. I know of a number of feral hives in my area (as well as where I used to live in Oregon) and I regularly catch feral swarms as well as ones which seem to come from kept hives. If the feral population rebounds as quickly as I've seen the kept population, the ferals have been fine for a decade.

As far as how varroa is treated, I believe you, but I don't have the numbers. I would like to see them. I hope its true.
 
#173 · (Edited by Moderator)
"Mike: The only solution to people who won't cooperate is to stop feeding them. He's not providing you with what you ask, so cut him loose.'

I answered his question. [Edit]

Sol:

You never did explain how you know that your treatment-free bees are disease resistant.

Sooo...

Perhaps you're the ones doing the trolling and refusing to answer questions?

WLC.
 
#174 ·
You never did explain how you know that your treatment-free bees are disease resistant.
Yes I did. If they weren't disease resistant they would be dying all over the place, but they are not. I have not treated for anything in nine and a half years. They keep telling me there's going to be a crash and it keeps not happening. Give me an alternate explanation.
 
#176 ·
Mark:

A little due diligence is in order.

How about getting the apiarist/bee inspector to come by and give an unbiased assessment?

A treatment-free beekeeper might cringe at the thought of an experienced, no-nonsense, inspector rating their hives.

But, frankly, it's like going to the doctor's. We all have to do it sometime.
 
#195 · (Edited)
I think that I'm addressing the conclusion of the paper rather directly.
You must be explicit and explain in terms we can understand. Take a sentence or paragraph from the paper (you mention the conclusion) and show how it bears on your thinking - or vice versa. At things stand you're building castles on thin air. That's a waste of our time and space, and a distraction from our topic. Start your own topic if you want to talk about a new mechanism beekeepers can experiment with to supplement the known routes to resistance.

We need to address how resistance evolves.
Resistance evolves due to natural selection for the fittest strains. What you seem to wish to talk about is the way resistance arises in the first place. It seems to me you wish to replicate what you believe to be a mechanism whereby some of the genetic material from the organism causing problems is somehow bought into service in the host's genetic structure, in a way that then supplies resistence to the host.

Is that what you are talking about?

Mike

PS from what Toofargone has written it seems that's about right. Its interesting. But it should be on a thread of its own, since our subject paper is directed at evolution working in the more common manner - by natural selection for the fittest strains. Your topic is related, but is getting in the way of this conversation. And this one is important - it deals directly with the mechanisms that will make the most difference to the great majority of beekeepers seeking to go treatment free. As the orginator of the thread I'm asking you to start your own. I'll subscribe to it and listen in and ask questions.
 
#180 ·
I am very interested in how resistance evolves. So I'll ask more questions in an effort to understand.

WLC says:

" Then you can make new queens [so that non-LTR, retrotransposon (the 'resistance gene')bearing RNPs (the package), can translocate from nurse cells to oocytes (the germ-line mechanism)]."

So I have to raise my own queens from the struggling stock. Is the word "nurse" in this sentence referring to nurse bees? If so, how does the resistance gene translocate from the nurse cells?

I want to run a treatment free operation, and am presently forulating my approach to next season. I am very much interested in whatever the group might offer to help me figure our my plan for the coming season.

Adam
 
#181 ·
Adam:

We're obviously looking at how egg cells (and possibly sperm cells) are made.

My understanding is that these RNP particles move into the oocyte along with other other components that are being transferred from the nurse cells.

You might have to look up gametogenesis to get a better feel for the process.

The RNP then makes it to the nucleus (possibly via the cytoskeleton) where it then reverse transcribes and integrates into the host genome.

So, the transposable element makes it to the nucleus during gamete formation and integrates.

After that, it's resistance via RNAi, as in the Maori paper.

This is the only example of Honeybee disease resistance by evolution, that I am aware of, that is so well documented.

I don't think that we can say the same for any of the other possible mechanisms being discussed. That's what makes it special.

--------------------------------------

Out of 8 splits from an obviously DWV infected hive (there was a funnel of dead bees, with shriveled wings, leading back to the hive), 1 was good enough to rehive.

Even though we're going to take a look for evidence for DWV integration, it might take a while before we actually know if the new hive is truly resistant.

Hunting for jumping genes is never an easy task.
 
#182 ·
Adam:

My understanding is that these RNP particles move into the oocyte along with other other components that are being transferred from the nurse cells. [within the reproductive organs of the queen] Right, WLC?

--------------------------------------

Out of 8 splits from an obviously DWV infected hive (there was a funnel of dead bees, with shriveled wings, leading back to the hive), 1 was good enough to rehive.

Even though we're going to take a look for evidence for DWV integration, it might take a while before we actually know if the new hive is truly resistant.

Hunting for jumping genes is never an easy task.
What did you do w/ the other 7 splits? What was their composition?

"we"?
 
#183 ·
This was DWV without mites, by the way, in VSH stock.

2 frames from the original hive, and an additional drawn frame for each split

No feeding or treatments.

4 came through, and I took the best looking one and rehived it. I allowed the other three to dwindle away.

The new hive was close to filling one deep when we took samples.

"we", Someone else gets to do the tests.
 
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