Tag Archives: DWV

Principles and practice

There’s a high level of ‘churn’ amongst new beekeepers. Beekeeping is relatively easy and inexpensive to start. The principles of beekeeping appear straightforward. But large numbers of beginners give up after a season or two.

Here I argue that the colonies and hives some of these beginners abandon pose a threat to other beekeepers, sometimes for years …

A better appreciation of the commitment required to successfully practice the principles of beekeeping might increase the success rates of beginners, though it might also dissuade some from starting in the first place.

Save the bees, save humanity

Supermarket bees

Supermarket bees …

Bees are popular. You only need to visit the supermarket, spend time on the High Street or browse the web, to find bees or pollinators mentioned. The plight of the honey bee is extensively documented in the press. In places some of these references are little more than thinly-veiled adverts … there are any number of beers or ales that now include ‘local honey’ to support bees and beekeeping.

So, public awareness is high.

A good thing

In some ways this is a good thing. The public are aware that, for a variety of reasons, our honey bees (and other pollinators, but I’m going to restrict myself to honey bees for the remainder of this post) are facing real problems. Habitat destruction, monoculture, disease, farming practices, global warming, mobile phone masts, parasites, imports and – the current favourite – neonicotinoids, are all/solely (delete as appropriate) to blame for the problems faced by our cute little bees.

Monoculture ... beelicious ...

Monoculture … beelicious …

It’s a good thing because you might get to sell more local honey which, as a consequence, means you’ll look after your bees carefully and manage them to make more honey next year. It’s a good thing – and I’ll declare a vested interest here – because the Government is encouraged to spend money on research to discover what the real threats to honey bees are (hint, it’s probably not mobile phone masts). This money will also help develop ways to mitigate these threats in due course.

There are a lots of other reasons why it’s a good thing. People are designing bee-friendly gardens, they’re planting wild-flower meadows, they’re reducing pesticide usage and favouring biological control or other pest management techniques. Farmers are being encouraged to leave wide field margins or build beetle banks … and some might even be doing this.

Too much of a good thing?

Some people are so concerned about the plight of the honey bee they decide to do the obvious thing and buy a hive and bees for the bottom of their garden. Obvious, because they’ve increased the number of hives and they’ll be getting lots of delicious honey at the end of the summer.

Some attend a winter ‘start beekeeping’ course (or fully intend to next year, once they’ve kept bees for the current season). Some think they’ll be OK with generous offer of telephone support from the person who sold them a midsummer nuc.

Others do this without any training, without any advice and without anyone to mentor them. 

What could possibly go wrong?

These new beekeepers are certainly well-intentioned. They fully intend to help bees. They really think they’re going to help. They love the idea of their own local honey.

Unfortunately, although many might think they appreciate the basic principles of keeping bees, they know very little about the practice of beekeeping.

Principles

Actually, the principles of beekeeping are a little more complicated than buying a hive, dumping a nuc into it and harvesting the honey at the end of the season.

The bees need to be fed when there’s a dearth of nectar, or in preparation for winter. They need to be protected from pests and diseases. They need space to expand. They need to be monitored in case they’re thinking of swarming. If they are, action is needed. And all this needs to be regularly and repeatedly checked throughout the Spring and Summer.

In short, they need to be properly managed. This management is the practice of successful beekeeping.

Without proper management I’d argue that one of the biggest threats to bees and beekeeping is the unmanaged colony (or hive) lurking in the corner of a field.

Practice

It’s easy to overgeneralise here. The following paragraphs are really describing beekeepers in their first few seasons. Experienced beekeepers can modify their management practices to one that suits their bees, environment, climate and strategy. Bear with me.

Inspections need to start before colonies build up too strongly in the Spring. Queens should ideally be found and marked (and clipped in my view, but some prefer not to do this). Inspections continue at 7 day intervals until the swarming season is well and truly over.

Not 11 day intervals … not when “the weather is better than today”, not when “I get back from the  fortnight in Crete”, not when “I can be bothered” … and certainly not only when “the neighbour is angry about the swarm clustered on their garden swing”.

Inspections have to be conducted thoroughly and with a purpose. It’s not a cursory glance in the top of the box. There’s a reason you’re doing it, so do it well.

Inspections must be done even if it’s 32°C in the shade and you’re melting in your beesuit, when the bees are stroppy as the OSR has just gone over and there’s no nectar coming in, when the weather is (again) miserable and all 50,000 will be ‘at home’ (and possibly tetchy as well) and even if you think “surely they’ll be OK for another day or two?”.

They probably won’t.

Hard labour

Beekeeping is hard work. If you’re lucky and the supers are bulging full it can be backbreaking.

You have to work reasonably fast and carefully. Manage only one of these two and, for different reasons, inspections can become tiresome.

You will get stung, though not often if you’re fast and careful and if you have well-tempered bees.

It can be hot as hell in summer and you can get wet, miserable and cold at any time of the season.

Uh oh ... swarming ...

Uh oh … swarming …

It’s not only physically hard, it is also mentally hard. Not like quantum physics, but it still requires quite a bit of thought. Bees are not ‘fit and forget’.

Using a combination of observation, experience and knowledge (and perhaps a little inspired guesswork) you need to determine what’s going on in a forty litre box containing over 50,000 bees. Is there disease present? Is it one you can do anything about? Is it notifiable? Is the queen present and laying well? Is the colony thinking of swarming (hint, a dozen sealed cells is usually an indication the colony has swarmed, not that it’s thinking of swarming 😉 ). Do they have enough stores? Do they need more space?

You need to be prepared for disappointment (and have a contingency plan). Despite your best efforts the colony may swarm. An extended period of lousy summer weather prevents the new queen from getting mated properly. The colony dwindles, is too weak to defend itself and is robbed out by another colony. Any number of things can go wrong.

Bees are managed, not domesticated.

That’s the reality of beekeeping. That’s the practice that underlies the principle of just dumping a nuc of bees in a box in late April and harvesting pound after pound of golden honey in early September.

If only it were that simple!

Beeless “beekeepers”

I regularly meet people who ‘once kept bees’. I’m sure you do to. Further discussion often shows that they certainly once had bees, but that they failed to keep them.

The colony died, was robbed out, repeatedly swarmed, absconded or – much more frequently – these beekeephaders simply lost interest.

Often they aren’t actually sure what happened to the colony. Have you ever asked them?

Their initial enthusiasm was tempered a bit by the first couple of inspections. The colony was getting much bigger, much faster than their experience made them comfortable with. They got a bit frightened but wouldn’t actually admit that. They missed an inspection (or two) as they were in Crete for the family holiday. The colony swarmed. They’d read somewhere that the colony shouldn’t be disturbed for a month, so they didn’t. They remembered again three months later but were then too late for the autumn Varroa treatment. Have you got any fondant to spare? They’ll have another go next year.

Definitely.

It’s not unusual for these hives to be simply abandoned. You find them in the corners of fields or tucked up against the hedge in a large sprawling garden.

Out of sight and out of mind.

Forgotten, but not gone

Forgotten, but not gone …

The gift that keeps on giving

Sometimes the colony limps on for a season or two. More often though it expires in the winter. The hive may then be repopulated the following year by a swarm. They flourish, or more likely perish and are repopulated again. Even if mice move in for winter and wax moth trashes the comb they still attract swarms.

duunnn dunnn ...

duunnn dunnn …

There’s a dozen or more hives like this on private land I know of. Some local beekeepers visit every year or so to collect any swarms that have moved in. I can’t imagine the state of the comb … or the colonies they collect.

But (queue Jaws music … duunnn dunnn… duuuunnnn duun… duuunnnnnnnn dun dun dun dun dun dun dun dun dun dun dunnnnnnnnnnn dunnnn) these abandoned and unmanaged hives mainly provide a great opportunity for Varroa to flourish. Together with both the foul broods, Nosema and goodness knows what else.

The abandoned hives effectively act as bait hives, attracting swarms which become established feral colonies. Most will eventually be decimated by Varroa and its viral payload, but many will chuck out a swarm or two first, or drones that drift from colony to colony. Some will get robbed out as they collapse – perhaps by one of your strong colonies – leading to a huge infestation with phoretic mites carried by the returning robbers.

They’re like a 40 litre cedar version of Typhoid Mary.


† And my extensive market research suggests they are very delicious too 😉

‡ After all, there’s no time like the present to start and the sooner you buy and populate that lovely cedar hive, the faster honey bee colonies numbers will increase. But they will definitely attend the beekeeping course next winter. Absolutely!

Telephone support. Really?! Have you ever tried to give telephone advice to a new beekeeper who’s standing by an open hive, mobile clamped to their ear, desperately looking for eggs, or deciding whether the queen cells are capped or uncapped? I’ve tried … don’t bother. Grab the beesuit and get to the apiary 😉

There are others I know of and have access to. The entrances to these have miraculously become stuffed tight with grass, so preventing their repopulation. How did that happen? 😉

A poor analogy, but it makes the point. Typhoid Mary (Mary Mallon) was an Irish immigrant  New York cook in the early part of the 20th Century. She was also an asymptomatic carrier of typhoid, a bacterial infection. During the period 1900-07 she infected at least 51 people, three of whom died. Investigative epidemiology traced a series of typhoid fever outbreaks to places where Mary Mallon worked. She was named Typhoid Mary in a 1908 article in the Journal of the American Medical Association.

Mary Mallon

Mary Mallon

Mary Mallon refused to accept that she was infected, was forcibly incarcerated (quarantined) twice and eventually died after three decades of isolation. The analogy is poor because Mary Mallon appeared in good health, whereas these abandoned hives (and the bees they contain) are often pretty skanky. However, the term “like Typhoid Mary” is often used to indicate a source of repeated infection … which is spot on.

 

 

The day job

It’s no secret that I have both amateur and professional interests in bees, bee health and beekeeping.

During the weekend I sweat profusely in my beesuit, rushing between my apiaries in Central and Eastern Fife, checking my colonies – about 15 at the autumn census this year – averting swarms, setting up bait hives, queen rearing and carrying bulging supers back for extraction.

Actually, not so much of the latter in 2017  🙁  I did get very wet though, much like all the other beekeepers in Fife.

The BSRC labs

The BSRC labs …

During the week I sit in front of a large computer screen running (or sometimes running to keep up with) a team of researchers studying the biology of viruses in the Biomedical Sciences Research Complex (BSRC) at the University of St. Andrews. Some of these researchers work on the biology and control of honey bee viruses.

During the winter the beekeeping stops, but the research continues unabated. The apiary visits are replaced with trips in the evenings and weekends to beekeeping associations and conventions to talk about our research … or sometimes to talk about beekeeping.

Or both.

This weekend I’m delighted to be speaking at the South Devon Beekeepers Convention in Totnes on the science that underpins rational and practical Varroa control.

Which came first?

I’ve been a virologist my entire academic career, but I’ve only worked on honey bee viruses for about 6 years. I’ve been a beekeeper for about a decade, so the beekeeping preceded working on the viruses of bees.

However, the two are inextricably entwined. Having a reasonable amount of beekeeping experience provides a unique insight into the problems and practicalities of controlling the virus diseases that bees get.

Being able to “talk beekeeping” with beekeepers has been very useful – both for the communication of our results to a wider audience and in influencing the way we approach our research.

Increasingly, the latter is important. Researchers need to address relevant questions, using their detailed understanding of the science to deliver practical solutions to problems1. There’s no point in coming up with a solution if there’s no way it’s implementation is compatible with beekeeping.

Deformed wing virus

DWV symptoms

DWV symptoms

The most important virus for most beekeepers in most years is deformed wing virus (DWV). This virus “does what it says on the tin” because, at high levels, it causes developmental defects in pupae that emerge with shrivelled, stunted wings. There are additional developmental defects which are slightly less obvious, but there are additional (largely invisible) changes which are of greater importance.

DWV reduces the lifespan of worker bees. This is probably not hugely significant in workers destined to live only a few weeks in midsummer. However, the winter bees that get the colony through from September through to March must live for months, not weeks. If these bees are heavily infected with DWV they die at a faster rate. Consequently, the colony dwindles and dies out in midwinter or early Spring. At best, it staggers through to March and then never builds up properly. It’s still effectively a winter loss.

Our research focuses on how Varroa influences the virus population. There’s very good evidence now that DWV transmission by Varroa leads to a significant increase in the amount of virus, and a considerable decrease in the diversity of the virus population.

So what?

Well, this is important because if we want to control the virus (i.e. to reduce DWV-associated disease and colony losses) it must help to know the proper identity of the virus we are trying to control. It will also help us measure how well our control works. We know we’re measuring the right thing.

We’re working with researchers around the world to define the important characteristics of DWV strains that cause disease and, closer to home, with entire beekeeping associations to investigate practical strategies to improve colony health.

Chronic bee paralysis virus

CBPV symptoms

CBPV symptoms

We’re about to start a large collaborative project on the biology and control of chronic bee paralysis virus (CBPV). This virus is becoming a significant problem for many beekeepers and is increasing globally. It’s a particular problem for some bee farmers.

CBPV causes characteristic symptoms of dark, hairless, oily-looking bees that sometimes shiver, dying in large smelly piles at the hive entrance. It typically affects very strong colonies in the middle of the season. It can be devastating. Hives that should be the most productive ones in the apiary fail catastrophically.

Why is a virus we’ve known about for decades apparently increasing in the amount of disease it causes? Are there new virulent strains of the virus circulating? Are there particular beekeeping practices that facilitate it’s spread? We’re working with collaborators in the University of Newcastle to try and address these and related questions.

I’ll write more about CBPV over the next year or so. It won’t be a running dialogue on the research (which would be crushingly dull for most readers), but will provide some background information on what is a really fascinating virus.

At least to a virologist 😉

And perhaps to beekeepers.

Grow your own

As virologists, we approach the disease by studying the virus. Although we maintain an excellent research apiary, we don’t do many experiments in ‘the field’. Almost all the work is done in test tubes in incubators in the laboratory … or in bees we rear in those incubators.

Grow your own

Grow your own …

We can harvest day-old larvae (or even eggs) from a colony and rear them to emergence as adult bees in small plastic dishes in the laboratory. We use an artificial diet of sugar and pollen to do this. It’s time consuming – they need very regular feeding – but it provides a tightly controllable environment in which to do experiments.

Since we can rear the bees, we can therefore easily test the ability of viruses to replicate in the bees. Do all strains of the virus replicate equally well? Do some strains outcompete others? Does the route by which the virus is acquired influence the location(s) in the bee in which the virus replicates? Or the strains it is susceptible to? Or the level of virus that accumulates?

And if our competitors are reading this, the answer to most of those questions is ‘yes’ 😉

We can even ask questions about why and how DWV causes deformed wings.

Again, so what? We suspect that DWV causes deformed wings because it stops the expression of a gene in the bee that’s needed to make ‘good’ wings. If we can identify that gene we might be able to investigate different strains of honey bee for variation in the gene that would render them less susceptible to being ‘turned off’ by DWV. That might be the basis for a selective breeding project.

It’s a simplistic explanation, but it’s this type of molecular interaction that explains susceptibility to a wide range of human, animal and plant diseases.

Bee observant

Bee health is important, and not fundamentally difficult to achieve. There are some basics to attend to … strong hives, good forage, good apiary hygiene etc. However, it primarily requires good powers of observation – does something look odd? Are there lots of mites present? How does the brood look?

If things aren’t right – and often deducing this means comparisons must be made between hives – then many interventions are relatively straightforward.

Not long for this world ...

Not long for this world …

The most widespread problems (though, interestingly, this doesn’t apply to CBPV) are due to high levels of Varroa infestation. There are effective and relatively inexpensive ways to treat these … if they’re used properly.

More correctly, they’re relatively inexpensive whether they’re used properly or not. However, they’re pretty ineffective if not used properly 😉

Regular checks, good record keeping, comparisons between hives and informed observation are what is needed. Don’t just look, instead look for specific things. Can you see bees with overt symptoms of DWV? Are there bees with Varroa riding around on their backs? The photo above has both of these in plain view. Are some hairless bees staggering around the top bars with glossy abdomens, or clinging to the side bars shaking and twitching?

Don’t wait, act

I’ve no doubt that scientists will be able to develop novel treatments to control or prevent virus infections of bees. I would say that … I’m a scientist 😉  However, I’m not sure beekeepers will be able to afford them, or perhaps even want to use them, or that they’d be compatible with honey production or of any use in Warré hives etc.

I’m also not sure how soon these sorts of treatments might become available … so don’t wait.

If there are signs of obvious DWV infection you need to do something. ‘Obvious’ because DWV is always present, but it’s usually harmless or at least tolerated by the bees. My lab have looked at thousands of bees and have yet to find one without detectable levels of DWV. However, healthy bees have only about 1/10,000 the level of DWV present in sick bees … and these are the ones that have obvious symptoms.

I’ve discussed Varroa control elsewhere, and will again.

Unfortunately, if your colony has signs of CBPV disease then Varroa control is not really relevant. The virus is transmitted from bee to bee by direct contact. This probably accounts for the appearance of the disease primarily in very strong colonies.

At the moment there’s little you can do to ‘cure’ a CBPV-afflicted colony. I hope, in 2-3 years we will have a better idea on what interventions might work. We have lots of ideas, but there are a lot of basic questions to be addressed before we can test them.

Field work

Field work

Business and pleasure

The half of my lab that don’t work on bee viruses study fundamental mechanisms of virus replication and evolution. They do this using human viruses, some of which are distant relatives of DWV. They work on human viruses as it’s only these that have excellent model systems to facilitate the types of elegant experiments we try to do. They’re also relatively easy to justify in funding applications, and it allows us to tap into a much bigger pot for funding opportunities (human health R&D costs probably total £2 billion/annum, bees might be £2 million/annum).

And no, my lab don’t get anything like that much per year for our research!

Importantly, the two activities on human and honey bee viruses are related. Our experience with the human viruses related to DWV made us well-qualified to tackle the bee virus. They replicate and evolve in very similar ways, we quantify them in the same way and there may be similarities in some ways we could approach to control them.

And with the bee viruses I can mix business with pleasure. If I’m going to the apiary I’ll get to see and handle bees, despite it being officially “work”. It doesn’t happen as much as I’d like as I’m usually sat behind the computer and all of the ‘bee team’ have been trained to work with bees by the ESBA.

However, at least when I talk to collaborators or to the beekeeping groups we’re fortunate to be working with we – inevitably – talk about bees.

And that’s fun  😀


Several years ago I delivered an enthusiastic and rather science-heavy talk at a Bee Farmers Association meeting. I thought it had gone reasonably well and they were kind enough to say some nice things to me … and then I got the question from the back of the room which went something like “That’s all very well young man … but what have you made NOW that I can put into my hives to make them healthy?”.

I’m sure my answer was a bit woolly. These days the presentation would have had a bit less science and bit more justification. We’ve also made some progress and it’s possible to now discuss practical strategies to rationally control viruses in the hive. It’s not rocket science … though some of the science it’s based on is reasonably fancy.

Kick ’em when they’re down

Out, damn'd mite ...

Out, damn’d mite …

Why bother treating colonies in midwinter to reduce Varroa infestation? After all, you probably treated them with Apiguard or Apivar (or possibly even Apistan) in late summer or early autumn.

Is there any need to treat again in midwinter?

Yes. To cut a long story short, there are basically two reasons why a midwinter mite treatment almost always makes sense:

  1. Mites will be present. In addition, they’ll be present at a level higher than the minimum level achievable, particularly if you last treated your colonies in late summer, rather than early autumn.
  2. The majority of mites will be phoretic, rather than hiding away in sealed brood. They’re therefore easy to target.

I’ll deal with these in reverse order …

Know your enemy

DWV symptoms

DWV symptoms

The ectoparasite Varroa feeds on honey bee pupae and, while doing so, transmits viruses (in particular DWV) that can completely mess up the development of the adult bee. Varroa cannot replicate anywhere other than on developing pupae. It’s replication cycle, and the resulting mite levels in the colony, are therefore tightly linked to the numbers and availability of hosts … honey bee pupae.

If developing brood is available the mite can replicate. Under these conditions, newly emerged adult, mated, female Varroa spend a few days as phoretic mites, riding around the colony on young bees. They then select a cell with a late-stage larvae in, enter the cell and wait until pupation occurs. If developing worker brood is available each infested cell produces 1 – 2 new mites (drone cells produce 3+) and mite numbers increase very rapidly in the colony.

In contrast, if there’s no developing brood available, the mites have to hang around waiting for brood to become available. They do this as phoretic mites and can remain like this for weeks or months if necessary.

Therefore, when brood is in abundance and the queen in laying freely mites can replicate to very high levels. In contrast, when brood is limiting and the queen has reduced her egg laying to a   v  e  r  y     s  l  o  w     r  a  t  e     the mite cannot replicate and must be predominantly phoretic.

When does this happen?

Lay Lady Lay … or don’t

Ambient temperature, day length and the availability of nectar and pollen likely influence whether the queen lays eggs. When it’s cold, dark and there’s little or no pollen or nectar coming into the hive the queen slows down, or even stops, laying eggs.

About 8 days after she stops laying there will be no more unsealed brood in the colony. About 13 days after that all the sealed brood will have emerged (along with any Varroa). Therefore, after an extended cold period in midwinter, the colony will have the lowest level of sealed brood … and the highest proportion of the mite population will be phoretic.

Under normal (midsummer) circumstances about 10% of the mite population is phoretic. It’s probably unnecessary to state that, if there’s no brood available, 100% of the mites must be phoretic.

All licensed miticides work extremely well against phoretic mites.

Caveats, guesstimates, global warming and the Gulf Stream

Global warming

Global warming …

Whatever the cause, the globe is warming (irrespective of what Donald Trump tweets). Long, hard winters are getting less common (or perhaps even rarer, as they were never particularly common in the UK). In Central, Southern or Eastern Britain it’s possible that the colony will have some brood present all year. In parts of the West, warmed by the Gulf Stream, I’d be surprised if a colony was ever broodless. Only in the North is it likely that there will be a brood break in midwinter.

Most of the paragraph above is semi-informed guesswork. I don’t think anyone has systematically analysed colonies in the winter for the presence of sealed brood. Sure, many (including me) have opened colonies for a quick peek. Others will have peered intently at the Varroa board to search for shredded wax cappings that indicate emerging brood. The presence of brood will vary according to environmental conditions and the genetics of the bees, so it’s not possible to be dogmatic about these things.

However, it’s safe to say that in midwinter, sealed brood – within which the mites can escape decimation by miticides – is at a minimal level.

Reducing mite levels and minimal mite levels

Within reason, the earlier you apply late summer miticides, the better you protect the all-important overwintering bees from the ravages of viruses, particularly deformed wing virus. This is explained in excruciating detail in a previous post, so I won’t repeat the text here.

However, I will re-present the graph that illustrates the modelled (using BEEHAVE) mite levels.

Time of treatment and mite numbers

Time of treatment and mite numbers

The gold arrow (days 240-300 i.e. September and October) indicates when the winter bees are being reared. These are the bees that need to be protected from mites (and their viruses). Mite numbers (starting with just 20 in the hive on day zero) are indicated by the solid coloured lines. The blue, black, red, cyan and green lines indicate modelled mite numbers when the colony is treated with a miticide (95% effective) in mid-July, August, September, October or November respectively.

The earlier you treat, the lower the mite levels are when the winter bees are being reared. Study the blue and black lines.

This is a good thing.

In contrast, by treating very late (the cyan and green lines) the highest mite numbers of the season occur at the same time as the winter bees are being reared. A bad thing.

But … look also at mite numbers after treatment

Look carefully at the mite numbers predicted to remain at the end of the year. Early treatment leaves higher mite levels at the start of the following year.

This is simply because mites escaping the treatment at the end of summer have had an opportunity to reproduce during the late autumn.

This is why the additional midwinter treatment is beneficial … it kills residual mites and gives the colony the best start to the new calendar year§.

Kick ’em when they’re down

Early treatment protects winter bees but risks exposing bees the following season to unnecessarily high mite numbers. However, in midwinter, these residual mites are much more likely to be phoretic due to a lack of brood in the colony. As I stated earlier, phoretic mites are relatively easy to target with miticides.

So, give the mites a hammering in late summer with an appropriate and effective miticide and then give those that remain another dose of the medicine in midwinter.

But not another dose of the same medicine

Since the majority of mites in a colony with little or no brood will be phoretic, you can easily reduce their numbers using a single treatment containing oxalic acid. This can be administered by sublimation (vaporisation) or by trickling (dribbling).

There’s no need to use any treatment that needs to applied for a month. Indeed, many (Apiguard etc.) are not recommended for use in winter because they work far less well on a largely inactive colony.

Trickle 2 - £1

Trickle 2 – £1

I’ve discussed sublimation previously. However, since this requires relatively expensive (£30 – £300) specialised delivery and personal protection equipment it may be inappropriate for the two hive owner. In contrast, trickling requires almost no expensive or special equipment and – reassuringly – has been successfully practised by UK beekeepers for many years. I did it for years before I bought my Sublimox vaporiser.

Therefore, in two further articles this autumn (well before you’ll need to treat your own colonies) I’ll describe the preparation and storage of oxalic acid solutions and its use.

Be prepared

If you want to be prepared you’ll need to beg, borrow or steal the following – sufficient oxalic acid (or Api-Bioxal), a Trickle 2 bottle sold by Thorne’s, a cheap vacuum flask (Tesco £2.50), granulated sugar and a pair of thin disposable gloves.

Do this soon. Don’t leave it until midwinter. You need to be ready to treat as soon as there’s a protracted cold spell (when brood will be at a minimum). Over the last few years my records show that this has been anywhere between the third week in November and the third week in January.

More soon …


† Only MAQS is effective against mites sealed in cells. This is why most miticides are used for extended periods in the late summer or early autumn … the miticide must be present as Varroa emerge from sealed cells.

‡ I’ll repeat the caveat that this is an in silico simulation of what happens in a beehive. Undoubtedly it’s not perfect, but it serves to illustrate the point well. It’s freely available, runs on PC and Mac computers, and is reasonably well-documented. In the simulations shown here the virtual colony was ‘primed’ with 20 mites at the beginning of the year. BEEHAVE was run using all the default settings – climate, forage etc. – with the additional application of a miticide (95% effective) in the middle of the months indicated. Full details of the modelling have already been posted.

§ The National Bee Unit recommend Varroa levels are maintained below 1000 throughout the season. Without treatment, 20 mites at the start of the season can easily replicate to ~750 in the autumn. If you start the season with 200 mites then levels are predicted to reach ~5000 in the following summer. The colony will almost certainly die that season or the next. There’s a more detailed account of the consequence of winter brood rearing and the level of mite infestation written by Eric McArthur and reproduced on the Montgomeryshire BKA website that’s worth reading.

¶ The cumulative (year upon year) effect of late summer treatment with no midwinter treatment has been discussed previously. I’ll simply re-post the relevant figure here – 5 years of bee (in blue, left axis) and mite (in red, right axis) numbers with only one treatment per season applied in late September. Within two years the higher mite numbers that are present at the start of the year reproduce to dangerously high levels.

Mid September

Mid September

Peaceful easy feeling

The 6-8 week period between late June and harvesting the summer honey is a quiet period in the beekeeping calendar. At least, it is in mine. My colonies aren’t going to the heather, so there’s nothing to prepare for that. Swarm control is complete and many colonies are now headed by new queens, so the chance of swarming is minimal. The spring honey – what little there was of it on account of the incessant rain – was extracted in late June. It’s now easy going until the summer honey is taken off and the colonies are prepared for winter.

Inspect, or just observe?

The 7 day cycle of inspections that are so important as the season builds up become much less critical. If there’s a new mated, laying queen in a box with ample space, sufficient supers and enough stores (for adverse periods of weather) there’s actually little to be achieved by rummaging through the box on a weekly basis.

Instead, I generally just observe things from the outside. If pollen is being taken in by foragers, if there are good numbers of bees on orientation flights during warm mornings and if the hive is reassuringly heavy, then there’s probably no need to inspect weekly. A peek through a perspex crownboard can give a pretty good idea of how much space the colony has and whether they’re fully utilising the super. With experience, hefting the hive (gently lifting the back an inch or two and judging the weight) is a good indication of whether they might need an additional super. And that’s it … I generally leave these strong, healthy colonies to simply get on with things during July and into August.

But inspect when appropriate

Of course, some hives will need checking. For example, any hives that are clearly below-strength for an unknown reason should be carefully checked for signs of disease. Varroa levels can be readily, albeit pretty inaccurately, determined by putting a Correx Varroa tray below the open mesh floor and the colony should be inspected for obvious signs of deformed wing virus (DWV) symptoms.

High levels of DWV

High levels of DWV …

If there’s any doubt about the health of the colony consult a good book on the subject (Ted Hooper’s Bees and Honey is a reasonable start though some of the more comprehensively illustrated newer books might be better), ask your mentor or an experienced local association beekeeper and contact the local bee inspector if necessary.

Chronic Bee Paralysis Virus (CBPV) is a high-season problem for big, strong colonies. Sick bees exhibit characteristic shaking or shivering symptoms, look oily or greasy and accumulate in a large smelly pile below the hive entrance. A very distressing sight. I’ll be discussing CBPV in more detail over the next few months as it appears to be an increasing problem.

Queen problems

The other colonies I keep a close eye on are those with known or potential queen problems. These include colonies where the queen may not have mated, or those in which the queen appears to have got mated but the colony shows signs of early supercedure, suggesting that all is not right.

Hopalong Cassidy ...

Hopalong Cassidy …

The queen in the (rather poor) photograph above has a paralysed left rear leg. She’s a 2017 queen and emerged in early/mid June during a period of very poor weather. I found her as a skittish virgin very soon after emergence (quite possibly the day of emergence) then left the colony to get on with things. She was mated by the first week in July. Eggs were present but I didn’t see her in the colony. However, she wasn’t laying particularly well, either in terms of number or pattern.

Since I was disappearing to Malaysia on business for 10 days in late July I thoroughly inspected the colony before leaving. I discovered her hobbling around the frame, clearly with very severely impaired abilities. There was very little open or sealed brood in the colony. In the several minutes I watched her she didn’t lay any eggs despite checking lots of cells that looked polished and ready to me (but I accept she’s probably a better judge of a suitable cell than I am). She clearly could lay, and you can see an egg at the tip of her abdomen. I suspect that, although her walking wasn’t grossly impaired, she was unable to properly ‘reverse’ into the cell.

Not a bee ...

Not a bee …

Don’t delay, act today

Mid-July, a strongish colony with almost no brood, a crippled queen and no means of checking things for a fortnight meant that prompt action was needed. I removed the queen and united the colony over the top of another strong colony. The alternative was to wait and see if the colony disposed of her, or tried to supercede her. Either would have imposed a delay of about a month after my return, there were limited numbers of larvae for the colony to start from, a rapidly ageing worker population and little chance of the colony building up strongly through the autumn to overwinter successfully. This was a case of using them or potentially losing them.

I’ve no idea how the queen came to have a gammy leg. I’d not seen her since she’d been mated. One possibility is that two queens emerged at or near the same time, duelled in the hive leaving one dead and the other partially crippled. Although damaged, the queen still managed to leave the hive to mate successfully, but then struggled to lay properly.

We’ll never know.

Late evening

Finally, if you’ve not visited your apiary late on a warm, calm summer evening then you really should. Strong colonies can be heard from some distance away, a sort of low humming sound. There’s the heady smell of warm honey in the air as they evaporate off water from stored nectar in preparation for capping stores off for the winter ahead. Highly recommended.


† Gammy meaning (especially of a leg) unable to function normally because of injury or chronic pain … in contrast to the fictional cowboy Hopalong Cassidy used to label the image. Hopalong Cassidy had a wooden leg.

Colophon

Peaceful easy feeling was the title of a song by the Eagles released in 1972 on their debut album (Eagles). The band, or what’s left of them after the recent death of Glenn Frey, continue to play live with four concerts last month.

Don Henley has just turned 70 and should really Take it Easy 😉

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.