Tag Archives: DWV

Apistan resistance

Apistan

Apistan

In an earlier article I discussed what Apistan is – a pyrethroid miticide – and the consequences of using it. These include decimation of the mite population if it is susceptible, coupled with the accumulation of long lasting residues in wax. These residues may adversely effect queen and drone development. I also discussed ways to avoid build-up of Apistan residues in comb.

The key phrase in the paragraph above is ‘if it is susceptible’. Unfortunately, resistance to Apistan and the related tau-fluvalinates develops very quickly. To understand why we’ll need to look in a little more detail at how Apistan and other pyrethroids work.

How does Apistan work?

Apistan, like other pyrethroids, works by blocking the activity of voltage gated sodium channels (VGSC) resulting in paralysis because the axonal membrane cannot repolarise.

What on earth does that mean?

Action potential

Action potential

Nerve transmissions – like the signal from the Varroa brain to tell the Varroa legs to move – travel along axons. These are usually very long thin cells. In the adjacent image the ‘brain’ is on the left and the leg muscles on the ‘right’. The nerve impulse (the moving arrow) travels down the axon ‘driven’ by a change in polarity (charge) across the membrane of the axon. In the resting state, when there is no impulse, this is positively charged on the outside and negatively charged on the inside. Sodium – remember the ‘S’ in the acronym VGSC – is positively charged and crosses the membrane (out to in) via a small pore or hole as the impulse passes. This makes the inside of the axon transiently positive. The pore or hole is the VGSC.

Top view of a VGSC

Top view of a VGSC

The VGSC is a transmembrane protein. It actually crosses the membrane multiple times and assembles to form a very narrow channel through which the sodium passes. The cartoon on the right shows the top view of a VGSC, looking “down” the pore into the inside of the axon. The blue bits can move to open or close the pore, allowing sodium to traverse – or not – the membrane into the axon. Apistan binds to the transmembrane protein and prevents the pore from closing. As a consequence, sodium continues to pass from the outside to the inside of the axon, the nerve cannot repolarise and no further impulses can be transmitted. As a consequence, Apistan paralyses the Varroa.

But I don’t suppose many beekeepers will feel much sympathy for the mite 😉

Why isn’t the beekeeper paralysed as well?

Nerve impulses in Varroa and humans are transmitted in essentially the same way. We also have VGSC’s that operate in a similar manner. Why doesn’t Apistan also paralyse careless beekeepers? More generally, why are pyrethroids the most widely used insecticides, available in all garden centres and supermarkets?

Two factors are at work here. The first is the specificity of binding. The VGSC is a protein. Proteins are made from building blocks termed amino acids. The precise sequence, or order, of amino acids is usually critical for protein function. However, two proteins with a similar function can exhibit differences in the amino acid sequence. Although the human and mite VGSC have a similar function they have a different amino acid sequence. Apistan binds much better to the mite VGSC than the human VGSC (this also explains why bees aren’t also paralysed by Apistan … the miticide is specific for the mite VGSC and binds poorly to the honey bee VGSC). In addition, many mammalian species have a number of detoxifying enzymes which deactivate pyrethroids, rendering them ineffective. Together, this explains the specificity of Apistan and other pyrethroids, and the low level of toxicity to humans.

So now you know how Apistan works we can address the much more important question …

Does Apistan work?

Unfortunately, usually not. Since the late-1990’s there have been a large number of publications of Apistan- or fluvalinate-resistant mites from many countries, including the USA (1998, 2002), Israel (2000), UK (2002), Spain (2006), Korea (2009) and Poland (2012). The National Bee Unit used to report Varroa resistance test results by geographic region in England and Wales. Resistance was first reported in mites from Cornwall and Devon (in 2001 and 2002). By 2006 resistance was very widely distributed throughout England. By then approximately a third of all mite samples tested were resistant. The number of tests conducted (or at least reported) then dwindled and there have been none reported since 2010. Not no resistance … no tests. Presumably it’s no longer worth reporting as resistance is so widespread.

The most up-to-date map on the distribution of Apistan resistance I could find is in the NBU booklet on Managing Varroa [PDF; page 28 of the 2015 edition], though the data presented is from 2009.

However, bee equipment suppliers continue to sell Apistan (even Vita, the manufacturer, states that resistance is widespread) and beekeepers continue to use it. Many do so without first testing whether the mite population in their colonies is sensitive to the miticide. How should this be done?

Testing for resistance

Vita suggest two tests. Their first (the “rule of thumb test”) is deeply flawed in my view. It suggests simply looking for a drop of 100’s of mites in the first 24 hours after treatment starts as indicative of a sensitive population.

This isn’t good enough. What if there were thousands of mites present? Perhaps 20% of the population are sensitive, with the remainder resistant. 20% of 5000 mites is 1000 … so you might expect a drop of 100-200 (the majority of the phoretic population) within the first 24 hours. Some might consider this drop indicates a sensitive population … it doesn’t.

It’s not sufficient to count the corpses … you need to know how many mites were unaffected by the treatment.

The second Vita-recommended test is a cut-down version of the “Beltsville” pyrethroid resistance test which is fully described in an NBU pamphlet (PDF). This is much more thorough. Essentially this treats ~300 bees with Apistan, counts the mites that are killed in 24 hours and then counts the unaffected mites remaining on the bees. It’s only by knowing the total number of mites at the start and by determining the percentage of mites sensitive that you can be sure that the treatment is effective.

What is the molecular basis of resistance?

We’re almost there … specific pyrethroids, like Apistan, bind to specific parts of the VGSC. The VGSC is a protein made up of a long connecting chain of amino acids. The binding of the pyrethroid requires an interaction with a small number of specific amino acids in the VGSC. If these particular amino acids change – through mutation for example – then the pyrethroid will no longer bind. If the pyrethroid does not bind the VGSC can open and close again, so the axon repolarises and the mite is not paralysed. The mite is resistant and can then go on to rear lots more resistant baby mites … which, in due course, transfer the viruses that kill your bees.

And that’s exactly what happens.

Leucine

Leucine

A single mutation that causes a substitution of amino acid number 925 in the Varroa VGSC, which is usually a leucine, to either a valine, a methionine or an isoleucine, is sufficient to prevent Apistan and other tau-fluvalinates from binding. At least 98% of mites resistant to Apistan have one of these substitutions. Apistan resistant mites with substitutions at position 925 have been found in the UK, eastern Europe and several sites in South-Eastern USA. It wouldn’t be surprising if the remaining ~2% of resistant mites had a mutation at one of the other amino acids involved in pyrethroid binding. Further studies will confirm this (there are alternative mechanisms that cause resistance, but the one described here is the most frequently seen).

Why aren’t all Varroa mites resistant to tau-fluvalinates?

Apistan resistance has clearly been demonstrated for the last two decades. Resistance is easy to acquire and selection – in the presence of the pyrethroid – is effectively absolute. Without the necessary mutation the mites die, with the mutation they survive.

Bees – and the phoretic mites that are associated with them – are moved around the place all the time, by migratory beekeepers, by importers and through robbing and drifting between colonies.

Why therefore aren’t all Varroa mites now resistant to Apistan and other tau-fluvalinates?

The answer to that is interesting and suggests strategies that could make Apistan an effective treatment again … but I’ll save that for another time.


Only transiently as the charge is reversed shortly afterwards by a similar, though not identical,  mechanism that does not use the VGSC. However, life is simply too short to describe this bit as it’s not needed to understand pyrethroid – or Apistan – activity and resistance.

 The incestuous life cycle of the Varroa mite is important here. This post is already too long to fully elaborate on this but the size of the mite population relative to available open brood (and whether you get single or multiple occupancy of cells) will likely influence the proportion of resistant, partially resistant and sensitive mites in a population.

Credits – the action potential GIF was created by Laurentaylorj from Wikipedia.

 

CSI: Forensics in Fife

This is a long post. If you can’t be bothered to read it in its entirety the conclusion is …

It’s the viruses wot done it … probably.

But the take home message is that you can learn from colonies lost in midwinter.

Introduction

I always have mixed feelings about midwinter hive losses, or deadouts as they’re called in the US. Of course, I regret losing the colony and wonder whether I could have managed them differently, or prepared them better, to increase their chances of survival. At the same time I’d much prefer a weak colony perishes in midwinter rather than having to mollycoddle them through the spring.

Winter colony losses in the UK vary from year to year but have averaged about 20% over the last decade (BBKA figures and SBA data). Whether these accurately reflect real losses is unclear to me – there are no statistics and they are usually by self-selected beekeeper reporting, so possibly unreliable.

Mollycoddling weak colonies in the Spring … a wasted effort?

The reality is that weak colonies in the spring require a lot of support and still may not survive. Even if they do, there’s little chance they will be strong enough to exploit anything other than the late season nectar flows.

If the colony is weak because of queen problems then they are likely to need re-queening. This requires a spare queen early in the season – not impossible, but it needs planning or is likely to be expensive. In my view you’d be better off using the ‘spare’ queen to make up a nuc from a prolific colony, rather than trying to rescue what might be a basket case.

If the colony is weak because of disease then having them limp on through the spring is a potential disaster for your other colonies. If it doesn’t recover quickly it’s likely that neighbouring colonies will rob it out, both destroying the weak colony and transferring whatever it was ailing from around the apiary.

Finally, the colony might be weak due to poor management e.g. insufficient stores in the early spring when the queen was gearing up to lay again. In this case you might be able to rescue the situation by boosting it with syrup, brood and bees. However, care is needed not to weaken your other colonies. Two half-strength colonies are more work and much less use – they will collect  less honey – than one full strong colony.

Learning from your losses

So, rather than pampering weak colonies in Spring – particularly if they’re struggling because of disease or queen problems – I’d prefer they expired in the winter. That sounds cruel but isn’t meant to. The reality is that a proportion of all colonies are likely to be lost in the winter … on average ~20%, but significantly more in long hard winters (or perhaps with more accurate surveys!). As beekeepers, all we can do is manage them in ways to minimise these losses – keep strong, healthy colonies and provide them with sufficient stores – and learn from those that are lost.

How do you learn from the losses? By examining the ‘deadout’ and trying to work out what went wrong. You then use this information in subsequent seasons to try and avoid a repeat performance.

For example …

A life in the year of a June swarm

Sometime in early/mid January a colony of mine died.

The colony was alive in early December when treated for mites. It was suspiciously quite at the end of that month when other colonies were flying. It looked moribund by mid-January on a quick visit to the apiary.

I took the hive apart on the 30th of January to see what might have gone wrong.

But before the autopsy, here’s the history of the deceased …

  • 7th June – a small to medium sized swarm arrives in a bait hive. The bait hive had foundationless frames so it was difficult to estimate the amount of bees in terms of ‘frames covered’. My notes state ” … 4-5 frames of bees (ish) …”.
  • 8th June – very brief inspection, two frames nearly drawn. Queen not seen.
  • 9th June – vaporised with an oxalic acid-containing treatment. 21 mites dropped in the first 24 hours. Not monitored after that as I replaced the solid floor of the bait hive with an open mesh floor.
  • 19th June – unmarked queen laying well. My notes state “… suspect this is a 2015 Q on account of the lousy weather we’ve had …”. There was already sealed brood present.
  • 27th June – clipped and marked the queen blue. At this point there were over 7 frames of brood in all stages – eggs, larvae and sealed brood – present.
  • Between then and mid-August the colony continued to build up very well … so well I ‘harvested’ three frames of brood and bees to make up nucs for circle splits.
  • In mid/late August I treated three times at five day intervals with a vaporised oxalic acid-containing miticide. My notes in August state ” … KEEP AN EYE ON THIS ONE … very high mite levels …” and (after a second round of treatment) in late September, ” … mite levels still high …”. Actual mite counts weren’t recorded.
  • In late September/early October the colony was fed with fondant. An additional block of fondant was left on into the late autumn.
  • Further miticide treatment was added in early December. Mite drop was high but not outrageous – about 44/day averaged over the first 5 days, dropping to 3/day over the subsequent five day period.
  • By late December the mite drop was less than one per day … however, by this time I was beginning to be concerned as there was very little activity from the colony on the warm days around Christmas.

The autopsy

I took the roof off the hive and removed the remaining fondant. Some of the fondant had dripped down between the frames but, in taking these apart, it was clear there were sufficient stores present.

The frames were clean. There were no sign of Nosema, which usually appears as distinctive faecal smearing and marking on the top bars, the face of the frames and – in a heavily infected colony – the front of the hive.

The frames were almost devoid of bees. There were a hundred of so clinging to the middle pair of frames. I brushed these away to reveal a dozen or so corpses stuck headfirst down in the cells. This is characteristic of starvation. These particular bees likely died of starvation, but the majority did not (or they would have also been wedged headfirst into the comb).

Having removed the frames the few hundred dead bees lying on the open mesh floor could be seen. Amongst these was the blue marked and clipped queen. The bees on the floor weren’t showing any obvious signs of disease – no characteristic shrivelled wings seen with overt deformed wing virus infection for example.

I’d walked to the apiary so couldn’t take the hive away with me. I therefore sealed up the entrance to prevent any robbing just in case there was disease present that could be transmitted to another colony. In due course I’ll burn old frames, I’ll treat some of the good drawn comb with acetic acid fumes and I’ll clean and sterilise the hive.

Elementary, my dear Watson

There’s no really obvious smoking gun, but there are some reasonably strong clues. I’m pretty sure why and how this colony succumbed.

But first, what didn’t kill off the colony? Well, Nosema didn’t and nor did starvation. Sure, a handful of bees in the middle frame died of starvation, but the majority were on the floor and there were ample stores in the hive and some fondant remaining. It had also been warm enough to move about within the colony to get to these stores.

It’s not possible to deduce much about the queen. The colony was strong in late August but not fully inspected after that. My notes state that brood levels were low in late September, but they were in all the colonies I peaked in at that time. She could have failed catastrophically soon afterwards. If she had I might have expected to find signs of attempted replacement e.g. a queen cell, as there were a few warm periods in the autumn. The fact that she was still present is far from conclusive, but suggests to me that she didn’t fail outright. The colony wasn’t full of drones late in the season suggesting she was poorly mated, though there are plenty of other ways the queen can fail. At least until late August she was laying very well.

I think the two main clues are the Varroa levels in autumn and December, coupled with the small number of bees present on the floor of the colony. Taking those in reverse order. There were far fewer bees than I would have expected from a colony that entered the autumn with about 8 frames of brood. This suggests to me that the bees were dying off at a faster rate than expected. Many bees that died off earlier in the winter would have been carried out and discarded on the warmer days.

The Varroa levels were very high in autumn and quite high (at least for my colonies) in December. In the autumn I didn’t record the numbers. A couple of hundred dropped after treatment in December isn’t huge … but I suspect that the colony was much reduced in size by now meaning the percentage infestation was likely significant.

The damage was already done …

Miss Scarlett in the ballroom with the lead piping

I think this colony died due to the viruses transmitted by Varroa, in particular deformed wing virus (DWV). DWV is known to shorten the life of overwintering honey bees – see this study by Dainat et al., for full details.

DWV symptoms

DWV symptoms

Why are there no symptomatic bees visible in the carpet of bees littering the floor of the hive? That’s easy … you only get these symptoms in very young bees that have emerged from Varroa-infested brood. In the winter there’s little or no brood (and there certainly wasn’t for some time in this colony). Any bees in this colony that had emerged with DWV symptoms would have been discarded from the colony months earlier. The colony was inspected every 7-10 days from mid-June to late July but there were no obvious signs of DWV symptomatic bees. They might have been missed, but I’m reasonably experienced at spotting them.

My interpretation is that the colony arrived with high Varroa levels and that – despite treatment shortly after arrival – these persisted through to mid-August. The mites transmitted the usual cocktail of pathogenic DWV strains within the colony. High Varroa levels are known to result in the massive amplification of virulent DWV strains in exposed bees. This late summer/early autumn period is a critical time for a colony. It’s when the overwintering bees are being reared. I discuss this at length in When to treat?. These overwintering bees, now infected with virulent strains of DWV, subsequently died off at a higher rate than normal. Despite the colony appearing reasonably strong in late August, many of the bees were carrying a lethal viral payload.

Bees that died in late autumn would have been carried out of the hive and discarded in the usual manner. Overall bee numbers continued to dwindle, leaving just a few hundred and the queen by the year end. We’ve had some hard frosts in the last month. The expired colony is in the same apiary as the bee shed which has a max/min thermometer inside. The lowest temperature seen was -6°C during this period. This probably finished them off.

So no crime scene … just another reminder that the viruses will get you if the Varroa levels are allowed to get too high.

Learning from my mistakes

I think I made one big mistake with this colony … way back on the 10th of June, just three days after it moved into the bait hive. I treated for mites, monitored mite drop after 24 hours and then left the colony with an open mesh floor. I should have monitored for longer (mite drop after vaporisation is often greater after the first 24 hours). I would have then realised how badly infested they were and could have taken greater care to reduce mite levels. By mid/late August mite levels were probably catastrophically high. They were hammered down with miticides but the damage was already done. I suspect that this is also a good example of why the timing of treatment is critical.

It’s sobering that an apparently minor oversight in midsummer probably resulted in the loss of the colony in midwinter.

If you got this far, well done. It wasn’t my intention to write so much. Swarms are a significant source of potential disease and carry a disproportionately high mite load … something I’ll discuss in the future.


 They are not unreliable because they are reported by beekeepers 😉  Not entirely anyway. They are unreliable because they are generally a self-selecting group that report them. The BBKA or SBA ask for beekeepers to complete a survey. Some do, many do not. The BBKA do not report – at least in their press releases – the number of respondents. Self-selecting bias in surveys means they may not be entirely (or at all) accurate. The SBA surveys by Magnus Peterson and Alison Gray are more thorough. For their 2014 report for example the sample size was 350, with a total of 213 respondents (for comparison, there are about 4000 beekeepers in Scotland). With this information, coupled with some additional data – for example, knowing that only 87% of respondents were actually keeping bees during the survey period! – you can determine how representative the survey is.

 Sherlock Holmes never uses this phrase in any of the books by Conan Doyle though he does use a number of similar expressions. The phrase “Elementary, my dear Watson” was first used by PG Wodehouse in Psmith, Journalist which was published contemperaneously (1909). The actor Clive Brook used the phrase in the 1929 film The return of Sherlock Holmes.

2016 in retrospect

The end of another year and another season’s beekeeping. Now is a good time to review what went well and what went badly.

The bee shed in autumn ...

The bee shed in autumn …

In terms of my beekeeping year in Scotland, the end of December isn’t even half way through the winter. Although I didn’t open many hives after mid-September (three and a half months ago), unless we get a warm, early Spring I don’t expect to do any inspections until mid-April. That’s another four and a half months to ruminate on the year passed and plan for the season ahead.

The high points

The great escape ...

The great escape …

This was the first full season using the bee shed and I’m already convinced of the advantages it offers. Colonies built up well in the late Spring, appreciably faster than colonies in the same apiary that didn’t benefit from the protection the shed offers. I was able to inspect whatever the weather. Only really warm days were a problem, and that was because it gets uncomfortably hot. The Up-and-Out™ windows (the bees crawl up and fly out) clear the shed very quickly, making it a good environment for grafting larvae when queen rearing without getting buzzed with bees all the time. It would benefit from power, better lighting, a kettle and an armchair … perhaps something to plan for 2017? It’s never going to resemble the palatial setups in some of those German bee houses, but in terms of secure, weatherproof and sheltered accommodation, it’s hard to beat.

Varroa control has worked well this year. A combination of timely applications of treatment and a significant brood break in the middle of the season, meant that colonies went into the winter with low to very low Varroa levels. Some broodless colonies dropped less than 20 mites after midwinter treatment which is very encouraging.

OSR ... can you believe it?!

OSR … can you believe it?!

I’ve also been pleased with the honey flavour this year. By missing the OSR – too cold (the photo above was taken at the end of April) – the early season honey was a heady mix of goodness knows what, and all the better for it. Great flavour and it has sold well. The switch to square jars with distinctive black lids looks good and, coupled with a very simple DIY label, it’s been popular with repeat customers. My honey is currently available – assuming they haven’t sold out over Christmas – from Mellis Cheese in St. Andrews and Edinburgh, and Luvians in Cupar.

The low points

The most significant problems were all related to queens. Firstly, queens from 2015 were poorly mated (as predicted way back in June 2015) and several gave up (stopped laying) or simply disappeared in May/June. Secondly, my own queen rearing coincided with shortfall and an extended period of very poor weather for queen mating. As a consequence, several hives developed laying workers and needed some significant interventions to rescue them.

Drone laying workers ...

Drone laying workers …

All of these problems – some of my own making, but some unavoidable – meant that production colonies weren’t really strong enough to exploit the summer nectar flow. Honey yields from the summer were the worst I’ve had for half a decade, though the flavour was outstanding. I’ve a couple of 30lb buckets left that I’m hoping to eke out over the next few weeks in the smallest possible portions. To add insult to injury … it was apparently one of the best years for heather honey and, because of the problems detailed above, I was singularly unprepared to take advantage of it. In all honesty, I’m not wildly disappointed about this as I’m not a great fan of heather honey. However, since I’m in Scotland and heather honey is considered by many as the crème de la crème, I feel I’ve missed a golden opportunity.

The new season

With the winter solstice now passed it’s time to make plans for the coming season. I’ll deal with these in the Spring as this article is already longer than intended.

www.theapiarist.org

It’s been a busy year with posts almost every Friday. This was more than I’d intended at the beginning of the year, but seems to have happened without too much contrivance. Although posted on a Friday, they’re written in the days and weeks preceding (hence explaining the butchered tenses often used).

Keeping it regular

Keeping it regular

I’ve always tried to avoid the diary-like cataloguing of what goes on in the apiary (as there are others who do this much better), instead focusing on a balance between topical items and more expansive posts – often written as separate linked articles (like on Varroa control or queen rearing) – that both reflect my interests and might help others improve their beekeeping … if only by avoiding my mistakes 😉

Page views and visitors

Page views and visitors

Other than a slightly odd dip in July – a belated “June gap”? – visitor numbers and page views showed the expected pattern of increasing interest in mid/late Spring, tailing off again as the season draws to a close. The peak figures in October reflect the interest in feeding fondant and mite treatments. Clearly there’s still some work to do … treating for mites in October is likely to be too late to protect the winter bees from the ravages of deformed wing virus. Over the entire year the original 2014 posting about honey warming cabinets remained the most popular, with articles on feeding fondant, vertical splits, steam wax extractors and foundationless frames getting lots of attention as well.

Search and ye shall find …

Google and most other search engines ‘hide’ the search terms used by viewers to reach a website. This is nominally valuable information, though looking at the terms that do get through the filters makes you wonder … each of the terms below led the viewer to this site (the typos are original) :

circular large 200 frame honey extractor plans … as opposed to a small 200 frame extractor?

wellies with honey bee pucturers on … puctures?

using laser printer in unheated wooden shed … electric heater needed I think

square drones frame homemaking striping images … random word generator?

foundationless sheds … understandable considering foundationless frames and bee sheds

poly queen beekeeping pdf … article on poly queen beekeeping in preparation for 2017

plastic nuc boxes for sale in manitoba … perhaps a little too geographically specialised

simple label design for honey sales in nigeria … see Manitoba

do i feed bees with apiguard … not exactly

is dettol effective against varroa mites … rigorous testing needed and possibly tainted honey?

how to treat a double brood hive with api bioxal … article on beekeeping bankruptcy to follow

houney bees kb shed bnati h or kb kha jays h … yes, that really was a search term

save humanity a topic covered in detail earlier this year

humanity save … there’s a theme emerging here

how do bees save humanity … by pretending to be wasps

Unsocial media

It’s clear that there are whole communities of beekeepers out there with very different online activities – some interchangeably use old-fashioned websites (like this site) and various types of social media, others restrict themselves to Twitter and Facebook. Posts to this site are now also ‘announced’ on Twitter (@The_Apiarist) and Facebook. I still have to get the hang of Facebook as I’ve not previously used it … I don’t even know how to properly link to it 🙁

Anyway … enough for the year. As I write this the winter solstice has now passed, the days will be getting longer and lighter, queens will – particularly now with the warmer winter weather – be starting to lay and mites will be starting to reproduce. There’s very little to do in the apiary, but the new season is definitely on its way …

For 2017 I hope your bees are gentle, your queens are prolific, your supers are heavy and your swarms end up in my bait hives 😉

Happy New Year

Frosty apiary

Frosty apiary

 

Get dribbling

There has been a prolonged spell of cold weather in Eastern Scotland. Temperatures have rarely risen above 5°C, with hard frosts overnight. However, a warm front moved in on Tuesday night and the last few days have been significantly warmer. The lack of activity at the hive entrances and a quick peek under the insulation through the perspex crownboards (where fitted) indicated the bees were all tightly clustered during the cold spell. Furthermore, the absence of debris on the removable Varroa monitoring trays fitted to many of the open mesh floors, suggested that little or no brood was being reared.

Ridiculous to the sublime

Ridiculous to the sublime

Varroa counts

Varroa trays ...

Varroa trays …

There was another clue that the colonies are likely broodless. I had been recording the natural Varroa drop of a few colonies over the last month. I did this by simply counting Varroa at each visit, calculated on a mites/day basis. Although generally low (and very low in a few colonies), it had been steadily increasing. This is a good indication there were more phoretic mites in the colony … again, presumably due to the absence of suitable brood for them to parasitise.

It’s worth noting that the natural mite drop is a notoriously unreliable method of accurately determining mite levels in a colony. For example, it’s dependent upon the amount of sealed brood in the colony. With no sealed brood all mites must be phoretic. In contrast, with limitless sealed brood 80-90% of the mites are within cells. However, although estimates from mite drop are not hugely accurate, they are a lot better than doing nothing. The National Bee Unit has published a Varroa calculator. This allows you to use a combination of the mite drop per day, the time of year, length of season and level of drone brood to predict the total numbers of mites in the colony. For some inexplicable reason this asks for the level of drone brood in December … with 0% not being an available option  🙁

Time to treat

With little or no brood in the colonies, now is a perfect time to treat with an oxalic acid-containing preparation to hammer down the remaining mite population. I’ve previously discussed the importance of this midwinter treatment (see Two treatments … a double whammy). In many ways it’s preparation for the season ahead, rather than for the protection of the bees already present in the colony. The lower the mite levels are at the beginning of the season, the longer it will take for the mite population to reach dangerously high levels.

BEEHAVE ...

BEEHAVE …

You can model these events using BEEHAVE. This is an interesting in silico model of a beehive. With mite numbers of ~10 at the beginning of the year, maximum levels reached are low to mid-hundreds by late summer, reducing to a couple of hundred the following winter. This assumes no intervening treatment and runs the model using all the default settings. In contrast, using the same parameters but starting the year with ~100 mites, levels peak at between 3000 and 4000 mites, returning to about 1800 in December.

Remember that the National Bee Unit recommends mite levels should not exceed 1000 or there is a risk of “significant adverse effects on the colony”. Therefore, the midwinter treatment is an important preparation for the year ahead, delaying the point at which these dangerously high mite levels are achieved.

Have your hives got less than 100 mites in them now?

Remember also that, with no sealed brood, midwinter is also the ideal time to expose as many mites as possible to the treatment. With the exception of prolonged treatment with hard chemicals like Apistan or Apivar, it’s probably the only time you’ll achieve greater than 95% reduction in mite numbers. With little or no brood present there’s nowhere for the mites to hide.

Dribbling or vaporisation?

An oxalic acid-containing treatment is recommended in midwinter. This can be delivered by dribbling or sublimation (vaporisation). Under optimal conditions, efficacy of the two methods is broadly similar (90%+) though there is some evidence that dribbled oxalic acid is slightly detrimental to colonies (when compared with sublimation, but not when compared to doing nothing).

Sublimox in use

Sublimox in use …

Api-Bioxal is the VMD-approved oxalic acid-containing treatment. If used for dribbling be aware that the suggested concentration on the side of the packet is higher than conventionally used in the UK. It’s also worth noting that it’s not available pre-mixed so has to be made up from powder. In this regard it’s a less useful product than the pre-mixed oxalic acid solution that Thorne’s (and possibly other suppliers) sold each winter. The one- or two-hive beekeeper needs to weigh out very small amounts accurately, or get together with others to make a large batch. Hardly what I’d call progress. Furthermore, the inclusion of glucose and powdered silica (as an anti-caking agent) in Api-Bioxal means it leaves a caramelised mess if used for vaporisation. Although a scouring pad and elbow grease will get rid of this mess, it’s another example of how the “approved” commercial product is actually less good – and no more effective – than the oxalic acid dihydrate that beekeepers have been using for 20 years or more.

Notwithstanding these negative comments, Api-Bioxal works well and is less expensive (per treatment) than most of the other VMD-approved Varroa treatments.

Don’t delay, get out and get dribbling …

The forecast for the next 7-10 days is for significantly warmer temperatures. This means that the queen – if she was having a break from egg-laying – will start laying again. There will be open brood by this weekend and sealed brood in your colonies by about the 15th of December. Dribbled oxalic acid is detrimental to – and may kill – open brood so if this is your preferred method of treatment then don’t delay. If you sublimate you’ve got a few days leeway, but don’t delay any longer than that.

Here are a couple of old videos showing trickling (dribbling) oxalic acid onto a large and small colony in the middle of winter. The Trickle bottle from Thorne’s makes administering the treatment very quick and easy.

Of course, sublimation using an active vaporiser like a Sublimox is even faster and doesn’t involve opening the colony. Here’s an example showing treatment of a recently hived swarm in midsummer … I could have removed the Sublimox after about 30 seconds.

The Daily Mail may be predicting the coldest winter since the last ice age (so perhaps there will be another broodless period§) but I wouldn’t rely on them to influence something as important as the midwinter treatment for reducing Varroa levels.


Here’s a perfect example of the problems encountered by the ‘topical blogger’. I wanted to write about midwinter Varroa treatment in the middle of winter, at a time when others – particular new beekeepers – should be treating their own colonies. Typically these treatments are made in late December or early January. However, the long-range (10 day) forecast in late November suggested the second week of December might be suitable. Some of this was therefore written in very late November, the Varroa drop comments added once I’d completed counting around the 4th to the 6th, and the post finished off the following day once I’d treated my own colonies.

This assumes that the queen started laying on the 7th, the first full day with elevated temperatures.

§ I didn’t open any colonies to confirm they were broodless. I was happy enough to take the clues from the increased mite drop on the Varroa trays and the absence of debris indicating uncapping of brood cells. However, I was told by friends that other colonies they opened on the 7th were broodless.

 

Helensburgh & District BKA talk

DWV symptoms

DWV symptoms

I’m very pleased to be speaking on the 24th of November (this Thursday) to members of the Helensburgh and District BKA. The talk will be at the rather splendid looking Rhu Parish Church at 7.15pm. The title of the talk is “Bees, viruses and Varroa: the biology and control of deformed wing virus (DWV)”. I’ll discuss aspects of the biology of DWV, particularly relating to its transmission by Varroa, and will then explore potential ways in which bees could be ‘protected’ using either high-tech or low-tech approaches. If you’re attending please introduce yourself when we’re all having a cuppa at the end of the evening … don’t leave it too late though, I’ve got a 2 hour drive home afterwards.

Update

The drive from the east coast to Helensburgh was stunning, with a fantastic pink-tinged sunset lighting up the snow-covered hills around Crainlarich (Stuc a’ Chroin, Ben Vorlich and Ben Ledi). It was bitterly cold and clear.

Stuc a' Chroin and Ben Vorlich ...

Stuc a’ Chroin and Ben Vorlich …

There was a slight delay due to an absentee projector. During this we discussed oxalic acid-containing treatments for Varroa control and the problems caused by the lack of a ready-mixed preparation of Api-Bioxal. Once the projector arrived we were up and running and I covered viruses and Varroa, why we treat when we treat (or perhaps more correctly ‘when should we treat for maximum effect?’) and the influence of drifting and robbing on parasite and pathogen transmission between colonies. That’s quite a lot to get through in an hour … and I didn’t. The audience were rewarded for their patience with a well-earned cup of tea and a question and answer session.

The return trip was less visually pleasing other than a great view of a barn owl ghosting along the verges of the A977 near Rumbling Bridge. With thanks to Cameron Macallum and colleagues for their hospitality and a very enjoyable evening.

Those pesky mites

DWV symptoms

DWV symptoms

If you haven’t yet treated your colonies to reduce Varroa levels before the winter arrives it may well be too late. High Varroa levels are known to result in the transmission of virulent strains of deformed wing virus (DWV). These replicate to very high levels and reduce the lifespan of bees. If this happens to the ‘winter bees’ raised in late summer/early autumn there’s a significant chance that the colony will die during the winter.

Mite levels in most of my colonies have been very low this year. Partly due to thorough Varroa management in the 2015/16 winter (the only thing I can take credit for), partly due to the relative sparsity of beekeepers in Fife, partly due to the late Spring and consequent slow build-up of colonies and partly due to an extended mid-season brood break when requeening. Most colonies yielded only a small number of mites (<50) during and after a 3 x 5 day treatment regime (to be discussed in detail in a later post) by sublimation.

Infested arrivals

The low mite drop definitely wasn’t due to operator error or vaporiser malfunction. At the same time I treated a swarm that had moved into a bait hive in early June …

Out, damn'd mite ...

Out, damn’d mite …

This is ~20% of the Varroa tray. Have a guess at the number of mites in this view only. Click on the image to read the full legend which includes the mite count.

The image above was taken on the 18th of September, a day or two after starting the second round of 3 x 5 day treatments. The colony really was riddled. When a colony swarms 35% of the mites in the colony leave with the swarm (or, in this case, arrives with it). For this reason the swarm was treated for mites shortly after it arrived in June. It did have a reasonably high mite load but subsequently built up very quickly and didn’t experience the mid-season brood break my other colonies benefitted from.

The colony now has an acceptable mite drop (<1 per day). Similar colonies are still rearing brood – I’ve not checked this one, but they are bringing in some pollen from somewhere – so there’s a possibility the majority of the remaining mites are tucked away in sealed cells. I’ll keep a close eye on this colony through the next few weeks and will be treating again midwinter to further reduce the parasite burden.

Treat ’em right

If you are treating this late in the season make sure you use a miticide that is appropriate for the conditions. Apiguard (a thymol-containing treatment) is almost certainly unsuitable unless you’re living in southern France as it needs a temperature of 15°C to be effective. MAQS has a recommended temperature minimum of 10°C which may be achievable.

Hard chemicals such as Apivar and Apistan can be used at lower temperatures but there’s little point in treating with Apistan unless you’re certain all your mites are sensitive. They almost certainly are not as Apistan/Bayvarol resistance is very widespread in the UK mite population. Just because you get an increased mite drop in the presence of Apistan does not mean treatment has been effective. Perhaps all you’ve done is killed the sensitive mites in the population, leaving the remainder untroubled. This is what’s known as a bad idea … both for your bees next season and for your neighbours.


 I’m posting this now due to the large number of searches for, and visits to, pages on use of Apiguard or other Varroa treatments. These are currently running second to ‘fondant‘ in one form or another.

Bee lining for Christmas

Bee hunting

Bee hunting

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

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.

Conclusions

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 ...

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.

Keep your distance

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 ...

Frey and Rosenkranz (2014) Mite invasion …

What can we conclude from these studies?

  1. 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.
  2. 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.
  3. 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?
  4. 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 ...

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 effective Varroa 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.

Gaffer tape apiary

Gaffer tape apiary …

Divide and conquer

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 One 11:e0150362).

Size matters

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

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

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.


§ at least in the good years 😉

When to treat?

Preparing Apiguard

Preparing Apiguard …

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 vaporiser etc. 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

DWV symptoms

DWV symptoms

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

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 ...

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?

The apiary in winter ...

The apiary in winter …

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.

In conclusion

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

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

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.


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 …

References

Overwintering honey bees: biology and management from the Grozinger lab.

Managing Varroa (PDF) by the National Bee Unit