If you follow some of the online discussions on Varroa you’ll see numerous examples of amateur beekeepers choosing not to treat so as to ‘select for mite-resistant bees’.
For starters it’s worth looking at the ‘treatment-free’ forums on Beesource.
The principle is straightforward. It goes something like this:
- Varroa is a relatively new 1 pathogen of honey bees who therefore naturally have no resistance to it (or the viruses it transmits).
- Miticide treatment kills mites, so favouring the survival of bees.
- Consequently, traits that confer partial or complete resistance to Varroa are not actively selected for (which would otherwise happen if an untreated colony died out).
- Treatment is therefore detrimental, at the population level if not the individual level, to the development of Varroa-resistant bees.
- Therefore, don’t treat and – with a bit of luck – a resistant strain of bees will appear.
A crude oversimplification?
Yes, I don’t deny it.
There are all sorts of subtleties here. These range from the open mating of queens, isolation of apiaries, desirable traits (with regards to both disease resistance and honey production 2), livestock management ethics, our responsibilities to other beekeepers and other pollinators. I could go on.
Instead I’ll discuss a short paper published in the Journal of Apicultural Research. It’s not particularly novel and the results are very much in the “No sh*t Sherlock” category. However, it neatly emphasises the futility of the ‘do nothing and expect evolution to find a solution’ approach.
But I’ll start with a simple question …
How many colonies have you got?
One? (in which case, get another)
Eight-two thousand? 3
Numbers matters because evolution is a numbers game. The evolutionary processes that result in alteration of genes (the genotype of an organism) that confer different traits or characteristics (the phenotype of an organism) are rare.
For example, viruses are some of the fastest evolving organisms and, during their replication, mutations (errors) occur at a rate of about 1 in 104 at the genetic level 4.
But so-called higher organisms (like humans or bees) have much more efficient replication machinery and make very many fewer errors. A conservative figure for bees might be about 10,000 times less than in these viruses (i.e. 1 in 108), though it could be as much as a million times less error-prone 5
There are lots of other evolutionary mechanisms in addition to mutation but the principle remains broadly the same. The chance changes that are acquired by copying or mixing up genetic material are very, very infrequent.
If they weren’t, most replication would result – literally – in a dead end.
OK, OK, enough numbers … what about my two colonies?
So, since the evolutionary mechanisms make small, infrequent changes, the chance of a beneficial change occurring is very small. If you start with small numbers of colonies and expect success you’re likely to be disappointed.
Where ‘likely to be’ means will be.
The chances of picking the Lotto jackpot is about 1 in 45 million for each ticket purchased. If you expect to win you will be disappointed.
If you buy two tickets (with different numbers!) your chances are doubled. But realistically, they’re still not great 6.
And so on.
Likewise, the more colonies you have, the more likely you’ll get one that might – by chance – acquire a beneficial mutation that confers some level of resistance to Varroa.
Of course, we don’t really know much about the genetic basis for resistance (or tolerance?) to Varroa in honey bees. We know that there are behavioural changes that increase survival. We also know that Apis cerana can cope with Varroa because it has a shorter duration replication cycle and exhibits social apoptosis.
There are certainly ‘hygienic’ and other traits in bees that may be beneficial, but at a genetic level I don’t think we know the number of genes that are altered to confer these, or how much each might contribute.
So we don’t know how many mutations will be needed … One? One hundred? One thousand?
If the benefit of an individual mutation is very subtle it might offer relatively little selective advantage, which brings us back to the numbers again.
Apologies. Let’s not go there.
Let’s cut to the chase …
Comparison of treated vs untreated colonies over 3 years
Miticides – whether hard chemicals like Amitraz or Apistan or organic acids like formic or oxalic acid – work by exhibiting differential toxicity to mites than to their host, the bee. They are not so specific that they only kill mites. They can harm other things as well … e.g. if you ingest enough oxalic acid (5 – 15g) it can kill you.
Jerzy Wilde and colleagues published their study 7 comparing colonies treated or untreated over a three year period. The underlying question addressed in the paper is “What’s more damaging, treating with potentially toxic miticides or not treating at all?”
The study was straightforward. They started with 100 colonies, requeened them and divided them randomly into 4 groups of 25 colonies each. Three received treatment and one was a control.
The ‘condition’ of the colonies was measured in a variety of ways, including:
- Colony size in Spring (number of combs occupied)
- Nosema levels (quantified by numbers of spores)
- Mite drop over the winter (dead mites per 100g of ‘hive debris’)
- Colony size in autumn (post-treatment) and egg laying rate by the queen
- Winter losses
The last one needs some explanation because in one group (guess which?) there were more winter losses than they started the experiment with.
Overwintering colony losses were made up from splits of colonies in the same group the following year, so that each year 25 colonies went into the winter i.e. surviving colonies were used to generate additional colonies for the same treatment group.
Treatment and seasonal variation
To add a little complexity to the study the authors compared three treatment regimes:
- Hard chemicals only – active ingredients amitraz or the pyrethroid flumethrin (the research group are Polish, so the particular formulations are those licensed in Poland – Apiwarol, Bayvarol and Biowar).
- Integrated Pest Management (IPM) – a range of treatments including Api Life Var (primarily a thymol-based treatment) in spring, drone brood removal early/mid season, hard chemical or formic acid in late summer/autumn and oxalic acid in midwinter.
- Organic (natural) treatments only – Api Life Var in spring, the same or formic acid in late summer and a midwinter oxalic acid treatment.
The fourth group were the untreated controls.
To avoid season-specific variation they conducted the experiment over three complete seasons (2010-2012).
The results of the study are shown in a series of rather dense tables with standard deviation and statistic significance … so I’ll give a narrative account of the important ones.
The strength of surviving colonies in Spring was unaffected by prior treatment (or absence of treatment) but varied significantly between seasons. In contrast, late summer colony strength was significantly worse in the untreated control colonies. In addition, the number of post-treatment eggs laid by the queen was significantly lower (by ~30%) in untreated control colonies 8.
Remember that early autumn treatment is needed to reduce Varroa infestation and so protect the winter bees that are being reared at this time from the mite-transmitted viruses.
The most dramatic effects were seen in winter losses and (unsurprisingly) mite counts.
Mites were counted in the hive debris falling through the open mesh floor during the winter. In the first year the treated and untreated controls had similar numbers of mites per 100g of debris (~12). In all treated colonies this remained about the same in each subsequent season. Conversely, untreated controls showed mite drop increasing to ~43 in the second year and ~114 in the final year of the study.
During the three years of the study 30 untreated colonies died. In contrast, a total of 37 colonies from the three treatment groups died.
The summary sentence of the abstract to the paper neatly sums up these results:
Failing to apply varroa treatment results in the gradual and systematic decrease in the number of combs inhabited by bees and condition of bee colonies and consequently, in their death.
… and some additional observations
Other than oxalic acid, none of the treatments used significantly affected the late season egg laying by the queen. Api Life Var contains thymol and many beekeepers are aware that the thymol in Apiguard quite often stops the queen from laying. Interesting …
I commented last week on queen losses with MAQS. In this Polish study, 8 of 50 colonies treated with formic acid suffered queen losses.
In the third season (2012) 45% of the 100 colonies died. More than half of these lost colonies were in the untreated controls. In contrast, overall colony losses in the first two years were only 9% and 13%. Survival of untreated colonies for a year or two is expected, but once the Varroa levels increase significantly the colony is doomed.
Overall, colonies receiving integrated pest management or hard chemical treatment survived best.
Remind yourself where the colonies came from that were used to make up the losses in the treatment (or control) groups … they were splits from colonies within the same group. So, colonies that survived without treatment were used to produce more colonies to not be treated the following season.
Does this start to sound familiar?
Jerzy Wilde and colleagues started with 25 colonies in the untreated group. They lost 30 colonies over a 3 year period and ended up with just two colonies. Had they wanted to continue the study they would have been unable to recover their losses from these two remaining colonies.
If you don’t treat you must expect to lose colonies.
Lots of colonies.
Actually, almost all of them.
… takes time
This study lasted only three years. That’s not very long in evolutionary terms (unless you are a bacterium with a 20 minute replication cycle).
It would be unrealistic to expect Varroa resistance to almost spontaneously appear. After all, there are about 91 million colonies worldwide, the majority of which are in countries with Varroa. Lots of these colonies will not be treated. If it was that easy it would have happened many times already.
What happens when you start with more colonies and allow more time to elapse?
Well, this ‘experiment’ has been done. There are a number of regions that have well-documented populations of feral honey bees that are living with, if not actually resistant to, Varroa.
One well known population are the bees in the Arnot Forest studied by Thomas Seeley. These bees have behavioural adaptations – small, swarmy colonies – that lessen the impact of Varroa on the colony 9.
Finally, returning to the title of this post, there is the so-called “Bond experiment” conducted on the island of Gotland in the Baltic Sea. Scientists established 150 colonies of mite-infested bees and let them get on with it with no intervention at all. Over the subsequent six years they followed the co-evolution of the mite and the bee 10.
It’s called the “Bond experiment” or the Live and Let Die study for very obvious reasons.
Almost all the colonies died.
Which is why the title of this post is more appropriate for those of us with only small numbers of colonies.
- In evolutionary terms one hundred years is the blink of an eye …
- Or whatever else floats your boat … pollination services, wax, royal jelly or propolis production etc.
- Adee Honey Farms is the largest commercial beekeeping operation in the USA (and therefore presumably the world). Unsurprisingly, they’re too busy doing colony inspections to update their website, but you can read more about Richard Adee here.
- I’m hoping to keep this simple by omitting pesky things like units … for those who are interested a virus, such as deformed wing virus, acquires 1 nucleotide change in ~10,000 nucleotides copied. Since the virus genome is ~10,000 nucleotides in length this means that every genome differs (randomly) by one nucleotide from every other genome.
- And, just so you appreciate the scale here … the honey bee genome contains 10,000 different genes and is ~23 million times larger than the genome of deformed wing virus.
- To put your 1 in 22 million chance in context … there’s a 1 in 10 million chance you’ll be struck by lightning and 1 in 250,000 chance of being killed at home by a crashing aeroplane. You might be wiser to spend your £2 on a hard hat … a hard rubber hat.
- Bak et al., (2018) The condition of honey bee colonies (Apis mellifera) treated for Varroa destructor by different methods. J. Apicultural Res. 57:674-681. PDF of Bak et al., available here for download.
- These could not be counted in oxalic acid treated colonies in late summer, presumably because they sprayed a 3.5% solution onto frames which would damage unsealed brood and eggs. This is not a treatment regime approved in the UK.
- In addition, there is evidence that the mite has evolved to be avirulent, rather than the bees acquiring resistance. Same overall result, very different reason. I’ll deal with this sometime in the future, it’s another interesting story.
- Since the word count has just crept over 2000 I’ll save a discussion of this interesting study for sometime in the future.
Surely if we keep treating the mites will form a resistance and the bees will just get weaker over time while the mites get stronger,there has to be some sort of a balance or do we just go on treating and end up like the resistance of viruses to antibiotics in humans so creating a super mite
I understand the concern. If we treat properly, by which I mean using appropriate, approved miticides at the right time and in the right way, we will significantly reduce the chance of resistant mites being selected. There’s no evidence that treatment makes the bees ‘weaker’, though – because mite-susceptible strains are ‘saved’ by treating – it probably will not encourage the development and selection of resistant strains.
However, the alternative isn’t pretty … if we choose not to treat most colonies will die. If you start with a couple, they’ll both probably die. If you start with a couple of dozen they’ll probably all die – some faster, some slower. If you start with a couple of hundred you might end up with a few colonies, after several years, which can at least tolerate mites.
We have some insights into what these bees could be like from Thomas Seeley’s studies … small colonies, very swarmy, unable to live in close proximity to other bees i.e. only one hive per apiary. These colonies are almost certainly no use for beekeeping and provide very little pollination activity.
Is that what we want?
There’s nothing inherently wrong with treating to prevent or cure disease. Quite the converse … I’d argue that it is grossly irresponsible not to try and prevent disease. There are parallels between those who choose not to treat because it ‘harms the bees’ and those who choose not to vaccinate their children against mumps or measles … not only do they put those ‘treated’ at risk, but they also put the population at large at increased risk of disease by acting as a source of infection.
As an aside, antibiotics are used to cure bacterial infections. Viral infections are prevented by vaccination and – in a relatively few cases – controlled and sometimes cured with antiviral drugs.
Please find attached a study of bees in North Co Dublin Ireland by Dr John McMullen published last year https://www.tandfonline.com/doi/full/10.1080/0005772X.2018.1431000,
Many thanks. I’m familiar with that work. Note that it’s a ‘self-contained’ area encouraging the co-evolution of bees and mite/virus complex. It would be interesting to know what happens to those bees moved out into another region with different viruses and mites.
There are insufficient details about the virus analysis but I’d be very surprised if these bees were truly DWV negative. Without knowing the limit of detection, or having any positive controls showing the sensitivity of the assay, you are not able to be sure that the virus is not present. We have tested bees that are Varroa-free and have been for 30+ years using an assay that can detect very low levels of DWV and always find the virus present.
If you slowly increase the ‘self contained’ area surely the same results will apply and the co-evolution will spread, and I do not think he is saying the bees are DVW truly negative but the amount is small and nearly irrelevant
Easier said than done I suspect … getting a small number of beekeepers to agree on anything is difficult enough in the first place!
My DWV comment was based on the statement made in the article which said “All samples of callow bees were negative for DWV”. What’s interesting is whether the mite and the virus populations are ‘attenuated’ as well as the bees having some resistance/tolerance traits.
The density of beekeepers in the UK (geographic density!) means that it is very difficult to define or create these self-contained areas I suspect.
Many senior bee scientists (Seeley, Neumann, Oliver, Beuchler etc…) are looking for the answer to the question of “Why some Apis mellifera colonies have adapted to varroa in the UK, continental Europe and North America”. Perhaps you could turn your own thoughts to that question. It is the only long term, sustainable solution.
It is not the only long term sustainable solution … but it’s certainly something I’ve thought about, and continue to think about. Many of these colonies have probably not ‘adapted to Varroa‘ at all. Most of them are in isolated locations – forests, islands, valleys in the mountains etc.
I’m going to write about this in the future so won’t go into a full discussion here. However, it’s worth thinking whether it’s only the bee that evolves …
Are any of these Varroa-adapted colonies able to be moved to a new environment, exposed to a different population of Varroa?
Watch this space
Local adaption is important. There are currently too many bees genetically unable to cope with varroa – a function of chemical treatments and lack of strategic thinking about the problem. The polyandry nature of mating in new areas undermines the better genetics of adapted bees. “Rapid parallel evolution overcomes global honeybee parasite” is a good piece of research shedding light on adaption of Apis mellifera bees to varroa. Hope you can get there….
I’m familiar with that paper by Neumann and colleagues. The capping/uncapping trait deserves more investigation. I’ll probably discuss it in a future post.
The ‘local adaptation’ is something a lot of beekeepers talk about though I’m not aware of any scientific studies that definitively show that locally adapted bees are at an advantage over imported stocks selected elsewhere. I’ve discussed imports previously and would prefer they weren’t needed … not primarily due to messing up the genetics of local stocks, but because it’s an obvious route by which new pests and pathogens will be introduced.
But, evolution doesn’t just occur by waiting for the lucky lottery of new mutations to appear – which, I agree, would be something of a long shot.
The constant driver of adaptation is an ongoing selective process that favours beneficial traits that already exist within a population.
For example, when myxomatosis wiped out over 90% of wild rabbits in the 70s, it wasn’t a random, lucky gene that happened to save them. It was the pre-existance of resistance in a small percentage of rabbits, which survived the carnage and went on to parent the ample population we have today.
So, sticking with the Bond theme, it could be argued that evolution is a bit less ‘Casino Royale’ and a bit more ‘Tomorrow never dies’.
Which makes a stronger case for Dr No (treatment)!
Very good! I’d tried to weave a couple more James Bond titles into the piece and those are much better than anything I could come up with.
You’re right about how evolution works, but so am I. It’s incremental, building upon what’s already there. If there was a small population that already had good levels of resistance we would probably have selected them … that there aren’t means what’s out there is probably insufficient and more evolution will be needed.
I have read many of your posts with interest. I have just two colonies at present – it’s great to have a mix of science and experience from your posts, on which I can base my colony management. I am keeping bees for the bees, so not taking honey. Thanks for all this timely and well informed info.
Nothing wrong with keeping bees for bees … they are fascinating creatures. In a poor year it’s worth making sure they have sufficient stores to overwinter. Even if you leave them with all their stores they may not have enough. And it’s certainly worth ensuring they are as disease-free as possible …
Enjoy your bees
Hi David, you are great author! Love your posts.
Special thanks for responsibilities link, I think this post should be printed and hung on the wall.
Many thanks … I’m never sure why it’s not always part of the winter training courses …
I have 6 colonies. Which open mate with others in the area. I know of 8 wild colonies and 8 hives in the area. A couple of the wild ones have persisted for over a decade. Bit difficult to treat them 30 feet up in a church wall, and they do NOT die out in winter or spring (I monitor them).
So there is a reservoir of survivor genes. Which spreads rapidly if you don’t treat.
What I found when I went no-treatment in 2012 was my Buckfasts died with high varroa loads that Spring. I repopulated with local swarms. No mite problems yet… hmm, no one year I had to do a shook swarm on one colony. But generally no problems.
I think this supports Mick King’s point that you CAN get mite resistant bees simply by allowing mating with whatever works in the area.
By the way, several BIBBA members I’ve spoken to reckon their bees are mite resistant. It seems to be a widely present trait all over the UK and simply needs to be allowed to express itself by accepting losses of nonresistant colonies.
I’ve got a couple more articles in the pipeline on Varroa resistance and host-pathogen co-evolution.
There is at least one good scientific study of the genetics of ‘feral’ bees by Thompson and Budge. I’ll try and dig it out as it suggests that most are regularly repopulated from lost (un)managed colonies swarming.
One of the key things most of the studies of mite resistance fail to do is to demonstrate resistance to mites other than those they have been reared in the presence of … if you sold a nuc to a beekeeper 50 miles away would they survive or perish? Maybe you’ve done this?
If they survive without treatment there then it’s very encouraging. If they don’t it suggests what you’re dealing with is a population of partially-resistant or mite-tolerant bees and – critically – a population of less virulent mites (or viruses).
Furthest our local non-treatment group has swapped swarms is about 20 miles. More significantly, we take swarms from towns to rural hives and vice-versa, depending on who wants one and where they pop up. This is generally successful (colony survives several years) though occasionally a queen fails to mate or, this year, we’ve seen several colonies absconding after hiving.
I’ve met Budge and respect him. Knows his stuff. I understand the genetics of an area reaches an equilibrium and so wild bees appear similar to ones from breeders if someone is importing lots of bees to an area. (For example about 15 miles from me is a vast-scale Buckfast breeder, you can see the effect in the wing morphometry of the colonies round here.) And talking to the chairman of the Devon BKA once, he mentioned there were zero wild colonies in Devon. Never having been to Devon I can’t say, but in this county there are old houses. And bees love old roofs. Also chimneys. And church towers. Maybe they don’t have those in Devon. Anyhow of the 6 (now 8 this year) ferals round here only one dies out each winter. As I said, I monitor them.
I’m pretty sure Devon is also full of old houses with old roofs and chimneys or churches 😉
You can read all the gory details about feral bees in Catherine Thompson’s PhD thesis (PDF) … I can’t find the paper and it may not yet be published.
I’ve acquired a couple of swarms this summer and – other than my own colonies – know of no other beekeeper within 2-3 miles of here. They’re not mine as all my queens are accounted for. Neither swarm had a significant Varroa load, though it’s still a bit early in the season for the mite levels to be dangerously high.
I certainly don’t dispute the existence of feral colonies, or that they can survive with Varroa. Thomas Seeley has demonstrated this in several compelling studies over the years. What remains unclear is whether their resistance/tolerance can cope with mite populations they have not co-evolved with.
Seeley’s new book – The Lives of Bees – arrived this morning in the post. In the jacket blurb it states that “The Lives of Bees is Thomas Seeley’s captivating story of what scientists are learning about the behavior, social life, and survival strategies of honey bees living outside the beekeeper’s hive-and how wild honey bees may hold the key to reversing the alarming die-off of the planet’s managed honey bee populations.”
I’ll read it with interest.
Are you aware of Melissa Oddie’s research on managed populations that have become varroa tolerant? The Norwegian beekeeper who achieved this did so by choosing not to treat, to the horror of other beekeepers. Instead of breeding from his best queens, he culled the 20-30% worst queens and colonies every year and attempted to build up a strong local gene pool. I can assure you that he’s not crazy, and not isolated on an island or in a forest. It’s not a secret who he is, he’s on social media now that more people are looking at what he’s doing: https://www.youtube.com/watch?v=OzYl4UssylY (english captions available)
The research of Oddie is a very interesting read:
I just read that she is returning to Norway next year, so there’s more to come.
I do get the cautious message of your article though. And I agree that beekeepers shouldn’t go “treatment free” just because they’ve read about it online. At least not blindly. One should always monitor the mite levels and act accordingly.
But I wouldn’t dismiss the idea of not treating all colonies all the time. I believe I saw a video where Randy Oliver was very excited about this research, and the prospect of selecting from colonies with proven mite tolerance while treating and requeening susceptible colonies.
The Norwegian beekeeper actually has a lot in common with Tom Seeley’s 10 suggestions for Darwinian beekeeping (https://www.naturalbeekeepingtrust.org/darwinian-beekeeping):
1. Locally adapted “street mix” (he has imported many queens over the years, including Elgon and Starline)
3. Single deep brood chamber
5. Insulated hives, which is standard in Norway
7. Doesn’t cull any drones (however he does take frames with drone brood and use them as part of his queen rearing and wax rotation practice, if I’m not mistaken)
8. Minimizes disturbance, as much as absolutely possible
9. Fairly stationary beekeeping, but does move some colonies to the heather
10. Hasn’t treated* for varroa since 1997
He also selects for a compact broodnest and the ability of the bees to be crammed tightly, which may be a contributing factor to his success. He does use 4.9mm, which may or may not be a factor. All in all, he thinks his results are due to three things: genetics, learned behaviour and the beekeeper. In other words: genes, “culture” and environment? There’s no silver bullet.
*) We only treat with organic acids in Norway. Here, treatment means only formic or oxalic acid.
Thank you for that comprehensive comment Joachim …
I’m aware of some of the work you cite. It’s some way from my own area of research so I’ll read it with interest. I am familiar with Seeley’s Darwinian beekeeping and intend to discuss it in the future.
The impression I get is that good colony management is a very important component in minimising or not needing treatment. The ability to identify problems in a colony and to take the appropriate action is not learnt overnight (or even over 2-3 years). In my experience there are a significant number of beekeepers who have yet to acquire some of these skills … they routinely cannot find the queen, they miss queen cells, they maintain colonies that are very weak and they suffer very high winter losses. Beekeeping is not easy. They like the idea of honey but not all the hard work (and disappointment) it takes to get the honey. The idea of “chemical free”, “natural” or “biodynamic” beekeeping appeals – whatever some of them actually mean! – and, after all, it’s additionally attractive as there’s less work involved.
However, it’s clear from the studies by Neumann, Conte etc. that, whilst evidence of resistance/tolerance exists, it is not achieved easily and it often involves several seasons of very heavy losses. You can embark on a selection strategy with a couple of hundred colonies, but not with two.
What remains to be determined is whether any of the bees that have come through this sort of selection process are compatible with ‘beekeeping as we know it’ … or whether we will have to make a fundamental change in the management of colonies and our expectations of their performance (and behaviour, pollination activity etc.).
Thanks again for the comment. I’ll get reading and write something more in the future.
Sorry for the late reply.
You’re absolutely right that resistance/tolerance often involves heavy losses, it did for the beekeeper I was talking about (though no more than he lost from his first application of formic acid, he claims).
I’m taking part in a local project where we try to achieve the same result without too many losses. We actively monitor mite levels through the season and only select queens from colonies with low levels, while either culling or requeening colonies that can’t cope with varroa, only treating with oxalic acid if mite levels get too high.
We’re also trying to copy the management practices of the Norwegian beekeeper I talked about, also basing our local population on his stock. Time will tell if we shall succeed, but there have already been others who have been successful in following his approach, so we’re hopeful.
The bees are highly productive, but they do require a lot of feed to get through our Norwegian winters. They’re also not as uniform in their qualities as for example Buckfasts or Carniolans, as his queen rearing is all about genetic depth. But I find them overall gentle and very easy to work with, you can have both gentleness and varroa tolerance.
I hope you’ll post an update when you have more information on your progress. The culling highly susceptible colonies is as aspect of Seeley’s Darwinian beekeeping that I suspect many who are keen on mite-tolerance may be unable to do. By the time you know they have very high mite loads it’s necessary to kill the colony, rather than just requeen. The mite and virus levels rapidly reach unmanageable levels and the colony is at risk of perishing overwinter.
Not all Buckfasts are uniform in my experience!
I’ll try to remember to post an update here, though I suspect it will take some years 🙂
Yes, only requeening is not enough. Sorry, I should have added that it should be done in combination with an oxalic acid treatment during an induced brood break. Randy Oliver has a good explanation of the method here (from page 49): http://scientificbeekeeping.com/scibeeimages/Oxalic-pdf-with-comments.pdf
I’m using the variation from page 55 onwards, where instead of just caging the queen you then introduce a new and hopefully better queen, treating with oxalic acid during the treatment window. You could also make splits, likewise making sure to treat when all mites are exposed.
I think these methods are doable for most beekeepers, as they are far easier (on the conscience) than having to cull a colony. I absolutely agree with your point on that in the article on Darwinian beekeeping. Killing colonies is among hardest things I’ve done in beekeeping, I wouldn’t want to do it regularly.
As you can tell, this is not treatment free or Darwinian beekeeping, but sort of a middle ground. I think the idea is to get as close as possible to the ideal while still remaining responsible beekeepers. While also taking into account the inevitable reinfestation from neighbouring apiaries. The long-term goal is to build up a local gene pool of varroa tolerant/resistant stock, as the Norwegian beekeeper in Oddie’s papers has achieved. Interestingly, he covers a lot of ground and sells a lot of queens to surrounding beekeepers. His bees’ gene pool is both genetically varied and geographically vast. That may be part of the answer to his success.
Thanks again for the interesting and thought-proviking articles on this blog!
I’ll wait for the follow-up with interest.