Following the Wild Bees† by Tom Seeley is an entertaining little book that would make an ideal Christmas present for a beekeeper. It describes the methods used to locate feral colonies (or any colonies actually) by bee hunting or bee lining, so called because you follow the line or direction they return to the colony from a nectar source you provide. It’s an ideal Christmas book for two main reasons; it’s a summer activity, so will remind the reader that balmy sunny days will – finally – replace the cold, dark days of winter and, secondly, it will allow the enthusiast the time to build the essential two-chambered ‘bee lining box’ which is used to trap, feed and mark the bees being ‘lined’.
I don’t intend to provide a précis of the method … you should buy and read the book for that. However, as a taster, you can visit the companion website to the book or watch a short video of Tom Seeley bee hunting …
Tom Seeley is a Professor in the Department of Neurobiology and Behaviour at Cornell University. He is a highly respected entomologist and, unlike many scientists, writes in an engaging and accessible manner. He explains complicated experiments in layman’s terms and makes parallels between his observations on honey bees and wider societal issues. Anyone who has read his book “Honeybee Democracy” will appreciate how simple and elegant his description of the science is.
His explanation of bee hunting is no less clear. Following the Wild Bees is really a ‘how to’ guide, rather than a popular science book, though each chapter does contain a separate section on the science behind the ‘how to’, together with lots of anecdotes. The book is subtitled “The craft and science of bee hunting”. If you’re not aware of feral colonies in your own area this book might help you find them … however, if you live in an area with lots of other beekeepers it will probably just help you find their apiaries (and you can also do that with Google maps).
Wild? They’re livid feral.
The most up-to-date review of feral colonies in the UK can probably be found in Catherine Thompson’s 2012 doctoral thesis (brace yourself … this links to PDF of the 173 page thesis!). Catherine surveyed a number of feral colonies in the UK and showed that, although there were limited but significant genetic differences between feral colonies and managed colonies, the feral colonies were no more ‘native’. Catherine also neatly demonstrates the limitations of studying wing veination (morphometry) as an indicator of genetic purity – it usually isn’t. Feral colonies are essentially relatively recent swarms lost by local beekeepers.
Why ‘relatively recent’?
High levels of DWV …
The feral bees Catherine studied had much higher levels of deformed wing virus (DWV), both indicative of – and as would be expected of – uncontrolled Varroa infestation. Therefore, whilst it might appear appealing to have colonies of wild bees in the local church tower they’re almost certainly riddled with DWV and Varroa. This presumably explains why so many of the feral colonies Catherine analysed died during the study period (2.5 years). The swarms lost by beekeepers (that occupy the church tower for example) quickly succumb to the detrimental effects of uncontrolled Varroa replication and the consequent transmission of viruses. Furthermore, through the activities of robbing and drifting that feral colony is likely to act as the generous donor of viruses and mites to the local managed beekeepers hives.
Perhaps not so appealing after all.
I recommend you read Following the Wild Bees. Do so sitting in front of a roaring log fire in mid-winter. Plan and build a ‘bee lining box’ (or buy one) and consider where you might go prospecting for ‘wild’ bees once the long summer days return.
But also plan to put out bait hives to catch swarms (yours or others) and clip your queens … every one ‘lost’ is an opportunity to establish a future source of Varroa and virus infestation.
Under offer …
† ISBN-10 0691170266 … it’s worth shopping around for a copy as the prices vary widely (at the time of writing). WH Smiths had it for well under a tenner recently.
A recent paper by Nolan and Delaplane (Apidologie 10.1007/s13592-016-0443-9) provides further evidence that drifting/robbing between colonies is an important contributor to Varroa transmission. In the study they established multiple pairs of essentially Varroa-free colonies 0, 10 or 100 metres apart and then spiked one of the pair with a known number of Varroa. They then monitored mite build-up in the paired colonies over several months. By comparison of the relative mite increases in colonies separated by different distances they showed that the more closely spaced, the more likely they were to acquire more Varroa, presumably through robbing or drifting.
This isn’t rocket science. However, it’s a nicely-conducted study and emphasises the importance of colony spacing on the transmission of phoretic mites between infested and uninfested colonies – through the normal colony activities such as robbing and drifting – as a primary cause of deformed wing virus (DWV) disease spread in the honey bee population. The paper only studies mite levels, but the association with DWV transmission is well established and unequivocal.
Related studies on the influence of colony/apiary separation
The introduction to the paper provides a good overview of the prior literature on the impact of drifting on disease and Varroa transmission, some of which has already been discussed here. However, some of these studies have not previously been mentioned and deserve an airing, for example:
Sakofski et al., (1990) showed that there was no difference in mite migration between colonies in closely-spaced rows from those located up to 10m apart.
Frey and Rosenkranz (2014) showed that high-density colonies (>300 within flight range [2.5 km] of the sentinel colonies) experienced approaching 4-fold greater inbound mite migration than when located in areas containing a low-density of treated colonies. Over a 3.5 month period the difference was 462 +/- 74 vs. 126 +/- 16 mites. This would have a very significant impact if allowed to subsequently replicate in the recipient colonies.
Frey et al., (2011) previously investigated mite transfer between colonies located 1m to 1500m apart. Strikingly, in this study (which was conducted during a dearth of nectar) mite transmission was effectively distance-independent, with the recipient colonies acquiring 85 – 444 mites over a 2 month period.
Frey and Rosenkranz (2014) Mite invasion …
What can we conclude from these studies?
Closely-spaced colonies – for example, the sort of distances used to separate colonies in an apiary – should really be viewed as a single location as far as mite infestation is concerned. A single heavily-infested colony in an apiary will quickly act as a source of mites to all other colonies.
High densities of beekeepers – assuming the usual range in both the timing and vigour with which Varroa control is practised – is probably detrimental to maintaining low mite levels in your own bees.
Significant mite transmission occurs over distances of at least 1.5 km … not just between hives in a single apiary. How many colonies are there within 1.5 km of your own apiary? Even if you are careful about controlling mite levels, what about all the beekeepers around you?
Colonies wth uncontrolled levels of mite infestation, abandoned colonies (or swarms that occupy abandoned hives) and feral colonies located at least 1.5 km away are potential sources from which your carefully-maintained hives get re-infested …
Recent experience with high and low density beekeeping
One mile radius …
I’ve moved in the last year from the Midlands to Fife. Beebase and my involvement with local beekeepers suggest that these represent areas of high and low colony-density respectively. For comparison, Beebase indicates that there were over 230 apiaries within 10 km of my home apiary in the Midlands and that there are currently 20 within a similar range in Fife. In the Midlands I was aware of at least 25 colonies (in several different apiaries) within a mile of one of my apiaries. Furthermore, apiaries might contain lots of hives … one of those previously within 10 km of my home apiary was our association apiary which held up to 30 colonies from ~15 beekeepers. In contrast, the closest beekeeper to my current home apiary is almost 3km away … though I acknowledge there may well be hives “under the radar” belonging to beekeepers that are not members of the local association or have not bothered to registered on Beebase (why not?). It’s far too early to be definitive but mite levels in my colonies have been reassuringly low this season. This includes uncapping hundreds of drone pupae – the preferred site for Varroa to replicate – without detecting a single mite. I’d like to think this was due to timely and effectiveVarroa control, but it is undoubtedly helped because my neighbours are further away … and perhaps better at controlling the mite levels in their own colonies.
This study provides further compelling evidence of the importance of either keeping colonies isolated (which may not be possible) and ensuring that all colonies in the same and adjacent apiaries are coordinately treated during efforts to control mite numbers.
Tom Seeley (of Honeybee Democracy fame) published an interesting paper in the journal PLoS One recently on “How honey bee colonies survive in the wild: testing the importance of small nests and swarming” – the paper is available as a PDF following this link (Loftus et al., 2016 PLoS One11:e0150362).
Using his normal elegant methodology Seeley formally tested the observed reduction in colony size and increased swarminess (is that a word?) of – feral or otherwise – colonies ‘selected’ to survive without Varroa treatment by simply abandoning them. The hypothesis – based on previous studies and an understanding of the biology of Varroa – was that colonies ‘forced’ to swarm by being confined in small hives would inevitably:
lose significant amount of Varroa through the act of swarming
experience a brood break so delaying Varroa replication while requeening
consequently survive better than large colonies in which pathogen levels inexorably increased to a level that would destroy the colony
Testing the hypothesis
He tested this by establishing adjacent apiaries (so they have the same microclimate) with either small (~40 litres … about the same as a National brood box) or large (~170 litre) volume hives and installing nucs in each which contained similar levels of brood, bees and Varroa. No Varroa control was performed. Those in the small hives were not managed to prevent swarming whereas those in the large hives were – with the caveat that the colony was kept together (i.e. queen cells were destroyed, brood frames were spread and ample supers were added). The study lasted two years, with regular monitoring of the colony strength, Varroa infestation level etc.
High levels of DWV …
To cut a long (but nevertheless interesting and worth reading) story short … the results support the original hypothesis. During the first year of the study the colonies developed in a broadly similar manner from transfer of the nuc to the large or small hive in June until the season’s end. However, by the following May the large hived colonies were almost twice as populous as those in the small boxes. This continued until August, with the average adult bee population in the small and large hives being ~10,000 and ~30,000 respectively. During this second season 10/12 small hives swarmed, whereas only 2/12 of the large hived colonies swarmed. In the latter mite levels dramatically increased to >6/100 adult bees (i.e. riddled with the little b’stards – my opinion, Seeley is too polite to comment). For comparison, the picture above has ~100 bees in it, with one visible Varroa, but has lots of overt deformed wing virus disease. In contrast, the small hived colonies – with the exception on one sampling point discussed later – had three to five times fewer mites than seen in the large hived colonies. By the second winter 10/12 large hived colonies had perished whereas only 4/12 small hived colonies had succumbed, and one of these was to a drone laying queen, not disease. Perhaps most tellingly, 7/12 large hived colonies had signs of overt deformed wing virus (DWV) disease – pathetic, tottering newly emerged workers with stunted abdomens and shrivelled wings – whereas none of those in small hives showed obvious disease.
Great … Varroa-tolerant colonies … where can I get some?
A small swarm
So, what does this mean in terms of practical beekeeping? Firstly, it suggests that it is possible to keep honey bee colonies without treatment or intervention. But – and it’s a biggy – the colonies will be too small to collect meaningful amounts of honey and will spend their time and energy swarming instead. 10,000 adult bees does not a colony make, as Aristotle didn’t say. Or at least not a colony that’s of any practical use for the honey-gathering goal of beekeeping. Ted Hooper (“Bees and honey“), and many others, have made the point that one big colony will gather more nectar than two smaller colonies. Secondly, these small colonies will chuck out loads of Varroa-riddled swarms. Seeley has previously demonstrated that swarming colonies lose ~35% of their Varroa load with the bees that leave the colony. Although this clearly benefits the original colony it potentially distributes Varroa-laden bees (and the smorgasbord of viral pathogens that are the real problem) to whichever local beekeeper finally hives them. This explains the need for prompt Varroa treatment of any swarms you might acquire.
On a more positive note this study clearly shows the benefit of a brood break in terms of restricting the replication and amplification of Varroa. Presumably this is primarily due to the 3+ week window with no sealed brood for Varroa to infest, though it may also mean that broodless colonies might get rid of Varroa at a faster rate with no brood present to distract them. It would be interesting to have compared mite levels immediately after swarming and in the subsequent weeks until the new queen starts laying. Randy Oliver has also discussed the benefits of a brood break during empirical development (and computer modelling) of his beekeeping methods for Varroa control. In his forthright manner he explains “Take home message: early splitting knocks the snot out of mite levels“.
Why discuss this if they’re no use for beekeeping … ?
There was one exception to the generally low mite levels in the small hived colonies and that was late summer in the second year when they all exhibited a large spike in Varroa numbers. This was attributed to robbing-out a collapsing, and soon to die-off completely, large hived colony in the adjacent apiary. The two study apiaries were in the same field. This emphasises the points made in earlier posts about the impact of drifting and robbing and the, at least theoretical benefits of, coordinated Varroa control. Of course, ~2 mites per 100 adult bees in the small hived colonies is not really a low number at all. Assuming a colony size of 10,000 adults with 80% of the mites in capped cells the total Varroa load would be ~1000 in the colony, the threshold level above which the NBU consider treatment is required to avoid loss of the colony.
Divide and conquer
The Varroa loss achieved by swarming, coupled with the break in brood rearing, help the colony conquer – or more correctly tolerate – Varroa levels that otherwise rapidly increase and destroy a colony. However, this is neither a practical or acceptable solution to the Varroa problem. ‘Beekeepers’ (an oxymoron surely?) that allow their colonies to swarm indiscriminately both reduce their chance of getting a good honey crop and impose their – potentially Varroa-ridden – swarms on the neighbourhood. This is irresponsible. In contrast, beekeepers who carefully monitor their colonies and use an effective combination of integrated pest management – for example, including an enforced brood break during the ‘June gap’, or a vertical split, perhaps – benefit from large, healthy, honey-laden§ colonies which overwinter better.
When and how do you treat colonies to have the greatest effect in minimising Varroa levels? At the end of this longer than usual post I hope you’ll appreciate that this is a different – and much less important – question than “When is the best time to treat?”.
You probably use one of the treatments licensed and approved by the Veterinary Medicines Directorate (VMD), which include Apistan, Apivar, Apiguard, MAQS and Api-Bioxal. I’ve discussed the cost-effectiveness of these treatments recently. If used correctly, all exhibit much the same efficacy, reducing phoretic mite levels by 90-95% under optimal conditions. That being the case the choice between them can be made on other criteria … the ease of administration, the cost/treatment, the likelihood of tainting the honey crop, the compatibility with brood rearing, whether they mess up your vaporiseretc. After using Apiguard for several years, with oxalic acid (OA) dribbled in midwinter, my current preference – used throughout the 2015 season – is OA sublimation or vaporisation. This change was based on four things – efficiency, cost, ease of administration and how well it is tolerated by a laying queen. The how? you treat is actually reasonably straightforward.
When, not how, is the question
OK, but what about when? Because, if the treatments are all much of a muchness if used correctly, the when is actually the more important consideration. When might be partly dictated by the treatment per se. For example, Apiguard needs an active colony to transfer the thymol throughout the hive so the recommendation is to use it when the ambient temperature is at least 15ºC (PDF guidance from Vita). It’s worth stressing that this is the ambient temperature, not the temperature in the colony, which in places will be mid-30’s even when it’s much colder outside. At low ambient temperatures the colony becomes less active, and in due course clusters, meaning that Apiguard is not spread well throughout the colony, and is therefore much less effective. If you’re going to use Apiguard you must not leave treatment too late.
For readers in Scotland it’s interesting to note that the SBA annual survey by Peterson and Gray shows significant numbers still use Apiguard in September and October, months in which the mean daily maximum temperature is ~14°C and 11°C respectively … so the average daily temperature will be well below the recommended temperature for effective Apiguard use.
However, the when should be primarily informed by the why you’re treating in the first place. It’s not really Varroa that’s the problem for bees, it’s the viruses that the mite transfers between bees when it feeds on developing pupae that cause all the problems. Most important of these is probably Deformed Wing Virus (DWV), but there are a handful of other viruses pathogenic to bees that are also transmitted. DWV causes the symptoms shown in the image above … these bees are doomed and will be ejected from the hive promptly. However, although apparently healthy (asymptomatic) bees have low levels of DWV, it’s been shown by Swiss researchers that DWV reduces the lifespan of worker bees, and that high levels of DWV in a colony are directly associated with – and causative of – overwintering colony losses. Therefore, the purpose of late summer/early autumn treatment is to reduce the Varroa levels sufficiently so that high levels of the virulent strains of DWV are not transmitted to the overwintering bees.When? therefore has to be early enough that this population, critical for overwinter survival, will live through to the spring – however long the winter lasts and however severe it is. However, before discussing when winter bees are reared it’s worth considering what happens if treatment is used early or late.
What happens if you treat early?
Mid June treatment …
For example, mid-season or after the first honey crop comes off. Nothing much … other than slaughtering many of the phoretic mites. This is what most beekeepers would call “a result” 😉 Aside from possible undesirable side effects of treatment – like tainting honey, or preventing the queen from laying or even, with some treatments, queen losses – early treatment simply reduces mite levels. It’s important to remember that the levels may well not be reduced sufficiently to negate the need for a treatment later in the season … as long as there is brood being raised the mites will be reproducing (for example, look at the mid-June treatment generated using BEEHAVE modelling – image above). Furthermore, avoiding those undesirable side effects might require some ‘creative’ beekeeping (for example, clearing the supers and moving them to another hive) and will certainly inform the choice of treatment but, fundamentally, if the mite levels are high then treating earlier than is usual will benefit the colony, at least temporarily. If the mite levels – estimated from the disappointingly inaccurate mite drop perhaps – are dangerously high you should treat the colony.
What happens if you treat late in the season?
Isolation starvation …
In midsummer workers only live for ~40 days. If mite levels are high, virus transmitted to these workers will shorten their lives, so reducing the colonies’ foraging ability and – possibly – ability to defend itself against wasps or robbing late in the season. However, if you delay treatment until very late the lifespan of bees raised at the end of the season – the overwintering bees – will be reduced with potentially more devastating consequences. The usual winter attrition rate of workers will be higher. The cluster size of the colony will shrink faster than a colony with low mite levels. At some point the colony will cross a threshold below which it becomes non-viable. The cluster is too small to move in cold periods to new stores, resulting in the beekeeper finding a pathetic little cluster of bees in a colony that’s succumbed to isolation starvation. A larger cluster, spread across a greater area and more frames, is much more likely to span an area of sealed stores and be able to exploit it.
When are winter bees reared?
In the Swiss study referred to above they looked at the longevity of winter bees. The title of the paper is “Dead or alive: deformed wing virus and Varroa destructor reduce the life span of winter honeybees”. We can use their data to infer when winter bees start to be reared in the colony and when mite treatments should therefore have been completed to protect these bees. Their studies were conducted in Bern, Switzerland, in 2007/08 where the average temperature in November/December that year was 3ºC. They first observed measurable differences in winter bee longevity (between colonies that subsequently succumbed or survived) in mid-November. This was 50 days after bees emerged and were marked to allow their age to be determined. By the end of November these differences were more pronounced. Therefore, by mid-November Varroa and virus-exposed winter bees are already exhibiting a reduced lifespan. Subtracting 50 days from mid-November means these bees must have emerged in late September. Worker development takes ~21 days, so the eggs must have been laid in the first week of September, and the developing larvae capped in mid-September.
To protect this population of overwintering bees in these colonies, mite treatments would have had to be completed by the middle of September, so that mite levels were sufficiently low that the developing larvae weren’t capped in a cell with a Varroa mite carrying a potentially lethal payload of DWV. For Apiguard treatment (which takes 2 x 14 days) this means treatment should have been started in mid-August. For oxalic acid vaporisation (which empirical tests suggest is best conducted three times at five day intervals) treatment would need to start no later than early September and preferably earlier as it is effective for up to a month.
Of course, these figures and dates aren’t absolute – the weather during the study would have influenced when the larvae would be raised as winter bees, with the increased fat deposits and other characteristics that are needed to support the colony survival through the winter. Despite the study being based in Switzerland my calculations on dates are probably broadly relevant to the UK … for example, the temperature during their study period is only about 1ºC lower than the 100 year average for Nov/Dec in Eastern Scotland where I now live.
That was all a bit protracted but it hopefully explains why it’s important to be selective about when you administer Varroa treatments. Chucking in a couple of trays of Apiguard in mid-August or mid-October has very different outcomes:
in mid-August the phoretic mite population should be decimated, reducing the transmission of virulent DWV to the all-important winter bees that are going to get the colony through the winter. This is a good thing.
in mid-October the mite population will be reduced (not decimated, as it’s probably too cool to effectively transfer the thymol around the hive – see above) but many of the winter bees will already have emerged, probably with elevated levels of DWV to which they will succumb in December or January. This is a bad thing.
Perhaps perversely, treating early enough to prevent the expected Varroa-mediated damage to developing winter bees is not be the best way to minimise mite numbers in the colony going into the winter. Using BEEHAVE I modelled the consequences of treating in the middle of each month between August and November¹. I used the default BEEHAVE setup as described previously. Figures plotted are the average of 3 simulations, each ‘primed’ with 20 mites at the start of the year.
Time of treatment and mite numbers
There’s a lot on this graph. To show colony development I plotted numbers of eggs, larvae and pupae (left axis) as dotted red, blue and black lines respectively. Mite numbers are shown in solid lines – treated with a generic miticide in mid-July (black), mid-August (blue), mid-September (brown), mid-October (cyan) and mid-November (green). In each case the miticide is considered to be 95% effective at killing phoretic mites. The gold arrowhead indicates the period during which winter bees are developing in the colony, based upon the data from Dainat.
Oxalic acid trickling
Treating at or before mid-August controls the late-summer build up of mites in the colony – look how the blue line changes direction. Mites that are not killed go on to reproduce in late September and early October, resulting in levels of ~200 at the year end. Remember that mites present in midwinter can, in the absence of sealed brood, be effectively controlled by trickling or vaporising oxalic acid (Api-Bioxal), and that this Christmas miticide application is particularly important if the autumn treatment has not been fully effective. In contrast, treating as late as October and November (cyan and green lines) exposes the developing winter bees to the highest mite levels that occur in the colony doing the year, and only then decimates the phoretic mite numbers, with those that remain being unable to reproduce effectively as the brood rearing period is almost over. Starting treatment in mid-September isn’t much different, in terms of exposing the winter bees to high mite levels, than starting later in the year.
So, within reason, treating earlier rather than later both reduces the maximum mite levels and helps protect the winter bees from virus exposure. Of course, treating as early as mid/late August may not be compatible with your main honey crop (particularly if you take hives to the heather) … but that’s another issue and one to be addressed in a future post.
STOP PRESS There is a very important follow-up article to this. Kick ’em when they’re down describes why it’s so important to treat during a broodless period in midwinter to minimise mite numbers at the start of the following year. Just treating in late summer is not sufficient … you’ll protect your winter bees, only for them to be targeted by mites the following Spring.
¹BEEHAVE makes a distinction between ‘infected’ and ‘uninfected’ Varroa, the proportions of which can be modified. This might (no pun intended) not accurately reflect the reality in the hive, where Varroa-mediated transmission of DWV results in the preferential amplification of virulent strains of the virus. I need to roll my sleeves up and delve into the code to see if the model can be altered to fully reflect our current understanding of the biology of the virus. This might take quite a while …
During previous research on deformed wing virus (DWV) biology and its transmission by Varroa I’ve moved known Varroa-free colonies (sourced from a region of the UK which the mite has yet to reach and maintained totally mite-free) into apiaries in the countryside. Within 2-3 weeks Varroa was detectable in sealed brood, showing that mite infestation occurs very readily. I know other researchers who have made very similar observations. Where do these mites come from?
They’re not all ‘your’ bees
The obvious source would be the phoretic mites transported on workers ‘drifting’ from nearby infested colonies, or on drones which are known to travel quite long distances and may be accepted by almost any colony. If you want to see how frequent this is try marking a few dozen drones with a dab of paint. To avoid confusion use the colour used to mark queens next year. There are unlikely to be 4+ year old queens in the apiary and the drones will all perish before the end of the current season. Over the next few days and weeks the drones will appear in adjacent colonies, and some will likely leave the apiary and be accepted in your neighbours colonies.
How to encourage drifting …
Beekeepers are usually aware that colonies at the ends of rows often ‘accumulate’ bees that have drifted when returning to the hive. In shared association apiaries some crafty beekeepers will site their colonies at the ends of rows to take advantage of the ‘generosity’ of other colonies. However, many beekeepers probably do not appreciate the extent to which drifting occurs. Pfeiffer and Crailsheim (1998) report that 13-42% of the population of a colony are ‘alien’ i.e. have drifted from adjacent hives, depending upon the time of season. Remember that drifting occurs in both directions simultaneously, so the overall numbers of bees in a colony may not be adversely affected (or boosted). In other studies Sekulja and colleagues (2014) showed that ~1% of marked bees drifted between colonies over a three day observation window. Interestingly, American foulbrood (AFB) infected bees drifted slightly more than uninfected bees. Spread of foulbroods during drifting is one reason the bee inspectors check nearby apiaries when there is an outbreak. These studies were all on workers where drifting primarily occurs during orientation flights before the bees become foragers. Drones drift two to three times more than workers (Free, 1958).
The likelihood of drifting must be closely related to the separation of hives and apiaries. Although workers will forage up to 2-3 miles from the hive I suspect the proportion of bees that drift this distance is extremely small. However, unless you’re very isolated I expect there are other apiaries within a mile or so of your own. Drones are known to fly up to about five miles to reach drone congregation areas for queen mating and are accepted by all colonies. I’ve regularly found drones appearing in (relatively) isolated mini-nucs. I’m not aware of studies that have formally tested drifting between apiaries (though it is reported in passing in the Sekulja et al., 2014 paper cited above).
Consequences of drifting
So, your hives probably contain workers and drones from other nearby colonies, and you can only really be sure that they’re all “your” bees if you live – as the sole beekeeper – on an isolated island. Not only does your neighbour generously exchange bees with you, he or she also kindly shares the phoretic mites those bees are carrying, the viral payload the bees and mites are infected with and – if you’re really unlucky – the Paenibacillus larvae spores responsible for causing AFB infection (and vice versa of course).
There are lessons here that should inform the way we conduct our integrated pest management to maintain healthy colonies.
This post provides background information for an article (“Viruses and Varroa: Using our current controls more effectively” by David Evans, Fiona Highet and Alan Bowman) in the December 2015 issue of Scottish Beekeeper, the monthly magazine for members of the Scottish Beekeepers Association.
Sublimation is the conversion of a substance in the solid phase into the gas phase without going via the intermediate liquid phase. With suitable heating oxalic acid (OA) powder can be converted into a vapour which, when spread through the hive, provides a quick and effective way to reduce the mite levels … hence it’s often referred to as oxalic acid vaporisation (or vaporization … if you search the web on this topic you’ll find at least four variant spellings). With too much heating OA decomposes to formic acid and carbon monoxide, so the temperature of the vaporiser is critical to generate the optimal cloud of OA vapour (or vapor!). I’ve been using a Sublimox vaporiser this season with good results and provide a description of the machine and its use here.
Vaporisation vs dribbling
Most beekeepers are familiar with midwinter treatment with 3.2% OA solution (in syrup), applied by ‘dribbling‘ 5ml per seam across the clustered colony. Under these conditions the colony needs to be broodless as a) it’s not effective against mites in capped cells and b) the OA dissolved in syrup is toxic to brood. It’s also reported that the ingested OA may be suppress subsequent brood rearing, at precisely the time the colony should be getting started for the upcoming season. Vaporisation or sublimation avoids this toxicity … the OA is introduced to the hive as a gas which permeates the entire colony, recrystallising as tiny crystals on all surfaces – bees, comb, internal walls etc. Studies of OA vaporisation has shown it is ~95% effective in reducing phoretic mite numbers. I recommend you read the extensive coverage by Randy Oliver @ Scientific Beekeeping who covers efficacy, mode of action and toxicity (though I’ll return to this last bit later).
This is an active vaporiser which blows a jet of vaporised OA through a small (8mm) nozzle. The machine consists of a handle, a box of electrickery (which I’ve not opened) and a heating pan surrounded with a safety guard. The machine is rated at 230V AC and 300W so you need either a car battery and inverter or a suitable generator (which is what I use). The vaporiser is simplicity itself to use. One gram of OA powder is placed into a small plastic ‘cup’, the preheated vaporiser is inverted and the ‘cup’ engaged with the heating pan. The nozzle is pushed through a hole in the hive body and the vaporiser is inverted again (so it’s now the correct way up – see the top photo on this page). The OA drops into the heating cup, immediately vaporises and is blown through the nozzle into the hive. It takes 40-50 seconds to use all the OA, at which point you can move on to the next hive.
This video shows the effect of dropping a few millilitres of water into the heating pan … it’s almost exactly the same when using OA, but less likely to cover my camera with a fine dusting of OA crystals 😉
Preparing the hive
Entrance block …
To fill the hive with vaporised OA it’s important that as little as possible leaks out during the short period of treatment. I use a Correx Varroa tray underneath the open mesh floor. In addition, the kewl floors I use are easy to block using a simple L-shaped piece of softwood (I use these when transporting hives; when screwed onto the front of the floor there’s no danger of bees escaping). Part of the beauty of OA vaporisation is that the hive does not even need to be opened. I’ve drilled 9mm holes just above the open mesh floor level, through either the side or back of my floors. This is a better location to insert the nozzle of the Sublimox as there’s space under the frames to allow the gas to spread evenly and quickly throughout the hive. This is easier than the alternatives of using an eke with a suitable hole in it, or drilling through the side wall of the brood box (this is too close to the frames and you get poor spread of the gas – I’ve tried this on hives with a perspex crown board and it’s very obvious).
Sublimox in use …
With a standard floor you could use a simple entrance block with a suitable hole in it. The nozzle gets hot … keep it away from poly hives or nucs! I treat my Everynuc poly nucs directly through the (cavernous) front entrance which I block using a thick piece of wood with a 9mm hole through the middle.
Preparing the beekeeper
OA vapour is pretty unpleasant and causes significant irritation to the eyes and lungs if exposed. Take care. You will need suitable eye protection and a mask of some sort. I use standard (and very inexpensive) safety goggles and a 3M dust/mist mask. You should also wear gloves when handling OA. It’s also wise to stand upwind of colonies being treated and to take care not to breath in any OA vapour that leaks out of gaps in the hive.
I’ve treated four swarms this year using OA vaporisation. Three had very low mite levels, but the small churchyard swarm dropped several hundred mites in the 2-3 days following treatment. I don’t routinely count the mite drop on each day post treatment (I have a life) but have noticed it can increase over the first 2-3 days and then tails off over the following week or so. In large scale studies in Europe 95% efficacy was reported with mite drop continuing for up to a fortnight. There are a number of useful references on the Scientific Beekeeping site if you want to follow this up further.
Inserted inverted …
There goes a few pence …
I’ve also used OA vaporisation on almost all my colonies this autumn, instead of Apiguard treatment. If the colony has sealed brood the usual estimate is that at least 80% of the mites are occupying capped cells. These mites are unaffected by OA vaporisation (until they emerge) and it is therefore necessary to perform repeat treatments. Taking account of the life cycle of the mite and empirical measurements made by Hivemaker reported on the Beekeeping Forum, three treatments at five day intervals are required to have the maximum effect. Ideally this should be on a day or at a time when most of the colony is ‘at home’ … though the crystallised OA continues to be effective for several days after initial treatment. Fortunately, OA vaporisation has little or no effect on the queen, unlike many other mite treatments. The colony gets mildly agitated during treatment but calms down again within minutes and resumes foraging. In the colonies I’ve looked at after treatment there appears to be no gap in egg laying (I’ve also treated casts with virgin queens that have gone on to mate successfully). This is ideal for the autumn treatment when you want the colony to raise as many bees for overwintering as possible. In contrast, Apiguard regularly stops the queen from laying.
And finally …
There are other OA vaporisers made, and instructions on the web for a variety of DIY items – some looking more dangerous (to the operator, not the mite) than others. The majority of these are passive vaporisers, in which the OA is placed in a cool heating pan which is then placed on the floor of the colony and heated up. I’ve not used this type. They have the advantage of being less expensive and only require a 12V supply. However, they are slower to use as the pan takes longer to heat up and then needs to be cooled in a bucket of water between applications. They are also incompatible with the kewl floors I use and I presume – depending on how hot they get – with poly hives and nucs. I think the efficacy of the two types is supposed to be broadly similar.
I listened to Bob Smith talk at the MSWCC conference last week on shook swarms. I sat there thinking that a shook swarm followed shortly afterwards by a single shot of OA vapour would give a colony a really good opportunity to build up well, free of pathogens that have accumulated in the comb and free of the majority of phoretic mites and their viral payload.
The Sublimox vaporiser is not inexpensive. It costs about €380 from Icko Apiculture. This is a lot, but is about the same as three 3kg tubs of Apiguard (C. Wynn Jones list this at £87 a tub at the time of writing) which is enough to treat 90 colonies with two treatments per colony. In contrast, OA dihydrate powder in bulk (not from Thorne’s) is about £20 for 5kg … enough for 1250 colonies (assuming 4 treatments per colony – 3 doses in the autumn and one midwinter). For beekeeping associations, particularly those with large shared apiaries when treatments could and should – see a later post – be coordinated, it might be a very good investment.
I spent last Friday and Saturday attending the Midland and South West Counties Convention at the Royal Agricultural University, Cirencester. It was a good venue for a meeting, complemented by an interesting and entertaining programme of talks. I presented our research on the influence of Varroa on the transmission of pathogenic strains of deformed wing virus, together with brief coverage of both high and low-tech solutions that might be useful in mitigating the detrimental impact of the mite on the virus population (and hence, the colony).
Queen rearing course
On the Saturday I donned my beekeepers hat (veil?) and discussed queenright queen rearing methods – a talk really aimed at encouraging beginners to ‘have a go’. I’m was aware there were people in the audience who earn their living from bees whereas I largely dabble at the weekends, and that they’ve probably forgotten more about queen rearing than I’m ever likely to learn. I’m always (silently) grateful they don’t ask tricky questions or interrupt with a “You don’t want to be doing that …” comment. I think only about 10% of beekeepers actively raise queens – by which I mean select suitable larvae and generate ‘spares’ for increase, sale or giving away. Without more learning how relatively easy it is to raise queen we cannot hope to be self-sufficient and will remain reliant on imported stocks, of largely unknown provenance (and with an unknown pathogen payload), particularly at the beginning and end of the season. There were excellent presentations on the analysis of pollen in forensic studies (Michael Keith-Lucas) and the use of the shook swarm (Bob Smith), together with a very interesting mead tasting event. I unfortunately missed the workshops and the Saturday afternoon presentations as I had to waste hours hanging around for three delayed trains to eventually get to Heathrow a few minutes after my flight back to Scotland departed 🙁
The MSWCC 2016 event will be running again next year (on the Gower) in mid-October hosted by Swansea and District BKA. The theme is “Meet the Natives” and – if this year is anything to go by – it promises to be a very worthwhile event.
I’m delighted to be sharing the programme with Michael Palmer and Celia Davies at the Somerset BKA lecture day in Cheddar this Saturday (21st February ’15). I’ll be adding a small bit of science to the day and no doubt benefiting significantly from their wealth of beekeeping expertise. It should be a very enjoyable event.
Update – it was a very enjoyable event. Aside from a few audio problems with a misbehaving microphone a packed hall enjoyed two talks by Celia Davies on Summer and Winter Bees and A World of Scents and a further two from Michael Palmer on the Sustainable Apiary and Queen rearing.
If you’ve not heard Michael talk about the importance of overwintering nucs for sustainable beekeeping then you should either try and catch him on his current UK tour or watch him deliver the talk at the 2013 National Honey Show on YouTube. I think I’ve heard this talk three times and have learnt something new every time. The methods Michael uses directly address the problems (lack of early-season queens, overwintering losses etc.) I’ve previously outlined in a post on the impact of imported bees and queens on the quality of UK beekeeping in Supply and Demand.
All the talks – including the science of Varroa and deformed wing virus I presented – generated lots of questions and discussions. With thanks to Sharon Blake for the invitation and organisation of the day.
Deformed wing virus (DWV) is probably the most important viral pathogen of honeybees. In the presence of Varroa the virus is amplified to very high levels in the colony, resulting in newly emerged workers – those that survive long enough to emerge – exhibiting the classic symptoms familiar to most beekeepers. These include deformed or atrophied wings, a stunted abdomen, additional deformities or paralysis of appendages and (not visible) learning impairment. There is a clear association between high Varroa levels, high levels of DWV symptomatic bees and overwintering colony losses.
Classic DWV symptoms
These images are of workers from a colony treated for a month with Apiguard to reduce mite numbers. Many bees remained with symptoms. I suspect the high levels of mites pre-treatment resulted in the amplification of virulent strains of DWV which continued to cause disease even after the mite numbers were reduced. This emphasises the need to monitor mite numbers and treat appropriately with Apiguard, oxalic acid or – during the season – other appropriate integrated pest management practices such as drone brood culling.