Category Archives: Diseases

Oxalic acid (Api Bioxal) preparation

This post updates and replaces one published three years ago (which has now been archived). The registered readership of this site has increased >200% since then and so it will be new to the majority of visitors.

It’s also particularly timely.

I will be treating my own colonies with oxalic acid in the next week or so.

Mites and viruses

Varroa levels in the hive must be controlled for successful overwintering of colonies. If you do not control the mites – and by ‘control’ I mean slaughter 😉 – the viruses they transmit to the overwintering bees will limit the chances of the colony surviving.

The most important virus transmitted by Varroa is deformed wing virus (DWV). At high levels, DWV reduces the lifespan of worker bees.

This is irrelevant in late May – there are huge numbers of workers and they’re only going to live for about 6 weeks anyway.

In contrast, reduced longevity is very significant in the winter where more limited numbers of overwintering bees must survive for months to maintain the colony through to the Spring. If these bees die early (e.g. in weeks, not months), the colony will dwindle to a pathetic little cluster and likely freeze to death on a cold winter night.

Game over. You are now an ex-beekeeper 🙁

To protect the overwintering bees you must reduce mite levels in late summer by applying an appropriate miticide. I’ve discussed this at length previously in When to treat? – the most-read post on this site.

I’d argue that the timing of this late summer treatment is the most important decision about Varroa control that a beekeeper has to make.

However, although the time for that decision is now long-gone, there are still important opportunities for mite control in the coming weeks.

In the bleak midwinter

Miticides are not 100% effective. A proportion of the mites will survive this late summer treatment 1. It’s a percentages game, and the maximum percentage you can hope to kill is 90-95%.

If left unchecked, the surviving mites will replicate in the reducing brood reared between October and the beginning of the following year. That means that your colony will potentially contain more mites in January than it did at the end of the late summer treatment.

Mid September

Late summer mite treatment and no midwinter treatment.

Over several years this is a recipe for disaster. The graph above shows modelled data that indicates the consequences of only treating in late summer. Look at the mite levels (in red, right hand vertical axis) that increase year upon year.

The National Bee Unit states that if mite levels exceed 1000 then immediate treatment is needed to protect the colony. In the modelled data above that’s in the second year 2.

In contrast, here is what happens when you also treat in “midwinter” (I’ll discuss what “midwinter” means shortly).

Two optimal treatments

Two optimal treatments

Mite numbers remain below 1000. This is what you are aiming for.

For the moment ignore the specific timing of the treatment – midwinter, late December etc.

Instead concentrate on the principle that determines when the second treatment should be applied.

During the winter the colony is likely to go through a broodless period 3.

When broodless all the mites in the colony must, by definition, be phoretic.

There’s no brood, so any mites in the colony must be riding around on the backs of workers.

A phoretic mite is an easy mite to kill 4.

A “midwinter” double whammy

A single oxalic acid based treatment applied during the winter broodless period is an ideal way to minimise the mite levels before the start of the following season.

Oxalic acid is easy to administer, relatively inexpensive and well-tolerated by the bees.

The combination – a double whammy – of a late summer treatment with an appropriate miticide and a “midwinter” treatment with oxalic acid should be all that is needed to control mites for the entire season.

However, “midwinter” does not mean midwinter, or shouldn’t.

Historically, winter mite treatments were applied between Christmas and New Year. It’s a convenient time of the year, most beekeepers are on holiday and it’s a good excuse to avoid spending the afternoon scoffing mince pies in front of the TV.

Or with the outlaws inlaws 😉

But by that time of year many colonies will have started brooding again.

With sealed brood, mites have somewhere to hide, so the treatment will be less effective than it might otherwise have been 5.

Why go to all the trouble of treating if it’s going to be less effective than it could be?

The key point is not the timing … it’s the broodlessness of the colony.

If the colony is broodless then it’s an appropriate time to treat. My Fife colonies were broodless this year by mid-October. This is earlier than previous seasons where I usually have waited until the first protracted cold period in the winter – typically the last week in November until the first week in December.

If they remain broodless this week I’ll be treating them. There’s nothing to be gained by waiting.

Oxalic acid (OA) treatment options

In the UK there are several approved oxalic acid-containing treatments. The only one I have experience of is Api-Bioxal, so that’s the only one I’ll discuss.

I also give an overview of the historical method of preparing oxalic acid as it has a bearing on the amount of Api-Bioxal used and will help you (and me) understand the maths.

OA can be delivered by vaporisation (sublimation), or by tricking (dribbling) or spraying a solution of the chemical.

I’ve discussed vaporisation before so won’t rehash things again here.

Trickling has a lot to commend it. It is easy to do, very quick 6 and requires almost no specialised equipment, either for delivery or personal protection (safety).

Trickling is what I always recommend for beginners. It’s what I did for years and is a method I still regularly use.

The process for trickling is very straightforward. You simply trickle a specific strength oxalic acid solution in thin syrup over the bees in the hive.

Beekeepers have used oxalic acid for years as a ‘hive cleaner’, as recommended by the BBKA and a range of other official and semi-official organisations. All that changed when Api-Bioxal was licensed for use by the Veterinary Medicines Directorate (VMD).

Oxalic acid and Api-Bioxal, the same but different

Api-Bioxal is the VMD-approved powdered oxalic acid-containing miticide. It is widely available, relatively inexpensive (when compared to other VMD-approved miticides) and very easy to use.

Spot the difference ...

Spot the difference …

It’s very expensive when compared to oxalic acid purchased in bulk.

Both work equally well as both contain exactly the same active ingredient.

Oxalic acid.

Api-Bioxal has other stuff in it (meaning the oxalic acid content is a fraction below 90% by weight) and these additives make it much less suitable for sublimation. I’ll return to these additives in a minute or two. These additives make the maths a bit more tricky when preparing small volumes at the correct concentration – this is the purpose of this post.

How much and how strong?

To trickle or dribble oxalic acid-containing solutions you’ll need to prepare it at home, store it appropriately and administer it correctly.

I’ve dealt with how to administer OA by trickling previously. This is all about preparation and storage.

The how much is easy.

You’ll need 5ml of oxalic acid-containing solution per seam of bees. In cold weather the colony will be reasonably well clustered and its likely there will be a maximum of no more than 8 or 9 seams of bees, even in a very strong colony.

Hold on … what’s a seam of bees?

Three seams of bees

Looking down on the colony from above, a seam of bees is the row visible between the top bars of the frames.

So, for every hive you need 5ml per seam, perhaps 45ml in total … with an extra 10% to cover inevitable spillages. It’s not that expensive, so don’t risk running out.

And the strength?

The recommended concentration to use oxalic acid at in the UK has – for many years – been 3.2% w/v (weight per volume) in 1:1 syrup. This is less concentrated than is recommended in continental Europe (see comments below on Api-Bioxal).

My advice 7 – as it’s the only concentration I’ve used – is to stick to 3.2%.

Calculators at the ready!

The oxalic acid in Api Bioxal is actually oxalic acid dihydrate. Almost all the powdered oxalic acid you can buy is oxalic acid dihydrate.

The molecular formula of oxalic acid is C2H2O4. This has a molecular weight of 90.03. The dihydrated form of oxalic acid has the formula C2H2O4.2H2O 8 which has a molecular weight of 126.07.

Therefore, in one gram of oxalic acid dihydrate powder (NOT Api Bioxal … I’ll get to Api Bioxal in a minute! Have patience Grasshopper) there is:

90.03/126.07 = 0.714 g of oxalic acid.

Therefore, to make up a 3.2% oxalic acid solution in 1:1 syrup you need to use the following recipe, or scale it up as needed.

  • 100 g tap water
  • 100 g white granulated sugar
  • Mix well
  • 7.5 g of oxalic acid dihydrate

The final volume will be 167 ml i.e. sufficient to treat over 30 seams of bees, or between 3 and 4 strong colonies (including the 10% ‘just in case’).

The final concentration is 3.2% w/v oxalic acid

(7.5 * 0.714)/167 * 100 = 3.2% 9.

Check my maths 😉

Recipe to prepare Api-Bioxal solution for trickling

Warning – the recipe on the side of a packet of Api-Bioxal makes up a much stronger solution of oxalic acid than has historically been used in the UK. Stronger isn’t necessarily better. The recipe provided is 35 g Api-Bioxal to 500 ml of 1:1 syrup. By my calculations this recipe makes sufficient solution at a concentration of 4.4% w/v to treat 11 hives. 

There’s an additional complication when preparing an Api-Bioxal solution for trickling. This is because Api-Bioxal contains two additional ingredients – glucose and powdered silica. These cutting agents account for 11.4% of the weight of the Api-Bioxal. The remaining 88.6% is oxalic acid dihydrate.

Using the same logic as above, 1g of Api-Bioxal therefore contains:

(90.03/126.07) * 0.886 = 0.633 g of oxalic acid.

Therefore, to make up 167 ml of a 3.2% Api-Bioxal solution you need to use the following recipe, or scale up/down appropriately:

  • 100 g tap water
  • 100 g white granulated sugar
  • Mix well
  • 8.46 g of Api-Bioxal

Again, check my maths … you need to add (7.5 / 0.886 = 8.46) grams of Api-Bioxal as only 88.6% of the Api-Bioxal is oxalic acid dihydrate.

Scaling up and down

8.46 g is not straightforward to weigh – though see below – and 167 ml may be too much for the number of hives you have. Here’s a handy table showing the amounts of Api-Bioxal to add to 1:1 syrup to make up the amount required.

Api-Bioxal recipes for 3.2% trickling in 1:1 syrup

The Api-Bioxal powder weights shown in bold represent the three packet sizes that can be purchased.

I don’t indicate the amounts of sugar and water to mix to make the syrup up. I’ll leave that as an exercise for the reader … remember that 100 g of sugar and 100 ml of water make 167 ml of 1:1 (w/v) syrup.

Weighing small amounts of Api-Bioxal

The amount of Api-Bioxal used is important. A few grams here or there matter.

If you are making the mix up for a limited number of hives you will have to weigh just a few grams of Api-Bioxal. You cannot do this on standard digital kitchen scales which work in 5 g increments.

Buy a set of these instead.

Digital scales … perfect for Api-Bioxal (and yeast)

These cost about a tenner and are perfect to weigh out small amounts 10 of Api-Bioxal … or yeast for making pizza dough.

A few words of caution

I don’t want to spoil your fun but please remember to take care when handling or using oxalic acid, either as a powder or when made up as a solution.

Oxalic acid is toxic

  • The lethal dose for humans is reported to be between 15 and 30 g. It causes kidney failure due to precipitation of solid calcium oxalate.
  • Clean up spills of powder or solution immediately.
  • Take care not to inhale the powder.
  • Store in a clearly labelled container out of reach of children.
  • Wear gloves.
  • Do not use containers or utensils you use for food preparation. A well rinsed plastic milk bottle, very clearly labelled, is a good way to store the solution prior to use.

Storage

Storage of oxalic acid syrup at ambient temperatures rapidly results in the acid-mediated breakdown of sugars (particularly fructose) to generate hydroxymethylfurfural (HMF). As this happens the colour of the oxalic acid-containing solution darkens significantly.

This breakdown happens whether you use oxalic acid or Api-Bioxal.

Stored OA solution and colour change

Stored OA solution and colour change …

HMF is toxic to honey bees at high concentrations. Studies from ~40 years ago showed that HMF concentrations below 30 mg/l were safe, but above 150 mg/l were toxic 11.

At 15°C HMF levels in OA solution can reach 150 mg/l in a little over a week. At room temperature this happens much faster, with HMF levels exceeding 150 mg/l in only 2-3 days. In the dark HMF levels build up slightly less quickly … but only slightly 12.

Therefore only make up OA solutions when you need them.

If you must store your oxalic acid-containing syrup for any length of time it should be in the fridge (4°C). Under these conditions HMF levels should remain well below toxic levels for at least one year. However, don’t store it for this long … use it and discard the excess.

Or prepare excess and share it with colleagues in your beekeeping association.

Don’t use discoloured oxalic acid solutions as they’ve been stored incorrectly and may well harm your bees.

Another final few words of caution

I assume you don’t have a fridge dedicated to beekeeping? That being the case please ensure that the bottle containing stored oxalic acid is labelled clearly and kept well out of the reach of children.


Notes

A quick trawl through the Veterinary Medicines Directorate database turns up several oxalic acid-containing solutions for managing Varroa. These include:

  • Oxuvar – approved for trickling or spraying, an aqueous solution of oxalic acid to which you add glucose if you intend to use it for trickling.
  • Oxybee – approved for trickling (and possibly other routes, but the paperwork was a minefield!), contains oxalic acid, glycerol and essential oils and is promoted as having a long shelf life.
  • VarroMed – approved for trickling, contains oxalic acid and formic acid and can be used throughout the year in one way or another.

I’ve not read the documentation provided with these and so don’t know the precise concentration of oxalic acid they contain. It will be listed as an active ingredient. I have not used these products. As with everything else on this site, I only write about methods or products I am familiar with. I therefore cannot comment on their relative efficacy compared to Api-Bioxal, to Apivar or to careful siting of your hives in relation to ley lines … or 5G phone masts.

 

Does DWV infect bumble bees?

Covid (the disease) is caused by a virus called SARS-Cov-2. SARS is an abbreviation of severe acute respiratory syndrome and the suffix ‘Cov’ indicates that it’s a coronavirus. The final digit (2) shows that it’s the second of this type of virus that has caused a pandemic. The first was in 2003, and was caused by a virus we now call SARS-Cov-1. That virus had a case fatality rate of 11%, but only infected ~8500 people worldwide. 

SARS-Cov-2 is not a human virus, by which I mean it’s not a virus that has been present in the human population for a long time. It’s actually a virus that most probably originated in bats.

We’re still not sure how SARS-Cov-2 jumped species from bats to humans.

SARS-Cov-1 made the same transition from bats and we do have a pretty good idea how this happened. Before the virus was found in bats it was detected in palm civets and raccoon dogs, both of which are farmed for food and sold in live game markets. Neither animal shows any symptoms when infected with SARS-Cov-1.

Bats were also sold in the same live game markets in Guangdong province in China and it seems likely that the virus either crossed directly from bats to humans, or went via a third species such as the palm civet.

Pathogen spillover

It’s likely that SARS-Cov-2 followed the same route. We are entering a second – likely extended – period of geographic lockdown due to Covid. Since SARS-Cov-2 made its cross-species jump from bats to humans it has infected at least 41 million people and killed over 1.13 million.

Pathogens that jump from one species to another can have catastrophic consequences for the recipient population 1 or, as in the case of palm civets, might cause no harm whatsoever.

The term ‘pathogen spillover’ is often used to describe the event when a pathogen – whether viral, bacterial or a parasite – escapes or spills over from its natural host to another species. 

CSI in the apiary … motive, opportunity, means

To make the species jump a number of criteria must occur. The pathogen has to be present at a high enough level to be infectious in the ‘donor’ species. For convenience, let’s consider this as the motive to jump species 2.

Secondly, the pathogen needs to have an opportunity to jump species. For example, because the donor and ‘recipient’ species share the same habitat or regularly come into contact.

Finally, it has to have the means to replicate in the recipient. If it cannot replicate it can never get established in the recipient population or cause disease.

In fact, this is an oversimplification. It also needs to be transmissible between individuals of the recipient species (or it will never spread in the recipient species).

So what has all this to do with the bumble bees in the title of this post?

Honey bees get a bad press from some scientists and environmentalists. They compete with native solitary and other bees and pollinators for environmental resources – like pollen and nectar. Increasingly, particularly in agricultural areas, these can be in limiting supply at certain times of the season. For examples, because all the hedgerows have been grubbed up and the wildflower meadows obliterated.

In addition, there are a number of studies that have suggested that honey bee viruses have spilled over into other pollinators, in particular bumble bees, and that this pathogen spillover has contributed to the decline in free-living bee populations.

Do honey bee viruses have the motive, opportunity and means to cause disease in bumble bees?

Are honey bee viruses responsible for the decline in bumble bee populations?

Correlation and causation

There are numerous studies showing that the most widespread honey bee virus, deformed wing virus (DWV), can be detected in wild-caught bumble bees.

Let me pose a quick question … does detection mean ‘replication’?

Deformed wing virus “does what it says on the tin” in honey bees. When transmitted by Varroa it causes developmental defects in pupae that appear as wing deformities in newly emerged workers.

DWV symptoms

DWV symptoms

There’s also one study that implicates DWV in directly causing disease in bumble bees.

This influential paper, published 15 years ago, demonstrated that some bumble bees had the characteristic crippled wings seen in symptomatic emerging honey bee workers. The ‘smoking gun’ was that DWV was also detected in these bumble bees.

Exhibit A : Evidence for DWV infection in bumble bees – click image for full legend.

This is the only figure in the paper and there have been no substantive follow-up papers. For some reason they showed ‘symptomatic’ Bombus terrestris (the buff-tailed bumble bee; panel A, left) and PCR detection data for B. pascorum (the common carder bee).

Nevertheless, this association between presence and symptoms was sufficient for the authors to conclude “we demonstrated that DWV is pathogenic to at least two bumble bee species … causing wing deformity similar to clinically DWV-infected honey bees”.

Here’s a second important question … does the detection of DWV in bumble bees demonstrate it is responsible for the symptoms observed? 3

As a virologist interested in the evolution, replication and transmission of viruses – and a beekeeper – this seemed like a worthwhile topic to explore in a bit more detail.

There might be a correlation between the presence of DWV in bumble bees, but does this account for causation of the DWV-like symptoms seen in the bumble bees?

Motive and opportunity

Let’s get these two out of the way quickly (though we’ll return to opportunity in the notes at the end).

Remember, viruses don’t want to do anything. I’m using motive as a hideously contrived reference to whether the pathogen, DWV, is present at high and infectious levels in honey bees.

It is.

Healthy, mite-naive (but reared in a hive with Varroa) workers can carry as little as ~1000 DWV viruses. Similar levels of DWV are also present in hives from Varroa-free regions – at least of the UK 4. In contrast, after parasitisation by Varroa, symptomatic or asymptomatic adult worker honey bees regularly have more that 109 (one trillion) viruses coursing through their little bodies. 

This virus is highly infectious. When injected into honey bees, as few as 10 viruses are sufficient to start a new infection and are replicated several million-fold within 24-48 hours.

Let’s agree that they have the ‘motive’ … to spread to other hosts.

They also have the opportunity, at least in the broadest sense of the word. Honey bees and bumble bees share the same environment. They collect nectar and pollen from the same flower species. They can even regularly be seen visiting the same flower simultaneously. In addition, it’s not unusual to see bumble bees trying to access honey bee hives to steal nectar.

I’d argue that the virus appears to have ample opportunity to move from one species to the other.

Does DWV replicate in bumble bees?

This is an important question. The data figure (‘Exhibit A’) shown above does not answer this question. Their assay simply detects the presence of DWV, with no indication of whether the virus is replicating.

And the reason this is important is really explained in the section on motive and opportunity above. DWV is ubiquitous and present at extraordinarily high levels in many honey bees. It’s present in honey bee faeces. It can be detected on flowers that honey bees have visited, or in pollen collected from those flowers.

DWV is absolutely everywhere.

So, if it is everywhere, there’s a good chance it might simply contaminate things … like bumble bees that look a bit sick for other reasons.

However, if DWV is involved in causing disease in bumble bees then the virus must replicate in bumble bees.

Virus replication – select for full size and legend.

I’ve used this figure before. To be certain that the virus is replicating you need to identify the intermediate replication products (the negative strand RNA shown as red arrows above).

Almost none of the large number of papers that have reported “DWV infected bumble bees” have identified these intermediate replication products.

Many studies didn’t even bother looking for these critical intermediate products.

So we did

There are two ways we could have investigated this. We could have collected large numbers of bumble bees from the fields and screened them in the lab for these replication intermediates. The problem with this approach is that DWV might be very rare in bumble bees, or might be common, but only replicate rarely. The additional problem is that it involves going out and collecting bees from the environment – that’s hard work 😉 5

An alternative approach is to buy a nest of bumble bees 6 and to inject a few bumble bee pupae and adults with DWV. This is what we did. In parallel, to ‘prove’ the virus used can replicate in honey bees, we injected a few honey bee pupae.

We injected the bees as it’s the definitive way we have of being sure that the virus was present.

‘Gene jockeys’

I’ve got some gifted molecular virologists in my lab. These are scientists who use genetic engineering or biotechnology techniques to address tricky questions (gene jockeys). They are particularly skilled at manipulating nucleic acids, such as the genomes of viruses.

If DWV is so common (it is – see above) how would we know that the replication intermediates were from the virus we injected into the bumble bees, rather than from a virus that was possibly already present?

To solve this puzzle Alex (the lead author on our recent paper) did two things. She engineered a unique genetic marker into the virus which we could look for (and that knew was absent from other similar viruses that might already be present in bumble bees). In addition, she ensured that the virus she injected into the bumble bees contained none of the negative strand RNA that is produced as the intermediate when the virus replicates. 

And … to cut a long story short, we could detect the negative strand RNA replication intermediate in injected bumble bees. In addition, the virus contained the unique genetic marker Alex had engineered into the virus genome, so we were absolutely certain it was the injected virus that was replicating. All of the controls worked exactly as expected.

DWV does replicate in bumble bees … at least under the conditions used in our experiment.

But it does not replicate very fast

The bumble bees we used for these experiments are commercially produced under very clean conditions. When we tested control bumble bees they contained no DWV at all, even using our most sensitive assays.

In contrast to injected honey bee pupae, DWV replicates rather slowly in bumble bees. In honey bees it will amplify a million-fold in 48 hours. However, in bumble bees, in 48 hours we only observed a 100-10,000 fold increase in DWV levels. It was only when we injected large amounts of DWV to bumble bees that we could recapitulate the virus levels seen in symptomatic honey bees.

This was a little puzzling as we’ve assumed that the very rapid replication of DWV in honey bees contributes to pathogenesis. The virus needs to replicate fast to spread through the pupa and infect the particular tissues and organs that, when damaged, result in the characteristic symptoms seen.

If it only replicates slowly in bumble bees how can it cause symptoms?

But hold on … does it cause symptoms?

Not as far as we can tell. 

We never found any injected bumble bees with deformed wings, or any that looked anything like the symptoms seen with DWV in honey bees. The actual quote from the paper is:

Strikingly, none of the eclosed bumble bees showed any signs of the wing deformities that are characteristic of DWV infection of honey bees”. 

Morbidity of DWV in bumble bees

Injected pupae developed until eclosion and were either non-viable, discoloured or apparently normal in appearance (see (c) above). We observed similar numbers of these three types whether the pupae were injected with DWV or mock-injected with buffer alone (see (b) above). What’s more, of those injected with the virus, the level of the virus was the same irrespective of the appearance (or viability) of the bumble bee (see (a) above).

We know that these bumble bees contain replicating DWV but see no evidence for overt disease. I acknowledge that they may have invisible symptoms. However, we see no evidence for the wing deformities reported in the 2005 paper from Genersch and colleagues (‘Exhibit A’, above).

Heavy going? But I’ve only just started … 

So, let’s briefly return to our “motive, opportunity, means” crime analogy and summarise where we’ve got to so far. 

DWV is present at very high levels in at least some honey bees. In addition, bumble bees are likely to regularly come into contact with DWV in the environment. This could happen through contaminated pollen, when attempting to rob hives, or by direct interaction with honey bees when both visit flowers. Finally, and most tellingly, DWV replicates in bumble bees.

So, if I was Peter Falk as Lieutenant Columbo, I’d argue that DWV has the motive, opportunity and means to potentially cause disease in bumble bees.

But, as is apparent from the figure above, it appears not to actually cause disease.

Which is puzzling. 

Just one more thing 7

There’s a major problem with the experiments I’ve discussed so far.

Like all experiments 8 they were tightly controlled, with single variables and lots of statistical analysis to demonstrate our confidence in their reproducibility.

The problem wasn’t technical, it was how well they recapitulated potential transmission in the environment.

We’re not aware of anything that goes around “injecting” bumble bee pupae or adults 9. They are not parasitised by Varroa and, although there are bumble bee mites (such as Parasitellus), they don’t feed on bumble bees in the same way that Varroa feeds on honey bees.

How else might bumble bees acquire DWV?

The obvious route is orally, while feeding. 

There are a few issues with feeding bees DWV. The method is simple enough … you add the virus to sugar syrup and they slurp it down. However, you have little control over how much individual bees consume. Do some bees feed directly and other acquire food when fed by other bees (trophallaxis)? It gets rather difficult control.

In addition, we knew from our studies of honey bees that they are far less susceptible to infection per os (by mouth) than by injection. And by far less I mean tens of thousands of fold less susceptible, at least as adults.

Feeding bumble bees DWV

We chose to investigate two routes of feeding.

The first was to directly feed individual bees in the laboratory. Using this approach we failed to detect any evidence for infection or DWV replication in fed adult bumble bees, even when fed 100 million DWV viruses.

Not an encouraging start. However, larvae generally have increased susceptibility to pathogens, so we also investigated feeding larvae in the laboratory. In these studies we did manage to establish infection. However, to do so we had to add 100 million DWV viruses to he food and only achieved a 50% infection rate. 

The second approach we used was direct feeding of complete bumble bee colonies maintained in the lab.

Bumble bees are easier to keep in the lab than honey bees as they don’t need to be free-flying. Each colony occupies a 30cm3 perforated plastic box, supplied with pollen and syrup. We fed three colonies 100 million DWV per bee per day for 4-6 weeks 10.

That’s a huge amount of virus for a protracted period. Our reasoning here was straightforward. Perhaps there was a particular developmental stage that had increased susceptibility? Perhaps adult bees feeding larvae would – for whatever reason – reduce their resistance to infection via the oral route?

We screened every egg, larva, pupa and adult bee for replicating DWV at the end of the experiment.

There was none present 🙁 ( or perhaps 🙂 , depending upon your viewpoint )

Summary and conclusions

We generated unequivocal evidence that DWV replicates in bumble bees. Specifically in Bombus terrestris, the buff tailed bumble bee. I’d be surprised if it did not replicate in other Bombus species, but that will need to be investigated. 

Infection of adult bees was only possible by injection, with no evidence for infection during feeding.

Bumble bee larvae can be infected with DWV while feeding, but only when fed very large amounts of virus directly. When larvae were reared by a colony supplied with DWV-laced food for several weeks the larvae did not become infected.

These results were recently published in Scientific Reports (Gusachenko et al., 2020) and are freely available. The title of the paper neatly sums up the study “Evidence for and against deformed wing virus spillover from honey bees to bumble bees: a reverse genetic analysis”

What does this mean in terms of our understanding of pathogen spillover from managed honey bee colonies to free living bees? 

If ecologists and environmental scientists are going to make the case that honey bees are threatening the survival of free-living solitary or bumble bees (due to pathogen spillover) they need to:

  1. formally demonstrate that the honey bee virus replicates in the free-living bee
  2. show that this replication is detrimental to the free-living bee
  3. provide evidence for a natural route of transmission by which infection can occur

In my view, and using legal terms again, it’s case proven for the first point in Bombus terrestris 11. In contrast, if I was the judge I’d throw out the other cases due to lack of evidence.

Monkey puzzles

There are viruses everywhere. Every living species has one or more viruses that infect it. Inevitably, because viruses replicate to very high levels, species other than the natural host may become exposed.

But almost always this has no consequences at all …

And to illustrate that I’ll briefly describe a study of monkey viruses infecting humans in Cameroon from several years ago. HIV is one of a very large group of viruses called immunodeficiency viruses. The ‘H’ stands for human, though the virus originated in chimpanzees and is very closely related to the simian immunodeficiency viruses (SIV).

A study of hunters living in the forests of Cameroon showed evidence for exposure to multiple different SIV isolates in tribespeople who hunted non-human primates or who were involved in butchering them or preparing them for market or cooking. There was no evidence these viruses were spreading in the human population, or that there was any sickness or disease associated with prior exposure. 

Environmental exposure happens all the time, and is relatively easy to detect. That’s exactly what had happened with these monkey viruses.

But evidence for environmental exposure, whilst easy to get, is not sufficient to support a claim that the virus causes disease at the level of the individual, or that it threatens an entire population.

As a virologist I think it’s interesting that DWV replicates in Bombus terrestris. However, I’ve yet to see any convincing evidence that DWV spillover from honey bees is responsible for the decline in wild bee populations.

Circumstantial evidence is not the same as convincing evidence.


Notes

What are the missing experiments that we didn’t do?

A key one is to determine whether long-term infection of bumble bees with DWV results in disease. We didn’t see overt deformed wing disease, but it’s possible that infection for weeks could have caused this or other symptoms. 

Although we fed bumble bee nests for weeks with DWV we saw no evidence of larval infection. This was despite previously demonstrating that larvae could be infected with high levels of DWV orally. One possibility is that DWV is inactivated by adult bees. I think it would be interesting to look at the level of infectious DWV in larval food.

Are there natural routes of exposure to DWV that result in bumble bee infection?

Does DWV ever cause environmental contamination at a high enough level to naturally infect bumble bees? For example, is the level of DWV in honey bee faeces high enough and does it ever contaminate pollen?

We are not going to do these studies so it will be interesting to see if others do … or whether simply the presence of the virus (whether replicating or not) will be proof’ that honey bee viruses are responsible for the decline in free-living bee populations.

Weed and feed

Weed and feed is a generic term that describes the treatment of lawns to simultaneously eradicate certain weeds and strengthen the turf.

It seemed an appropriate title for a post on eradicating mites from colonies and feeding the bees up in preparation for the winter ahead.

Arguably these are the two most important activities of the beekeeping year.

Done properly they ensure you’ll still be a beekeeper next year.

Ignored, or done too little and too late, you’ll join the unacceptably large number of beekeepers who lose their colonies during the winter.

They think it’s all over

In Fife, on the east coast of Scotland, my beekeeping season effectively finishes with the midsummer ‘mixed floral’ nectar sources. This is a real mix of lime, blackberry, clover and Heinz nectars 1 … many of which remain to be identified.

There’s no reliable late nectar flow from himalayan balsam around my apiaries are and not enough rosebay willowherb (fireweed) to be worthwhile, though in a good year the bees continue to collect a bit from both into early September.

But by then the honey supers are off and extracted. Anything the bees find after that they’re welcome to.

The contrast with the west of Scotland is very marked. Over there my bees are still out collecting reasonable amounts of late heather nectar, though the peak of the flow is over.

Storing supers

Once the honey supers are extracted they can be returned to the colonies for the bees to clean up prior to storing them overwinter. However, this involves additional trips to the apiary and usually necessitates using the clearer boards again to leave them bee-free before storage.

I used to do this and quite enjoyed the late evening trips back to the apiary with stacks of honey-scented supers. More recently I’ve stopped bothering and instead now store the supers ‘wet’. The main reasons for this are:

  • laziness lack of time
  • unless you’re careful it can encourage robbing, by wasps or bees. You need to return supers to all the colonies in the apiary and if you have the hives open too long it can induce a frenzy of robbing 2
  • the honey-scented supers encourage the bees to move up faster when they’re used the following season

If you do store the supers ‘wet’ make sure the stacked boxes are bee and wasp-tight. Mine go in a shed with a spare roof on the top. If there are any gaps the wasps, bees or ants will find them and it then becomes very messy. 

I know many beekeepers who wrap their supers in clingfilm. Not the 30 cm wide roll you use in the kitchen but the sort of metre wide swathe they used to wrap suitcases in at London Heathrow.

Dated super frames

The drawn super comb is a really valuable resource and can be used again and again, year after year. I usually record the year a frame was built on the top bar. Many are now over a decade old and have probably accommodated at least 80 lb of honey in their lifetime 3.

The timing of late season Varroa management

During the brood rearing season the Varroa levels in the colony will have been rising inexorably. Without intervention the mites will continue to replicate on developing pupae that would otherwise emerge as the all-important overwintering bees. These are critical to get the colony through to the following spring.

When Varroa feeds on a developing pupa it transmits the viruses – primarily deformed wing virus – it acquired from the last bee is fed on. These viruses amplify by about a million-fold within 24-48 hours. Pupae that do not die before eclosion may have developmental defects. Importantly, those that appear normal have a reduced lifespan.

The overwintering bees should live for months, but might only live for weeks if their virus levels are high.

And if enough overwintering bees have high viral loads and die prematurely, the probability is the the colony will perish in the winter.

You therefore need to reduce mite levels before the overwintering bees are exposed to Varroa

The full details and justification are in a previous post logically entitled When to treat?

TL;DR 4late August to early September is the best time to treat to protect the winter bees from the worst of the ravages of mite-transmitted DWV.

Use an appropriate treatment

You need to reduce the mite levels in the colony by at least 90% to protect the winter bees.

To achieve this you need an appropriate miticide used properly. 

I use Apivar

Apivar is an Amitraz-containing miticide. Although there are reports of mite resistance in some commercial apiaries, the pattern is very localised (individual hives within an apiary, which is difficult to understand) and in my view it is currently the best choice.

What are the alternates?

  • MAQS – active ingredient formic acid – poorly tolerated at high temperatures, but can be used with the supers present
  • Apiguard – active ingredient thymol – ineffective at lower temperatures (it needs an ambient temperature of 15°C to work – that’s not going to happen in Scotland in September).
  • Apistan – active ingredient a synthetic pyrethroid – unsuitable as there is widespread resistance in the mite population.

Using Apivar

Apivar treatment is temperature-independent. It cannot be used when the honey supers are present. You simply hang two strips in the hive for 6 to 10 weeks and let them do their work. The bees tolerate it well and, unlike MAQS or Apiguard, I’ve not seen any detrimental effects on the queen who continues to lay … making more of those important winter bees.

Apivar strips

Each strip consists of an amitraz-impregnated piece of plastic tape with a V-shaped tab that can be pushed into the comb to hold it in place. 

This generally works well as the frames are usually not moved much as there’s no need for inspections this late in the season.

Apivar strip pushed into comb

However, the strips can be a little fiddly to remove (or fall off during frame handling) and some of our research colonies will continue to be used for at least another month. I’ve therefore used a short piece of bent wire to hang the strips from in these hives.

Apivar strip on wire hanger

I place the strips in opposite corners of the hive, set two frames in from the sides. 

Apivar, wax and honey contamination

Although Amitraz is not wax soluble 5 there are recent reports on BEE-L that one of its breakdown products are, including one that has some residual miticide activity 6

I therefore try and get all the bees into the brood box before starting treatment (I described nadiring supers with unripe honey last week).

Very rarely I’ll leave the bees with a super of their own unripe honey. Usually this happens when the brood box is already packed with stores and overflowing with bees. In this case I’ll mark the super and melt down the comb next season rather than risking tainting the honey I produce.

I attended a Q&A session by the Scottish Beekeeping Association last month in which the chief bee inspector discussed finding Apivar strips in honey production hives. He described the testing of honey for evidence of miticide contamination and potential subsequent confiscation.

This is clearly something to be avoided.

Remember to record the batch number of Apivar used and note the date in your hive records. I just photograph the packet for convenience. The date is important as the strips must be removed after 6 weeks and before 10 weeks have elapsed. 

It’s finally worth noting that the instructions recommend scraping the strip with a hive tool part way through the period if they are being used for the full ten week course of treatment. The strips usually get propolised into the frame and the scraping ‘reactivates’ them to ensure that the largest possible number of mites are killed off.

And, after all, that’s what they’re being used for.

Apivar is expensive

Well … yes and no.

Yes it feels expensive when walking out of Thorne’s of Newburgh clutching one small foil packet and being £31 poorer. 

But think about it … that packet is sufficient to treat 5 colonies.

Is £6.20 too much to spend on a colony?

My 340 g jars of honey cost more than £6.20 and my productive colonies produce at least one hundred times that amount of honey. 

I don’t think 1% of the honey value is too much to spend on protecting the colony from mites and the viruses they carry.

Mite drop

Varroa killed by the miticide 7 fall to the bottom of the hive. If you have an open mesh floor (OMF) they fall through … onto the ground or the intervening neatly divided Varroa tray, enabling you to easily count them

Varroa trays ...

Varroa trays …

Remember that amitraz, the active ingredient of Apivar, works by direct contact. This is why you place the strips diametrically opposite one another so that as many bees as possible contact them. Unlike Apiguard, it makes no difference whether the Varroa tray is present or not.

It is useful to ‘count the corpses’ to get an idea of the infestation level and the efficacy of the treatment.

I’m going to discuss what you might expect in terms of mite drop in the winter (I need to plot some graphs first). However, this is something you could think about before then … knowing Apivar kills mites in less than three hours after exposure, what do you think the mite drop should look like over the 6-10 weeks of treatment?

Enough weeding, what about feeding?

I treat and feed colonies on the same day.

I also do the final hive inspection of the season. At this I look for evidence of a laying queen, the general health of the colony, the amount of brood present and the level of stores in the brood box. 

If the colony is queenless (how did that happen without me noticing earlier?) I simply unite the colony with a strong, healthy queenright colony. I don’t bother testing it with a frame of eggs … time is of the essence.

It’s too late to get a queen mated (at least in Fife … when I lived in the Midlands I got a few September queen matings but they could not be relied upon) and I rarely, if ever, buy queens.

I only feed with fondant in the autumn.

Convenience food

I described fondant last week as a convenience food

A spade's a spade ...

A spade’s a spade …

I’ve described in detail many of the benefits of fondant in numerous previous posts. Essentially these can be distilled to the following simple points:

  • zero preparation; no syrup spillages in the kitchen, no marital strife.
  • bucket- and feeder-free; no need to carry large volumes of syrup to the apiary and no feeders to store for the remaining 11 months of the year. All you need to feed fondant is a queen excluder and an empty super … and you’ve got those already.
  • easy to store; unopened it keeps for several years 8.
  • super speedy; I can feed a colony, including cutting the block in half, in less than 2 minutes.
  • good for queen and colony; perhaps that’s stretching it a bit. What I mean is that the bees take the fondant down more slowly than syrup, consequently the queen continues to lay uninterrupted as the brood nest does not get backfilled with stores. This is good for the colony as it means the production of more winter bees.
  • an anti-theft device; you can’t spill fondant so there is much less chance of encouraging robbing by neighbouring bees or wasps.
  • useful boxes; the empty boxes are a good size to store or deliver jarred honey in – each will accommodate sixteen 1 lb rounds.

I’ve fed nothing but fondant for about a decade and can see no downsides to its use.

Money, money, money

I’ve never used anything other than commercially purchased “baker’s” fondant … don’t believe the rubbish (about ‘additives’) some of the bee equipment suppliers use to justify their elevated prices.

You should be paying about £1/kg … any more and you’re being robbed. This year (2020) I paid less than 90p/kg.

Do not use the icing fondant sold by supermarkets for Christmas cakes. I’m sure there’s nothing much wrong with it, but – at £2/kg – you’ll soon go bankrupt. 

Tips for feeding fondant

Fondant blocks are easier to slice in half if they are slightly warm.

Use a sharp bread knife and don’t slice your fingers off. 

You can cut the blocks in half in advance in the warmth of your kitchen and then cover the cut faces with clingfilm to prevent them reannealing, but I just do it in the apiary.

Take care with sharp knives … much easier with a slightly warm block of fondant

Alternatively, use a clean spade 9.

Always place the block cut face down on a queen excluder directly over the top bars of the brood frames. With a full block, it’s like opening a book and laying it face down. Do not place it above a crownboard with a hole in it.

You want the bees to have unfettered access to the open face of the fondant block.

Fondant on queen excluder with eke

Ideally, use a framed wire queen excluder.

These are easier to lift off should you need to go into the colony.

Which you don’t 😉

There’s no need to continue inspections this late into the season. Go and enjoy a week or two away in Portugal … or perhaps not 🙁

If you need to store an unused half block of fondant wrap the cut face in clingfilm.

All my colonies get one full block (12.5 kg) and many get a further half block, depending upon my judgement of the level of the stores in the hive.

Insulation

The bees will take the fondant down over 2 – 4 weeks. They do store it, rather than just using it as needed. By late September or early October all that will remain is the blue plastic husk. The photo below is from mid-October. This colony has had a ‘topup’ additional half block after already storing a full block of fondant.

They fancied that fondant

With cooler days and colder nights, you want to reduce heat loss by the colony and minimise the dead space above the bees into which the heat escapes.

Although bees take fondant down at lower temperatures than they do syrup, there’s no point in giving the colony more additional space to heat than they need.

Poly super and fondant ...

Poly super and fondant …

Depending upon the availability of equipment I do one or a combination of the following:

  • use a poly super to provide space for the fondant
  • compress the fondant (use your boot) into as little space as possible and you squeeze it into a 50 mm deep eke, which (conveniently) is the same depth as the rim on my insulated polcarbonate/perspex crownboards 10.
  • use an eke and an inverted perspex crownboard with no need to compress the fondant
  • add a 50 mm thick block of insulation above the crownboard, under the roof (which may also be insulated)

Fondant block under inverted perspex crownboard – insulation block to be added on top is standing at the side

Oh yes … before I forget … completely ignore any advice you might read on using matchsticks to provide ventilation to the hive 11.

They think it’s all over … it is now

That’s the end of the practical beekeeping for the season 🙁

If your colonies are strong and healthy, if the mite levels are low and they have sufficient stores, there’s almost nothing to do now until March 12

Now really is a good time for a beekeeper to take a holiday.

Make a note in your diary on the date you need to remove the Apivar strips

Write up your notes, pour a large glass of Shiraz and make plans for next season 🙂


 

A virus that changes bee behaviour

Particle physicists might not agree, but I think that evolution is the most powerful force in the universe. It is responsible for the fabulous diversity of life, for everything from the 6,000,000 kg Pando clonal colony of quaking aspen covering 43 hectares of the Fishlake National Forest in Utah, to the teeniest of tiniest of viruses.

As a microbiologist I’m acutely aware of the role evolution has played in the genetic arms race between hosts and pathogens. This is what is responsible for the multi-faceted immune system higher organisms carry – the antibodies, the lymphocytes, the complement and interferon responses, and everything else.

In turn, the fast replicating bacteria and viruses have evolved countermeasures to subvert these immune mechanisms, to switch them off entirely or to decoy them into targeting the wrong thing. This ‘arms race’ has gone on since well before the evolution of multicellular organisms (~600 million years ago) … and continues unabated.

Evolution is powerful for one simple reason; if a particular genetic combination 1 ‘works’ it will be passed on to the progeny. If a virus evolves a way to resist the immune response of the host, or to spread between hosts more efficiently, then the trait will be inherited.

Molecular mechanisms and behavioural changes

Some of changes work at the molecular level, invisible without exquisitely sensitive in vitro analysis; protein A binds to protein B and, in doing so, stops protein B from doing whatever it should have be doing. These are important but often very subtle.

Rabies: Slaying a mad dog, 1566 illustration from Wellcome Images

Other changes are far more obvious. Take rabies for example (or don’t, it’s not recommended as it has a near-100% case fatality rate) … the primary host of the rabies virus are carnivorous mammals. Infection causes gross behavioural changes that facilitate virus transmission. The animal becomes bolder and much more aggressive, resulting in virus transmission through biting.

Recent studies have elegantly demonstrated that this (also) is an example of protein A binding to protein B at the molecular level, it’s just that the phenotype 2 is very much more marked.

A protein on the surface of the virus resembles a snake venom toxin and has the ability to bind to nicotinic acetylcholine receptors present in the central nervous system of the mammalian host. These receptors ‘do what they say on the tin’ and bind the neurotransmitter acetylcholine. If the virus protein binds the receptor the response to acetylcholine is blunted and this, in turn, leads to hyperactivity, one of the key behavioural responses caused by rabies viruses.

That’s enough about mad dogs.

If virus-induced behavioural changes are so obvious, why haven’t lots of different examples already been identified and characterised?

Sniffles

Part of the problem is the blurring of distinctions between overt behavioural changes and the direct symptoms induced due to the virus replicating.

Human rhinovirus, the aetiological agent of the common cold, causes upper respiratory tract infections. You get a runny nose and you sneeze a lot.

Gesundheit

Your behaviour changes.

However, it’s generally accepted that the sneezing and runny nose are a result of the physiological response to infection, rather than a virus-induced behavioural response to facilitate transmission.

It’s worth noting that all that “stuff” that comes out of your nose contains infectious virus, so it’s perhaps an artificial distinction between the general symptoms of sickness and evolutionarily-selected host behavioural changes caused by the virus.

Which in a roundabout way …

… allows me to finally introduce the topic of bee viruses that cause host behavioural changes involved in their transmission.

Or, rather, one bee virus that does this … though I’m certain that there will be more.

Israeli Acute Paralysis Virus (IAPV) is an RNA virus transmitted horizontally by direct contact between bees, or while feeding on developing pupae, by the parasitic mite Varroa destructor. It was implicated as a causative agent of Colony Collapse Disorder (CCD), though really compelling evidence supporting it as the primary cause never materialised.

It’s a virus UK beekeepers should be aware of, but unworried by, as it is extremely rare in the UK.

A recent paper has shown two behavioural changes in response to IAPV infection in honey bees. One of them – that facilitates horizontal transmission between colonies – is also partially explained at the molecular level.

The paper was published a couple of months ago:

Geffre et al., (2020) Honey bee virus causes context-dependent changes in host social behavior. Proc. Natl. Acad. Sci. USA 117:10406-10413. 3

I’m going to focus on the results, rather than the methods, though the methods are rather cool. They used barcoded bees to allow the automated image analysis of every bee in a colony for some of the studies where they had introduced known IAPV infected individuals.

Responses of nestmates to IAPV infected bees

Imagine watching a few hundred waggle dances and being able to recount the position, distance and response of every bee ‘watching’ 4 the dance, and then being able to summarise the results.

Over five days.

Non-stop.

Including nights (and yes, bees do still waggle dance at night – a subject for the future).

The scientists orally infected groups of 30 bees with a sub-lethal dose of IAPV, marked them and released them into an observation hive. They then recorded their movements around the hive and their interactions with other bees in the colony. In particular, they focussed on trophallaxis interactions where one bee ‘feeds’ another.

Trophallaxis is also considered to be a method of communication in the hive and has been implicated in disease transmission.

The authors love their whisker plots and statistical analysis.

Who doesn’t? 😉

However, they generally make for rather underwhelming images in a bee blog for entertaining reading. Here .. see what I mean …

Number of trophallaxis interactions per hour.

Suffice to say that the results obtained were statistically significant.

They showed that the infected bees in the colony actually moved about the colony more than their nestmates. Conversely, they were engaged in fewer trophallaxis interactions i.e. it appeared as though they were being ‘ignored’ by their nestmates.

Were they really being ignored altogether or did their nestmates approach them, detect something was amiss and move away?

Antennation

Antennation is the mechanism by which bees recognise nestmates. They use the sensitive chemoreceptors on their antenna to detect cuticular hydrocarbons (CHC) which are distinctive between bees from different hives.

Antennation is a precursor to trophallaxis.

After all, bees do not want to feed a foreigner, or exchange chemicals involved in communications, or even potentially risk being exposed to a new pathogen.

Good as the barcoding and camera system is, it’s not good enough to record antennation within the observation hive. To do this they manually 5 recorded antennation events between IAPV-infected bees and nestmates in cages in the laboratory 6.

In these studies IAPV-infected bees were engaged in the same number of antennation events as control bees. This strongly suggests that the nestmate could detect there was something ‘wrong’ with the IAPV-infected individuals. In support of this conclusion, the authors also demonstrated that bees inoculated with a double stranded RNA (dsRNA) stimulator of the honey bee immune response were also also antennated equally, but engaged in less trophallaxis interactions.

Therefore, these studies appear to show that nestmates exhibit a behavioural response to IAPV-infected bees (and bees with elevated immune responses, recapitulating their response to pathogen infection) that is likely to be protective, reducing the transmission of horizontally acquired viruses.

It’s worth noting two things here.

  1. There were no virus transmission studies conducted. It’s assumed that the lack of trophallaxis reduces virus transmission. That still needs to be demonstrated.
  2. This response is not induced by the virus on the host. It’s a response by nestmates of the host to virus infected individuals (or individuals that present as ‘sick’). As such it’s not the same as the rabies example I started this post with.

Virus-induced behavioural responses

But do the IAPV-infected bees behave differently when they come into contact with other bees who are not their nestmates?

After all, IAPV is a pathogenic virus and its continuing presence within a population (not just a single hive) depends upon it being spread from hive to hive.

For a highly pathogenic virus this is very important. If you spread from bee to bee within a hive and kill the lot you also go extinct … this partly explains the mechanism by which highly virulent viruses become less virulent over time.

But back to IAPV. What happens when IAPV-inoculated bees interact with bees from a different hive?

For example, what would happen if they drifted from one hive to another in a densely populated apiary? Drifting is a significant contributor to the spread of bees between adjacent colonies – studies show that 1% of marked bees drift to adjacent hives over a 3 day window. This partially accounts for the genetic mix of workers (up to 40% are unrelated to the queen that heads the colony) in a hive, a fact generally unappreciated by beekeepers.

The authors first showed that IAPV-infected bees could apparently leave and return to the hive with a similar frequency as uninfected foragers. Their flying was not compromised.

They then resorted again to recording interactions in the laboratory between IAPV-infected bees or control dsRNA-inoculated bees and workers from a different hive.

This was where it gets particularly interesting.

Hello stranger

The dsRNA-immunostimulated bees (remember, these induce a generalised immune response characteristic of a ‘sick’ bee) were treated aggressively by unmatched workers from a different hive.

In contrast, the IAPV-infected bees (which were ‘sick’ and would have been undergoing immunestimulation caused by the IAPV infection) experienced significantly less aggression than both uninoculated workers (which induced an intermediate response) and the dsRNA-inoculated.

This strongly suggests that IAPV is somehow able to modulate the appearance or behaviour (and one often determines the other) of the host to make it more acceptable to an unmatched worker.

They extended this study to conduct “field-based assays at the entrances of three normally managed honey bee colonies”, monitoring whether IAPV-infected bees were more likely to be accepted by the guard bees at the entrance of the hive.

They were. The IAPV-infected bees received a less aggressive reception and/or entered the hives much more easily than the controls.

But what about proteins A and B?

Good question.

The behavioural alterations described above must be explainable in terms of the molecular changes that IAPV induces in the bees. By that I mean that the virus must make, or induce the making of, a chemical or protein or other molecule, the presence of which explains their acceptance by the foreign guard bees.

And the obvious candidates are the cuticular hydrocarbons (CHC) that are recognized during antennation, which I introduced earlier.

And here the story leaves us with some tantalising clues, but no definitive answer.

The scientists demonstrate that there were marked differences between the CHC profile of IAPV-infected and control bees. Again, they used their favoured whisker plots to show this, but collated all of the CHC data into an even more difficult to explain scatter plot of linear discriminant analysis.

CHC profiles (relative abundance) shown using linear discriminant analysis.

The key take home message here is that for each of the CHC’s analysed there were differences in both the quality and relative abundance between the control bees, bees immunestimulated with dsRNA and the IAPV-infected bees.

These differences were so marked that you can see distinct clustering of points in the analysis above … these bees ‘look’ 7 different to the guard bees that antennate them.

This is a great story.

It’s as yet incomplete. To complete the understanding we will need to know which of those CHC’s, or which combination, when suppressed (or overrepresented) induce the guard bees to say “Welcome, step this way … “.

We’ll then of course need to find out how IAPV induces the change in CHC profile, which takes us right back to protein A and protein B again.

Ever the pedant

Much as I like this science I’d perhap argue that, again, the virus isn’t directly inducing a behavioural change in the host.

What it’s doing is inducing a behavioural change in the response to the infected host (by the guard bee). So perhaps this again isn’t quite the same as the rabies example we kicked off with.

A behavioural change in the host might include IAPV-infected bees drifting more, or drifting further. Alternatively, perhaps a colony with widespread IAPV infection could more easily indulge in robbing neighbouring colonies as they would experience less aggression from guard bees.

Smaller is better ...

Reduced entrance to prevent robbing …

I can see immediate evolutionary benefits to a virus that induced these types of behavioural changes. It’s not an original idea … the late Ingemar Fries suggested it in a paper two decades ago 8.

I’m also certain that researchers are looking for evidence supporting these types of directly-induced behavioural changes caused by viral pathogens in honey bees.

All religion, my friend, is simply evolved out of fraud, fear, greed, imagination, and poetry

Edgar Allen Poe may or may not have said this.

However, while we’re on the thorny subject of pathogen-induced behavioural changes in the host, it might be worth mentioning a couple of more controversial areas in which it has been proposed.

In the snappily titled paper “Assortative sociality, limited dispersal, infectious disease and the genesis of the global pattern of religion diversity” Fincher and Thornhill argue 9 that the wide diversity of religions in the tropics (compared to temperate regions) is driven by infectious disease selecting for three anti-contagion behaviours; in-group assortative sociality; out-group avoidance; and limited dispersal. It’s an interesting idea and I’m pleased I don’t have to test it experimentally. Their argument is that these three behavioural changes select for fractionation, isolation and diversification of the original culture … and hence the evolution of religions.

Conversely, perhaps microorganisms induce religious behaviours (rather than religion per se) that facilitate their transmission. This is exemplified in the entertainingly titled paper “Midichlorians – the biomeme hypothesis: is there a microbial component to religious rituals?” by Panchin et al., (2014). They argue that microbes – and they are really thinking about the gut microbiota here – might be able to influence their hosts (humans) to gather for religious rituals at which both ideas (memes) and infections are more easily transmitted.

Perhaps something to think about when mindlessly spinning out all that summer honey in the next few weeks?

Party, party

I think it’s fair to say that both the papers in the section above have some way to go until they achieve mainstream acceptance … if they ever do.

Furthermore, the general area in which parasites, bacteria and viruses, induce changes in the behaviour of their hosts’ is really in its infancy. We are aware of a lot of behavioural changes, but few are understood at the molecular level 10. As such, we often don’t know whether the association is correlative or causative.

Evolution is certainly a powerful enough selective force to ensure that even extremely subtle benefits to the pathogen may become a genetically-fixed feature of the complex interaction it has with the host.

Respiratory viruses, such as the common cold, Covid-19 and influenza infect millions of people globally and are readily transmitted by direct or indirect contact.

That’s why most of the readers of this post have a face mask nearby and a bottle of hand sanitizer ‘at the ready’. Or should.

Direct transmission benefits the virus as it does not have to survive on a door handle, milk bottle or petrol filling pump.

But direct transmission requires that people meet and are in close contact.

And a paper 10 years ago demonstrated that infection with influenza virus resulted in increased social interactions in the 48 hours post-exposure, compared with the same period pre-exposure 11.

It’s amazing what viruses can do … or might do … or (just look around you) are doing.


 

Barcoding bees

Every jar of honey I prepare carries a square 20mm label that identifies the apiary, batch, bucket and the date on which is was jarred. The customer can scan it to find out about local honey … and hopefully order some more.

The label looks a bit like this:

Scan me!

This is a QR code.

You’ll find QR codes on many packaged goods in the supermarket, on bus stop adverts, on … well, just about anything these days.  QR codes were first used in 1994 and are now ubiquitous.

QR is an abbreviation of quick response.

It’s a machine-readable two-dimensional barcode that is used to provide information about the thing it’s attached to.

QR codes contain positional and informational content. In the image above the three corners containing large squares allow the orientation to be unambiguously determined.

Within the mass of other, much smaller, black and white squares are several alignment points, an indication of the encoding 1 and the ‘information payload’. 

Large QR codes can contain more information and more error correction (so they can be read if damaged 2 ). Conversely, small QR codes contain reduced amounts of information and less error correction, but can still be used to uniquely identify individual things in a machine-readable manner.

A barcoded bee and barcode diagram.

And those ‘things’ include bees.

I am not a number 3

I had intended to write a post on how pathogens alter honey bee behaviour. This has been known about in general terms for some time, but only at a rather crude or generic level. 

To understand behavioural changes in more detail you need to do two things:

  • observe bees in a ‘natural setting’ (or at least as natural as can be achieved in the laboratory)
  • record hundreds or thousands of interactions between bees to be able to discriminate between normal and abnormal behaviour. 

And that isn’t easy because they tend to all look rather similar.

Lots of bees

How many of the bees above are engaging in trophallaxis?

Does the number increase or decrease over the next five minutes? What about the next hour?

And is it the same bees now and in an hour?

And what is trophallaxis anyway? 

I’ll address the last point after describing the technology that enables these questions to be answered.

And, since it’s the same technology that has been used to monitor the behavioural changes induced by pathogens, I’ll have to return to that topic in a week or two. 

Gene Robinson and colleagues from the University of Illinois at Urbana–Champaign have developed a system for barcoding bees to enable their unique identification 4.

Not just a few bees … not just a couple of dozen bees … every bee in the colony.

Though, admittedly, the colonies are rather small 😉

Each barcode carries a unique number, readable by computer, that can be tracked in real time.

So, unlike Patrick McGoohan, these bees are a number.

bCode

The scientists designed a derivative of the QR code that could be printed small enough to be superglued to the thorax of a worker bee. They termed these mini-QR-like codes bCodes 5. The information content of a bCode was limited by its size and the reference points it had to carry that allowed the orientation of the bee to be determined.

In total the bCode could carry 27 bits of data. Eleven bits (each essentially on or off, indicated by a black or white square) encoded the identification number, allowing up to 2048 bees to be uniquely numbered. The remaining 16 bits were the error-correction parity bits that had to be present to ensure the number could be accurately decoded.

If you’re thinking ahead you’ll realise that the maximum number of bees they could therefore simultaneously study was 2048. That’s about 1/25th of a very strong colony at the peak of the season, or the number of bees covering both sides of a two-thirds full frame of sealed brood.

It’s enough bees to start a one frame nucleus hive, which will behave like a mini-colony 6 and, in due course, expand to be a much larger colony.

And if you’re thinking a long way ahead you’ll realise the every barcode must be affixed to each bee in the same orientation. How otherwise would you determine whether the bees were head to head or abdomen to abdomen?

Labelling bees

This is the easy bit.

Each bCode was 2.1mm square and weighed 0.6mg i.e. ~0.7% of the weight of a worker bee. Honey bees can ‘carry’ a lot more than that. When they gorge themselves before swarming they ingest ~35mg of honey. 

The bCode therefore should not be an encumbrance to the bee (and they confirmed this in an exhaustive series of control studies).

A single frame of sealed brood was incubated and the bees labelled within a few hours of emergence. Typically, two batches of ~700 bees each were labelled from a single frame for a single experiment.

Each bee was anaesthetised by chilling on ice, the bCode glued in place (remember … in the same orientation on every bee) and the bee allowed to recover.

Labelling a single bee took 1-2 minutes.

Labelling 1400 bees takes several people a long time.

I said it was easy.

I didn’t say it was interesting.

Smile for the camera

I’ve not yet discussed the goal of the study that needed barcoded bees. It’s not really important while I’m focusing on the technology. Suffice to say the scientists wanted to observe bees under near natural conditions.

Which means a free-flying colony, on a frame of comb … in the dark.

Free-flying because caged bees do not behave normally.

On a frame of comb because they were interested in the interactions between bees under conditions in which they would normally interact.

And in the dark because that’s what it’s like inside a beehive (and it’s one of the features that scout bees favour when selecting a site for a swarm).

Camera and hive setup.

The scientists used an observation hive with a difference. It had an entrance to allow the bees to fly and forage freely and it contained a single sided, single frame. In front of the frame was a sheet of glass separated by 8mm from the comb. This prevented the bees from clambering over each other, which would have obscured the bCodes 7. Behind the frame was an 850nm infrared lamp to increase contrast, and the front was illuminated by several additional infrared lamps.

Bees cannot see light in the infrared range, so they were effectively in the dark.

The camera used (an Allied Vision Prosilica GX6600 … not your typical point and shoot) recorded ~29MP images every second. A typical experiment would involve the collection of about a million images occupying 4-6 terabytes of hard drive space 8.

The recorded images were processed to determine the temporal location of every bee with a visible (and readable) bCode. This was a computationally interesting challenge and involved discarding some data – e.g. barcodes that moved faster than a bee can walk or barcodes that fell to the bottom of the hive and remained motionless for days (i.e. dead bees). About 6% of the data was discarded during this post-processing analysis.

Trophallaxis

Which finally gets us to the point where we can discuss trophallaxis. 

Honey bees and other social insects engage it trophallaxis.

It involves two insects touching each other with their antennae while orally transferring liquid food. It occurs more frequently than would be required for just feeding and it has been implicated in communication and disease transmission

bCoded bees and trophallaxis

So, if you are interested in trophallaxis, how do you determine which bees are engaging in it, and which are just facing each other head to head?

In the image above the two bees in the center horizontally of the insert 9 are engaged in trophallaxis. The others are not, even those immediately adjacent to the central pair.

Image processing to detect trophallaxis – head detection.

This required yet more image processing. The image was screened for bees that were close enough together and aligned correctly. An additional set of custom computer-vision algorithms then determined the shape, size, position and orientation of the bees’ heads. To be defined as trophallaxis the heads had to be connected by thin shapes representing the antennae or proboscis.

And when I say the image … I mean all million or so images.

Bursty behaviour

And after all that the authors weren’t really interested in trophallaxis at all.

What they were really interested in was the characteristics of interactions in social networks, and the consequences of those interactions.

This is getting us into network theory which is defined as “Well out of my depth”

Transmission of things in a network depends upon interactions between the individuals in the network.

Think about pheromones, or honey, or email … or Covid-19.

It’s only when two individuals interact that these can be transmitted between the individuals. And the interaction of individuals is often characterised by intermittency and unpredictable timing. 

Those in the know – and I repeat, I’m not one of them – call this burstiness. 

If you model the spread of ‘stuff’ (information, food, disease) through a bursty human communication network it is slower than expected.

Is this an inherent characteristic of bursty networks?

Are there real bursty networks that can be analysed.

By analysing trophallaxis Gene Robinson and colleagues showed that honey bee communication networks were also bursty (i.e. displayed intermittent and unpredictable interactions), closely resembling those seen in humans.

However, since they had identified every trophallaxis interaction over several days they could follow the spread of ‘stuff’ through the interacting network.

By simply overlaying the real records of millions of interactions over several days of an entire functional community with an event transmitted during trophallaxis they could investigate this spread..  

For example, “infect” (in silico) bee 874 in the initial second and follow the spread of the “infection” from bee to bee through the real network of known interactions.

In doing this they showed that in a real bursty network, interactions between honey bees spread ‘stuff’ about 50% faster than in randomised reference networks. 

Why isn’t entirely clear (certainly to me 10, and seemingly to the authors as well). One obvious possibility is that the topology of the network i.e. the contacts within it, are not random. Another is that the temporal features of a bursty network influence real transmission events. 

Scientists involved in network theory will have to work this out, but at least they have a tractable model to test things on …

… and at a time when some remain in lockdown, when others think it’s all a hoax, when social distancing is 2m 11, when some are wearing masks and when prior infection may not provide protective immunity anyway, you’ll appreciate that ‘how stuff spreads’ through a network is actually rather important.

Stay safe


 

Aristotle’s hairless black thieves

Aristotle not in his beesuit

Almost every article or review on chronic bee paralysis virus 1 starts with a reference to Aristotle describing the small, black, hairless ‘thieves‘, which he observed in the hives of beekeepers on Lesbos over 2300 years ago 2.

Although Aristotle was a great observer of nature, he didn’t get everything right.

And when it came to bees, he got quite a bit wrong.

He appreciated the concept of a ‘ruling’ bee in the hive, but thought that the queen was actually a king 3. He also recognised different castes, though he thought that drones (which he said “is the largest of them all, has no sting and is stupid”) were a different species.

He also reported that bees stored noises in earthenware jars (!) and carried stones on windy days to avoid getting blown away 4.

However, over subsequent millenia, a disease involving black, hairless honey bees has been recognised by beekeepers around the world, so in this instance Aristotle was probably correct.

Little blacks, maladie noire, schwarzsucht

The names given to the symptomatic bees or the disease include little blacks or black robbers in the UK, mal nero in Italy, maladie noire in France or schwarzsucht (black addiction) in Germany. Sensibly, the Americans termed the disease hairless black syndrome. All describe the characteristic appearance of individual diseased bees.

Evidence that the disease had a viral aetiology came from Burnside in the 1940’s who demonstrated the symptoms could be recapitulated in caged bees by injection, feeding or spraying them with bacterial-free extracts of paralysed bees. Twenty years later, Leslie Bailey isolated and characterised the first two viruses from honey bees. One of these, chronic bee paralysis virus (CBPV), caused the characteristic symptoms described first by Aristotle 5.

CBPV causes chronic bee paralysis (CBP), the disease first described by Aristotle.

CBPV infection is reported to present with two different types of symptoms, or syndromes. The first is the hairless, black, often shiny or greasy-looking bees described above 6. The second is more typically abnormal shivering or trembling of the wings, often associated with abdominal bloating 7. These bees are often found on the top bars of the frames during an inspection. Both symptoms can occur in the same hive 8.

CBP onset appears rapid and the first thing many beekeepers know about it is a large pile (literally handfuls) of dead bees beneath the hive entrance.

It’s a distressing sight.

Despite thousands of bees often succumbing to disease, the colony often survives though it may not build up enough again to overwinter successfully.

BeeBase has photographs and videos of the typical symptoms of CBPV infection.

Until recently, CBP was a disease most beekeepers rarely actually encountered.

Emerging and re-emerging disease

I’ve got a few hundred hive year’s worth 9 of beekeeping experience but have only twice seen CBP in a normally-managed colony. One was mine, another was in my association apiary a few years later.

A beekeeper managing 2 to 3 colonies might well never see the disease.

A bee farmer running 2 to 3 hundred (or thousand) colonies is much more likely to have seen the disease.

As will become clear, it is increasingly likely for bee farmers to see CBP in their colonies.

Virologists define viral diseases as emerging if they are new in a population. Covid-19, or more correctly SARS-CoV-2 (the virus), is an emerging virus. They use the term re-emerging if they are known but increasing in incidence.

Ebola is a re-emerging disease. It was first discovered in humans in 1976 and caused a few dozen sporadic outbreaks 10 until the 2013-16 epidemic in West Africa which killed over 11,000 people.

Often the terms are used interchangeably.

Sporadic and rare … but increasing?

Notwithstanding the apparently sporadic and relatively rare incidence of CBP in the UK (and elsewhere; the virus has a global distribution) anecdotal evidence suggested that cases of disease were increasing.

In particular, bee farmers were reporting increasing numbers of hives afflicted with the disease, and academic contacts overseas involved in monitoring bee health also reported increased prevalence.

Something can be rare but definitely increasing if you’re certain about the numbers you are dealing with. If you only have anecdotal evidence to go on you cannot be certain about anything very much.

If the numbers are small but not increasing there are probably other things more important to worry about.

However, if the numbers are small but definitely increasing you might have time to develop strategies to prevent further spread.

Far better you identify and define an increasing threat before it increases too much.

With research grant support from the UKRI/BBSRC (the Biotechnology and Biological Sciences Research Council) to the Universities of Newcastle (Principle Investigator, Prof. Giles Budge) and St Andrews, and additional backing from the BFA (Bee Farmers’ Association), we set out to determine whether CBPV really was increasing and, if so, what the increase correlated with (if anything).

This component of the study, entitled Chronic bee paralysis as a serious emerging threat to honey bees, was published in Nature Communications last Friday (Budge et al., [2020] Nat. Comms. 11:2164 https://doi.org/10.1038/s41467-020-15919-0).

The paper is Open Access and can be downloaded by anyone without charge.

There are additional components of the study involving the biology of CBPV, changes in virus virulence, other factors (e.g.environmental) that contribute to disease and ways to mitigate and potentially treat disease. These are all ongoing and will be published when complete.

Is chronic bee paralysis disease increasing?

Yes.

We ‘mined’ the National Bee Units’ BeeBase database for references to CBPV, or the symptoms associated with CBP disease. The data in BeeBase reflects the thousands of apiary visits, either by call-out or at random, by dedicated (and usually overworked) bee inspectors. In total we reviewed almost 80,000 apiary visits in the period from 2006 to 2017.

There were no cases of CBPV in 2006. In the 11 years from 2007 to 2017 the CBP cases (recorded symptomatically) in BeeBase increased exponentially, with almost twice as much disease reported in commercial apiaries. The majority of this increase in commercial apiaries occured in the last 3 years of data surveyed.

Apiaries recorded with chronic bee paralysis between 2006 and 2017.

BeeBase covers England and Wales only. By 2017 CBPV was being reported in 80% of English and Welsh counties.

During the same period several other countries (the USA, several in Europe and China) have also reported increases in CBPV incidence. This looks like a global trend of increased disease.

But is this disease caused by CBPV?

It should be emphasised that BeeBase records symptoms of disease – black, hairless bees; shaking/shivering bees, piles of bees at the hive entrance etc.

How can we be sure that the reports filed by the many different bee inspectors 11 are actually caused by chronic bee paralysis virus?

Or indeed, any virus?

To do this we asked bee inspectors to collect samples of bees with CBPV-like symptoms during their 2017 apiary visits. We then screened these samples with an exquisitely sensitive and specific qPCR (quantitative polymerase chain reaction) assay.

Almost 90% of colonies that were symptomatically positive for CBP were also found to have very high levels of CBPV present. We are therefore confident that the records of symptoms in the historic BeeBase database really do reflect an exponential increase of chronic bee paralysis disease in England and Wales since 2007.

Interestingly, about 25% of the asymptomatic colonies also tested positive for CBPV. The assay used was very sensitive and specific and allowed the quantity of CBPV to be determined. The amount of virus present in symptomatic bees was 235,000 times higher than those without symptoms.

Further work will be needed to determine whether CBPV is routinely present in similar proportions of ‘healthy’ bees, and whether these go on and develop or transmit disease.

Disease clustering

Using the geospatial and temporal (where and when) data associated with the BeeBase records we investigated whether CBPV symptomatic apiaries were clustered.

For example, in any year were cases more likely to be near other cases?

They were.

Across all years of data analysed together, or for individual years, there was good evidence for spatial clustering of cases.

We also looked at whether cases in one year clustered in the same geographic region in subsequent years.

They did not.

Clustering of CBPV – spatial and temporal analysis.

This was particularly interesting. It appears as though there were increasing numbers of individual clustered outbreaks each year, but that the clusters were not necessarily in the same geographic region as those in previous or subsequent years.

The disease appears somewhere, increases locally and then disappears again.

Apiary-level disease risk factors

The metadata associated with Beebase records is relatively sparse. Details of specific colony management methods are not recorded. Local environmental factors – OSR, borage, June gap etc. – are also missing. Inevitably, some of the factors that may be associated with increased risk are not recorded.

A relatively rare disease that is spatially but not temporally clustered is a tricky problem for which to define risk factors. Steve Rushton, the senior author on the paper, did a sterling job of analysing the data that was available.

The two strongest apiary-level factors that contributed to disease risk were:

  1. Commercial beekeeping – apiaries run by bee farmers had a 1.5 times greater risk of recording CBP disease.
  2. Importing bees – apiaries which had imported bees in the two preceding years had a 1.8 times greater risk of recording CBP disease.

Bee farming is often very different from amateur beekeeping. The colony management strategies are altered for the scale of the operation and for the particular nectar sources being exploited. For example, colonies may already be booming to exploit the early season OSR. This may provide ideal conditions for CBPV transmission which is associated with very strong hives and/or confinement.

Bee imports does not mean disease imports

There are good records of honey bees imported through official channels. This includes queens, packages and nucleus colonies. Between 2007 and 2017 there were over 130,000 imports, 90% of which were queens.

An increased risk of CBP disease in apiaries with imported bees does not mean that the imported bees were the source of the disease.

With the data available it is not possible to distinguish between the following two hypotheses:

  1. imported honey bees are carriers of CBPV or the source of a new more virulent strain(s) of the virus, or
  2. imported honey bees are susceptible to CBPV strain(s) endemic in the UK which they were not exposed to in their native country.

There are ways to tease these two possibilities apart … which is obviously something we are keen to complete.

All publicity is good publicity …

… but not necessarily accurate publicity 🙁

We prepared a press release to coincide with the publication of the paper. Typically this is used verbatim by some reporters whereas others ask for an interview and then include additional quotes.

Some more accurately than others 🙁

The Times, perhaps reflecting the current zeitgeist, seemed to suggest a directionality to the disease that we certainly cannot be sure of:

The Times

Its sister publication, The Sun, “bigged it up” to indicate – again – that bees are being wiped out.

The Sun

And the comments included these references to the current Covid-19 pandemic:

  • “Guess its beevid – 19. I no shocking”
  • “It’s the radiation from 5g..google it”
  • Local honey is supposed to carry antibodies of local virus and colds – it helps humans to eat the stuff or so they say. So it could be that the bees are actually infected by covid. No joke.

All of which I found deeply worrying, on a number of levels.

The Telegraph also used the ‘wiped out’ reference (not a quote, though it looks like one). They combined it with a picture of – why am I not surprised? – a bumble bee. D’oh!

The Telegraph

The Daily Mail (online) had a well-illustrated and pretty extensive article but still slipped in “The lethal condition, which is likely spread from imports of queen bees from overseas …”. The unmoderated comments – 150 and counting – repeatedly refer to the dangers of 5G and EMFs (electric and magnetic fields).

I wonder how many of the comments were posted from a mobile phone on a cellular data or WiFi network?

😉

Conclusions

CBPV is causing increasing incidence of CBP disease in honey bees, both in the UK and abroad. In the UK the risk factors associated with CBP disease are commercial bee farming and bee imports. We do not know whether similar risk factors apply outside the UK.

Knowing that CBP disease is increasing significantly is important. It means that resources – essentially time and money – can be dedicated knowing it is a real issue. It’s felt real to some bee farmers for several years, but we now have a much better idea of the scale of the problem.

We also know that commercial bee farming and bee imports are both somehow involved. How they are involved is the subject of ongoing research.

Practical solutions to mitigate the development of CBP disease can be developed once we understand the disease better.


Full disclosure:

I am an author on the paper discussed here and am the Principle Investigator on one of the two research grants that funds the study. Discussion is restricted to the published study, without too much speculation on broader aspects of the work. I am not going to discuss unpublished or ongoing aspects of the work (including in any answers to comments or questions that are posted). To do so will compromise our ability to publish future studies and, consequently, jeopardise the prospects of the early career researchers in the Universities of St Andrews and Newcastle who are doing all the hard work.

Acknowledgements

This work was funded jointly by BBSRC grants BB/R00482X/1 (Newcastle University) and BB/R00305X/1 (University of St Andrews) in partnership with The Bee Farmers’ Association and the National Bee Unit of the Animal and Plant Health Agency.

The scent of death

It’s late May. Outside it’s dark, so you’re trapped inside until sunrise. Inside it’s warm, dark and humid. You and your sisters are crowded together with barely enough space to turn around.

And your mother keeps laying more eggs … perhaps 2000 a day. If it wasn’t for the fact that about 2000 of your sisters perish each day you’d have no space at all.

Most of them die out in the fields. Missing in action.

I counted them all out and I didn’t count them all back, as the late Brian Hanrahan did not say in 1982 😉

But some die inside. And in the winter, or during prolonged periods of poor weather, your sisters all die inside.

Which means there’s some housekeeping to do.

Bring out your dead

Dead bees accumulating in the hive are a potential source of disease, particularly if they decompose. Unless these are removed from the colony there’s a chance the overall health of the colony will be threatened.

Not all bees die of old age. Many succumb to disease. The older bees in the colony may have a higher pathogen load, reinforcing the importance of removing their corpses before disease can spread and before the corpses decompose.

Corpses

Honey bees, like many other social insects, exhibit temporal polyethism i.e. they perform different tasks at different ages.

One of the tasks they perform is removing the corpses from the colony.

The bees that perform this task are appropriately termed the undertaker bees.

Gene Robinson in Cornell conducted observational studies on marked cohorts of bees. In these he identified the roles and activities of the undertaker bees. At any one time only 1-2% of the bees in the colony are undertakers 1.

These are ‘middle aged’ bees i.e. 2-3 weeks after eclosion, similar to guard bees. Although called undertakers, they do not exclusively remove corpses. Rather they are generalists that are more likely to remove the corpses, usually depositing them 50-100m from the hive and then returning.

They preferentially occupy the lower regions of the hive – presumably because gravity means the corpses accumulate there – where they also perform general hive cleansing roles e.g. removing debris.

Bees, like all of us, are getting older all the time. Some bees may spend only one day as undertakers before moving on to foraging duties. Presumably – I don’t think we know this yet – the time a bee remains as an undertaker is influenced by the colony’s need for this activity, the laying rate of the queen and, possibly, the numbers of other bees performing this role 2.

No no he’s not dead, he’s, he’s restin’!

Dead parrot

In Monty Python’s Dead Parrot sketch Mr. Praline (John Cleese) argues with the shop owner (Michael Palin) that the Norwegian Blue parrot he’d purchased was, in fact, dead.

The shop owner tries to persuade Mr. Praline that the parrot is resting.

Or stunned.

Or pining for the fjords.

The inference here is that it’s actually rather difficult to determine whether something is dead or not 3.

So if you struggle with an unresponsive parrot how do you determine if a bee is dead?

More specifically, how do undertaker bees in a dark, warm, humid hive determine that the body they’ve just tripped over is a corpse?

As opposed to a resting bee 4.

The scent of death

Almost forty years ago Kirk Visscher at Cornell studied necrophoresis (removal of the dead) in honey bees 5.

He noted that it had two distinct characteristics; it happened rapidly (up to 70 times faster than debris removal) and dead bees that were solvent-washed or coated in paraffin-wax were removed very much more slowly.

Kirk Visscher concluded that the undertaker bees “probably use chemical cues appearing very rapidly after the death of a bee” to identify the corpses.

Visscher studied honey bees, Apis mellifera. I’m not aware of any recent studies in A. mellifera that have better defined these ‘chemical cues’. However, a very recent preprint has been posted on bioRχiv describing how the closely related Eastern honey bee, Apis cerana, undertakers identify the dead.

As an aside, bioRχiv (pronounced bioarkive) is a preprint server for biology. Manuscripts published there have not been peer reviewed and will potentially be revised and/or withdrawn. They might even be wrong. Many scientists increasingly use bioRχiv to post completed manuscripts that have been submitted for publication elsewhere. The peer review and publication process is increasingly tortuous and long-winded. By posting preprints on bioRχiv other scientists can read and benefit from the study well before full publication elsewhere.

It’s also used as a ‘marker’ … we did this first 😉

The preprint on bioRχiv is Death recognition by undertaker bees by Wen Ping, submitted on the 5th of March 2020.

Odours and pongs

Death recognition in honey bees is rapid. Visscher demonstrated that a dead worker bee was usually removed within 30 minutes, well before it would have started producing the pong associated with the processes of decay.

Corpse recognition occurs in the dark and in the presence of lots of other bees. Logically, an odour of some sort might be used for identification. Both visual and tactile signals would be unlikely candidates.

In searching for the odour or chemical clues (the term used by Visscher), Ping made some assumptions based on prior studies in social insects. In Argentine ants a reduction in dolichodial and iridomyrmecin is associated with corpse recognition, and addition of these compounds (respectively a dialdehyde and a monoterpene) prevented necrophoresis.

Conversely, some social insects produce signals associated with death or disease. Dead termites give off a mix of 3-octanone, 3-octanol and the combination of β-ocimene and oleic acid production is a marker of diseased brood in honey bees.

What else could be assumed about the chemicals involved? Corpse removal is an individual effort. There’s only one pallbearer. Therefore the chemical, whatever it is, doesn’t need to be a recruitment signal (unlike the alarm pheromone for example).

Finally, the signal needs to operate over a very short range. There’s no point in flooding the hive with a persistent long-range chemical as that would make the detection of the corpse impossible.

Cuticular hydrocarbons

Cuticular hydrocarbons (CHC) are widely used in insect communication. They are long chain hydrocarbons (chemicals composed solely of carbon and hydrogen) that have many of the characteristics expected of a ‘death chemical’.

Nonacosane – a long chain CHC with 29 carbons and 60 hydrogen atoms

They are generally short-range, low volatility compounds. Honey bees use CHC’s for communication during the waggle dance and to distinguish colony mates by guard bees. They also have structural roles, being a major component of wax comb and, in the cuticle, they help maintain water balance in bees.

As would be expected from chemicals with a wide variety of roles, there’s a huge range of CHC’s. Taking all the above together, Wen Ping searched for CHC’s that functioned during necrophoresis.

Cool corpses and cuticular hydrocarbons

Wen studied undertakers removing segments of dead bees and determined that the chemical signal was most probably a component of the cuticle.

Living bees in his studies had a body temperature of ~44°C. In contrast, dead bees rapidly cooled to ambient temperatures. Wen demonstrated that corpse removal was significantly delayed if the corpses were warmed to ~44°C, but then occurred rapidly once they were allowed to cool. Finally, dead bees washed with hexane (which removes CHC’s) were removed even if the corpse was warm.

Taken together, these results suggest that a cuticular hydrocarbon that was produced and released from warm bees, but reduced or absent in cold bees, was a likely candidate for the necrophoresis signal.

But which one?

Gas chromatography

A gas chromatograph analyses volatile gases. Essentially gas vapour is passed through a thin coated tube and gaseous compounds of different molecular weights bind and elute at different times. It’s a very precise technique and allows all the components of a mixture to be identified by comparison with known standards.

Gas chromatography of volatiles from live (red) and dead (blue) bees.

Ping studied the volatile CHC’s in the airspace immediately surrounding dead bees or live bees using gas chromatography. There were some significant differences, shown by the absence of peaks in the blue trace of gases from the cold, dead bees. All of the peaks were identified and nine of the twelve peaks were CHC’s.

CHC’s with chain lengths of 27 or 29 carbons exhibited the greatest difference between live warm bees and cool dead bees and synthetic versions of these and the other CHC’s were tested to see which – upon addition – delayed the removal of dead bees.

Three had a significant impact in the dead bee removal assay – with chain lengths of 21, 27 and 29 carbons. These include the compounds heptacosane (C27H56)and nonacosane (C29H60).

Summary

The results section rather fizzles out in the manuscript posted to bioRχiv and I wouldn’t be surprised to see modifications to this part of the paper in a peer reviewed submission.

The overall story can be summarised like this. Live bees are warm and produce a range of CHC’s. Dead bees cool rapidly and some of the volatile CHC levels decrease in the immediate vicinity of the corpse. The undertaker bees specifically monitor the levels of (at least) heptacosane and nonacosane 6 as a means of discriminating between live and dead bees. Within 30 minutes of death local heptacosane and nonacosane levels have dropped below a level associated with life and the undertaker bee removes the corpse.

One final point worth making again. This study was conducted on Apis cerana. Our honey bees, A. mellifera, may use the same necrophoresis signals. Alternatively, they might use different chemicals in the same way.

Or they might do something else entirely.

Personally, I bet it’s a similar mechanism, potentially using different chemical.

There are mixed species colonies of A. mellifera and A. cerana. Do the undertakers only remove same-species corpses?

Global warming and hive cooling

The discussion of the bioRχiv paper raises two interesting points, both of which are perhaps a little contrived but still worth mentioning.

We’re living in a warming world.

Temperatures are rising

Dead bees cooling to ambient temperature lead to reduced CHC production. If global temperatures rise, so will the ambient temperature. Potentially this could decrease the reduction in the levels of CHC’s i.e. the dead bees might not look (er, smell!) quite so dead. This could potentially reduce corpse removal, with the concomitant potential for pathogen exposure.

I suspect that we’ll have much bigger problems to worry about than undertaker bees if the global temperatures rise that high …

But Wen also points out that the rise in global temperatures is also associated with more extreme weather, including very cold weather. Perhaps cold anaesthetised or weak bees will be prematurely removed from the hive under these conditions because their CHC levels have dropped below a critical threshold?

Finally, do dead bees lying on open mesh floors (OMFs) cool more rapidly and so trigger more efficient undertaking? Perhaps OMFs contribute more to hive hygiene than just allowing unwanted Varroa to drop through?


 

Time to deploy!

It’s early April. The weather is finally warming up and the crocus and snowdrops are long gone. Depending where you are in the UK the OSR may start flowering in the next fortnight or so.

All of which means that colonies should be expanding well and will probably start thinking of swarming in the next few weeks.

So … just like any normal season really.

Except that the Covid-19 pandemic means that this season is anything but normal.

Keep on keeping on

The clearest guidelines for good beekeeping practice during the Covid-19 pandemic are on the National Bee Unit website. Essentially it is business as usual with the caveats that good hygiene (personal and apiary) and social distancing must be maintained.

Specifically this excludes inspections with more than one person at the hive. Mentoring, at least the really useful “hands-on” mentoring, cannot continue.

A veil is no protection against aerosolised SARS-CoV-2. Don’t even think about risking it.

This means that there will be a lot of new beekeepers (those that acquired bees this year or late last season) inspecting colonies without the benefit of help and advice immediately to hand.

Mistakes will be made.

Queen cells will be missed.

Colonies will swarm 1.

Queen cells

Queen cells …

It’s too early to say whether the current restrictions on society are going to be sufficient to reduce coronavirus spread in the community. It’s clear that some are still flouting the rules. More stringent measures may be needed. For beekeepers who keep their bees in out apiaries, the most concerning would be a very restrictive movement ban. In China and (probably) Italy these measures proved to be effective, although damaging to beekeeping, so the precedent is established.

Many hives and apiaries are already poorly managed 2. I would expect that additional coronavirus-related restrictions would only increase the numbers of colonies allowed to “fend for themselves” over the coming season.

Which brings me back to swarming.

Swarmtastic

The final point of advice on the NBU website is specifically about swarms and swarm management:

You should use husbandry techniques to minimise swarming. If you have to respond to collect a swarm you need to ensure that you use the guidelines on social distancing when collecting the swarm. If that is not possible, then the swarm then should not be collected. Therefore trying to prevent swarms is the best approach. 

Collecting swarms can be difficult enough at the best of times 3. And cutouts of established colonies are even worse.

In normal years I always prefer to reduce the swarms I might be called to 4 by setting out bait hives.

Swarm recently arrived in a bait hive with a planting tray roof …

Let the bees do the work.

Then all you need do is collect them once they’re all neatly tucked away in a hive busy drawing comb.

This year, with who-knows-what happening next, I’ll be setting out more bait hives than usual with the expectation that there may well be additional swarms.

If they’re successful I’ll have more bees to deal with when the ‘old normal’ finally returns. If they remain unused then all I’ve lost is the tiny investment of time made in April to set them out.

Not just any dark box

I’ve discussed the well-established ‘design features’ of a good bait hive several times in the past. Fortunately the requirements are easy to meet.

  • A dark empty void with a volume of about 40 litres.
  • A solid floor.
  • A small entrance of about 10cm2, at the bottom of the void, ideally south facing.
  • Something that ‘smells’ of bees.
  • Ideally located well above the ground.

I ignore the last of these. I’d prefer to have an easy-to-reach bait hive to collect rather than struggle at the top of a ladder. If I wanted to do some vertically-challenging beekeeping I’d go out and collect more swarms 😉

So, ignoring the final point, what I’ve described is the nearly perfect bait hive.

Those paying attention at the back will realise that it’s also a nearly perfect description of a single brood National hive.

How convenient 🙂

All of my bait hives are either single National brood boxes or two stacked National supers. The box does need a solid floor and a crownboard and roof. If you haven’t got a spare solid floor you can easily build them from Correx 5 for a few pence.

Inside ...

Bait hive floor

Alternatively, simply tape down a piece of cardboard or Correx over the mesh of an open mesh floor 6. In some ways this is preferable as it’s convenient to be able to monitor Varroa levels after a swarm arrives.

Do not be tempted to use a nuc box as a bait hive. You can easily fit a small swarm into a brood box, but a really big prime swarm will not fit in a 5 frame nuc box.

Big swarms are better 🙂 7

More to the point, bees are genetically programmed to search for a void of about 40 litres, so many swarms will simply overlook your nuc box for a more spacious nest site.

What’s in the box?

No, this has nothing to do with Gwyneth Paltrow in Se7en.

How do you make your bait hive even more desirable to the scout bees that search out nest sites? How do you encourage those scouts to advertise the bait hive to their sister scouts? Remember, that it’s only once the scouts have reached a democratic consensus on the best local nest site that the bivouacked swarm will move in.

The brood box ideally smells of bees. If it has previously held a colony that might be sufficient.

Bait hive ...

Bait hive …

However, a single old, dark brood frame pushed up against one sidewall not only provides the necessary ‘bee smell’, but also gives the incoming queen space to immediately start laying 8.

You can increase the attractiveness by adding a couple of drops of lemongrass oil to the top bar of this dark brood frame. Lemongrass oil mimics the pheromone produced from the Nasonov gland. There’s no need to Splash it all over … just a drop or two, replenished every couple of weeks. I usually soak the end of a cotton bud, and lay it along the frame top bar.

Lemongrass oil and cotton bud

The old brood frame must not contain stores – you’re trying to attract scouts, not robbers.

The incoming swarm will be keen to draw fresh comb for the queen to lay up with eggs. Whilst you can simply provide some frames and foundation, this has two disadvantages:

  • the vertical sheets of foundation effectively make the void appear smaller than it really is. The scout bees estimate the volume by walking around the perimeter and taking short internal flights. If they crash into a sheet of foundation during the flight the box will seem smaller than it really is.
  • foundation costs money. Quite significant amounts of money if you are setting out half a dozen bait hives. Sure, they’ll use it but – like putting a new carpet into a house you’re trying to sell – it’s certainly not the deal-clincher.

No foundation for that

Rather than filling the box with about £10 worth of premium foundation, a far better idea is to use foundationless frames. Importantly these provide the bees somewhere to draw new comb whilst not reducing the apparent volume of the brood box.

If you’ve not used foundationless frames before, a bait hive is an ideal time to give them a try.

There are two things you should be on the lookout for. The first is that the bait hive is horizontal 9. Bees draw comb vertically down, so if the hive slopes there’s a good chance the comb will be drawn at an angle to the top bar.

And that’s just plain irritating … because it’s avoidable with a bit of care.

Bamboo foundationless frames

Bamboo foundationless frames

The second thing is that the colony needs checking as it starts to draw comb. Sometimes the bees ignore your helpful lollipop stick ‘starter strips’ and decide to go their own way, filling the box with cross comb.

Beautiful … but equally irritating 🙂

Final touches

For real convenience I leave my bait hives ready to move from wherever they’re sited to my quarantine apiary (I’ll deal with both these points in a second).

Wedge the frames together with a small block of expanded cell foam so that they cannot shift about when the hive is moved.

Foam block ...

Foam block …

And then strap the whole lot up tight so you can move them easily and quickly when you need to.

Bait hive location and relocation

Swarms tend to move relatively modest distances from the hives they, er, swarmed from. The initial bivouac is usually just a few metres away. The scout bees survey a wide area, certainly well over a mile in all directions. However, several studies have shown that bees generally choose to move a few hundred yards or less.

It’s therefore a good idea to have a bait hive that sort of distance from your own apiaries.

Or even tucked away in the corner of the apiary itself.

I’ve had bees move out of one box, bivouac a short distance away and then occupy a bait hive on a hive stand adjacent to the original hive.

It’s probably definitely poor form to position a bait hive a short distance from someone else’s apiary 😉

But there’s nothing stopping you putting a bait hive at the bottom of your garden or – whilst maintaining social distancing of course – in the gardens of friends and family.

If you want to move a swarm that has occupied a bait hive the usual “less than 3 feet or more than 3 miles” rule applies unless you move them within the first couple of days of arrival. Swarms have an interesting plasticity of spatial memory (which deserves a post of its own) but will have fully reorientated to the bait hive location within a few days.

So, if the bait hive is in grandma’s garden, but grandma doesn’t want bees permanently, you need to move them promptly … or move them over three miles.

Or move grandma 😉

Lucky dip

Swarms, whether dropped into a skep or attracted to a bait hive, are a bit of a lucky dip. Now and again you get a fantastic prize, but often it’s of rather low value.

The good ones are great, but even the poor ones can be used.

But there’s an additional benefit … every one that arrives self-propelled in your bait hive is one less reported to the BBKA “swarm line” or that becomes an unwelcome tenant in the eaves of a house 10.

As long as they’re healthy, even a bad tempered colony headed by a queen with a poor laying pattern, can usefully be united to create a stronger colony to exploit late season nectar.

Varroa treatment of a new swarm in a bait hive…

But they must be healthy.

Swarms will potentially have a reasonably high mite count and will probably need treating within a week of arrival in the bait hive 11. Dribbled or vaporised oxalic acid/Api-Bioxal would be my choice; it’s effective when the colony has no sealed brood 12 and requires a single treatment.

But swarms can bring even more unwelcome payloads than Varroa mites. If you keep bees in an area where foulbroods are established be extremely careful to confirm that the arriving swarm isn’t affected. This requires letting the colony rear brood while isolated in a quarantine apiary.

How do you know whether there are problems with foulbroods in your area? Register your apiary on Beebase and talk to your local bee inspector.

My bait hives go out in the second or third week of April … but I’m on the cool east coast of Scotland. When I lived in the Midlands they used to be deployed in early April. If you’re in the balmy south they should probably be out already 13.

What are you waiting for 😉 ?


 

Darwinian beekeeping

A fortnight ago I reviewed the first ten chapters of Thomas Seeley’s recent book The Lives of Bees. This is an excellent account of how honey bees survive in ‘the wild’ i.e. without help or intervention from beekeepers.

Seeley demonstrates an all-too-rare rare combination of good experimental science with exemplary communication skills.

It’s a book non-beekeepers could appreciate and in which beekeepers will find a wealth of entertaining and informative observations about their bees.

The final chapter, ‘Darwinian beekeeping’, includes an outline of practical beekeeping advice based around what Seeley (and others) understand about how colonies survive in the wild.

Differences

The chapter starts with a very brief review of about twenty differences between wild-living and managed colonies. These differences have already been introduced in the preceding chapters and so are just reiterated here to set the scene for what follows.

The differences defined by Seeley as distinguishing ‘wild’ and ‘beekeepers’ colonies cover everything from placement in the wider landscape (forage, insecticides), the immediate environment of the nest (volume, insulation), the management of the colony (none, invasive) and the parasites and pathogens to which the bees are exposed.

Some of the differences identified are somewhat contrived. For example, ‘wild’ colonies are defined fixed in a single location, whereas managed colonies may be moved to exploit alternative forage.

In reality I suspect the majority of beekeepers do not move their colonies. Whether this is right or not, Seeley presents moving colonies as a negative. He qualifies this with studies which showed reduced nectar gathering by colonies that are moved, presumably due to the bees having to learn about their new location.

However, the main reason beekeepers move colonies is to exploit abundant sources of nectar. Likewise, a static ‘wild’ colony may have to find alternative forage when a particularly good local source dries up.

If moving colonies to exploit a rich nectar source did not usually lead to increased nectar gathering it would be a pretty futile exercise.

Real differences

Of course, some of the differences are very real.

Beekeepers site colonies close together to facilitate their management. In contrast, wild colonies are naturally hundreds of metres apart 1. I’ve previously discussed the influence of colony separation and pathogen transmission 2; it’s clear that widely spaced colonies are less susceptible to drifting and robbing from adjacent hives, both processes being associated with mite and virus acquisition 3.

Abelo poly hives

50 metres? … I thought you said 50 centimetres. Can we use the next field as well?

The other very obvious difference is that wild colonies are not treated with miticides but managed colonies (generally) are. As a consequence – Seeley contends – beekeepers have interfered with the ‘arms race’ between the host and its parasites and pathogens. Effectively beekeepers have ‘weaken[ed] the natural selection for disease resistance’.

Whilst I don’t necessarily disagree with this general statement, I am not convinced that simply letting natural selection run its (usually rather brutal) course is a rational strategy.

But I’m getting ahead of myself … what is Darwinian beekeeping?

Darwinian beekeeping

Evolution is probably the most powerful force in nature. It has created all of the fantastic wealth of life forms on earth – from the tiniest viroid to to the largest living thing, Armillaria ostoyae 4. The general principles of Darwinian evolution are exquisitely simple – individuals of a species are not identical; traits are passed from generation to generation; more offspring are born than can survive; and only the survivors of the competition for resources will reproduce.

I emphasised ‘survivors of the competition’ as it’s particularly relevant to what is to follow. In terms of hosts and pathogens, you could extend this competition to include whether the host survives the pathogen (and so reproduces) or whether the pathogen replicates and spreads, but in doing so kills the host.

Remember that evolution is unpredictable and essentially directionless … we don’t know what it is likely to produce next.

Seeley doesn’t provide a precise definition of Darwinian beekeeping (which he also terms natural, apicentric or beefriendly beekeeping). However, it’s basically the management of colonies in a manner that more closely resembles how colonies live in the wild.

This is presumably unnnatural beekeeping

In doing so, he claims that colonies will have ‘less stressful and therefore more healthful’ lives.

I’ll come back to this point at the end. It’s an important one. But first, what does Darwinian mean in terms of practical beekeeping?

Practical Darwinian beekeeping

Having highlighted the differences between wild and managed colonies you won’t be surprised to learn that Darwinian beekeeping means some 5 or all of the following: 6

  • Keep locally adapted bees – eminently sensible and for which there is increasing evidence of the benefits.
  • Space colonies widely (30-50+ metres) – which presumably causes urban beekeepers significant problems.
  • Site colonies in an area with good natural forage that is not chemically treated – see above.
  • Use small hives with just one brood box and one super – although not explained, this will encourage swarming.
  • Consider locating hives high off the ground – in fairness Seeley doesn’t push this one strongly, but I could imagine beekeepers being considered for a Darwin Award if sufficient care wasn’t taken.
  • Allow lots of drone brood – this occurs naturally when using foundationless frames.
  • Use splits and the emergency queen response for queen rearing i.e. allow the colony to choose larvae for the preparation of new queens – I’ve discussed splits several times and have recently posted on the interesting observation that colonies choose very rare patrilines for queens.
  • Refrain from treating with miticides – this is the biggy. Do not treat colonies. Instead kill any colonies with very high mite levels to prevent them infesting other nearby colonies as they collapse and are robbed out.

Good and not so good advice

A lot of what Seeley recommends is very sound advice. Again, I’m not going to paraphrase his hard work – you should buy the book and make your own mind up.

Sourcing local bees, using splits to make increase, housing bees in well insulated hives etc. all works very well.

High altitude bait hive …

Some of the advice is probably impractical, like the siting of hives 50 metres apart. A full round of inspections in my research apiary already takes a long time without having to walk a kilometre to the furthest hive.

The prospect of inspecting hives situated at altitude is also not appealing. Negotiating stairs with heavy supers is bad enough. In my travels I’ve met beekeepers keeping hives on shed roofs, accessed by a wobbly step ladder. An accident waiting to happen?

And finally, I think the advice to use small hives and to cull mite-infested colonies is poor. I understand the logic behind both suggestions but, for different reasons, think they are likely to be to the significant detriment of bees, bee health and beekeeping.

Let’s deal with them individually.

Small hives – one brood and one super

When colonies run out of space for the queen to lay they are likely to swarm. The Darwinian beekeeping proposed by Seeley appears to exclude any form of swarm prevention strategy. Hive manipulation is minimal and queens are not clipped.

They’ll run out of space and swarm.

Even my darkest, least prolific colonies need more space than the ~60 litres offered by a brood and super.

Seeley doesn’t actually say ‘allow them to swarm’, but it’s an inevitability of the management and space available. Of course, the reason he encourages it is (partly – there are other reasons) to shed the 35% of mites and to give an enforced brood break to the original colony as it requeens.

These are untreated colonies. At least when starting the selection strategy implicit in Darwinian beekeeping these are likely to have a very significant level of mite infestation.

These mites, when the colony swarms, disappear over the fence with the swarm. If the swarm survives long enough to establish a new nest it will potentially act as a source of mites far and wide (through drifting and robbing, and possibly – though it’s unlikely as it will probably die – when it subsequently swarms).

A small swarm

A small swarm … possibly riddled with mites

Thanks a lot!

Lost swarms – and the assumption is that many are ‘lost’ – choose all sorts of awkward locations to establish a new nest site. Sure, some may end up in hollow trees, but many cause a nuisance to non-beekeepers and additional work for the beekeepers asked to recover them.

In my view allowing uncontrolled swarming of untreated colonies is irresponsible. It is to the detriment of the health of bees locally and to beekeepers and beekeeping.

Kill heavily mite infested colonies

How many beekeepers reading this have deliberately killed an entire colony? Probably not many. It’s a distressing thing to have to do for anyone who cares about bees.

The logic behind the suggestion goes like this. The colony is heavily mite infested because it has not developed resistance (or tolerance). If it is allowed to collapse it will be robbed out by neighbouring colonies, spreading the mites far and wide. Therefore, tough love is needed. Time for the petrol, soapy water, insecticide or whatever your choice of colony culling treatment.

In fairness to Seeley he also suggests that you could requeen with known mite-resistant/tolerant stock.

But most beekeepers tempted by Darwinian ‘treatment free’ natural beekeeping will not have a queen bank stuffed with known mite-resistant mated queens ‘ready to go’.

But they also won’t have the ‘courage’ to kill the colony.

They’ll procrastinate, they’ll prevaricate.

Eventually they’ll either decide that shaking the colony out is OK and a ‘kinder thing to do’ … or the colony will get robbed out before they act and carpet bomb every strong colony for a mile around.

Killing the colony, shaking it out or letting it get robbed out have the same overall impact on the mite-infested colony, but only slaying them prevents the mites from being spread far and wide.

And, believe me, killing a colony is a distressing thing to do if you care about bees.

In my view beefriendly beekeeping should not involve slaughtering the colony.

Less stress and better health

This is the goal of Darwinian beekeeping. It is a direct quote from final chapter of the book (pp286).

The suggestion is that unnatural beekeeping – swarm prevention and control, mite management, harvesting honey (or beekeeping as some people call it 😉 ) – stresses the bees.

And that this stress is detrimental for the health of the bees.

I’m not sure there’s any evidence that this is the case.

How do we measure stress in bees? Actually, there are suggested ways to measure stress in bees, but I’m not sure anyone has systematically developed these experimentally and compared the stress levels of wild-living and managed colonies.

I’ll explore this topic a bit more in the future.

I do know how to measure bee health … at least in terms of the parasites and pathogens they carry. I also know that there have been comparative studies of managed and feral colonies.

Unsurprisingly for an unapologetic unnatural beekeeper like me ( 😉 ), the feral colonies had higher levels of parasites and pathogens (Catherine Thompson’s PhD thesis [PDF] and Thompson et al., 2014 Parasite Pressures on Feral Honey Bees). By any measurable definition these feral colonies were less healthy.

Less stress and better health sounds good, but I’m not actually sure it’s particularly meaningful.

I’ll wrap up with two closing thoughts.

One of the characteristics of a healthy and unstressed population is that it is numerous, productive and reproduces well. These are all characteristics of strong and well-managed colonies.

Finally, persistently elevated levels of pathogens are detrimental to the individual and the population. It’s one of the reasons we vaccinate … which will be a big part of the post next week.


 

Which is the best … ?

It’s (slowly) approaching the start of the beekeeping season.

From draughty church halls across the land newly trained beekeepers are emerging (or eclosing, to use the correct term), blurry-eyed from studying their Thorne’s catalogues, desperate to get their hands on some bees and start their weekly inspections.

Their enthusiasm is palpable 1.

The start of the beekeeping season, any season, after the long winter is always a good time. Longer days, better weather, more light 🙂 . For current beekeepers we can stop fretting over stores or winter losses. The long days with plentiful forage are getting nearer. We’ll soon be doing inspections in our shirtsleeves and thinking about swarm prevention.

New beekeepers, those who haven’t had to worry about Storm Ciara wrecking their apiaries or subsequent flooding washing hives away, simply want to get started as soon as possible.

Moving to higher ground ...

Moving to higher ground …

But, of course, they want to do things properly.

They don’t want to cut corners, they don’t want to skimp or make false economies. They want the best for their (as yet, non-existent) bees.

They’re committed and serious and determined to make a success of beekeeping … and get a great honey crop.

It needs to be great as they’ve already ‘promised away’ half of it to friends and family 🙂

Which is the best …?

If you look on the online beekeeping discussion fora, or questions to the BBKA Q&A monthly column or listen to discussions at local association meetings, many start with the words “Which is the best …”.

Which is the best hive, the best strain of bees, the best fuel for your smoker etc.

These questions reflect a couple of things:

  1. A lack of experience coupled with an enthusiasm to properly care for their charges.
  2. The generally misguided belief that these things make any substantive difference to the welfare or productivity of the bees.

Neither of these are criticisms.

All beekeepers should want the best for their bees.

Inexperienced beekeepers don’t know what works and what does not work, but they want to ensure that – whatever they do – the bees do not suffer (or fail to thrive).

They want the best bees, presumably defined as those that are calm, frugal, populous and productive and they want the best hive so these bees are warm enough in winter and cool enough in summer, or have enough space, or are easiest to manipulate, or best resembles a tree trunk.

And the smoker fuel should be the best so that it’s easy to light, never goes out and calms the bees quickly.

The best smoker fuel

Logic dictates that if there was a ‘best’ smoker fuel then almost everyone would be using it.

The septuagenarian ‘expert’ with 50 years experience would have said “Stuff your smoker with XYZ” when describing hive inspections on the beginners course. Other experienced beekeepers around the room would nod sagely and that would be the end of the matter.

If a beginner were to ask “Why don’t you use hessian rather than XYZ?” over a cuppa and a digestive afterwards there would be an awkward silence and a simple “Because XYZ is the best smoker fuel you can use” response.

The group would then move on to talk about something else.

Fuel bucket

XYZ …

And that happens … precisely never.

What actually happens is that eight beekeepers (with varying levels of expertise) contribute eleven different opinions of their personal view of the ‘best’ smoker fuel.

The only thing vaguely in common in these opinions is that some of the recommended fuels burn.

Note that I said ‘some’ 😉

The point I’m trying to make is that the ‘best’ smoker fuel does not exist. It’s what works for you when you need it … dried horse manure (yes, really), grass, wood chips, Thorne’s cardboard packaging, rotten dried wood etc.

It’s what’s in your bag, it’s what you carefully collected last month, it’s what you find in the car glove compartment when you can’t find anything else.

If it burns – ideally slowly and gently – producing good amounts of smoke, if it’s easy to light, light to carry, stays lit and is available when you need it, it’ll do.

The best hive

I’ve previously discussed the ridiculously wide range of hives and frames available to UK beekeepers.

Knowing that, or spending just half an hour perusing the Thorne’s catalogue, shows that there is clearly no ‘best’ hive. Any, and probably all, of the hives work perfectly satisfactorily. In the right conditions and with sympathetic and careful beekeeping all are capable of housing a colony securely and productively.

It’s the hive type that is compatible with those used by your mentor 2, it’s the type you have a stack of in the corner of the shed, it’s what you can borrow at short notice when you’ve run out of broods or supers.

It’s what’s available in the end of season sales or it’s what you started with (or your mother started with) and it ‘just works’.

If there was a best hive type, or hive tool or smoker fuel the Thorne’s catalogue would be about 3 pages long.

It’s not, it’s approaching 100 pages in length, with 12 pages of hive types alone (including a nice looking Layens hive). The 2020 catalogue has even more hive tools than the seventeen I counted in 2019 🙁

If there’s no ‘best’, will anything do?

Just because there might not be the perfect hive, smoker fuel or hive tool does not mean that it doesn’t matter what you use.

There are some that are unsuitable.

Smoker fuel that doesn’t stay lit, or that burns too fiercely. Hive tools with blunt edges, or that rust badly and are difficult to sterilise, or that bend 3. Hives with incorrect dimensions, ill-fitting floors, overly fussy designs or a host of other undesirable ‘features’.

Just because there’s no single best whatever definitely does not mean that anything will do.

Anthropocentrism

But, before we move on, note that all the things I used to define a smoker fuel or hive as ‘the best’ were anthropocentric 4 criteria.

It’s what suits us as beekeepers.

And, since there are a wide range of beekeepers (by education, age, height, intellect, shoe size, strength, wealth, petty likes and dislikes etc.) there is inevitably a very wide choice of stuff for beekeeping.

Which also emphasises the irrelevance of the ‘best type of ‘ question.

The full version of the question is “Which is the best type of hive tool for beekeepers” 5.

But what’s best for the bees?

None, or any, of the above.

Clearly no single hive tool is better than any other as far as the bees are concerned.

Take your pick ...

The bees do not care …

Likewise, as long as the smoker fuel generates cool, not-too-acrid, smoke, as far as the bees are concerned it’s just smoke. It masks the smell of the alarm pheromones and encourages the bees to gorge on honey, so they remain calm. Used judiciously, which is nothing to do with the fuel and everything to do with the beekeeper, one type of smoker fuel should be as good as any other.

And the same thing applies to hives. Assuming they’re secure, wind and watertight, large enough to fill with stores, have a defendable entrance and proper bee space around the frames, they’ll suit the bees perfectly well.

Think about the trees that wild-living bees naturally choose … do they prefer oak or lime, tall chimney-like cavities or largely spherical hollows?

Oak … preferred by bees. Or not.

Do they do better in one species of tree over another, one shape of space over another?

No.

Doing better …

How do we tell if the bees are ‘doing better’ anyway?

We can’t ask them.

We cannot, despite the assurances of the so-called bee-centric or bee-friendly beekeepers, tell whether they’re happy or not.

I’m a very bee-friendly beekeeper, but I don’t anthropomorphize and attribute feelings like happy or sad to my bees 6.

I determine whether a colony is doing well (or better) by very similar criteria to those you would use to judge whether a colony in a tree was flourishing.

Are they building up well, are they storing sufficient pollen and honey stores, is there overt disease, are they going to swarm?

The hive tool, smoker fuel or any one of a dozen or more hive types, have little or no influence on these measurable definitions of ‘doing well’.

What is it that determines the success or otherwise of a colony?

Essentially it comes down to two things – forage and colony health.

Bees ‘do well’ when they have ample and varied forage and when they are (largely) free of disease 7.

A healthy colony with ample forage will do better irrespective of the hive tool, hive type or smoker fuel used. You could house them in a plastic dustbin, prize the lid off with a screwdriver and waft a smouldering egg box across the entrance and they’ll still ‘do well’.

Egg box smoker

Smouldering egg box …

Conversely, put a disease-weakened colony in an area of poor forage and they’ll do badly (probably very badly) … again irrespective of the hive type, tool or smoker fuel.

Good forage does not just mean lots of it (though that helps). It means early-season pollen for colony build-up, it means late-season nectar and pollen to help develop a strong population of winter bees, it means a varied diet and it means season-long availability.

A healthy colony is one that has no overt disease. It has low levels of parasites and pathogens 8 and is able to survive periods of nectar shortages without succumbing to disease. In addition, it is resilient and genetically diverse.

And so back to those eclosing trainee beekeepers … the real ‘best’ questions they should be asking are:

  • Where is the best place to site my colonies to ensure good, season-long forage availability?
  • How to I best keep my colonies as disease-free as possible so that they can exploit that forage?

Focusing on these questions will help ensure the honey crop really is great so you can provide all those friends and family with the jars they have been promised 😉

Exceptions to the above

Inevitably there are exceptions.

It wouldn’t be beekeeping without qualifications and caveats.

The best bees are almost certainly local bees. There are several studies that demonstrate locally-adapted bees do better than imported bees. This does not mean that imported (and not necessarily from abroad) bees cannot do well. I’ve discussed some of these studies recently.

Finally, whilst the smoker fuel is irrelevant, the smoker is not.

The best smoker is the large Dadant smoker. The small Dadant is pretty good, but the large one is the bee’s knees 9.

Large Dadant smoker

I know, because my happy bees told me so 🙂