Category Archives: Varroa control

The flow must go on

Except it doesn’t ūüôĀ

And once the summer nectar flow is over, the honey ripened and the supers safely removed it is time to prepare the colonies for the winter ahead.

It might seem that mid/late August is very early to be thinking about this when the first frosts are probably still 10-12 weeks away. There may even be the possibility of some Himalayan balsam or, further south than here in Fife, late season ivy.

However, the winter preparations are arguably the¬†most important time in the beekeeping year. If you leave it too late there’s a good chance that colonies will struggle with disease, starvation or a toxic combination of the two.

Long-lived bees

The egg laying rate of the queen drops significantly in late summer. I used this graph recently when discussing drones, but look carefully at the upper line with open symbols (worker brood). This data is for Aberdeen, so if you’re beekeeping in Totnes, or Toulouse, it’ll be later in the calendar. But it will be a broadly similar shape.

Seasonal production of sealed brood in Aberdeen, Scotland.

Worker brood production is down by ~75% when early July and early September are compared.

Not only are the numbers of bees dropping, but their fate is very different as well.

The worker bees reared in early July probably expired while foraging in late August. Those being reared in early September might still be alive and well in February or March.

These are the ‘winter bees‘ that maintain the colony through the cold, dark months so ensuring it is able to develop strongly the following spring.

The purpose of winter preparations is threefold:

    1. Encourage the colony to produce good numbers of winter bees
    2. Make sure they have sufficient stores to get through the winter
    3. Minimise Varroa levels to ensure winter bee longevity

I’ll deal with these in reverse order.

Varroa and viruses

The greatest threat to honey bees is the toxic stew of viruses transmitted by the Varroa mite. Chief amongst these is deformed wing virus (DWV) that results in developmental abnormalities in heavily infected brood.

DWV is well-tolerated by honey bees in the absence of Varroa. The virus is probably predominantly transmitted between bees during feeding, replicating in the gut but not spreading systemically.

However, Varroa transmits the virus when it feeds on haemolymph (or is it the fat body?), so bypassing any protective immune responses that occur in the gut. Consequently the virus can reach all sorts of other sensitive tissues resulting in the symptoms most beekeepers are all too familiar with.

Worker bee with DWV symptoms

Worker bee with DWV symptoms

However, some bees have very high levels of virus but no overt symptoms 1.

But they’re not necessarily healthy …

Several studies have clearly demonstrated that colonies with high levels of Varroa and DWV are much more likely to succumb during the winter 2.

This is because deformed wing virus reduces the longevity of winter bees. Knowing this, the increased winter losses make sense; colonies die because they ‘run out’ of bees to protect the queen and/or early developing brood.

I’ve suggested previously that isolation starvation may actually be the result of large numbers of winter bees dying because of high DWV levels.¬†If the cluster hadn’t shrunk so much they’d still be in contact with the stores.

Even if they stagger on until the spring, colony build up will be slow and faltering and the hive is unlikely to be productive.

Protecting winter bees

The most read article on this site is When to treat? This provides all the gory details and is worth reading to get a better appreciation of the subject.

However, the two most important points have already been made in this post. Winter bees are being reared from late August/early September and their longevity depends upon protecting them from Varroa and DWV.

To minimise exposure to Varroa and DWV you must therefore ensure that mite levels are reduced significantly in late summer.

Since most miticides are incompatible with honey production this means treating very soon after the supers are removed 3.

Time of treatment and mite numbers

Time of treatment and mite numbers

Once the supers are off there’s nothing to be gained by delaying treatment … other than more mite-exposed bees ūüôĀ

In the graph above the period during which winter bees are being reared is the green arrow between days 240 and 300 (essentially September and October). Mite levels are indicated with solid lines, coloured according to the month of treatment. You kill more mites by treating in mid-October (cyan) but the developing winter bees are exposed to higher mite levels.

In absolute numbers more mites are present and killed because they’ve had longer to replicate … on your developing winter bee pupae ūüôĀ

Full details and a complete explanation is provided in When to treat?

So, once the supers are off, treat as early as is practical. Don’t delay until late September or early October 4.

Treat with what?

As long as it’s effective and used properly I don’t think it matters too much.

Amitraz strip placed in the hive.

Apiguard if it’s warm enough. Apistan if there’s no resistance to pyrethroids in the local mite population (there probably will be ūüôĀ ). Amitraz or even multiple doses of vaporised oxalic acid-containing miticide such as Api-Bioxal¬†5.

This year I’ve exclusively used Amitraz (Apivar). It’s readily available, very straightforward to use and extremely effective. There’s little well-documented resistance and it does not leave residues in the comb.

The same comments could be made for Apiguard though the weather cannot be relied upon to remain warm enough for its use here in Scotland.

Another reason to not use Apiguard is that it is often poorly tolerated by the queen who promptly stops laying … just when you want her to lay lots of eggs to hatch and develop into winter bees 6.

Feed ’em up

The summer nectar has dried up. You’ve also removed the supers for extraction.

Colonies are likely to be packed with bees and to be low on stores.

Should the weather prevent foraging there’s a real chance colonies might starve 7 so it makes sense to feed them promptly.

The colony will need ~20 kg (or more) of stores to get through the winter. The amount needed will be influenced by the bees 8, the climate and how well insulated the hive is.

I only feed my bees fondant. Some consider this unusual 9, but it suits me, my beekeeping … and my bees.

Bought in bulk, fondant (this year) costs £10.55 for a 12.5 kg block. Assuming there are some stores already in the hive this means I need one to one and a half blocks per colony (i.e. about £16).

These three photographs show a few of the reasons why I only use fondant.

  • It’s prepackaged and ready to use. Nothing to make up. Just remove the cardboard box.
  • Preparation is simplicity itself … just slice it in half with a long sharp knife. Or use a spade.
  • Open the block like a book and invert over a queen excluder. Use an empty super to provide headroom and then replace the crownboard and roof.
  • That’s it. You’re done. Have a holiday ūüėČ
  • The timings shown above are real … and there were a couple of additional photos not used. From opening the cardboard box to adding back the roof took¬†less than 90 seconds. And that includes me taking the photos¬†and cutting the block in half ūüôā
  • But equally important is what is¬†not shown in the photographs.
    • No standing over a stove making up gallons of syrup for days in advance.
    • There is no specialist or additional equipment needed. For example, there are no bulky syrup feeders to store for 48 weeks of the year.
    • No spilt syrup to attract wasps.
    • Boxed, fondant keeps for ages. Some of the boxes I used this year were purchased in 2017.
    • The empty boxes are ideal for customers to carry away the honey they have purchased from you ūüėČ
  • The final thing not shown relates to how quickly it is taken down by the bees and is discussed below.

I’m surprised more beekeepers don’t purchase fondant in bulk through their associations and take advantage of the convenience it offers. By the pallet-load delivery is usually free.

Fancy fondant

Capped honey is about 82% sugar by weight. Fondant is pretty close to this at about 78%. Thick syrup (2:1 by weight) is 66% sugar.

Therefore to feed equivalent amounts of sugar for winter you need a greater weight of syrup. Which – assuming you’re not buying it pre-made – means you have to prepare and carry large volumes (and weights) of syrup.

Meaning containers to clean and store.

But consider what the bees have to do with the sugar you provide. They have to take it down into the brood box and store it in a form that does not ferment.

Fermenting stores can cause dysentry. This is ‘a bad thing’ if you are trapped by adverse weather in a hive with 10,000 close relatives … who also have dysentry. Ewww ūüėĮ

To reduce the water content the bees use space and energy. Space to store the syrup and energy to evaporate off the excess water.

Bees usually take syrup down very fast, rapidly filling the brood box.

In contrast, fondant is taken down more slowly. This means there is no risk that the queen will run out of space for egg laying. Whilst I’ve not done any side-by-side properly controlled studies – or even improperly controlled ones – the impression I have is that feeding fondant helps the colony rear brood into the autumn 10.

Whatever you might read elsewhere, bees do store fondant. The blocks I added this week will just be crinkly blue plastic husks by late September, and the hives will be correspondingly heavier.

You can purchase fancy fondant prepared for bees with pollen and other additives.

Don’t bother.

Regular ‘Bakers Fondant’ sold to ice Chelsea buns is the stuff to use. All the colonies I inspect at this time of the season have ample pollen stores.

I cannot comment on the statements made about the anti-caking agents in bakers fondant being “very bad for bees” … suffice to say I’ve used fondant for almost a decade with no apparent ill-effects 11.

It’s worth noting that these statements are usually made by beekeeping suppliers justifying selling “beekeeping” fondant for ¬£21 to ¬£36 for 12.5 kg.

Project Fear?


Colophon

The title of this post is a mangling of the well-known phrase The show must go on. This probably originated with circuses in the 19th Century and was subsequently used in the hotel trade and in show business.

The show must go on is also the title of (different) songs by Leo Sayer (in 1973, his first hit record, not one in my collection), Pink Floyd (1979, from The Wall) and Queen (1991).

Droning on

This post was supposed to be about¬†Varroa resistance in¬†Apis mellifera – to follow the somewhat controversial ‘Leave and let die’ from a fortnight ago. However, pesky work commitments have prevented me doing it justice so it will have to wait for a future date.

All work and no play …

Instead I’m going to pose some questions (and provide some partial answers) on overwintering mites and the use of drone brood culling to help minimise mite levels early in the season.

Imagine the scenario

A poorly managed colony goes into the winter with very high mite levels. Let’s assume the beekeeper failed to apply a late summer/early autumn treatment early enough and then ignored the advice to treat again in midwinter when the colony is broodless.

Tut, tut …

The queen is laying fewer and fewer eggs as the days shorten and the temperature drops. There are decreasing amounts of the critical 5th instar larvae that the mite must infest to reproduce.

At some point the colony may actually be broodless.

What happens to the mites?

Do they just hang around as phoretic mites waiting for the queen to start laying again?

Presumably, because there is nowhere else they can go … but …

What about the need for nurses?

During the Varroa reproductive cycle newly emerged mites preferentially associate with nurse bees for ~6 days (usually quoted as 4-11 days) before infesting a new 5th instar larva.

Mites that associate with newly emerged bees or bees older than nurse bees exhibit reduced fecundity and fitness i.e. they produce fewer progeny and fewer mature progeny 1 per infested cell.

I’m not aware of studies showing the influence of the physiologically-distinct winter bees on mite fecundity.

Similarly, I’m not sure if there are any studies that have looked at the types of bees phoretic mites associate with during the winter 2, or the numbers of bees in the colony during November to January 3 that might be considered to be similar physiologically to nurse bees.

Whilst we (or at least I) don’t know the answer to these questions, I’m willing to bet – for reasons to be elaborated upon below – that during the winter the fecundity and fitness of mites decreases significantly.

And the number of the little blighters …

Mite longevity

How long does a mite live?

The usual figure quoted for adult female mites is 2-3 reproductive cycles (of ~17 days and ~11 days for the first and subsequent rounds respectively). So perhaps about 40 days in total.

But, in the absence of brood (or if brood is in very short supply) this is probably longer as there is data linking longevity to the number of completed reproductive cycles i.e. if there is no reproduction the mite can live longer.

It is therefore perhaps reasonable to assume that mites should be able to survive through a broodless period of several weeks during midwinter. However, remember that this increases the chance the mite will be removed by grooming or other physical contacts within the cluster, so reducing the overall population.

Spring has sprung

So, going back to the scenario we started with …

What happens in late winter/early spring when the queen starts laying again?

Does that 5cm patch of early worker brood get immediately inundated with hundreds of mites?

If so, the consequences for the early brood are dire. High levels of mite infestation inevitably mean exposure to a large amount of deformed wing virus (DWV) which likely will result in precisely the developmental deformities you’d expect … DWV really “does what it says on the tin”.

Worker bee with DWV symptoms

Worker bee with DWV symptoms

My hives are carefully managed to minimise mite levels. I don’t really have any personal experience to help answer the question. However, in colonies that have higher (or even high) mite levels I don’t think it’s usual to see significant numbers of damaged bees in the very earliest possible inspections of the season 4.

My (un)informed guess …

My guess is that several things probably happen to effectively reduce exposure of this earliest brood to Varroa:

  1. Varroa levels in the colony drop due to the extended winter phoretic phase. More opportunities for grooming or similar physical contact (perhaps even clustering) increase the loss of mites.
  2. Mites that remain may have reduced access to brood simply due to the mathematical chance of the bee they are phoretic on coming into contact with the very small numbers of late stage larvae in the colony.
  3. Mites that do infest brood have reduced fecundity and fitness and may not rear (m)any progeny.

There are a lot of assumptions and guesswork there. Some of these things may be known but discussions I’ve had with some of the leading¬†Varroa researchers suggest that there are still big gaps in our knowledge.

OK, enough droning on, what about drones?

Back to the imagined scenario.

What happens next?

Well, perhaps not next, but soon?

The colony continues to contract (because the daily loss of aged workers still outnumbers the daily gain of new bees) but the laying rate of the queen gradually increases from a few tens, to hundreds to a couple of thousand eggs per day.

And the colony starts to really expand.

And so do the mite numbers …

Pupa (blue) and mite (red) numbers

And at some point, depending upon the expansion rate, the climate and (probably) a host of factors I’ve not thought of or are not known, the colony begins to make early swarm preparations by starting to rear drones.

Drones take 24 days to develop from the egg and a further 12-16 days to reach sexual maturity. If the swarming period starts in the first fortnight of May, the drones that take part were laid as eggs in late March.

And drone larvae are very attractive to Varroa.

9 out of 10 mites prefer drones

Varroa replicates ‘better’ in association with drone pupae. By better I mean that more progeny are produced from each infested cell. This is because the drone replication cycle is longer than that of worker brood.

The replication cycle of Varroa

The replication cycle of Varroa

On average 2.2 new mites are produced in drone cells¬†vs only 1.3 in worker cells 5. From an evolutionary standpoint this is a significant selective pressure and it’s therefore unsurprising that Varroa have evolved to preferentially infest drone brood.

Irrespective of the mite levels, given the choice between worker and drone, Varroa will infest drone brood at 8-11 times the level of worker brood 6.

Significantly, as the amount of drone brood was reduced (typically it’s 5-15% of comb in the hive) the¬†drone cell preference increased by ~50% 7.

I hope you can see where this is now going …

Early drone brood sacrifice

As colony expansion segues into swarm preparation the queen lays small amounts of drone brood. These cells are a very small proportion of the overall brood in the colony but are disproportionately favoured by the mite population.

And the mite population – even in a poorly managed colony – should be less (and less fit) in the Spring than the preceding autumn for reasons elaborated upon above (with the caveat that some of that was informed guesswork).

Therefore, if you make sure you remove the earliest capped drone brood you should also remove a significant proportion of the viable mites in the colony.

Drone brood is usually around the periphery of the brood nest, along the bottom of frames with normal worker foundation, or on the ‘shoulders’ near the lugs. The drone brood is often scattered around the brood nest.

As a consequence, if you want to remove all the earliest capped drone brood you have to rummage through the frames and ‘fork out’ 8 little patches here and there.

It can be a bit of a mess.

Is there an easier way to do this?

Drone cells

Beekeepers who predominantly use foundationless frames will be aware that they usually have significantly more drones (and drone comb) in their colonies than equivalent sized colonies using embossed worker foundation.

Depending upon the type of foundationless frames used the drone comb is drawn out in different positions on the frames.

Horizontally wired foundationless frames can be all drone brood or a mix of drone and worker. However, the demarcation between the brood types is often inconveniently located with regard to support wires.

In contrast, foundationless frames constructed using vertical¬†bamboo supports are often built as ‘panels’ consisting entirely of drone¬†or worker comb.

Drone-worker-drone

Drone-worker-drone …

Which makes slicing out one or more complete panels of recently capped drone brood simplicity itself.

There are no wires in the way.

You can sometimes simply pull it off the starter strip.

Drone brood sacrifice

Check the brood for Varroa 9, feed the pupae to your chickens and/or melt out the wax in your steam wax extractor.

The bees will rapidly rebuild the comb and will not miss a few hundred drones.

They’ll be much healthier without the mites. Importantly, the mites will have been removed from the colony¬†early in the season so preventing them going through repeated rounds of reproduction.

This is the final part of the ‘midseason mite management‘ triptych 10, but I might return to the subject with some more thoughts in the future … for example, continuous culling of drone brood (in contrast to selective culling of the very earliest drone brood in the colony discussed here) is not a particularly effective way of suppressing mite levels in a colony.


 

 

 

 

 

Window of opportunity

I’ve recently discussed problems faced by beekeepers trying to control high Varroa¬†levels in colonies during the ‘body’¬†of the beekeeping season.¬†Essentially the problems are two-fold:

  • Many miticides need to be used for several weeks to target mites in capped cells.
  • The soft or hard chemicals used for¬†Varroa control are – with the exception of the formic acid in MAQS – incompatible with honey production.

This type of midseason mite management should not be needed if parasite levels are controlled in late summer and midwinter.

If it is needed it suggests that the treatment(s) failed or that mites are being acquired through robbing or drifting from other colonies in the neighbourhood (either your own, a nearby apiary or a feral colony).

Opportunity knocks

However, all is not lost. Most seasons offer at least one opportunity to intervene and control mite levels.

Knowing when and how to exploit it requires an appreciation of the development cycle of the bee.

Honey bee development

Honey bee development

The important numbers are the 21 and 24 day development cycle of workers and drones respectively, the 16 day development cycle of the queen and the time it takes for eggs to hatch, grow as larvae and pupate in capped cells.

Not shown is the maturation period after emergence for the queen (5 to 6 days) before she goes on a mating flight, or the delay after returning before she starts laying (2-3 days) 1.

Swarms

The easiest scenario to discuss is when the colony swarms.

Consider the swarm first. A prime swarm is broodless, contains a mated queen and ~35% of the mites that were present in the issuing colony. All the mites will be phoretic. Assuming there’s drawn comb available the queen will start laying soon after the swarm is hived (or conveniently moves into your bait hive).

Eight days later the first eggs will have hatched, the larvae grown and the brood will be capped.

At which point the majority of the mites will start to become inaccessible again.

However, during those 8 days it’s ‘open season’ for those phoretic mites.

It is sensible to quarantine swarms from an unknown source and treat for mites in the first 8 days if needed.

If the swarm is a cast with an unmated queen you’ve got a bit more time. The virgin queen needs to get out and mate, mature and start laying. This tends to happen in just a few days if the weather is accommodating, so don’t leave things too long.

The swarmed colony

Now consider what’s left in the colony that swarmed 2. There will be sealed and unsealed brood and – notwithstanding the reduced egg laying by the queen as she’s slimmed down in preparation for swarming – there are also likely to be some eggs.

There will also be a sealed queen cell (and, in a strong colony, several sealed and unsealed queen cells).

Queen cells ...

Queen cells …

Without intervention the queen(s) will start emerging about 9 days later. If you intervene, knocking down all the sealed cells and leaving just one good charged open cell 3, it will be a couple more days before the queen emerges.

Weather permitting it will be a further 8 days before the newly mated queen starts laying. In reality, this is the absolute minimum and is rarely achieved in a full hive 4.

Simultaneously, in the requeening hive, the open brood is maturing and being capped and the capped brood is emerging (releasing more mites).

About eight days after the swarm leaves all the worker brood in the hive will be capped.

Twenty one (or 24 in the case of drone brood) days after the last egg was laid by the queen all the brood will have emerged.

Consequently all the mites in the colony will be phoretic.

The window of opportunity

So, if you need to treat 5 the window of opportunity is between the last of the brood from the old queen emerging and the first of the larvae from the new queen being capped.

You can determine when this is likely to be based upon the known activities of the old and new queen during the swarming period.

The window of opportunity

The diagram above makes a number of assumptions. As presented, all minimise the duration of the minimum broodless period:

  • The old queen continues laying until the day she swarms
  • The colony swarms on the day the queen cell is sealed
  • The beekeeper does not intervene to leave an open, charged cell of a known age
  • The new queen takes the minimum amount of time to mature, go on a mating flight and start laying

It should be self-evident that more realistic timings applied to these will only increase the length of the minimum broodless period.

For example, the weather will have a significant impact. Swarming may be delayed due to adverse conditions. During this time the slimmed-down queen will probably lay very few eggs.

Similarly, only 8 days are shown for maturing, mating and starting to lay. Mating flights are very weather-dependent and this period could easily take a week longer (or more).

Splits and artificial swarms

If you practice swarm control using the nucleus method, vertical splits or the classic Pagden artificial swarm the same types of calculations apply.

These three methods all share two features:

  • They involve the physical separation of the box with the old queen and the new developing queen
  • The old queen is isolated with a very small amount of brood – either open brood or emerging brood

The queenright component of the split (whether nuc box or new brood box left on the old site) will follow the right hand part of the diagram above i.e. everything to the right of the vertical red line labelled laying. Here it is expanded a bit:

Queenright splits and the window(s) of opportunity

The queen should start laying almost immediately if drawn comb is provided meaning this new brood will be sealed in a further 8-9 days. The timing and duration of the minimum broodless period depends upon whether you prime the queenright split with a small amount of open or emerging brood.

  • Open brood will be capped within about 6 days of the eggs hatching. If the frame contains nothing older than 3rd instar larvae (about mid-size) you will only have about 3 days before the cells are capped – indicated by bracketed region labelled (A) above, with capped pupae shown by the dark shaded arrow.
  • Emerging brood offers a bit more flexibility. If all the brood emerges in the first 2-3 days after the split (shown with the pale shaded arrow) then the duration of the broodless period, shown in (B) above, lasts about 5 days.

Queenless colonies after splitting

The queenless part of the split will behave like the swarmed colony in the upper line diagram. All capped worker brood will have emerged 21 days after the split (drones after 24 days).

Capped brood arising from eggs laid by the new queen in this colony will depend upon the origin of the queen.

If the colony is left to rear its own queen then the timing will be similar to the upper line diagram plus the additional time required to create a capped queen cell (which rather depends upon the state of the colony when split).

However, if you add a mature queen cell a day off emergence you will reduce the time to the appearance of new capped brood by ~8 days. Consequently the colony will probably never go through a phase with no capped brood present. This is the same, but even more so, if you requeen the colony with a mated queen.

The miticide of choice

Of all the (rather limited range of) miticides available, an oxalic acid-containing treatment is the most appropriate. Oxalic acid (OA) is well-tolerated and, if used on a colony that lacks capped brood, over 90% effective. In addition, and critical for treatment in a narrow window of opportunity, only one treatment is required.

OA can be administered by trickling or sublimation. I’ve covered both methods in detail previously so won’t repeat what’s required, or the recipes, here.

Note that in many cases although the colony will have no capped brood it will not be broodless. For example, larvae from eggs laid by the new queen will be present but uncapped.

This is important because trickled oxalic acid-containing treatments are toxic to open brood. Under these conditions the treatment of choice would be sublimated oxalic acid.

Sublimox vaporiser

Sublimox vaporiser …

Finally, note that if you are going to sublimate Api-Bioxal you’ll either have to spend ages cleaning the pan of the vaporiser, or line it with aluminium foil in advance.

The treatments outlined here are not intended for routine use. They should be used only if needed based upon mite counts or overt signs of DWV-mediated disease.

However, if you do need to treat make sure you do it when the treatment will be most effective.


 

Leave and let die

If you follow some of the online discussions on Varroa¬†you’ll see numerous examples of amateur beekeepers choosing not to treat so as to ‘select for mite-resistant bees’.

For starters it’s worth looking at the ‘treatment-free’ forums on Beesource.

DWV symptoms

DWV symptoms

The principle is straightforward. It goes something like this:

  • Varroa is a relatively new 1 pathogen of honey bees who therefore naturally have no resistance to it (or the viruses it transmits).
  • Miticide treatment kills mites, so favouring the survival of bees.
  • Consequently, traits that confer partial or complete resistance to¬†Varroa are not actively selected¬†for (which would otherwise happen if an untreated colony died out).
  • Treatment is therefore detrimental, at the population level if not the individual level, to the development of¬†Varroa-resistant bees.
  • Therefore, don’t treat and – with a bit of luck – a resistant strain of bees will appear.

A crude oversimplification?

Yes, I don’t deny it.

There are all sorts of subtleties here. These range from the open mating of queens, isolation of apiaries, desirable traits (with regards to both disease resistance and honey production 2), livestock management ethics, our responsibilities to other beekeepers and other pollinators. I could go on.

But won’t.

Instead I’ll discuss a short paper published in the Journal of Apicultural Research. It’s not particularly novel and the results are very much in the “No sh*t Sherlock” category. However, it neatly emphasises the futility of the ‘do nothing and expect evolution to find a solution’ approach.

But I’ll start with a simple question …

How many colonies have you got?

One? (in which case, get another)

Two?

Ten?

One hundred?

Eight-two thousand? 3

Numbers matters because evolution is a numbers game. The evolutionary processes that result in alteration of genes (the genotype of an organism) that confer different traits or characteristics (the phenotype of an organism) are rare.

For example, viruses are some of the fastest evolving organisms and, during their replication, mutations (errors) occur at a rate of about 1 in 104 at the genetic level 4.

This is why we treat ...

This is why we treat …

But so-called higher organisms (like humans or bees) have much more efficient replication machinery and make very many fewer errors. A conservative figure for bees might be about 10,000 times less than in these viruses (i.e. 1 in 108), though it could be as much as a million times less error-prone 5

There are lots of other evolutionary mechanisms in addition to mutation but the principle remains broadly the same. The chance changes that are acquired by copying or mixing up genetic material are very, very infrequent.

If they weren’t, most replication would result – literally – in a dead end.

OK, OK, enough numbers … what about my two colonies?

So, since the evolutionary¬†mechanisms make small, infrequent changes, the¬†chance of a beneficial change occurring is very small. If you start with small numbers of colonies and expect success you’re likely to be disappointed.

Where¬†‘likely to be’¬†means¬†will be.

The chances of picking the Lotto jackpot is about 1 in 45 million for each ticket purchased. If you expect to win you will be disappointed.

It could be you … but it’s unlikely

If you buy two tickets (with different numbers!) your chances are doubled. But realistically, they’re still not great 6.

And so on.

Likewise, the more colonies you have, the more likely you’ll get one that might – by chance – acquire a beneficial mutation that confers some level of resistance to¬†Varroa.

Of course, we don’t really know much about the genetic basis for resistance (or tolerance?) to¬†Varroa in honey bees. We know that there are behavioural changes that increase survival. We also know that¬†Apis cerana can cope with¬†Varroa because it has a shorter duration replication cycle and exhibits¬†social apoptosis.

There are certainly ‘hygienic’ and other traits in bees that may be beneficial, but at a genetic level I don’t think we know the number of genes that are altered to confer these, or how much each might contribute.

So we don’t know how many mutations will be needed … One? One hundred? One thousand?

If the benefit of an individual mutation is very subtle it might offer relatively little selective advantage, which brings us back to the numbers again.

Apologies. Let’s not go there.

Let’s cut to the chase …

Comparison of treated vs untreated colonies over 3 years

Miticides – whether hard chemicals like Amitraz or Apistan or organic acids like formic or oxalic acid – work by exhibiting differential toxicity to mites than to their host, the bee. They are not so specific that they only kill mites. They can harm other things as well … e.g.¬†if you ingest enough oxalic acid (5 – 15g) it can kill you.

Amitraz

Amitraz …

Jerzy Wilde and colleagues published their study 7¬†comparing colonies treated or untreated over a three year period. The underlying question addressed in the paper is “What’s more damaging, treating with potentially toxic miticides or not treating at all?”

The study was straightforward. They started with 100 colonies, requeened them and divided them randomly into 4 groups of 25 colonies each. Three received treatment and one was a control.

The ‘condition’ of the colonies was measured in a variety of ways, including:

  • Colony size in Spring (number of combs occupied)
  • Nosema levels (quantified by numbers of spores)
  • Mite drop over the winter (dead mites per 100g of ‘hive debris’)
  • Colony size in autumn (post-treatment) and egg laying rate by the queen
  • Winter losses

The last one needs some explanation because in one group (guess which?) there were more winter losses than they started the experiment with.

Overwintering colony losses were made up from splits of colonies in the same group the following year, so that each year 25 colonies went into the winter i.e. surviving colonies were used to generate additional colonies for the same treatment group.

Treatment and seasonal variation

To add a little complexity to the study the authors compared three treatment regimes:

  1. Hard chemicals only – active ingredients amitraz or the pyrethroid flumethrin (the research group are Polish, so the particular formulations are those licensed in Poland – Apiwarol, Bayvarol and Biowar).
  2. Integrated Pest Management (IPM) – a range of treatments including Api Life Var (primarily a thymol-based treatment) in spring, drone brood removal early/mid season, hard chemical or formic acid in late summer/autumn and oxalic acid in midwinter.
  3. Organic (natural) treatments only – Api Life Var in spring, the same or formic acid in late summer and a midwinter oxalic acid treatment.

The fourth group were the untreated controls.

To avoid season-specific variation they conducted the experiment over three complete seasons (2010-2012).

The apiary in winter ...

The apiary in winter …

The results of the study are shown in a series of rather dense tables with standard deviation and statistic significance … so I’ll give a narrative account of the important ones.

Results …

The strength of surviving colonies in Spring was unaffected by prior treatment (or absence of treatment) but varied significantly between seasons. In contrast, late summer colony strength was significantly worse in the untreated control colonies. In addition, the number of post-treatment eggs laid by the queen was significantly lower (by ~30%) in untreated control colonies 8.

Remember that early autumn treatment is needed to reduce Varroa infestation and so protect the winter bees that are being reared at this time from the mite-transmitted viruses.

Out, damn'd mite ...

Out, damn’d mite …

The most dramatic effects were seen in winter losses and (unsurprisingly) mite counts.

Mites were counted in the hive debris falling through the open mesh floor during the winter. In the first year the treated and untreated controls had similar numbers of mites per 100g of debris (~12). In all treated colonies this remained about the same in each subsequent season. Conversely, untreated controls showed mite drop increasing to ~43 in the second year and ~114 in the final year of the study.

During the three years of the study 30 untreated colonies died. In contrast, a total of 37 colonies from the three treatment groups died.

The summary sentence of the abstract to the paper neatly sums up these results: 

Failing to apply varroa treatment results in the gradual and systematic decrease in the number of combs inhabited by bees and condition of bee colonies and consequently, in their death.

… and some additional observations

Other than oxalic acid, none of the treatments used significantly affected the late season egg laying by the queen. Api Life Var contains thymol and many beekeepers are aware that the thymol in Apiguard quite often stops the queen from laying. Interesting …

I commented last week on queen losses with MAQS. In this Polish study, 8 of 50 colonies treated with formic acid suffered queen losses.

In the third season (2012) 45% of the 100 colonies died. More than half of these lost colonies were in the untreated controls. In contrast, overall colony losses in the first two years were only 9% and 13%. Survival of untreated colonies for a year or two is expected, but once the Varroa levels increase significantly the colony is doomed.

Overall, colonies receiving integrated pest management or hard chemical treatment survived best.

Evolution …

March of Progress

Evolution …

Remind yourself where the colonies came from that were used to make up the losses in the treatment (or control) groups … they were splits from colonies within the same group. So, colonies that survived without treatment were used to produce more colonies to not be treated the following season.

Does this start to sound familiar?

Jerzy Wilde and colleagues started with 25 colonies in the untreated group. They lost 30 colonies over a 3 year period and ended up with just two colonies. Had they wanted to continue the study they would have been unable to recover their losses from these two remaining colonies.

If you don’t treat you must expect to lose colonies.

Lots of colonies.

Actually, almost all of them.

… takes time

This study lasted only three years.¬†That’s not very long in evolutionary terms (unless you are a bacterium with a 20 minute replication cycle).¬†

It would be unrealistic to expect Varroa resistance to almost spontaneously appear. After all, there are about 91 million colonies worldwide, the majority of which are in countries with Varroa. Lots of these colonies will not be treated. If it was that easy it would have happened many times already.

What happens when you start with more colonies and allow more time to elapse?

Well, this ‘experiment’ has been done. There are a number of regions that have well-documented populations of feral honey bees that are living with, if not actually resistant to,¬†Varroa.

One well known population are the bees in the Arnot Forest studied by Thomas Seeley. These bees have behavioural adaptations Рsmall, swarmy colonies Рthat lessen the impact of Varroa on the colony 9.

Finally, returning to the title of this post, there is the so-called “Bond experiment” conducted on the island of Gotland in the Baltic Sea. Scientists established 150 colonies of mite-infested bees and let them get on with it with no intervention at all. Over the subsequent six years they followed the co-evolution of the mite and the bee 10.

It’s called the “Bond experiment” or the¬†Live and Let Die¬†study for very obvious reasons.

Almost all the colonies died.

Which is why the title of this post is more appropriate for those of us with only small numbers of colonies.


 

Midseason mite management

The Varroa mite and the potpourri of viruses it transmits are probably the greatest threat to our bees. The number of mites in the colony increases during the spring and summer, feeding and breeding on sealed brood.

Pupa (blue) and mite (red) numbers

In early/mid autumn mite levels reach their peak as the laying rate of the queen decreases. Consequently the number of mites per pupa increases significantly. The bees that are reared at this time of year are the overwintering workers, physiologically-adapted to get the colony through the winter.

The protection of these developing overwintering bees is critical and explains why an early autumn application of a suitable miticide is recommended … or usually¬†essential.

And, although this might appear illogical, if you treat early enough to protect the winter bees you should also treat during a broodless period in midwinter. This is necessary because mite replication goes on into the autumn (while the colony continues to rear brood). If you omit the winter treatment the colony starts with a higher mite load the following season.

And you know what mites mean

Mites in midseason

Under certain circumstances mite levels can increase to dangerous levels 1 much earlier in the season than shown in the graph above.

What circumstances?

I can think of two major reasons 2. Firstly, if the colony starts the season with higher than desirable mite levels (this is why you treat midwinter). Secondly, if the mites are acquired by the colony from other colonies i.e. by infested bees drifting between colonies or by your bees robbing a mite infested colony.

Don’t underestimate the impact these events can have on mite levels. A strong colony robbing out a weak, heavily infested, collapsing colony can acquire dozens of mites a day.

The robbed colony may not be in your apiary. It could be a mile away across the fields in an apiary owned by a treatment-free 3 aficionado or from a pathogen-rich feral colony in the church tower.

How do you identify midseason mite problems?

You need to monitor mite levels, actively and/or passively. The latter includes periodic counts of mites that fall through an open mesh floor onto a Varroa board. The National Bee Unit has a handy Рthough not necessarily accurate Рcalculator to determine the total mite levels in the colony based on the Varroa drop.

Out, damn'd mite ...

Out, damn’d mite …

Don’t rely on the NBU calculator. A host of factors are likely to influence the natural¬†Varroa¬†drop. For example, if the laying rate of the queen is decreasing because there’s no nectar coming in there will be fewer larvae at the right stage to parasitise … consequently the natural drop (which originates from phoretic mites) will increase.

And vice versa.

Active monitoring includes uncapping drone brood or doing a sugar roll or alcohol wash to dislodge phoretic mites.

Overt disease

But in addition to looking for mites you should also keep a close eye on workers during routine inspections. If you see bees showing obvious signs of deformed wing virus (DWV) symptoms then you need to intervene to reduce mite levels.

High levels of DWV

High levels of DWV …

During our studies of DWV we have placed mite-free 4 colonies into a communal apiary. Infested drone cells were identified during routine uncapping within 2 weeks of our colony being introduced. Even more striking, symptomatic workers could be seen in the colony within 11 weeks.

Treatment options

Midseason mite management is more problematic than the late summer/early autumn and midwinter treatments.

Firstly, the colony will (or should) have good levels of sealed brood.

Secondly, there might be a nectar flow on and the colony is hopefully laden with supers.

The combination of these two factors is the issue.

If there is brood in the colony the majority (up to 90%) of mites will be hiding under the protective cappings feasting on sealed pupae.

Of course, exactly the same situation prevails in late summer/early autumn. This is why the majority of approved treatments – Apistan¬†(don’t), Apivar, Apiguard¬†etc. – need to be used for at least 4-6 weeks. This covers multiple brood cycles, so ensuring that the capped¬†Varroa are released and (hopefully) slaughtered.

Which brings us to the second problem. All of those named treatments should not be used when there is a flow on or when there are supers on the hive. This is to avoid tainting (contaminating) the honey.

And, if you think about it, there’s unlikely to be a 4-6 week window between early May and late August during which there is not a nectar flow.

MAQS

The only high-efficacy miticide approved for use when supers are present is MAQS 5.

The active ingredient in MAQS is formic acid which is the only miticide capable of penetrating the cappings to kill Varroa in sealed brood 6. Because MAQS penetrates the cappings the treatment window is only 7 days long.

I have not used MAQS and so cannot comment on its use. The reason I’ve not used it is because of the problems many beekeepers have reported with queen losses or increased bee mortality. The Veterinary Medicines Directorate MAQS¬†Summary of the product characteristics provides advice on how to avoid these problems.

Kill and cure isn’t the option I choose ūüėČ 7

Of course, many beekeepers have used MAQS without problems.

So, what other strategies are available?

Oxalic acid Api-Bioxal

Many beekeepers these days Рif you read the online forums Рwould recommend oxalic acid 8.

I’ve already discussed the oxalic acid-containing treatments extensively.

Importantly, these treatments only target phoretic mites, not those within capped cells.

Trickled oxalic acid is toxic to unsealed brood and so is a poor choice for a brood-rearing colony.

Varroa counts

In contrast, sublimated (vaporised) oxalic acid is tolerated well by the colony and does not harm open brood. Thomas Radetzki demonstrated it continued to be effective for about a week after administration, presumably due to its deposition on all internal surfaces of the hive. My daily mite counts of treated colonies support this conclusion.

Consequently beekeepers have empirically developed methods to treat brooding colonies multiple times with vaporised oxalic acid Api-Bioxal to kill mites released from capped cells.

The first method I’m aware of published for this was by¬†Hivemaker on the Beekeeping Forum. There may well be earlier reports. Hivemaker recommended three or four doses at five day intervals if there is brood present.

This works well 9 but is it compatible with supers on the hive and a honey flow?

What do you mean by compatible?

The VMD Api-Bioxal Summary of product characteristics 10 specifically states “Don‚Äôt treat hives with super in position or during honey flow”.

That is about as definitive as possible.

Another one for the extractor ...

Another one for the extractor …

Some vapoholics (correctly) would argue that honey naturally contains oxalic acid. Untreated honey contains variable amounts of oxalic acid; 8-119 mg/kg in one study 11 or up to 400 mg/kg in a large sample of Italian honeys according to Franco Mutinelli 12.

It should be noted that these levels are significantly less than many vegetables.

In addition, Thomas Radetzki demonstrated that oxalic acid levels in spring honey from OA vaporised colonies (the previous autumn) were not different from those in untreated colonies. 

Therefore surely¬†it’s OK to treat when the supers are present?

Absence of evidence is not evidence of absence

There are a few additional studies that have shown no marked rise in OA concentrations in honey post treatment. One of the problems with these studies is that the delay between treatment and honey testing is not clear and is often not stated 13.

Consider what the minimum potential delay between treatment and honey harvesting would be if it were allowed or recommended.

One day 14.

No one has (yet) tested OA concentrations in honey immediately following treatment, or the (presumable) decline in OA levels in the days, weeks and months after treatment. Is it linear over time? Does it flatline and then drop precipitously or does it drop precipitously and then remain at a very low (background) level?

Oxalic acid levels over time post treatment … it’s anyones guess

How does temperature influence this? What about colony strength and activity?

Frankly, without this information we’re just guessing.

Why risk it?

I try and produce the very best quality honey possible for friends, family and customers.

The last thing I would want to risk is inadvertently producing OA-contaminated honey.

Do I know what this tastes like? 15

No, and I’d prefer not to find out.

Formic acid and thymol have been shown to taint honey and my contention is that thorough studies to properly test this have yet to be conducted for oxalic acid.

Until they are – and unless they are statistically compelling – I will not treat colonies with supers present … and I think those that recommend you do are unwise.

What are the options?

Other than MAQS there are no treatments suitable for use when the honey supers are on. If there’s a good nectar flow and a mite-infested colony you have to make a judgement call.

Will the colony be seriously damaged if you delay treatment further?

Quite possibly.

Which is more valuable 16, the honey or the bees?

One option is to treat, hopefully save the colony and feed the honey back to the bees for winter (nothing wrong with this approach … make sure you label the supers clearly!).

Another approach might be to clear then remove the supers to another colony, then treat the original one.

However, if you choose to delay treatment consider the other colonies in your own or neighbouring apiaries. They are at risk as well.

Finally, prevention is better than cure. Timely application of an effective treatment in late summer and midwinter should be sufficient, particularly if all colonies in a geographic area are coordinately treated to minimise the impact of robbing and drifting.

I’ve got two more articles planned on midseason mite management for when the colony is broodless, or can be engineered to be broodless 17.


 

Pedantically not phoresy

The life cycle of the ectoparasitic mite Varroa destructor essentially consists of two stages. The first is within the capped cell, where reproduction takes place. The second occurs outside the capped cell when the recently-mated female progeny mites matures while riding around the colony attached to a nurse bee.

Almost without exception this second stage is termed the phoretic phase.

It isn’t.

Phoresy

Phoretic is an adjective of the word phoresy. Phoresy is derived from the French¬†phor√©sie¬†which, in turn, has its etymological origins in the Ancient Greek word¬†ŌÜőŅŌĀő∑ŌÉőĻŌā.

And¬†ŌÜőŅŌĀő∑ŌÉőĻŌā means¬†being carried.

Which partly explains why the correct definition of the word phoresy is:

An association between two organisms in which one is carried on the body of the other, without being a parasite [OED]

Phoresy has been in use for about a century, with the word phoretic first being recorded in the Annals of the Entomological Society of America (25:79) in 1932:

It is possible, as suggested by Banks (1915), that such young mites are phoretic, being carried about from place to place on the host’s surfaces.

And, no, they weren’t discussing¬†Varroa.

“Without being a parasite”

These are the critical words in the dictionary definition of phoresy which makes the use of the word phoretic incorrect when referring to mites on nurse bees.

Because mites on nurse bees are feeding Рor at least a significant proportion 1 of them are.

They are therefore being¬†parasitic and so shouldn’t be described as phoretic.

Om, nom, nom 2

Last week I discussed the recent Samual Ramsey paper presenting studies supporting the feasting of Varroa on the fat body of bees.

In the study they harvested bees from a heavily mite-infested hive and recorded the location on the bee to which the mite was attached.

The majority were attached to the left underside of the abdomen. More specifically, the mite was wedged underneath the third abdominal tergite 3.

What were they doing there? Hiding?

Yes … but let’s have a closer look.

Ramsey and colleagues removed some of the mites and used a scanning electron microscope to examine the attachment point on the bee. Underneath the tergite there is a soft membrane. The imprint of the body of the mite was clearly visible on the membrane.

Varroa feeding location on adult bee

Scanning EM of Varroa feeding location on adult bee

The footpads of the mite were left attached to the membrane (left image, white arrows), straddling an obvious wound where the mouthparts had pierced the membrane (black arrow). Between them, the inverted W shape is presumably the imprint of the lower carapace of the mite.

The close-up image on the right even shows grooves at the wound site consistent with the mouthparts of the mite.

These mites were feeding.

Extraoral digestion

Varroa belongs to the order (a level of classification) Mesostigmata. Most mesostigmatids feed using a process termed extraoral digestion.

Extraoral digestion has also been termed ‘solid-to-liquid’ feeding. It involves the¬†injection of potent hydrolytic enzymes which digest solid tissue, converting it to a semi-solid that can be easily ingested. It can reduce the time needed to feed and it increases the nutrient density of the consumed food.

If¬†Varroa fed on haemolymph it wouldn’t need to use extraoral digestion. Instead it would need all sorts of adaptations to a high volume, low nutrient diet. Varroa¬†doesn’t have these. It has a simple tube-like gut parts of which lack enzymatic activity … implying that digestion occurs elsewhere.

A picture is worth a thousand words

Do the images of feeding mites support the use of extraoral digestion?

EM cross-section of Varroa feeding

EM cross-section of Varroa feeding

The image above 4 shows the cross-section of a Varroa (V), wedged under the tergite (Te), feeding through a hole (arrow in the enlargement on the right) in the membrane (M). The fat body (FB) is immediately underneath the membrane. The scale bar is incorrectly labelled 5.

A close-up of the wound site shows further evidence for extraoral digestion.

Feeding wound at higher magnification

Feeding wound at higher magnification

Beneath the wound site (C, arrow) are remnants of fat body cells (white arrow) and bacteria (black arrow; of two types, shown in D). A closer look still at the remnants of the fat body (E and F) shows cell nuclear debris (blue arrows) and lipid droplets (red arrows).

These images are entirely consistent with extraoral digestion of fat body tissue by feeding Varroa. The presence of bacteria near the wound suggests that bacterial infection may result from Varroa feeding, possibly further contributing to disease in bees.

So, pedantically it’s not phoresy

So-called phoretic mites, unless they’re on the thorax or head of the bee, are not really phoretic. They are being carried about, but they are also likely¬†feeding. By definition that excludes them from being phoretic.

Instead they are ectoparasites of adult bees.

What are the chances that beekeepers will stop using the term phoretic?

Slim to none I’d predict 6.

And, of course, it doesn’t really matter what the correct term for them is.

What’s more important is that beekeepers remember that it’s at this stage that mites are susceptible to all miticides.

The June gap

But it’s also worth thinking about the potential impact of brood breaks.

During brood breaks all the mites in the colony must be ‘phoretic’.

Generally, the majority of the mites in a hive are in capped cells. Depending upon the stage of the season, the egg-laying rate of the queen and other factors, up to 90% of the mites are associated with developing pupae.

But as the laying rate dwindles more and more mites are released from cells and become ‘phoretic’, unable to find a suitable late-stage larva to infest.

And which bees do the mites associate with?

Nurse bees primarily, for reasons I’ll discuss in the future. But – spoiler alert – one of the reasons is likely to be that they have a larger fat body.

So, a mid-season brood break (e.g. the ‘June gap’) is likely to result in lots more nurse bees becoming both the carriers¬†and¬†the dinner of the mite population.

Some or many of the nurse bee cohort may perish, perhaps from damage to the fat body or from the viruses acquired from the mite. However, bees exhibit phenotypic plasticity, meaning that older bees can revert to being nurse bees when the queen starts laying again.

Late season brood breaks

In late summer mite levels are usually at their highest in the hive. A brood break occurring now will release a very large number of mites to parasitise the adult bee population.

Presumably these mites select the bees best able to support them 7.

And which bees are these? The nurse bees of course. But it’s also worth remembering that there are¬†key physiological similarities between nurse bees and winter bees. Both have low levels of juvenile hormone and high levels of vitellogenin (stored in the fat body).

So I’d bet that the ‘phoretic’ mites during a late season brood break would also preferentially associate with any early-produced winter bees.

Furthermore, once the queen starts laying again – perhaps in early/mid-autumn – the winter bees being produced would be subjected to the double-whammy of high levels of mite infestation and potential damage from ‘phoretic’ mites.

Practical considerations

More work is required to model or actually measure the impact of late season brood breaks, high levels of ‘phoretic’ mites, nurse bee numbers and winter bee development.

Compare two colonies of a similar size with a similar mite load, treated at the same time in early autumn with an appropriate miticide. If one of them experienced a late summer brood break (pre-treatment) and consequent high levels of ‘phoretic’ mites, does this reduce the chances of the colony surviving overwinter?

Who knows? Lots and lots of variables …

Fundamentally, it remains important to treat colonies early enough to protect the winter bee population. You’ve heard this from me before and you’ll hear it again.

However, it’s something to think about and I can see ways in which it might influence the strategy and timing of mite control used. I’ll return to this sometime in the future.


 

Convenience or laziness?

It’s cold and dark and all is quiet in the apiary. Hives appear somnolent. Colonies are clustered 1 and, other than the odd corpse or two on the landing board, I’ve not seen a bee for at least a fortnight.

The apiary in winter ...

The apiary in winter …

Based upon previous experience I suspect colonies are – or very soon will be – broodless. I usually reckon that the first extended (2-3 weeks) period of cold weather 2 in the winter is the most likely time for the colony to be broodless.

In 2016/17 this was the first week in December.

In 2017/18 it was just a day or two later.

In both instances, when the hives were checked, they had no brood.

What’s all this about being broodless?

If a colony is broodless there are no capped cells in which the Varroa mite can ‘hide’. As a consequence¬†it’s an¬†ideal time to apply a miticide like a trickled solution of Api-Bioxal 3.

There are very good reasons why a midwinter OA treatment is necessary, particularly if you treated early enough in the autumn to protect the overwintering workers from the ravages of Deformed Wing Virus (DWV). High DWV levels reduce the lifespan of bees and contribute to many (possibly most) winter colony losses. I’ve even suggested here that “isolation starvation” might actually be due to Varroa-transmitted viral disease.

Time of treatment and mite numbers

Time of treatment and mite numbers

Early autumn treatment protects the winter bees but also leaves the long autumn for the residual mites to continue replicating.

And there will be residual mites. No treatment is 100% effective.

So, paradoxically, if you treated early enough in the autumn to really help protect the winter bees, your mite levels will be higher at the end of the year.

Which also means they’ll be higher at the beginning of next year.

Not a good start to the 2019 season ūüôĀ

Convenience or laziness?

Many beekeepers, for convenience, laziness or historical precedent, choose to apply the winter OA treatment between Christmas and New Year. I suspect that this is often too late. If the queen starts laying again around the winter solstice there will be sealed brood – and therefore unreachable Varroa – by the end of the month.

I’d prefer to have a cold and damp afternoon in the apiary slaughtering¬†Varroa now¬†than the convenience of treating them less effectively¬†during the Christmas holiday period.

The latter might be more convenient … the office will be closed, I’ll be replete with turkey and sprouts and it will be a good excuse to ‘escape’ visiting relatives and yet more mince pies 4.

But is it the best time for your bees?

We have the technology

We have a couple of hives with Arnia hive monitors fitted 5. These have a temperature probe inserted into the brood nest. Brood rearing temperature is around 34¬įC. Here is a trace of one colony over the last month.

Arnia hive monitor temperature

Arnia hive monitor temperature

The colony temperature was pretty stable (around 33-35¬įC) until about the 19th of November and has dropped about 10¬įC since then. Although I’ve not opened the colony I think that this is additional evidence that the colony is broodless 6.

Beekeeping by numbers

Keeping bees properly involves being aware of the seasons, the available forage and the state of the colony. This varies from month to month and year to year 7.

You can’t mechanically (‘by the numbers’) add supers on the 5th of May and harvest honey on the 15th of June. Sure, it might work some years, but is it the¬†best time to do it?

Similarly, you can’t¬†optimally treat a colony for Varroa¬†on the 30th of December¬†unless the climatic conditions and state of the colony coincide to make that the best time to treat.

It might be, but I suspect that generally it’s a bit late if there is a brood break.

If you’re going to the trouble of preparing the OA treatment, donning the beesuit and disturbing the colony you might as well do it at the right time for the bees.

I’ll be treating in between the predicted sleet showers and sunny periods this weekend.

Time to treat

Time to treat

Isn’t evolution a wonderful thing? This post started with a working title of¬†Know your enemy”¬†and was on a different topic altogether. I’ll save that for next week.


STOP PRESS

The above was written at the beginning of the week. Now the weekend is closer it’s clear the weather is going to be cold with heavy snow predicted. Unless the forecast is wrong (and how often does that happen?!) I’ll hold off treating until a) it’s over 5¬įC, and b) the roads are safe.

Resistance is not futile

Apivar ...

Apivar …

Amitraz-containing miticides are sold in the UK as Apivar and Apitraz.

Until recently they were only available with a veterinary prescription. I expect – though I have not yet seen data to support this – that their usage in the UK will increase now they are off-prescription. These miticides are now widely available and so there is greater opportunity to use –¬†and misuse – them.

If you’re using Apivar 1 for the first time this year you will soon have to remove the strips from the hive.

That’s assuming you started treating early enough to protect the all-important winter bees from Varroa and its deadly viral payload.

This post is a reminder to remove the strips at the right time. The alternative – leaving them in place until the first Spring inspections – risks help the development of resistance to amitraz, so further reducing our opportunity to control mites effectively.

Leave and let die

Without careful integrated pest management (IPM) 2 Varroa levels build up in the hive. Varroa transmits viruses Рmost important of which is deformed wing virus (DWV) Рto developing pupae. High levels of DWV either kills the pupa or results in emergence with or without significant developmental defects. Even those bees that are apparently normally developed have a reduced lifespan 3.

Winter bees with a reduced lifespan prevent the colony from surviving through the winter until the queen starts laying again. I’ve also proposed recently that high levels of DWV, and the resulting increased rate of winter bee die-offs, probably accounts for some cases of¬†isolation starvation.

So … intervention is needed to reduce mite levels, protect your bees and save your colonies.

Follow the instructions!

Apivar is one solution to reduce mite levels. It is an easy-to-apply chemical treatment that is very effective in reducing the Varroa load by ~95%. For a National hive it is applied as two polymer strips, each containing 500mg of slow-release Amitraz. Strips are hung between brood frames for 6-10 weeks and Рfor maximum efficacy Рshould be scratched with a hive tool and repositioned half way through the treatment period.

Amitraz

Amitraz …

Unlike some other miticides (e.g. Apiguard and MAQS) there are no temperature restrictions for Apivar usage. The colony does not need to be broodless (a requirement for trickled oxalic acid-based treatments) as the treatment period covers multiple brood cycles.

Other than not using it with supers present the only contraindication for Apivar is to not use it if Amitraz-resistant mites are present.

How does resistance develop?

When discussing parasites and pathogens, resistance 4 is a consequence of two things:

  1. A selective pressure that kills the pathogen
  2. A population which exhibits genetic diversity

The selective pressure could be anything … heat for example, antibiotics prescribed by your GP, an antiviral against HIV or – of relevance here – Apivar against Varroa.

Killing – at the population level – is not absolute. Some individuals within the population survive longer than others. They could be exposed to a slightly lower dose, or be located in a protected niche for example. However, treat for long enough and the majority will be killed.

But there’s more …

Pathogen populations are not genetically invariant. Actually, many are quite diverse and have replication cycles that – deliberately 5 – generate diversity.

Therefore some pathogens are genetically slightly less resistant and some are genetically slightly more resistant to a selective pressure. We can ignore the former as they’ll rapidly be killed off … but we must be concerned about the more resistant ones.

Keep taking the pills

All of this is a ‘numbers game’, better represented with graphs and equations. However, the take-home message is simple … to effectively control a pathogen you need to treat for long enough and with a high enough dose to kill the vast majority of the population.

That’s why you’re encouraged to “complete the course” of antibiotics … or to remove the Apivar strips after 10 weeks and not leave them in over the winter.

Because both courses of action result in selection of more resistant pathogens.

If you stop taking antibiotics too soon, you won’t have treated for long enough and with a high enough dose. You end up selecting for the more genetically resistant pathogens.

Similarly, if you leave Apivar strips in overwinter you’ll be “treating” the remaining mites 6 with a lower dose of the miticide, which is an ideal situation to favour the growth of the slightly more genetically resistant mites.

How does Amitraz resistance develop?

Resistance to Amitraz in¬†Varroa is well documented. It’s been described in a number of countries including the USA and Europe, Mexico and Argentina 7. Generally resistance is defined in terms of a reduced level of mite killing, or – in laboratory experiments – an increased dose required to kill a certain proportion of mites.

However, I’m unaware of any studies defining the¬†genetic basis of Amitraz resistance in¬†Varroa.

But Amitraz is a widely-used acaricide 8 and the genetic basis of resistance in¬†cattle ticks is well understood. In these, ticks resistant to Amitraz carry a mutation in the¬†RMő≤AOR gene 9.

What 10 is the¬†RMő≤AOR gene?

I’m glad you asked ūüėČ

This gene encodes the¬†ő≤-adrenergic octopamine receptor protein and readers with good memories will recall that this is one of the targets that Amitraz binds to and inactivates 11.

If the protein carries a mutation the Amitraz cannot bind to it and so the mite – or more correctly the tick as it’s yet to be formally demonstrated in mites – is therefore¬†resistant.

(Bad) practical beekeeping

What does all this mean in terms of practical beekeeping?

It means use the correct number of Apivar strips for the colony and leave them in for the right length of time.

Do not …

  • Use one strip on a full colony mid-season to¬†‘knock back the mites a bit’¬†
  • Re-use the strips in another colony (yes really!)
  • Use improperly stored strips (or out of date strips) in which the effective Amitraz dose is reduced

I’ve heard examples of these types of¬†misuse¬†this season. All increase the chance of selecting for Amitraz-resitant mites.

And (the real reason for posting this at this time of year) …

  • Do not leave the strips you added in late summer in the colony throughout the winter

Removing the strips takes seconds. Prize off the crownboard, grab the tab projecting above the top bars, gently withdraw the strip and close the hive up again.

Finally, because of the incestuous lifestyle 12 of Varroa the genetic diversity (and therefore potential presence of more resistant mites) in the population is likely to be increased by the high mite levels that prevail late in the season.

All the more reason to use the effective treatments we currently have in a way that helps ensure they remain effective.


Colophon

Resistance is futile

Resistance is futile

Resistance is futile is the title of a 2018 album by the Welsh rock band the Manic Street Preachers.

More specifically, in the context of this post, it was the phrase routinely used by the Borg – the alien cyborgs sharing a collective mind – in the Star Trek franchise. Borgs rarely speak, but when they do they usually include this phrase. For example¬†“We are the Borg. Lower your shields and surrender your ships. We will add your biological and technological distinctiveness to our own. Your culture will adapt to service us. Resistance is futile.” The warning about resistance being futile was usually accompanied by the threat that the target would be¬†assimilated”.

I’d started writing this post using the title ‘Resistance is futile’ but realised late on that – as far as¬†Varroa are concerned – resistance is¬†anything but futile¬†13.

Resistance Рto miticides Рgives Varroa a reason to live. Literally.

Let’s not help them ūüôā

Survival of the fattest

Winter bees have high levels of vitellogenin, a glycolipoprotein 1, deposited in their fat bodies which act as a food reservoir for the long winter.

These fat winter bees are essential for the successful overwintering of the colony.

Last week I discussed the major points that need attention for overwintering i.e. strong, healthy colonies with ample food in a weathertight hive.

This week I want to explore the relationship between colony strength, health – specifically with regard to Varroa and deformed wing virus (DWV) – and isolation starvation.

Isolation starvation describes the phenomenon where a small colony of tightly clustered honey bees gets isolated from the honey stores laid down in autumn, resulting – typically during protracted cold periods – in the colony starving to death.

Isolation starvation ...

Isolation starvation …

It’s both a pathetic and distressing sight. Bees, with their heads crammed into the bottom of cells searching for food, dying from starvation when literally inches away from capped stores.

Deaths and births

In temperate climates the winter is characterised by low temperatures and little or no forage for the bees. The queen usually stops laying sometime in autumn and starts again around the turn of the year. During the intervening period she may lay intermittently, but generally in limited amounts.

The fat bodied winter bees that are reared in late summer and early autumn are long-lived (about 6 months) and are responsible for getting the colony through the winter. They protect the queen, thermoregulate the hive and they help rear the brood raised in the autumn and through the winter.

In their absence – or if there are just too few of them – the colony will perish.

Winter bees do not all live for 6 months. The usual figure quoted is ~175 days 2. Some live shorter lives, some longer … up to 9 months under certain conditions.

Importantly, in studies I’ve discussed at length previously, high levels of DWV¬†reduces the lifespan of winter bees. We know this because, in¬†Varroa-infested colonies, researchers 3¬†have shown that the winter bees die off faster 4.

Live fast, die young

Winter bees with high levels of DWV don’t really live fast … but they do die young. In the studies above the average lifespan of winter bees was reduced by 20% in the colonies that died overwinter.

There are a couple of important things to note here. Dainat and colleagues were not looking at bees in the presence or absence of Varroa, or in the presence or absence of high or low levels of DWV. They simply looked at hives that succumbed in the winter or that survived, then measured DWV and¬†Varroa levels. It’s a subtle but important difference. Their surviving colonies still had¬†Varroa and DWV.

From analysis of hives that died or survived, and having marked known numbers of bees in late summer, they could determine the life expectancy of workers – in their surviving colonies it was ~88 days, in those that died it was ~71 days.

Healthy colonies

The gradual death of bees through the winter coupled with the reduced lifespan of winter bees with high levels of DWV explains why colonies need to be strong and healthy.

The following graphs are based upon modelled data 5, but show the influence of colony size and winter bee lifespan.

The first graph – the least important – simply shows the lifespan of bees. The graph plots the number of bees (on the vertical axis) in a population that die at a particular time (on the horizontal axis) after the start of the experiment. The blue bees have a longer average lifespan than the red bees 6.

Lifespan of winter bees

Lifespan of winter bees

In the following graphs remember that the blue bees are healthy, with low levels of Varroa and Рconsequently Рlow levels of DWV. The red bees are unhealthy and have high levels of Varroa and DWV.

Using this lifespan data we can look at the influence on the total number of winter bees in a colony (on the vertical axis) over time (horizontal). Imagine that the horizontal axis is the long, dark, wet and cold months of winter. Starting in early September and running through until late March.

Brrrr ūüôĀ

Winter bee numbers in healthy (blue) and unhealthy (red) colonies

Winter bee numbers in healthy (blue) and unhealthy (red) colonies

It is clear, and of course entirely predictable, that the numbers of bees in the healthy (blue) colony are higher than those in the unhealthy colony at each time point. If the average lifespan is reduced (by disease) more bees will have died by a particular time point when compared with a healthy colony at the same timepoint.

Finally, consider that the shaded section of the graph represents the lower limit of bee numbers for viability. If the number of bees in the colony drops into this region the colony will perish.

Simplistically – and in reality – starting with similar numbers of bees a healthy colony will survive longer than an unhealthy colony.

Strong colonies

Using a similar approach we can also look at the influence of the average lifespan of winter bees on the survival of strong or weak colonies.

The following graph shows the numbers of bees in the colony over time for a strong colony (solid line) and a weak colony (dashed line) where worker bee lifespan is identical 7.

Winter bee numbers in strong and weak colonies.

Winter bee numbers in large (strong) and small (weak) colonies with the same average lifespan.

The shaded section of the graph again represents colony oblivion.

Large (strong) colonies take longer to drop below the threshold for viability and so – all other things being equal – will survive longer 8.

Mix’n’match

A strong colony with high levels of Varroa and DWV might actually survive less well than a weak but healthy colony.

Strong unhealthy colonies might survive less well than weak healthy colonies.

Large unhealthy colonies might survive less well than small healthy colonies.

In this graph the weak but healthy colony drops below the ‘viability threshold’ after the strong but unhealthy colony¬†9.

Winter bees and brood rearing

This is modelled data, but it makes the point clearly. Large and/or healthy colonies retain more of the all-important winter bees and so survive longer.

Simples.

The differences might not appear marked.¬†However, for convenience 10 I’ve omitted the influence of winter bee numbers on the ability of the colony to rear brood.

If there are more winter bees, the colony is able to thermoregulate the hive better. It’s therefore able to keep any brood present warm. It’s therefore able to rear more brood.

As a consequence, the differences in bee numbers between the large or small, or the healthy and unhealthy, colonies will be much more striking.

Critically 11 the strength of the colony coming out of the winter is often the rate-limiting determinant for spring build-up to exploit early season nectar flows. Weak colonies develop less well.

Isolation starvation

Finally, returning to that pathetic little cluster of starving bees in the image at the top of the page. What is the relationship between colony health, strength and isolation starvation?

It’s now time to dust off my weak-to-non-existent Powerpoint skills …

Isolation starvation schematic

Isolation starvation schematic

Again, it’s straightforward. A large (strong) overwintering colony (A above) only has to move a short distance to access stores in midwinter. In contrast, a small (weak) overwintering colony has to move much further.

Consequently, small colonies become isolated from their stores during long, cold periods when the colony is clustered.

Prediction

Many beekeepers will be familiar with isolation starvation of overwintering colonies.

Most would explain this in terms of “very cold weather and the cluster was unable to reach its stores”.

Some would explain this in terms of¬†“the colony was far too small to reach the stores when¬†clustered”.

Very few would explain this in terms of¬†“the Varroa and DWV levels were too high because of poor disease management last autumn. Inevitably most of my winter bees died off early in the winter,¬†leaving a very small cluster of bees that were unable to reach the stores..

I suspect the real cause of isolation starvation is probably disease … specifically poor management of¬†Varroa levels and consequently high levels of DWV in the colony.


Colophon

Herbert Spencer

Herbert Spencer

Another post, another poor pun in the title. Survival of the fittest encapsulates the Darwinian evolutionary principle that the form of an organism that survives is the one able to leave the most copies of itself in future generations. Darwin didn’t actually use the term until the 5th edition (1869) of his book¬†On the origin of the species. Instead, the phrase was first used by Herbert Spencer in 1864 after reading Darwin’s book. Whilst ‘survival of the fittest’ suggests natural selection, Spencer was also a proponent of the inheritance of acquired characteristics, Lamarckism.

Apivar & Apitraz = Amitraz

The range of miticides available ‘off the shelf‘ to UK beekeepers has recently been increased by the introduction of Apitraz and Apivar.

‘Off the shelf’ because, until recently, these were only available with a veterinary prescription.

Considering the extensive coverage on this site of oxalic acid-containing miticides and more recent posts about the – regularly ineffective – Apistan, it seemed fair and appropriate to write something on the active ingredient and mode of action of these new products.

Mites on drone pupae ...

Mites on drone pupae …

Conveniently, because the active ingredient is identical, these can be dealt with together in a single post. The similarities don’t end there. The amount of the active ingredient is the same and the way it is administered is very similar. They¬†are different commercial products; Apitraz is distributed by¬†Laboratorios Calier, SA and sold by BS Honeybees, Amitraz is distributed by Veto Pharma and sold by Thorne’s. The strips have a different appearance and a slightly different mechanism by which they are hung in the hive.

They even cost about the same Рa single packet of 10 strips (sufficient to treat 5 hives) costs £30.50 and £31 respectively for Apitraz and Apivar.

Amitraz

The active ingredient in both Apitraz and Apivar is Amitraz.

Yes … I find these three names confusing similar as well ūüėČ

Amitraz is a synthetic acaricide – a pesticide that kills mites and ticks. It was discovered and developed almost 50 years ago by the Boots Co. (the drug development predecessor of the Boots the Chemist 1 found in most high streets). Amitraz is the active ingredient in a range of medicines approved by the Veterinary Medicine Directorate, including Aludex and Certifect, both of which are used to treat mange in dogs.

Amitraz

Amitraz …

For completeness I should add that Amitraz used to be used by US beekeepers and was sold as a generic pesticide under the name Taktic, though this was withdrawn in about 2014. I believe that Apivar is now available as a slow-release Amitraz-containing Varroa treatment in the US.

Mechanism of action

Amitraz has to be metabolised (essentially ‘modified’) before it is active. This modification occurs much less well in bees than in mites. In fact, the toxicity of Amitraz for bees has been determined to be about 7000 times less than in mites.

Once converted into an ‘active’ form the most important mechanism of action for Amitraz is through interaction with the alpha-adrenoreceptor and¬†octopamine receptors of¬†Varroa 2.

OK, since you asked … octopamine receptors normally bind a neurotransmitter called – rather unimaginatively – octopamine. Quelle surprise as an¬†apiculteur would say. It’s likely that occupancy of these receptors by Amitraz triggers a series of so-called downstream events that change the behaviour of¬†Varroa. Similarly, amitraz also acts as an agonist 3 when binding to the¬†alpha-adrenoreceptor which normally interacts with¬†catecholamines. This results in neurotoxicity and preconvulsant effects.

That all sounds a bit vague. Essentially, amitraz binds and activates receptors that are critically important in a range of important aspects of the¬†Varroa activity and behaviour. Remember here that the mite is entirely dependent upon proper interaction with the bee to complete the life cycle. For example, if the mite fails to enter a cell at the correct time or doesn’t hitch a ride on a passing nurse bee for a few days, it will likely perish.

Amitraz changes behaviour and so exhibits miticidal activity. It has additional activities as well … these multiple routes of action may explain why resistance to amitraz is slow to develop. More on this later.

Usage of Apitraz and Apivar

Both Apitraz and Apivar are formulated as plastic strips impregnated with amitraz. The bees must come into contact with the strips to transmit the amitraz around the hive. Two strips are therefore placed between frames approximately one-third of the way in from each side of the brood box – typically between frames 4 & 5 and 7 & 8 of an 11 frame box. This assumes the bees occupy the entire box. If they don’t, arrange the strips in the appropriate part of the box with 2 frames separating them. Both types of amitraz-containing strips have a means of securing them hanging between the frames.

The recommended treatment period is 6 (Apitraz, or Apivar with little/brood present) to 10 weeks (Apivar with brood present). As with Apistan, treatment should not be applied during a honey flow or when honey supers are present. Further details are included on the comprehensive instructions provided with both products. There’s also a reasonable amount of information on this New Zealand website for Apivar.

Efficacy

This is the good bit … very, very effective. When used properly, amitraz-containing miticides can kill up to 99% of the Varroa in a colony.

Toxicity and wax residues

The good news first. Amitraz does not accumulate in wax to any significant extent. It is not wax-soluble. This is in contrast to Apistan which is found as a contaminant in most commercially-available beeswax foundation.

And now the bad news. Beekeepers also have alpha-adrenoreceptors and octopamine receptors. So do dogs and fish and bees. Although amitraz has increased specificity for the receptors in mites and ticks, it can also interact with the receptors in other organisms. Consequently, amitraz can be toxic. In fact, if you ingest enough it can be very toxic. Symptoms of amitraz intoxication include CNS depression, respiratory failure, miosis, hypothermia, hyperglycemia, loss of consciousness, vomiting and bradycardia.

And it can kill you.

Admittedly, the doses required to achieve this are large, but it’s worth being aware of what you’re dealing with. Amitraz-containing strips should be used only as described in the instructions for use, handled with gloves and discarded responsibly after use.

Resistance

Multiple modes of action makes it much more difficult for resistance to evolve. But it can and does. Resistance to amitraz is well-documented and is understood at the molecular level. However, this is in cattle ticks, not Varroa.

At least, not yet, though there are numerous anecdotal reports of Varroa resistance.

I’ll deal with resistance in a separate post. It’s an important subject and avoiding it is a priority if amitraz-containing compounds are going to remain effective for¬†Varroa control.

Cost

At about £6 per colony, amitraz-containing treatments are not significantly more expensive than the majority of other approved miticides, perhaps with the exception of Api-Bioxal which is appreciably less expensive (though more restricted in the ways it can effectively be administered 4).

Apivar ...

Apivar …

When you purchase a couple of packets of Apivar – enough for 10 colonies – it might feel expensive 5. However, it’s worth remembering that this is still less than the likely ‘profit’ on a couple of jars of your fabulous local honey per colony per year, which seems pretty reasonable in the overall scheme of things.

And, if you look after your colonies well, you are maximising the potential yield of honey in the future … so you’ll be able to afford it ūüėČ