Category Archives: Science

Mites equal viruses

Healthy bees are happy bees ūüôā

Sounds good doesn’t it?

Actually, there’s¬†no evidence that bees display or perceive most of the emotions often attributed to them 1.

Happy? Who knows? But certainly not healthy ...

Happy? Who knows? But certainly not healthy …

A more accurate statement might be¬†“Healthy¬†bees are more¬†productive, they are less likely to die overwinter, less likely to be robbed out by wasps or neighbouring strong colonies and their parasites and pathogens cannot threaten the health of other honey bee colonies or, through so-called-pathogen overspill, the health of other pollinators.”

More accurate?

Yes … but it doesn’t exactly trip off the tongue ūüėČ

Whether it makes the bees happy or not, beekeepers have a responsibility to look after the health of their livestock. This includes controlling Varroa numbers to reduce the levels of pathogenic viruses in the hive.

How well are virus levels controlled if mite levels are reduced?

I’ll get to that in due course …

Midwinter mite massacre

The 2018 autumn was relatively mild through until mid/late November. In the absence of very early frosts colonies continued rearing brood.

We opened colonies in mid-November (for work) and found sealed brood, though it was clear that the laying rate of the queen was much-reduced.

These are ideal conditions for residual mite replication. Any mites that escaped the late summer/early autumn treatment (the ideal time to treat to protect the overwintering bees) continue to replicate, resulting in the colony starting the following season with a disappointingly high level of mites.

I’ve noted before that midwinter mite levels are paradoxically¬†higher if you treat¬†early enough in the autumn to protect the all-important winter bees.

Consequently, to start the year with minimal mite levels, I treat in midwinter with a trickled or vaporised oxalic acid-containing (OA) treatment.

A combination of colder weather (hard frosts in late November) and brood temperature measurements 2 indicated mid-December was a good time to treat.

Midwinter mite massacre

Midwinter mite massacre

18th December

In one of my apiaries ten colonies were treated. Some were definitely broodless (based upon Arnia hive monitoring). Others may have had brood, but colonies were not routinely checked.

Over the four day period after vaporising these ten colonies dropped a total of 92 mites. More than 50% of these were from just one double-brooded colony. Overwintering nucs 3 dropped no mites at all in the 12 days following treatment.

This was very encouraging. These are lower midwinter mite levels than I’ve seen since returning to Scotland in 2015.

The one colony with ‘high’ mite levels received two further treatments (on the 22nd and 27th) in an attempt to minimise the mite levels for the start of the season. Going by the strength of the colony and the debris on the¬†Varroa¬†tray it was presumed that this colony was still rearing brood.

Mite drop following the third treatment was negligible 4.

Why are mite levels so low?

I think it’s a combination of:

  • Luck
  • Use of natural, organic, bee-centric and biodynamic beekeeping methods
  • Varroa-resistant bees
  • Very tight control of mite numbers in the 2017/18 season, primarily by correctly timing the¬†winter¬†and the late-season¬†autumn¬†treatments. This is simply good colony management. Anyone can achieve this.
  • A brood break midseason and/or a broodless period when splitting colonies (both give opportunities for more phoretic mites to be lost through grooming). Undoubtedly beneficial but season-dependent. I’ll be discussing ways to exploit these events in posts next year.
  • A low density of beekeepers in Fife, so relatively little¬†drifting or robbing¬†of poorly managed colonies from neighbouring apiaries. Geography-dependent. Much easier in Fife than Warwickshire … and easier still in Lochaber.

And what do less mites mean?

Varroa is a threat to bee health because it transmits pathogenic viruses when feeding on developing pupae.

The most important of these viruses is deformed wing virus (DWV).

Generally, the higher the level of infestation with mites, the higher the viral load 5. This has been repeatedly demonstrated by studies from researchers working in the UK, Europe and the USA.

It is well-established that colonies with high viral loads have an increased chance of dying overwinter, due to the decreased longevity of bees infected with high levels of virus.

DWV symptoms

DWV symptoms

In our work apiaries we regularly measure DWV levels. For routine screening our limit of detection is around 1,000 viruses per bee.

We don’t actually count the viruses. They’re too small to see without an electron microscope 6.

Instead, we quantify the amount of the virus genetic material present 7, compare it to a set of standards and express it as ‘genome equivalents (GE)’.

Many of the bees tested this year contained ~103 (i.e. 1000) GE, which is extremely low. Bees from Varroa-free regions (e.g. Colonsay) carry similar levels of DWV.

Most of our colonies were at or close to this level of virus much of the 2018 season. This is 100-1,000 times lower than we often see even in apparently perfectly healthy colonies in other years or other apiaries.

For comparison, using the same assay we usually detect about 1010 (ten billion) DWV GE per bee in symptomatic adult bees from heavily mite-infested colonies.

So, less mites means less viruses which means healthier bees ūüôā

And they might even be happier bees ūüėČ

And your point is?

It’s worth remembering that the purpose of treating a colony with miticides is to reduce the transmission of viruses between bees. This transmission results in the amplification of DWV. This is why the¬†timing of treatments is so important.

Yes, it’s always good to slaughter a few (or a few thousand ūüôā ) mites. However, far better massacre them when you need to protect particular populations of bees.

This includes the overwintering bees, raised in September, that get the colony through to the Spring.

Remember also that it ‘takes bees to make bees’¬†i.e.¬†the rearing of new brood requires bees. Therefore strong colony build-up in Spring requires healthy workers rearing healthy brood.

This is why it’s important to minimise mite levels in midwinter when colonies are broodless.

What do most beekeepers do?

Fifteen months ago I published a post on the preparation of oxalic acid solutions for trickling colonies in midwinter.

Whatever the vapoholics on the online forums claim, trickling remains the easiest, quickest and least expensive way to treat colonies in midwinter 8.

The best time to treat in the winter is when the colony is broodless. Here in Fife, and often elsewhere, I believe that this usually occurs¬†earlier in the winter than many beekeepers treat (if it happens at all … or if they treat at all).

I usually treat between the end of the third week in November and mid-December, at the end of the first extended cold period.

Oxalic acid preparation recipe page views

Oxalic acid preparation recipe page views

Looking at the page views for these oxalic acid recipes it looks as though many beekeepers treat after Christmas 9¬†… which may be suboptimal if colonies had a broodless period and now started rearing brood again.

Mine have.

This winter has been quite mild (at least at the time of writing) so there may yet be opportunities to treat really effectively during a broodless period.

Or the chance may have gone …


 

Know your enemy

What less appropriate time is there, as we enter the festive season of goodwill, to provide a brief account of the incestuous and disease-riddled life cycle of the Varroa mite?

Happy Christmas ūüôā

Scanning electron micrograph of Varroa destructor

Scanning electron micrograph of Varroa destructor

Varroa is the biggest enemy of bees, beekeepers and beekeeping. During the replication cycle the mite transfers a smorgasbord of viruses to developing pupae. One of these viruses, deformed wing virus (DWV), although well-tolerated in the absence of Varroa 1, replicates to devastatingly high levels and is pathogenic when transferred by the mite.

Without colony management methods to control Varroa, mite and virus replication will eventually kill the colony.

I’ve written extensively on ways to control¬†Varroa. Most of these have focused on early autumn and midwinter treatment regimes. However, next season I’m hoping to discuss some alternative strategies and will need to reference aspects of the life cycle of¬†Varroa … hence this post.

What is Varroa?

Varroa destructor is a distant relative of spiders, both being members of the class¬†Arachnida … the joint-legged invertebrates (arthropods). It was originally (and remains) an external parasite (ectoparasite) of¬†Apis cerana (the Eastern honey bee) and – following cross-species transfer a century or so ago –¬†Apis mellifera, ‘our’ Western honey bee.

Apis cerana, having co-evolved with Varroa, has a number of strategies to minimise the detrimental consequences of being parasitised by the mite.

Apis mellifera¬†doesn’t. Simple as that 2.

One hundred years is the blink of an eye in evolutionary terms and, whilst there are bees that have partial solutions – largely behavioural (small colonies and very swarmy) – they’re probably unable to collect meaningful amounts of honey 3.

Varroa-resistant honey bees will probably evolve (as much as anything is predictable in evolution) but not in my time as a beekeeper … or possibly not until Voyager 2 leaves the Oort Cloud¬†4.

And there’s no guarantee they’ll be any use whatsoever for beekeeping …

The replication cycle of Varroa

Varroa has no free-living stage during the life-cycle. The adult mated female mite exhibits two distinct phases during the life-cycle. It has a phoretic phase on adult bees and a reproductive phase within sealed (‘capped’) worker and drone brood cells. Male mites only ever exist within sealed brood cells.

I’m going to discuss phoretic mites in a separate post. I’ll concentrate here on the replication cycle.

The mated female mite enters a cell 15-50 hours before brood capping. Drone brood is chosen preferentially (at ~10-fold greater rates than worker brood) and entered earlier. Depending upon the time of the season and the levels of mites and brood, up to 70-90% of mites in the colony occupy capped cells.

The first egg is laid ~70 hours after cell capping. This egg is unfertilized and develops into a haploid male mite. Subsequent eggs are fertilised, diploid, and so develop into female mites. These are laid at ~30 hour intervals.

The replication cycle of Varroa

The replication cycle of Varroa

Worker and drone brood take different times to develop. Therefore a typical reproductive cycle involves five eggs being laid in worker brood and six in drone brood. Not all of these eggs mature, their development being curtailed by the bee emerging as an adult.

There are all sorts of developmental stages involved in getting from an egg to a mature unfertilised mite, but these are not important in terms of the overall outcome. Mite-geeks love this sort of detail 5, but we need to cut to the chase …

Keeping it in the family

The foundress ‘mother’ mite and her progeny all share a single feeding hole through the cuticle of the developing pupa.

What a lovely scene of family ‘togetherness’.¬†

Male and female mites take 6.6 and 5.8 days respectively to develop to sexual maturity. Therefore the male mite reaches sexual maturity before the first of his sisters.

He then lurks around the attractive-sounding “faecal accumulation site” and mates with each of the (sister) females in turn.

What a little charmer ūüėČ

Male mites are short lived and the eclosion of the adult worker or drone curtails further mating activity, releasing the foundress mite and the mated mature daughters 6.

Reproductive rate (mites per cell)

The three day difference in the duration of worker and drone development means that more mites are produced from drone cells than worker cells. Depending on conditions the reproductive rate is 1.3 – 1.45 in worker brood and 2.2 – 2.6 in drone brood.

Remember that the foundress is also released from the cell. She can go on to initiate one or two further reproductive cycles (or up to 7 in vitro). Consequently, the average yield of mature, mated female mites from worker and drone cells is a fraction over 2 and 3 respectively.

Before entering a fresh cell containing a late stage (5th instar) larva the newly-mated mites need to mature. They do this during the phoretic phase which lasts 5-11 days. Therefore the full replication cycle of the mite probably takes a minimum of about 17 days.

Exponential growth

Two to three mites per infested cell doesn’t sound very much. However, under ideal conditions this leads to exponential growth of the mite population in the colony. Assuming 10 reproductive cycles in 6 months, a single mite would generate a population of >1,000 in worker brood and >59,000 in drone brood 7.

Fortunately (for our bees, not for the mites), ideal conditions don’t actually occur in reality.

Lots of things contribute to the reduction in reproductive potential. For example, only 60% of male mites achieve sexual maturity due to developmental mortality, drone brood is only available at certain times in the season, brood breaks interrupt the availability of any suitable brood and grooming helps rid adult bees of phoretic mites.

Out, damn'd mite ...

Out, damn’d mite …

However, these reductions aren’t enough. Without proper management mite levels still reach dangerously high levels, threatening the long-term viability of the colony.

In the next few months I will discuss some additional opportunities for reducing the mite population.

In the meantime, as we reach the winter solstice, colonies in temperate regions may well be broodless and – as emphasised last week – this is an ideal time to apply a midwinter oxalic acid-containing treatment. This will effectively reduce mite levels for the start of the coming season.

Happy Christmas … unless you’re a mite ūüėČ


Colophon

Today is the¬†winter solstice in the Northern hemisphere. This is actually the precise¬†time when¬†the Earth’s Northern pole has its maximum tilt away from the Sun. However, the term is usually used for the day with the shortest period of daylight and the longest period of night.¬†In Fife, sunrise is at 08.44 and sunset at 15.37, meaning the day length is 6 hours and 53 minutes long.

With increasing day length queens will start laying again … but there’s a long way to go until winter is over.

 

The eyes have it

We’re entering the not beekeeping end-of-season phase of the beekeeping year.¬†There’s been a marked reduction in¬†visitor numbers to ‘The Apiarist’ over the last few weeks and –¬†with the weather gradually deteriorating1 – the ‘shack nasties‘ are starting to develop. The online forums (fora?) are filled with increasingly¬†bad-tempered arguments discussions and it might be too soon to be thinking about 2019 (it isn’t).

Wasted words

So, rather than write a series of erudite, well-argued, coherent, logical and persuasive posts about evolution of¬†Varroa resistance in¬†Apis mellifera, or rational mid-season mite-management strategies, or the 75:25 rule for queen and stock-improvement, or an exhaustive review of Swienty¬†vs. Abelo poly Nationals …

Some chance !2

… I’m instead going to spend the next few weeks on a variety of odds and ends. Some interesting and amusing science, some ‘teasers’ on grow-your-own-denim-knit-your-own-yoghurt beekeeping, an introduction to why people keep bees and why they shouldn’t and a long and apologetic explanation of where the site disappeared to when I tried to move it to another server.

Actually, of these only the first exists (see below). The last I hope not to use, though I will be switching servers to accommodate changes in security and to speed things up and to introduce site-wide intrusive advertising and a subscription model to fund my seemingly-unstoppable purchasing of essential beekeeping stuff from Brian at Thorne’s of Newburgh.

Oops.

The eyes have it

The eyesight of bees is remarkable.

Actually, eyesight alone is not enough. It’s the combination of eyesight with the neuronal processing of the received images that’s truly remarkable.

Remember that the brain of a bee is about 1mm3 and contains about one million neurones 3. With this brain the bee is able to undertake a series of complex mental tasks involving learning and memory, image processing and visual generalisation.

Bees soon learn that particular flowers yield lots of pollen or nectar. They can return to them time and again, recognising them at relatively short distances from their appearance. How do they determine that other flowers – of different shapes, sizes or colours – might also have valuable pollen or nectar? What about tree flowers that have a different appearance again?

It turns out that bees are generalists, at least where flowers are concerned. They recognise things that are flower-like. They have evolved to associate reward (pollen, nectar) with things that have the appearance of flowers.

More general generalists?

Do they only have the ability to identify flower-like ‘things’. Are bees generalists when just identifying flowers and flower-like things, albeit of different colours, sizes and shapes? Is there some sort of hardwiring in the brain of the bee that has evolved this exquisite combination of flower-recognising sensitivity and flexibility?

Alternatively, perhaps bees have a more adaptable image processing capability? For example, we know through simple experiments that bees can rapidly learn to associate very unflower-like shapes with a syrup ‘reward’.

You can train bees to repeatedly return to a distinctively coloured/shaped item with a syrup reward. Over short distances you can move the item and the bees return to the new location, with the final approach being guided by vision, pattern recognition and associated image processing.

The item doesn’t need to look much like a flower.

They can also identify ‘diamond-shaped things’ (again, for example, other shapes are available at a bee lab near you) of a different colour, or even no colour, to those they’ve been trained on.

Shape recognition by bees

Shape recognition by bees …

This suggests that – at least for simple ‘not-flower’ shapes like these – a degree of generalisation is still possible.

But bees operate in a very busy and variable environment filled with shapes and colours that form wildly variable complex images. Generalisation might well be a problem with all of this variation and complexity.

Facial recognition

Bees are good at discriminating between images of simple shapes. How good are they are at recognising the sorts of complex shapes and images that are found in the environment?

What about something that our bees see every week?

Something they might associate with disruption and/or reward?

Like your face …¬† ūüėÄ

It turns out that bees can distinguish between faces. Very well. When trained to a syrup reward on one face (top left in image below), they can distinguish it from a different face (second row) about 80% of the time (graph).

Facial recognition by bees ...

Facial recognition by bees …

There’s a distinct possibility your bees recognise you. An interesting twist on the comment many non-beekeepers make about whether we can identify ‘our’ bees.

However, bees trained to recognise a face the ‘right way up’ failed to identify the face if it was inverted (column¬†v above).

Don’t do your hive inspections standing on your head.

Complex image generalisation

Bees can certainly discriminate well between complex images like faces. Are they also able to generalise when it comes to complex image analysis?

For example, could you train bees to associate reward with a range of female faces? Then challenge them with discriminating between a pair of new (never seen before) male and female faces? Would they pick the female face significantly more than 50% of the time?

That’s a pretty tough test.¬†Without the labels how well do¬†you¬†cope with this training set?

Faces

Faces

OK, if that’s too hard, how about an analysis of image generalisation based upon the¬†style of the image?

Humans are pretty good at this sort of thing. We can easily discriminate between the Impressionist painters (e.g. Degas, Monet, Manet, Renoir) and those in the early 20th Century Cubist art movement (e.g. Picasso, Metzinger, Braque, Gleizes, Léger).

For example, is the Picasso (below) Cubist or Impressionist?

We can tell … can the bees?

Monet or Picasso?

Wu and colleagues4 recently attempted to answer this question.

They took pairs of paintings matched for luminance, colour and spatial frequency information, one by Monet (Impressionist) and one by Picasso (Cubist). Bees were trained to associate either the Monet or the Picasso with a syrup reward.

When subsequently tested, bees were able to easily identify the painting they had been trained on from one by the other artist. After 30 training blocks bees made the correct choice about 75% of the time … approximately the same accuracy with which they identify faces (above).

This is not fundamentally a different experiment to the face recognition study as both involved the discrimination between just one complex image and another.

Monets or Picassos?

Using five different pairs of luminance, colour and spatial frequency-matched paintings from Monet and Picasso Рwith five days of training Рthey demonstrated that bees could simultaneously discriminate between them up to 75% of the time.

The more training the bees received, the better they were at picking the correct painting each time.

Impressionist or Cubist?

Having trained the bees on multiple Picasso or Monet paintings they then challenged them with new¬†(to the bees … you’ll appreciate that these artists no longer produce new work ūüėČ ) paintings by the same artists.

Could bees that were able to discriminate between¬†The Cliff at √Čtretat after the Storm (Monet) from Le R√™ve (Picasso)¬†and between¬†Water Lilies and the Japanese bridge¬†(Monet) from¬†Girl before a Mirror (Picasso)¬†and three other pairs correctly select a previously unseen Picasso or Monet?

In all honesty, not very well ūüôĀ

The statistics are poor. For one of the novel pairs tested it appeared as though the bees could discriminate as well as they could one of the training pairs. However, the most positive statement that could be made by the authors was “Notably, for both groups the percentage of correct choices for novel pairs was above chance (i.e., above 50 %) in six out of the eight tests, indicating that a weak generalization may have occurred”.

Underwhelming … in this sort of science the stats wins every time, and this type of statement isn’t very compelling.

Finally, the scientists repeated the entire training regime with greyscale versions of the same training pairs of images. With this training, generalization to the novel pairs was quite a bit better with¬†“only marginal or no significant difference between training pairs and most novel pairs”.

Better, but still not really statistically compelling. However, don’t underestimate the complexity of the task. The results showed that insects with a sesame-seed-sized brain could often discriminate between previously unseen Cubist or Impressionist paintings after a few days training on only 5 pairs of paintings of the same style.

That’s remarkable.

Bird brains

Pigeons live in the same visually complex environment as bees. They have to undertake similar visually demanding tasks during foraging. They can discriminate between Monets and Picassos. They can correctly (and statistically convincingly) determine whether a new Monet or Picasso is more Impressionist-like or Cubist-like.

In addition, when challenged with other paintings of similar styles by different artists (e.g. a Degas or a Braque), pigeons can again generalise in their selection of Cubist or Impressionist 5.

However, to achieve this remarkable visual feat, pigeons need to be trained to hundreds of exemplar paintings over many, many weeks.

Could bees do as well if trained for the same period?

We don’t know.

And we’re unlikely to find out as the lifespan of a worker bee is probably too short ūüôĀ


Colophon

This post was written as the political fallout of the draft Brexit deal was occupying 110% of the news. By the time it appears online it’s not clear the UK will have a Prime Minister or even a functioning Government.

Be that as it may, there will be a Parliamentary vote on it.

Historically, there is a division of the assembly into those that support the motion (the ‘ayes’ i.e. ‘yes’) and those that do not (the ‘noes’). Once the vote is taken – typically by members of parliament traipsing into the appropriate division lobby – the Speaker counts the votes and announces¬†The Ayes have it … assuming the motion was supported.

Considering the timing, a pun on The Ayes have it seemed appropriate.

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

Ouch, that hurt

If you keep bees you’ll inevitably get stung.

Not necessarily often and not necessarily badly, but getting stung goes with the territory.

You’ll probably get stung more often if your bees are stroppy, or if you are clumsy. But even if you’re careful and the bees are calm there’s always the chance of being stung.

I moved a very feisty colony late one evening last week 1. The hive was sealed, moved and re-located to an out apiary. Knowing they were, er, rather temperamental I let them settle for 15 minutes, then gently lifted the entrance block.

Out they boiled … as I beat a very hasty retreat ūüôĀ

I thought I’d got away with it, but driving home 20 minutes later I was stung on the ankle by a stowaway in my boot.

Ouch! That hurt.

I’ve only been stung a few times all season. Most didn’t hurt much at the time and were forgotten within minutes. That sting on the ankle¬†hurt like hell and was sore for a further 48 hours.

Why does it hurt when you’re stung? Furthermore, assuming stings are inevitable, which parts of the body hurt¬†more when stung … and so deserve additional protection?

Why do bee stings hurt?

The honey bee sting is a hollow barbed tube used to deliver the venom. About 50% of bee venom by weight is the small protein mellitin.

It’s fair to say that mellitin is small but potent. It’s only 26 amino acids 2 long and forms a tetramer in aqueous solution. The ‘noughts and crosses’ shape it adopts hides the hydrophobic parts of the peptide and therefore allows it to ‘dissolve’ in venom. However, the tetramer dissociates at or near cell membranes into which monomeric mellitin embeds itself.

Mellitin

Mellitin

And this is where the pain and damage start …

Membrane-association causes cell lysis 3. This results in the release of all sorts of cytokines from the cells which signal ‘damage’ to the body, leading to the inflammatory response usually associated with bee stings. That’s the long-term effect of a bee sting. However, simultaneously, mellitin triggers the expression of proteins known as sodium channels in pain receptor cells. These allow large amounts of sodium to flow across the membrane. It is this that is directly responsible for the pain sensation when you are stung.

So, if being stung is almost inevitable and if bees have evolved stings to cause pain (which they have), in which parts of the body is the pain sensation most marked?

Measuring pain

Pain is a subjective response.¬†What’s painful to me might hardly be noticed by someone with a higher pain threshold. Two individuals receiving the same sensory input can experience very different sensory responses 4.

As an aside it’s well documented that there are differences in the pain felt by males and females 5. All the pain reported in this article is from studies – or personal experience – by males.

Therefore, to meaningfully determine how much pain a sting causes, from a particular insect or at a particular location for example, it’s essential that the studies are properly controlled. This includes taking account of variation between individuals and variation within an individual on a day to day basis.

These are not the sorts of studies that attract large numbers of volunteers ūüėČ

Perhaps unsurprisingly, the scientific work in this field is often published in single author papers in which the author alone is the ‘volunteer’.

The Schmidt Sting Pain Index

Before discussing honey bees specifically a brief diversion must be made to introduce the seminal studies by Justin Schmidt.

Schmidt is an entomologist at the Carl Hayden Bee Research Centre in Arizona. He’s interested in haemolysis (the cell lysis caused by mellitin and other constituents of insect venom) and whether the evolution of sociality in hymenopterans (bees, ant and wasps) required the evolution of toxic and painful stings.

Over about twenty years Justin Schmidt published a number of papers on hymenopteran venoms and the pain that they cause. In his early papers he rated stings on a scale of 1 – 4 (actually 0 upwards, but 0 was totally painless to humans).

Only a very few insects scored 4, including bullet ants¬†about which Schmidt comments “Paraponera clavata stings induced immediate, excruciating pain and numbness to pencil-point pressure, as well as trembling in the form of a totally uncontrollable urge to shake the affected part“.

You can’t fault his commitment, but you might question his sanity.

Schmidt published his¬†magnum opus in 1990 in which he ranked stings by 78 hymenopteran species covering 41 genera 6. His descriptions of the pain induced are often entertaining. ¬†The aforementioned bullet ant is “pure, intense, brilliant pain…like walking over flaming charcoal with a three-inch nail embedded in your heel“.

Another sting scoring 4, that of Synoeca septentrionalis (the warrior wasp) is accompanied by the statement “Torture. You are chained in the flow of an active volcano. Why did I start this list?”.

Why indeed?

Standing on the shoulders of giants

Bees and wasps scored 2 on the Schmidt Sting Pain Index. What Schmidt didn’t investigate was the influence of the¬†location of the sting on the pain experienced.

Which brings me to Michael Smith. In 2014 Smith published an entertaining paper entitled¬†Honey bee sting pain index by body location. It’s published in the journal¬†PeerJ and the full paper is available for¬†download.

It’s a well controlled study written in an engaging style that most readers will appreciate.

Building on the landmark studies by Schmidt, Michael Smith rated the pain endured from honey bee stings in 25 different locations.

Some of these locations should really be protected with a bee suit.

Sting locations tested

Sting locations tested

Smith controlled the study by always including an “internal control”¬†i.e. comparing two test locations with three stings to his forearm.

Every time.

All locations were tested in triplicate (randomly). This meant that Smith was stung a minimum of five times for 38 consecutive days. Ouch.

There are some excellent quotes in the paper … “Some locations required the use of a mirror and an erect posture during stinging (e.g., buttocks)“. Scientists involved in studies that require ethical approval will appreciate the comments made in the paper on self-experimentation.

And the results? To quote directly from the paper “The three least painful locations were the skull, middle toe tip, and upper arm (all scoring a 2.3). The three most painful locations were the nostril, upper lip, and penis shaft (9.0, 8.7, and 7.3, respectively)” 7.¬†Interestingly, skin thickness did not correlate with the pain experienced.

My experience of stings is limited. Those I’ve had to the face (including the lower lip) have been relatively painless, but the subsequent inflammatory response has been dramatic. Smith only scored immediate pain … I think a follow-up study on inflammation and its duration is needed.

I’m not going to conduct it.

Points pain means prizes

You can’t fault the dedication shown by Justin Schmidt and Michael Smith 8. That sort of dedication should be recognised with prizes and honours.

And it was.

Schmidt and Smith shared the 2015 Ig Nobel prize for Physiology and Entomology. The Ig Nobels – a parody of the Nobel prizes – recognise unusual or trivial achievements in scientific research.

The list of Ig Nobel prizes awarded is eclectic and highly entertaining … Medicine (2013) “for treating “uncontrollable” nosebleeds, using the method of nasal-packing-with-strips-of-cured-pork“, Economics (2005) for¬†the inventors of “Clocky, an alarm clock that runs away and hides, repeatedly, thus ensuring that people get out of bed, and thus theoretically adding many productive hours to the workday” and Psychology (1995)¬†for “their success in training pigeons to discriminate between the paintings of Picasso and those of Monet9.

Sir Andre Geim received the Physics Ig Nobel in 2000 for levitating a frog by magnetism. Yes, really. Ten years later he was awarded the Nobel prize in Physics for his studies on graphene. He’s the only holder of a Nobel and Ig Nobel.

Marc Abrahams, the founder of the Ig Nobel awards, regularly tours giving talks on Improbable Research and the Ig Nobel prizes.

Go if you get the chance … it’s highly entertaining.


 

 

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.

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¬† ūüôĀ ¬†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 ūüėČ

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’ ūüėČ

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 ūüėČ

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 ūüėČ ¬†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 Warr√© 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¬† ūüėÄ


1¬†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.

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Honey and hay fever

300 jars of honey

300 jars of honey

I’m conflicted.¬†As a beekeeper I appreciate offsetting the cost of indulging my hobby from honey sales. In a good year I get much more honey than I could ever give away to friends and family. Despite making some of my own equipment, there are the costs of purchasing (yet more) boxes, miticides, extraction equipment and winter feed. There’s also an ever-growing wishlist of things that, whilst not essential, would be very welcome. Abelo’s heated honey creamer looks very nice ūüėČ ¬†Bottling, labelling and then selling honey – either from the door or from local shops – provides a few quid to help … a sort of self-perpetuating process in which I transfer all that summer effort by the bees into the coffers of Thorne’s and C. Wynne Jones.

However, I regularly get asked for local honey to ‘prevent the symptoms of hay fever’. Emails or phone calls go something like this:

“My son/daughter/husband/wife suffers really badly from hay fever and I read that locally produced honey could help her symptoms” … followed by a request to confirm that what they’ve read is correct and could I sell them some honey.

As a¬†scientist I can’t do the former and so usually fail to achieve the latter. No way to run a business perhaps, but honesty is the best policy‚ąĎ.

Achoo!

Bless you

Bless you

Hay fever is an allergic reaction to pollen in the air. About 20% of the population have, or will develop, hay fever. I never had it as a child, but in my 30’s developed a strong reaction to some grass pollens that still makes a fortnight or so in mid/late June pretty miserable. Hive inspections with bad hay fever are really miserable.

Symptoms are characteristic – itchy eyes, sneezing and a runny nose (where does all that stuff come from?!). Anti-histamines, either prescription or over-the-counter, help prevent the allergic reaction from occurring. Usually this is sufficient to make the symptoms bearable.

Severe hay fever symptoms, where anti-histamines or corticosteroids are insufficient, can be treated by immunotherapy. Over several months, the patient is exposed sub-cutaneously or orally, to low and increasing doses of the allergen (the compound that causes the allergy) to help develop immunity. Full desensitisation takes about three years.

Honey contains pollen

Honey contains small amounts of pollen. The presence of the pollen forms the basis for lots of tricky questions in the BBKA examinations and is a feature used by food standards to discriminate between flavoured sugar syrup and real honey.

This is probably where the ‘honey prevents hay fever” stories originate. It’s this small amount of pollen that is supposed to stimulate the immune system of hay fever sufferers. A sort of DIY desensitisation course using toast or porridge to help deliver the allergen. Tasty ūüėČ

All this seems pretty logical and straightforward. Honey contains pollen. Low doses of pollen are used to stimulate immunity that, in turn, stops hay fever from developing. Local honey prevents hay fever¬†… I must get this printed on my labels to boost sales further.

Don’t let the facts get in the way of a good theory‚ąě

Unfortunately, there are a couple of irritating facts that scupper this nice little theory. The first is  a sort of error of omission, the second is the absence of evidence supporting the theory (or, more accurately, the evidence that the theory is wrong).

Honey certainly contains pollen. At least, real honey does. Melissopalynologists Рthose who study the pollen in honey Рcan identify the genus of plants that the bees have been visiting and so may be able to deduce the geographic origin of the honey.

The key part of that last sentence is¬†“that the bees have been visiting”. The vast majority of pollens in honey are from the flowers and trees that they visit to gather nectar. These pollens are usually large and sticky so they adhere to the passing bee and are then transferred to another plant when the bee moves on.

What’s missing are any significant quantities of pollens from wind-pollinated plants such as grasses. Studies have shown that almost all pollens that cause allergies such as hay fever are from these wind-pollinated species‚Ć. It’s logical that these pollens are largely absent … since the flowers, grasses and trees that produce them are anemophilous (wind-pollinated) they don’t need to generate nectar to attract bees, so the bees don’t visit. So there’s little or none of this type of pollen in honey.

No bees legs ...

No bees legs …

Testing, testing …

So that’s the error of omission. What about scientific support, or otherwise, for the theory that local honey prevents hay fever? After all, this must be an easy (and tasty) experiment to do. Feed a group of people honey and compare their hay fever symptoms with a group fed synthetic honey (or perhaps imported pseudo-honey sold from a supermarket near you).

Researchers in Connecticut did this experiment in 2002. They published their results in a snappily-titled paper “Effect of ingestion of honey on symptoms of rhinoconjunctivitis” published in the Annals of Allergy, Asthma and Immunology.

Rhinoconjunctivitis, or perhaps more correctly, allergic rhinoconjunctivitis, is the symptoms of hay fever – the itchy eyes, sneezing and runny nose. Three groups of a dozen hay fever sufferers, pre-screened for reactivity to common wind-borne allergens, were randomly assigned to receive local ‘raw‘ honey, filtered non-local honey and honey-flavoured syrup (the placebo group). They took one tablespoon of honey, or substitute, a day and recorded their hay fever symptoms. The abstract of the paper neatly summarises the results:

Neither honey group experienced relief from their symptoms in excess of that seen in the placebo group.

… leading the authors to conclude that:

This study does not confirm the widely held belief that honey relieves the symptoms of allergic rhinoconjunctivitis.

Absence of evidence does not mean evidence of absence

So, this study does not confirm (prove) that honey prevents hay fever. What about the opposite? Can we use it as evidence that honey does not prevent hay fever symptoms?

1934 Loch Ness haox

1934 Loch Ness hoax

Tricky … as the skeptic James Randi asserted, you can’t prove a negative. I can’t prove that the Loch Ness Monster doesn’t exist. However, in the absence of convincing evidence that it does exist, I can be reasonably sure that Nessie is a 6th Century tale, embellished in the 19th Century and blatantly exploited by the 21st Century tourist industry.

Of course, lake monsters are ‘found’ worldwide, which isn’t evidence that any of them actually exist ūüėČ

We’re getting into the messy intersection of science and philosophy here. I think it’s sufficient to say that there’s no scientific evidence that honey prevents hay fever. The Connecticut experiment was a properly controlled random study. To my mind (as a scientist) this is much more compelling evidence than any amount of anecdotal stories to the contrary.

An abbreviated version of which is what I tell potential customers who want me to confirm that buying my local honey will help alleviate their hay fever symptoms. Essentially, it won’t.

Sure, they might not get hay fever after eating my honey, but that’s almost certainly a coincidence. It’s a coincidence I’m happy to live with, but not one I’m happy to promote as a reason to buy my local honey.

Why buy local honey?

I don’t think it’s necessary to cite dubious medical benefits when encouraging people to buy local honey.

Why claim something that’s probably not true?

Far better to claim the things that are true, some of which are also clearly demonstrable:

  • It’s local, from the hedges and fields within 3 miles of the apiary. It wasn’t imported by the tonne from a location or locations unknown‚Ä°.
  • It’s a very high quality product – clearly to claim this you need to ensure it looks wonderful and that there are no legs or antennae lurking in the jar.
  • It hasn’t been excessively heated before jarring – all the goodness is still present, including pollen, just not the sort of pollen that will prevent hay fever.
  • The honey hasn’t been micro-filtered, pasteurised or tampered with in any way.
  • It varies during the season as the forage changes – a jar of spring OSR honey is very different ¬†in flavour from a jar of mid-summer floral (hedgerow) honey. It’s a wonderful edible snapshot of the changing seasons.
  • Buying it supports a local cottage industry.
  • It tastes fantastic – clearly demonstrable.

The ‘taste test’ is usually the deciding factor. A couple of tester jars – clearly labelled – a limitless supply of plastic coffee stirrers and a discard pot will allow customers ample opportunity to ‘try before they buy’.

Which they surely will … ūüôā


‚ąĎ¬†Honesty is the best policy is an idiom dating back to the late 16th Century when¬†Sir Edwin Sandys, a founder of the Virginia Company and one of the first settlers in America, stated¬†“Our grosse conceipts, who think honestie the best policie”.

‚ąě A corruption of the saying by Mark Twain “Don’t let the facts get in the way of a good story”.¬†

‚Ƭ†Jean Emberlin (2009). “Grass, tree, and weed pollen”. In Kay et al. The Scientific Basis of Allergy. Allergy and Allergic Diseases. 1:942-962. John Wiley & Sons. ISBN¬†9781444300925

‚Ä°¬†This isn’t xenophobia. The UK is a net importer of honey. 95% of the honey eaten in the UK is imported – 50% of the 34,000 tonnes imported in 2012 came from China. Most honey on the supermarket shelves contains some rather vague term like¬†Produce of EU and non-EU countries. You don’t know where it came from, and probably nor does the supermarket. There have been bans on imported honey due to it being not honey (just doctored corn syrup), or being contaminated with antibiotics.

Small cell foundation

In a recent monthly newsletter Thorne’s announced they were now supplying small cell foundation. This foundation has a cell diameter¬†of 4.9mm, rather than the standard 5.2-5.4mm. Under the¬†ambiguous heading 4.9 mm foundation for varroa control”¬†they have the following text:

Wired foundation

Wired foundation

“It is claimed varroa mites struggle to reproduce in the slightly smaller cell size. 4.9 mm being close to what bees produce in comb width in nature. Many beekeepers in the USA who have experimented with small cell have reported encouraging results. Moving over to small cell however can be difficult and must be done at the correct time of year. It cannot be done either by simply putting 10 frames of small cell foundation in the hive. The bees must first be subject to regression over a period of several months.”

Do mites struggle to reproduce?

No. There’s compelling scientific evidence that¬†Varroa levels in hives on small cell foundation may actually have¬†higher mite levels than those on standard foundation. These are from¬†properly conducted and controlled studies involving dozens of hives.

It certainly is claimed that mites struggle to reproduce in small cell foundation. The evidence actually directly contradicts these claims. Undoubtedly beekeepers in the USA have reported encouraging results, but scientists doing side-by-side comparisons clearly demonstrate that mite levels are at best not changed or at worst appreciably higher on small cell foundation.

Actually, it’s not the mites but our bees that struggle to reproduce in small cells. This explains the phrase¬†“subject to regression over a period”¬†above. You have to select smaller bees that can reproduce well in¬†small cell foundation. Once this is done, the bee size is measurably smaller and the density of brood cells in the hive is greater.

Is¬†this is a one-off study –¬†where is the independent verification?

No. They were repeated at least three times by labs at the University of Georgia. Similar studies were conducted by Florida Department of Agriculture and Consumer services. In addition, the Ruakura Research Centre in Hamilton, New Zealand, conducted their own study Рusing a different experimental format Рbut achieving the same conclusions. Small cell foundation increased mite levels when compared with conventional or standard diameter foundation. There are now several additional independent studies which essentially reach the same conclusion Рsmall cell foundation does not restrict Varroa replication and may actually increase it.

Has this new research been published?

Apidologie

Apidologie

After all, perhaps Thorne’s aren’t completely up-to-date about these studies? If the work is really new then perhaps they can be excused for¬†trying to flog something for which there’s no compelling evidence of benefit.

Well, it was¬†published … in some¬†cases seven¬†to nine¬†years ago:

  1. Taylor, M.A., Goodwin, R.M., McBrydie, H.M., Cox, H.M. (2008) The effect of honeybee worker brood cell size on Varroa destructor infestation and reproduction. Journal of Apiculture Research¬†47, 239‚Äď242 …¬†summary, a higher proportion of cells from small foundation were mite infested.
  2. Ellis, A.M., Hayes, G.W., Ellis, J.D. (2009) The efficacy of small cell foundation as a Varroa mite (Varroa destructor) control. Experimental and Applied Acarology¬†47, 311‚Äď316 … summary, no difference in mite levels between small cell and conventional foundation.
  3. Berry, J.A., Owens, W.B., Delaplane, K.S. (2010) Small-cell comb foundation does not impede Varroa¬†mite population growth in honey bee colonies. Apidologie 41, 40‚Äď44 …¬†summary, small cell colonies had ~40% higher mite infestation levels when compared with conventional foundation.
  4. Seeley, T.D., Griffin, S.R. (2011) Small-cell comb does not control Varroa mites in colonies of honeybees of European origin. Apidologie¬†42,¬†526-532 …¬†summary, no difference in mite infestation levels between small cell and conventional foundation.

If you want an accessible and readable account of small cell foundation studies Jennifer Berry has written one for Bee Culture which includes experimental details of the work in references 1-3 above.

In denial

A recent thread on Beesource discussed the reported benefits of small cell foundation and the scientific evidence that contradicts these claims. It’s notable that supporters of small cell foundation generally criticise the ‘agenda’ they claim scientists have, rather than providing scientific evidence that supports¬†the ‘benefits’.¬†I’ve not been able to find a single peer-reviewed and properly controlled study that supports the beneficial claims for small cell foundation.

Hives on small cell foundation may have manageable levels of¬†Varroa. If they do it’s in spite of the use of small cell foundation, not because of it. I am very willing to accept that there are some very competent beekeepers using splits, rational miticide treatment or other strategies¬†and small cell foundation, who have low or manageable¬†Varroa levels. However, it’s their beekeeping skill and experience not the choice of foundation size¬†that is important here.

Indeed, you could argue that the detrimental enhancement to mite reproduction of small cell foundation, means that they must have truly exceptional beekeeping talents.

Or an agenda perhaps ūüėČ

Ambiguous and misleading titles

In the opening paragraph I stated that the title¬†4.9 mm foundation for varroa control” was ambiguous. The scientific evidence presented above is that small cell foundation does control¬†Varroa. Assuming you use the word ‘control’ when defined as¬†the power to influence or direct the course of events. Small cell foundation does exert control … but almost certainly in the opposite direction to¬†the way implied in the title.

What turns an ambiguous into a misleading title is this implication that small cell foundation reduces Varroa levels. The text that accompanies makes this implication without providing any sort of balanced view based upon the published evidence to the contrary.

Beekeepers, particularly beginners, looking for effective ways to reduce their mite levels are not being provided with the facts and are likely to be misled.

But wait … were all these scientific studies flawed?

Thorne’s partly justify the sale of small cell foundation in their newsletter by citing a UK research project that involves its use:

“The University of Reading has just started an exciting new research project examining the highly problematic issue of varroa mites and whether the use of small cell foundation (4.9 mm) can help. This is being carried out with volunteer beekeepers in the local area as well as in an apiary at the University. The study will evaluate the use of small cell foundation alongside regular-sized (5.4mm) foundation and compare the varroa loads during next spring and summer.

This is an interesting topic to research as beekeepers around the world have had success with the use of small cell foundation whereas many others have not. Some previous studies have also found that varroa counts increase in the short term when small cell foundation is first used. The new study will evaluate what happens once the bees have fully adjusted to small cell foundation and if there is a significant impact on varroa loads.”

The implication here is that the previous studies (above) are flawed because they failed to use bees that were properly adapted to small cell foundation. Thorne’s do clearly state that the bees have to be properly adapted – subjected to regression – for several months before benefits are seen (or claimed to be seen). To their credit also, they acknowledge that some studies show increases in mite levels. This text is from the newsletter and unfortunately does not appear on the webpage of their catalogue that describes the foundation.

Call me sceptical …

If it looks like a duck ...

If it looks like a duck …

As you can tell from the tone of this post, I remain sceptical.

If it looks like a duck, if it swims like a duck and if it quacks¬†like a duck … it is a duck. As a scientist I’m influenced by controlled studies, not hearsay or beliefs.

The Berry study (ref 3 above) did use bees reared on small cell foundation for their comparative studies, the other studies did not as far as I can tell.¬†However, remember the original hypothesis about why small cell foundation is beneficial. The mites do not develop properly within the cell as they are ‘crowded’ by the abdomen of the developing honey bee pupa i.e. there’s too little space for the mite.

What does regression lead to? Smaller bees. In the Berry¬†et al., study the weights of adult bees reared on small cell and conventional foundation was 129 and 141 mg respectively. This seems to be contradictory … if properly regressed bees on small cell foundation are significantly smaller than those on conventional foundation how is the space for the mite development restricted? I acknowledge that the cell size is proportionately smaller than the reduction in adult bee weight.¬†Conversely, if small cell foundation is supposed to restrict mite development, why are levels apparently higher when ‘normal’ sized bees are first forced to use smaller cells? Surely there should be a greater reduction in mite reproduction before the bees have regressed?

I hope the study being conducted by the University of Reading is thorough and properly controlled. These are difficult studies to conduct, particularly at the scale needed to be statistically convincing and when not under the direct control of a single beekeeper in a single apiary. I wish them every success with the experiments and look forward to reading about it once it is peer-reviewed and published.

Until then I suggest you save your ¬£11.60 for ten sheets of small cell wired brood foundation … you’d be far better off preparing foundationless frames and controlling¬†Varroa by rational and judicious use of hive manipulations and approved miticides.


Additional reading (far from exhaustive):

The late and still unbeatable Dave Cushman has an article by Philip Denwood reproduced from the 2003 BIBBA magazine on cell size. Recommended for a historical perspective.

A 2013 article from the New Hampsha’ Bees blog¬†Small cell doesn’t work (but please don’t tell my bees describing typical¬†evidence that small cell foundation does work¬†… anecdotal and not controlled, but nevertheless enthusiastic and – unusually – acknowledging the evidence against.

Michael Bush on small cell bees and foundation.

Dee Lusby – one of the originators of the ‘small cell’ movement – in an early article from ABJ reproduced on the Beesource forums. Be warned … there’s some misleading¬†nonsense in this article.¬†For example¬†“it is a known fact that both honey bees and mites have been on this Earth many millions of years together and survived quite nicely”.¬†I don’t disagree that both mites and bees have been around for millennia. However, they have only been together for a century or so. I think I’ll have to write something about natural beekeeping in the future …

It’s notable that top Google ‘hits’ for small cell foundation provide no scientific support for the claims that are made¬†… caveat emptor.

 

 

 

You’ve spilt wax in the kitchen … again

cover_natureThere’s an interesting article in yesterday’s¬†Nature on the detection of beeswax residues in crockery shards dating back at least¬†9000 years i.e. since the development of agriculture.¬†This suggests that humans have been exploiting bees and bee products since the Neolithic Revolution when the first animals were domesticated, though evidence for beekeeping (from wall engravings in Egypt) only exists for about 4500 years. Samples of crockery almost 6000 years old from Southern/Eastern England¬†were found containing traces of wax, but more northerly samples were free from residues. This suggests that there was a northerly/westerly ecological limit to the distribution of honeybees (Apis mellifera) but confirming – assuming Neolithic pastoralists weren’t plagued with imports – that honeybees aren’t a recent introduction to the British Isles.