Category Archives: Science

Strong hives = live hives

Science and beekeeping make for interesting contrasts and can be awkward bedfellows 1.

Science is based upon observation of tested single variables. multiple repeats and statistical analysis. It builds on what has gone before but has accepted processes to challenge well-established theories. Some of the greatest advances are made by young researchers willing to test – and subsequently overturn – established dogma.

Over the last three generations science – both how we do it and what we understand – has changed almost beyond recognition.

In contrast, beekeeping is steeped in history, has multiple variables – climate, forage, ability – and very small sample sizes. It tends to be taught by the most experienced, passing down established – though often not rigorously tested 🙁 – methods 2.

As a consequence our beekeeping has barely changed over the last three decades. Established dogma tends to stay established.

Local bees are better adapted to local conditions

So let’s look in a little more detail at one of these established ‘facts’ … that locally reared bees are better adapted to local conditions.

The suggestion here is that locally reared bees, because they’re ‘better adapted’ (whatever that means) are more likely to flourish when the going is good, and more likely to survive when the going gets tough.

Furthermore, the implication is that they’re more likely to do better in that environment than bees reared elsewhere (and that are therefore adapted to a different environment).

This sounds like common sense.

Locally bred queen ...

Locally bred queen …

As Brexit looms and the never-ending supply of early-season Greek or Slovenian queens disappears perhaps it’s also fortunate, rather than just being common sense.

But, as a scientist, I’ve spent a career questioning things.

Every time I read the “locally adapted bees survive better (or perform better, or whatever better)” 3 two questions pop into my head …

  1. What’s local?
  2. How did they prove – or how would I test – this?

Spoiler alert

There is evidence that local bees show adaptive changes to their local environment. There is also evidence that local bees do better in their local environment.

Formally, I don’t think scientists have demonstrated that the former explains the latter. This might seem trivial, but it does mean that our understanding is still incomplete.

However, I’m not going to discuss any of these things today – but I will in the future.

Instead I’m going to deal with those two questions that pop into my head.

If we tackle those I think we’ll be better placed to address that dogmatic statement that local bees are better adapted to local conditions in due course.

But perhaps we’ll first discover that other things are more important?

What’s local?

I live most of the time in central Fife. It’s a reasonably dry, relatively cool, largely arable part of the UK with a beekeeping season that lasts about 5 months (from first to last inspections).

Are my (fabulous 😉 ) locally bred queens adapted for central Fife, or the east of Scotland, or perhaps north-west maritime Europe, or Europe?

Where have all my young girls gone?

What a beauty

Would these locally adapted bees do better here (in Fife) than bees raised in the foothills of the Cairngorms, or the Midlands, or Devon or East Anglia … or Portugal?

If you measure the environment you’ll find there’s significant overlap in terms of the climate, the temperature, the forage, the day length (or a hundred other determinants) with other regions of the UK.

The temperature or rainfall extremes we experience in central Fife aren’t significantly different to those in the Midlands. The season duration is different (because of latitude), but I had lots of short seasons in the Midlands due to cool springs and early autumns.

Local is an ill-defined and subjective term.

But there are differences of course. Are Ardnamurchan bees better able to cope with the rain (and the fantastic scenery) than Fife bees? Are Fife bees better able to exploit arable crops than those foraging on the heather and Atlantic rainforests that cloak the hills in the far west of Scotland?

I don’t know 🙁

And there’s something else I don’t know

I also don’t know how I would meaningfully test this.

Just thinking about these types of experiments makes me nervous. Think of the year to year variation – in weather, forage etc. – compounded by the hive to hive variation.

Then multiply that by the variation between beekeepers.

This last one is a biggy. Two beekeepers of differing abilities will experience very different levels of success – quantified in terms of honey yield or hives that survive for example – in the same season and environment.

Doing a study large enough to be statistically relevant without having such enormous variation that the results are essentially meaningless is tricky.

What a nightmare.

Which, in a roundabout way, brings me to a paper earlier this year by Maryann Frazier and Christina Grozinger from Penn State University.

Ask the question in a different way

The title of the paper tells you most of what you need to know about the study.

Colony size, rather than geographic origin of stocks, predicts overwintering success in honey bees (Hymenoptera: Apidae) in the northeastern United States. 4

But don’t stop reading … let’s look in a bit more detail at what they did.

They approached the question (that local bees are better adapted) from a slightly different angle.

Essentially the question they asked was “Does the geographic origin of the bees influence the overwintering survival of bees in a temperate region?”

This question is easier to answer.

They defined the parameters of the experiment a bit more clearly. For example:

  • Rather than looking at several regions they just studied bees in one area  – Pennsylvania (the temperate region in the title of the paper).
  • The bees came from four sources; two were from a hot geographic region of the USA and two from a cold region.
  • They scored ‘doing better’ only in terms of overwintering survival.

By simplifying the question they could reduce some of the variables. They could therefore increase the quantification of the parameters (colony weight, strength/size etc.) that might influence the ‘doing better’.

And in doing so, they came up with an answer.

The study

Sixty colonies were established in three apiaries in Pennsylvania. Two of the apiaries (A & B) were within 1 mile of each other, with the third (C) about 15 miles away. Colonies were generally established from packages 5, to which a queen was introduced from one of four different queen breeders.

Two of the queen breeders were from southern USA (Texas or Florida) and two from northern USA (Vermont and West Virginia 6.

The authors used microsatellite analysis to confirm that the queens – after introduction – headed genetically distinct colonies by midsummer 7.

So far, so good …

They then used standard beekeeping methods to manage the colonies – regular inspections, Varroa treatments as appropriate, feeding them up for winter etc.

They scored colonies for a variety of ‘parameters’; net weight, frames of brood, adult bees and stores.

Four queens failed before winter.

And then they overwintered the remaining 56 colonies …

The results

… of which only 39 survived until April 🙁

39/56 sounds a pretty catastrophic loss to me but it’s actually about the same (~30%) as the average winter losses reported each year in the USA.

So, did the ‘cold-adapted’ 8 Vermont queens survive and prosper? Did the ‘Southern Belles’ 9 from Texas all perish in the cold Pennsylvanian winter?

No.

That’s no to both questions.

There was no significant difference in survival of colonies headed by queens from the north or the south.

The geographic ‘origin’ of the bees did not determine colony survival.

They may have been ‘locally adapted’ (to Vermont, or Texas or wherever) and they were certainly genetically distinct, but it made no difference to whether the colony perished or not in Pennsylvania.

So if the source of the queen didn’t influence things, what did?

Weighty matters

This is the key figure from the paper.

Overwintering success is significantly associated with colony weight.

The heavier a colony was in October, the more likely that the colony survived until April.

The left hand panel shows the probability of a colony surviving (vertical axis, solid line) plotted against the net weight of the colony.

Below about 30 kg colony survival dropped significantly.

The right hand panel shows that net weight alone was not the only determinant. This plots colonies ranked by weight (vertical axis) and indicates whether they survived or not. An underweight (i.e. under 30 kg) colony in apiary C was much more likely to survive than a similar weight colony from the other two apiaries.

Allee, Allee 10

The heavier the colony, the greater the chance it survived. Furthermore, it wasn’t simply the amount of stores available.

Heavier colonies were also larger colonies.

This indicates a so-called Allee effect 11 which is a positive correlation between population density and individual fitness.

This has been shown before for honey bees (and other social insects). For bees we know that the larger the winter cluster the better they are able to maintain the correct overwintering temperature. These large clusters show lower per capita honey consumption to maintain the same temperature when compared to small clusters.

However, in addition to not running out of stores (due to more frugal usage) 12, large colonies will also be better able to rear brood in early spring … ‘it takes bees to make bees’.

Taken together these results demonstrate that colony size and weight, rather than geographic adaptation, is probably the most important determinant of overwintering colony survival.

Disease interlude

These studies were conducted in 2013 (and published in 2019 … a feature of some of my science 🙁 ). In the previous year the authors set up a similar study but did not manage Varroa levels.

Under these conditions only 12% of the colonies survived.

There’s a lesson there I think 😉

This disastrous 2012 study used the same queen breeders to source their queens (from Texas, Florida, West Virgina and Vermont). Some of these queens were described and sold as ‘Varroa-resistant’.

There was no difference in survival (or, more accurately, death) rates between colonies headed by queens described as ‘Varroa-resistant’ or not.

Another lesson perhaps?

Is there a geographic component to Varroa-resistance? Are Varroa-resistant Vermont colonies only actually resistant to mites from Vermont?

Or their viruses? 13

OK, we’re getting distracted … let’s return to apiary C.

Forage diversity and abundance is also important

Colonies in apiary C survived better at lower overall net weights than colonies from other apiaries. In addition, average colony weights were higher in apiary C than in the other two apiaries.

Apiary location significantly affected colony weight and survival.

And the abundance and range of nectar sources was significantly different between the three apiaries used in this study, with colonies from apiary C – located in a less forested and more agricultural area – surviving better.

The proportion of land cover/land use types surrounding apiaries.

The authors suggest that the forage diversity and abundance around apiary C increased the size of the colonies (by boosting brood rearing, adult longevity and colony growth) and that it was this larger adult population, rather than colony weight per se, that was important.

Are we getting the message?

This is the second time in a month that I’ve discussed the importance of strong colonies.

A few weeks ago I discussed how strong colonies are more profitable because they generate a surplus of honey or bees, both of which are valuable.

In this post I show that the primary determinant of overwintering success is the strength and weight of the colony. The source of the queen – whether from the balmy south or the frosty north – had no significant influence on colony survival.

This doesn’t mean local bees aren’t better adapted to local conditions. That wasn’t what was being tested.

However, it does suggest that other things that may be as important, or perhaps more important.

The take home message from this study is keep strong colonies in a forage-rich environment.

In a future post I’ll discuss the evidence that local bees are better adapted … and I’ll make the suggestion that some of these adaptations might be explained because the local genotype actually produces stronger colonies 😉


Note

This was originally published with the title Correlates of winter survival on 8/11/2019 but a hamster running amok in the server meant that the email to those registered to receive announcements of new posts was never sent. Rather than let the post disappear into digital oblivion – as the take home message is an important one – I’m re-posting it again.

With apologies to those who read the original …

Spotty brood ≠ failing queen

I thought I’d discuss real beekeeping this week, rather than struggle with the high finance of honey sales or grapple with the monetary or health consequences of leaving supers on the hive.

After all, the autumn equinox has been and gone and most of us won’t see bees for several months 🙁

We need a reminder of what we’re missing.

Beekeeping provides lots of sensory pleasures – the smell of propolis on your fingers, the taste of honey when extracting, the sound of a full hive ‘humming’ as it dries stored nectar … and the sight of a frame packed, wall-to-wall, with sealed brood.

Brood frame with a good laying pattern

This is a sight welcomed by all beekeepers.

Nearly every cell within the laid up part of the frame is capped. All must therefore have been laid within ~12 days of each other (because that’s the length of time a worker cell is capped for).

However, the queen usually lays in concentric rings from the middle of the frame. Therefore, if you gently uncap a cell every inch or so from the centre of the frame outwards, you’ll see the oldest brood is in the centre and the most recently capped is at the periphery.

It’s even more reassuring if the age difference between the oldest and the youngest pupae is significantly less than 12 days. Hint … look at the eye development and colouration.

This shows that the queen was sufficiently fecund to lay up the entire frame in just a few days.

What are these lines of empty cells?

But sometimes, particularly on newly drawn comb, you’ll see lines of cells which the queen has studiously avoided laying up.

That'll do nicely

That’ll do nicely …

It’s pretty obvious that these are the supporting wires for the sheet of foundation. Until the frame has been used for a few brood cycles these cells are often avoided.

I don’t know why.

It doesn’t seem to be that the wire is exposed at the closed end of the cell. I suspect that either the workers don’t ‘prepare’ the cell properly for the queen – because they can detect something odd about the cell – or the queen can tell that there’s something awry.

However, after a few brood cycles it’s business as usual and the entire frame is used.

Good laying pattern ...

Good laying pattern …

All of these laid up frames contain a few apparently empty cells. There are perhaps four reasons why these exist:

  • Workers failed to prepare the cell properly for the queen to lay in
  • The queen simply failed to lay an egg in the cell
  • An egg was laid but it failed to hatch
  • The egg hatched but the larvae perished

Actually, there’s a fifth … the cell may have been missed (for whatever reason) but the queen laid in it later and so it now contains a developing larva, yet to be capped.

What are all these empty cells?

But sometimes a brood frame looks very different.

Worker brood 1 is present across the entire frame but there are a very large number of missed cells.

Patchy brood pattern

Patchy brood & QC’s …

Note: Ignore the queen cells on this frame! It was the only one I could find with a poor brood pattern.

This type of patchy or spotty brood pattern is often taken as a sign of a failing queen.

Perhaps she’s poorly mated and many of the eggs are unfertilised (but they should develop into drone brood)?

Maybe she or the brood are diseased, either reducing her fecundity or the survival and development of the larvae?

Sometimes spotty brood is taken as a sign of inbreeding or poor queen mating.

Whatever the cause, colonies producing frames like that shown above are clearly going to be less strong than those towards the top of the page 2.

So, if the queen is failing, it’s time to requeen the colony …

Right?

Perhaps, perhaps not …

Which brings me to an interesting paper published by Marla Spivak and colleagues published in Insects earlier this year 3.

This was a very simple and straightfoward study. There were three objectives, which were to:

  • Determine if brood pattern was a reliable indicator of queen quality
  • Identify colony-level measures associated with poor brood pattern colonies
  • Examine the change in brood pattern after queens were exchanged into a colony with the opposite brood pattern (e.g. move a ‘failing queen’ into a colony with a good brood pattern)

If you are squeamish look away now.

Inevitably, measuring some of the variables relating to queen quality and mating success involve sacrificing the queen, dissecting her and counting ‘stuff’ … like viable sperm in the spermathecae.

Unpleasant, particularly for the queen(s) in question, but a necessary part of the study.

However, in the long run it might save some queens, so it may have been a worthwhile sacrifice … so, on with the story.

Queen-level variables in ‘good’ and ‘poor’ queens

By queen level variables I mean things about the queen that could be measured – and that differ – between queens with a good laying pattern or a poor laying pattern.

Surprisingly, good and poor queens were essentially indistinguishable in terms of sperm counts, sperm viability, body size or weight.

Poor queens i.e. those generating a spotty brood pattern, weren’t small queens, or poorly mated queens. They were also not more likely to have fewer than 3 million sperm in the spermathecae (a threshold for poorly mated queens in earlier studies).

Furthermore, the queens had no statistical differences in pathogen presence or load (i.e. amount), including viruses (DWV, Lake Sinai Virus, IAPV or BQCV), Nosema or trypanosomes (Crithidia). 

Hmmm … puzzling.

Colony-level variables

So if the queens did not differ, perhaps colonies with spotty brood patterns had other characteristics that distinguished them from colonies with good brood patterns?

Spivak and colleagues measured pathogen presence and amount in both the good-brood and poor-brood colonies.

Again, no statistical differences.

So what happens when queens laying poor-brood patterns are put into a good-brood pattern hive?

And vice versa …

Queen exchange studies

This was the most striking part of the study. The scientists exchanged queens between colonies with poor-brood and good-brood and then monitored the change in quality of the brood pattern 4.

Importantly, they monitored brood quality 21 days after queen exchange. I’ll return to this shortly.

Changes in sealed brood pattern after queen exchange

Queen from good-brood colonies showed a slight decrease in brood pattern quality (but not so much that they’d be considered to now generate poor brood patterns).

However, surprisingly, queens from poor-brood colonies exhibited a greater improvement in brood quality (+11.6% ± 9.9% more sealed cells) than the loss observed in the reverse exchange (-8.0% ± 10.9% fewer sealed cells).

These results indicate that the colony environment has a statistically significant impact on the sealed brood pattern.

Admittedly, a 10-20% increase (improvement) in the sealed brood pattern on the last frame photograph (above) might still not qualify as a ‘good brood pattern’ queen, but it would certainly be an improvement.

Matched and mismatched workers

Since exchanged queens were monitored just 21 days after moving them all the workers in the receiving hive were laid – and so genetically related to – the previous queen.

The authors acknowledge this and comment that it would be interesting to extend the period until surveying the hive to see if ‘matched’ workers reverted to the poor brood pattern (assuming that was what the queen originally laid).

This and a host of other questions remain unanswered and will undoubtedly form the basis of future studies.

The authors conclude that “Brood pattern alone was an insufficient proxy of queen quality. In future studies, it is important to define the specific symptoms of queen failure being studied in order to address issues in queen health.”

Notwithstanding the improvements seen in some brood patterns I suspect they would be insufficient to justify not replacing an underperforming queen … when considering the issue as a practical beekeeper i.e. there may be improvements but they were much less than could be achieved by replacing the queen from a known and reliable source.

But it might be worth thinking twice about this …

Insufficient storage space

In closing it’s worth noting that I’ve seen spotty or incomplete brood patterns when there’s a very strong nectar flow on and the colony is short of super storage space.

Under these conditions the bees start to backfill the brood box, taking up cells that the queen would lay in.

Usually this is resolved just by adding another super or two.

If there remains any doubt (about the queen) and you’ve provided more supers you can determine the quality of the laying pattern by putting a new frame of drawn comb into the brood nest.

The queen should lay this up in a day or two if she’s “firing on all cylinders”.

In which case, definitely keep her 🙂


 

Crime doesn’t pay

At least, sometimes it doesn’t.

In particular, the crime of robbery can have unintended and catastrophic consequences.

The Varroa mite was introduced to England in 1992. Since then it has spread throughout most of the UK.

Inevitably some of this spread has been through the activities of beekeepers physically relocating colonies from one site to another.

However, it is also very clear that mites can move from colony to colony through one or more routes.

Last week I described the indirect transmission of a mite ‘left’ by one bee on something in the environment – like a flower – and how it could climb onto the back of another passing bee from a different colony.

Mite transmission routes

As a consequence colony to colony transmission could occur. Remember that a single mite (assuming she is a mated female, which are the only type of phoretic mites) is sufficient to infest a mite-free hive.

However, this indirect route is unlikely to be very efficient. It depends upon a range of rather infrequent or inefficient events 1. In fact, I’m unaware of any formal proof that this mechanism is of any real relevance in inter-hive transmission.

Just because it could happened does not mean it does happen … and just because it does happen doesn’t mean it’s a significant route for mite transmission.

This week we’ll look at the direct transmission routes of drifting and robbing. This is timely as:

  • The early autumn (i.e. now) is the most important time of year for direct transmission.
  • Thomas Seeley has recently published a comparative study of the two processes 2. As usual it is a simple and rather elegant set of experiments based upon clear hypotheses.

Studying phoretic mite transmission routes

There have been several previous studies of mite transmission.

Usually these involve a ‘bait’ or ‘acceptor’ hive that is continuously treated with miticides. Once the initial mite infestation is cleared any new dead mites appearing on the tray underneath the open mesh floor must have been introduced from outside the hive.

All perfectly logical and a satisfactory way of studying mite acquisition.

However, this is not a practical way of distinguishing between mites acquired passively through drifting, with those acquired actively by robbing.

  • Drifting being the process by which bees originating from other (donor) hives arrive at and enter the acceptor hive.
  • Robbing being the process by which bees from the acceptor hive force entry into a donor hive to steal stores.

To achieve this Peck and Seeley established a donor apiary containing three heavily mite-infested hives of yellow bees (headed by Italian queens). These are labelled MDC (mite donor ccolony) A, B and C in the figure below. This apiary was situated in a largely bee-free area.

They then introduced six mite-free receptor colonies (MRC) to the area. Three were located to the east of the donor hives, at 0.5m, 50m and 300m distance. Three more were located – at the same distances – to the west of the donor apiary. These hives contained dark-coloured bees headed by Carniolan queens.

Apiary setup containing mite donor colonies (MDR) and location of mite receptor colonies (MRC).

Peck and Seeley monitored mite acquisition by the acceptor hives over time, fighting and robbing dynamics, drifting workers (and drones) and colony survival.

Test a simple hypothesis

The underlying hypothesis on the relative importance of robbing or drifting for mite acquisition was this:

If drifting is the primary mechanism of mite transmission you would expect to see a gradual increase of mites in acceptor colonies. Since it is mainly bees on orientation flights that drift (and assuming the egg laying rate of the queen is constant) this gradual acquisition of motes would be expected to occur at a constant rate.

Conversely, if robbing is the primary mechanism of mite transmission from mite-infested to mite-free colonies you would expect to see a sudden increase in mite number in the acceptor hives. This would coincide with the onset of robbing.

Graphically this could (at enormous personal expense and sacrifice) be represented like this.

Mite acquisition by drifting (dashed line) or robbing (solid line) over time (t) – hypothesis.

X indicates the time at which the mite-free acceptor colonies are introduced to the environment containing the mite-riddled donor hives.

These studies were conducted in late summer/early autumn at Ithaca in New York State (latitude 42° N). The MDC’s were established with high mite loads (1-3 mites/300 bees in mid-May) and moved to the donor apiary in mid-August. At the same time the MRC’s were moved to their experimental locations. Colonies were then monitored throughout the autumn (fall) and into the winter.

So what happened?

Simplistically, the three mite donor colonies (MDC … remember?) all collapsed and died between early October and early November. In addition, by mid-February the following year four of the six MRC’s had also died.

In every case, colony death was attributed to mites and mite-transmitted viruses. For example, there was no evidence for starvation, queen failure or moisture damage.

But ‘counting the corpses‘ doesn’t tell us anything about how the mites were acquired by the acceptor colonies, or whether worker drifting and/or robbing was implicated. For this we need to look in more detail at the results.

Mite counts

Mite counts in donor (A) and receptor (B, C) colonies.

There’s a lot of detail in this figure. In donor colonies (A, top panel) phoretic mite counts increased through August and September, dropping precipitously from mid/late September.

This drop neatly coincided with the onset of fighting at colony entrances (black dotted and dashed vertical lines). The fact that yellow and black bees were fighting is clear evidence that these donor colonies were being robbed, with the robbing intensity peaking at the end of September (black dashed line). I’ll return to robbing below.

In the receptor colonies the significant increase in mite numbers (B and C) coincided with a) the onset of robbing and b) the drop in mite numbers in the donor colonies.

Phoretic mite numbers in receptor colonies then dropped to intermediate levels in October before rising again towards the end of the year.

The authors do loads of statistical analysis – one-way ANOVA’s, post-hoc Wilcoxon Signed-Rank tests and all the rest 3 and the data, despite involving relatively small numbers of colonies and observations, is pretty compelling.

Robbery

So this looks like robbing is the route by which mites are transmitted.

A policeman would still want to demonstrate the criminal was at the scene of the crime.

Just because the robbing bees were dark doesn’t ‘prove’ they were the Carniolans from the MRC’s 4. Peck and Seeley used a 400+ year old ‘trick’ to investigate this.

To identify the source of the robbers the authors dusted all the bees at the hive entrance with powdered sugar. They did this on a day of intense robbing and then monitored the hive entrances of the MRC’s. When tested, 1-2% of the returning bees had evidence of sugar dusting.

Returning robbers were identified at all the MRC’s. Numbers (percentages) were small, but there appeared to be no significant differences between nearby and distant MRC’s..

Drifting workers and drones

The evidence above suggests that robbing is a major cause of mite acquisition during the autumn.

However, it does not exclude drifting from also contributing to the process. Since the bees in the MDC and MRC were different colours this could also be monitored.

Yellow bees recorded at the entrances of the dark bee mite receptor colonies.

Before the onset of significant robbing (mid-September) relatively few yellow bees had drifted to the mite receptor colonies (~1-2% of bees at the entrances of the MRC’s). The intense robbing in late September coincided with with a significant increase in yellow bees drifting to the MRC’s.

Drifting over at least 50 metres was observed, with ~6% of workers entering the MRC’s being derived from the MDC’s.

If you refer back to the phoretic mite load in the donor colonies by late September (15-25%, see above) it suggests that perhaps 1% of all 5 the bees entering the mite receptor colonies may have been carrying mites.

And this is in addition to the returning robbers carrying an extra payload.

Since the drones were also distinctively coloured, their drifting could also be recorded.

Drones drifted bi-directionally. Between 12 and 22% of drones at hive entrances were of a different colour morph to the workers in the colony. Over 90% of this drone drifting was over short distances, with fewer than 1% of drones at the receptor colonies 50 or 300 m away from the donor apiary being yellow.

Discussion and conclusions

This was a simple and elegant experiment. It provides compelling evidence that robbing of weak, collapsing colonies is likely to be the primary source of mite acquisition in late summer/early autumn.

It also demonstrates that drifting, particularly over short distances, is likely to contribute significant levels of mite transmission before robbing in earnest starts. However, once collapsing colonies are subjected to intense robbing this become the predominant route of mite transmission.

There were a few surprises in the paper (in my view).

One of the characteristics of colonies being intensely robbed is the maelstrom of bees fighting at the hive entrance. This is not a few bees having a stramash 6 on the landing board. Instead it involves hundreds of bees fighting until the robbed colony is depleted of guards and the robbers move in mob handed.

As a beekeeper it’s a rather distressing sight (and must be much worse for the overwhelmed guards … ).

I was therefore surprised that only 1-2% of the bees returning to the mite receptor colonies carried evidence (dusted sugar) that they’d been involved in robbing. Of course, this could still be very many bees if the robbing colonies were very strong. Nevertheless, it still seemed like a small proportion to me.

It’s long been known that mites and viruses kill colonies. However, notice how quickly they kill the mite receptor colonies in these studies.

The MRC’s were established in May with very low mite numbers. By the start of the experiment (mid-August) they had <1% phoretic mites. By the following spring two thirds of them were dead after they had acquired mites by robbing (and drifting) from nearby collapsing colonies 7.

It doesn’t take long

The science and practical beekeeping

This paper confirms and reinforces several previous studies, and provides additional evidence of the importance of robbing in mite transmission.

What does this mean for practical beekeeping?

It suggests that the late-season colonies bulging with hungry bees that are likely to initiate robbing are perhaps most at risk of acquiring mites from nearby collapsing colonies.

This is ironic as most beekeepers put emphasis on having strong colonies going into the winter for good overwintering success. Two-thirds of the colonies that did the robbing died overwinter.

The paper emphasises the impact of hive separation. Drifting of drones and workers was predominantly over short distances, at least until the robbing frenzy started.

This suggests that colonies closely situated within an apiary are ‘at risk’ should one of them have high mite levels (irrespective of the level of robbing).

If you treat with a miticide, treat all co-located colonies.

However, drifting over 300 m was also observed. This implies that apiaries need to be well separated. If your neighbour has bees in the next field they are at risk if you don’t minimise your mite levels … or vice versa of course.

And this robbing occurred over at least 300 m and has been reported to occur over longer distances 8. This again emphasises both the need to separate apiaries and to treat all colonies in a geographic area coordinately.

Most beekeepers are aware of strategies to reduce robbing i.e. to stop colonies being robbed. This includes keeping strong colonies, reduced entrances or entrance screens.

But how do you stop a strong colony from robbing nearby weak colonies?

Does feeding early help?

I don’t know, but it’s perhaps worth considering. I don’t see how it could be harmful.

I feed within a few days of the summer honey supers coming off. I don’t bother waiting for the bees to exploit local late season forage. They might anyway, but I give them a huge lump of fondant to keep them occupied.

Do my colonies benefit, not only from the fondant, but also from a reduced need to rob nearby weak colonies?

Who knows?

But it’s an interesting thought …

Note there’s an additional route of mite transmission not covered in this or the last post. If you transfer frames of brood from a mite-infested to a low mite colony – for example, to strengthen a colony in preparation for winter – you also transfer the mites. Be careful.


Colophon

The idiom “Crime doesn’t pay” was, at one time, the motto of the FBI and was popularised by the cartoon character Dick Tracy.

Woody Allen in Take the Money and Run used the quote “I think crime pays. The hours are good, you travel a lot.”

Flower mites

Where do all those pesky mites come from that transmit pathogenic viruses in and between colonies?

Unless you are fortunate enough to live in the remote north west of Scotland 1 or the Isle of Man then bees, whether managed or feral, in your area have the parasitic mite Varroa destructor.

And if you take a mite-free colony from, say, north west Scotland and stick it in a field in Shropshire 2 it will, sooner or later, become mite-infested.

Sooner rather than later.

In our studies we see mite infestation (capped drone pupae with associated mites) within a few days of moving mite-free colonies to out apiaries.

Where did these mites originate and how did they get there?

Direct or indirect? Active or passive?

They don’t walk there.

Mites are blind and have no directional abilities over long distances.

Essentially therefore there are just two routes, both involving the host honey bee 3.

Direct, in which phoretic mites are transferred on honey bees between colonies, or indirect, in which they are transferred via something that isn’t a bee in the environment.

Like a flower.

Mite transmission routes

With an infested hive (the Donor) and a mite-free hive (the Acceptor 4) the direct routes involve the well-established processes of drifting and robbing.

As far as the acceptor hive is concerned, drifting is a passive process. The bees just arrive at the entrance and are allowed access.

In contrast, robbing is an active process by the acceptor hive. The foragers that rampage around pillaging weak colonies bring the phoretic mites back with them.

There have been two recent papers that have considered the relative importance of these routes and, in the case of indirect transmission, whether there is evidence that it can occur.

Both papers are from Thomas Seeley and colleagues at Cornell University. Seeley conducts simple and elegant experiments and, apart perhaps for the statistics, both papers are pretty readable, even without a scientific background.

I’ll deal with indirect transmission here and return to drifting and robbing in the future.

Say it with flowers … send her a mite

There is quite a bit of circumstantial evidence that horizontal transmission via flowers may occur. This includes evidence that mites can survive on flowers for several days (in the absence of bees). If ‘presented’ with live or dead bees these mites could then climb onto the bee.

But clambering aboard a dead bee held in a pair of tweezers is very different from boarding a live bee making a transient visit to a flower.

Like this.

This short video is by David Peck, the lead author on a 2016 manuscript on acquisition of mites by bees visiting flowers 5. The paper is open access and freely available so I’ll cut to the chase and just present the key details.

The mites and bees came from the same colony. Mites were harvested by sugar roll and placed on flower petals. Different flower species were baited with the same anise-flavoured sugar solution to make them equally attractive to foraging bees.

Video recording of bee visits enabled the scientists to determine whether the mite attached to a bee, if it was subsequently groomed off (in the vicinity of the flower) and how long any interaction took. The latter was measured in bee seconds i.e. the cumulative number of seconds a bee was present before the mite attached.

Mite transmission to bees from flowers

In 43 independent tests, using a total of three different flower species, every mite successfully managed to clamber onto a visiting bee. Of these, 41 left the flower with the bee (the two that didn’t fell off or were groomed by the bee).

Speed and efficiency

It took on average just two minutes of bee visits for the mite to climb aboard. In one test the mite successfully attached in just 2 seconds.

About 50% of the mites attached after the first contact with a bee. The average number of contacts needed was just over two (usually to the same bee).

We’ve all watched bees visiting flowers. They approach, orientate, land, take off again, reorientate, land again. Sometimes they walk across the inflorescence.

That’s all it takes.

The mites didn’t move about the flower much. They didn’t chase the bee around the flower. None moved more than 1 cm.

They simply waited for the bee to come close enough.

Mites haven’t got eyes but they have exquisitely sensitive chemosensory receptors on their forelegs (not four legs, they have eight 😉 ). They use these to detect the approaching bee and are then nimble enough to embark, as the video above shows.

Mites on daisy (Bellis sp.) or speedwell (Veronica sp.) relocated to a bee much more rapidly than those placed on an Echinacea flower. It’s not clear why – the flowers are larger on Echinacea so perhaps it’s something to do with the way a bee interacts with these when foraging?

Case proven m’lud?

Mites are transferred between colonies via flowers … it’s a fact.

Not quite.

What this study shows was that mites on flowers can readily attach to a visiting bee.

Specifically to a visiting bee from the same hive that the mite was ‘harvested’ from for the experiments.

Mites absorb the cuticular hydrocarbon profile of their host hive i.e. they smell like the bees do. Perhaps they were less readily detected by the visiting mite-free bee? Would they transfer to bees from a foreign colony less efficiently?

Conversely, host-parasite theory would suggest that the mite would have evolved mechanisms to preferentially infest ‘foreign’ visiting bees 6. At least they should if this route provided a suitable selective pressure, which would involve it providing an advantage to the mite (over other routes like robbing or drifting, for example). This remains to be tested.

But there’s something else missing until we can be certain that mites are transferred indirectly between colonies via flowers.

Have you ever seen a flower with a mite on it?

I haven’t either.

Which of course doesn’t help support or refute a role for flowers in mite transmission.

Absence of evidence is not evidence of absence.

A limited survey of flowers around apiaries also failed to detect Varroa 7 which is as little help as our own observations (see above).

So we’re left with half a story. Mites can transfer (quite efficiently) from flowers to bees. What we don’t know is whether – or how – they get from infested bees to the flower in the first place.

And if they do, whether it happens frequently enough to be of any real relevance as a mite transmission route between hives.

Next week I’ll revisit robbing and drifting as mite transmission routes to discuss some recent studies looking at their relative importance.

One last thing … one of the co-authors of the 2016 study described above is Michael L. Smith. In 2014 he published the honey bee sting pain index. I’m pleased to see he’s moved on to less painful scientific studies 🙂


Colophon

Flour mite (c) Joel Mills

The flour mite (Acarus siro), a distant relative of Varroa destructor, is a contaminant of grain and – unsurprisingly – flour which “acquires a sickly sweet smell and becomes unpalatable”.

Which isn’t a huge recommendation for Mimolette cheese. This cheese originates from Lille in France. It has a grey crust and an orange(ish) flesh, looking a bit like a cantaloupe. The crust hardens over time.

The appearance, the hardening (?) and certainly the flavour of the crust is due to the addition of flour mites (aka cheese mites) which are intentionally introduced during production of the cheese. Yummy.

Virus resistant bees?

In the early/mid noughties there was a lot of excitement about a newly discovered pathogen of honey bees, Israeli Acute Paralysis Virus (IAPV). This virus was identified and initially characterised in 2004 and, a couple of years later, was implicated as the (or at least a) potential cause of Colony Collapse Disorder (CCD) 1..

CCD is, and remains (if it still exists at all), enigmatic 2. It is an oft-misused term to describe the dramatic and terminal reduction in worker bee numbers in a colony in the absence of queen failures, starvation or obvious disease. It primarily occurred in the USA in 2006-07 and was reported from other countries in subsequent years 3.

Comparisons of healthy and CCD-affected colonies showed a correlation between the presence of IAPV and colony collapse, triggering a number of additional studies. In this and a future post I’m going to discuss two of these studies.

I’ll note here that correlation is not the same as causation. Perhaps IAPV was detected because the colony was collapsing due to something else? IAPV wasn’t the only thing that correlated with CCD. It’s likely that CCD was a synergistic consequence of some or all of multiple pathogens, pesticides, poor diet, environmental stress, migratory beekeeping, low genetic diversity and the phase of the moon 4.

IAPV

Israeli Acute Paralysis Virus is an RNA virus. That means the genome is made of ribonucleic acid, a different sort of chemical to the deoxyribonucleic acid (DNA) that comprises the genetic material of the host honey bee, or the beekeeper. The relevance of this will hopefully become clear later.

RNA viruses are not unusual. Deformed wing virus (DWV) is also an RNA virus as is Sacbrood virus and Black Queen Cell Virus. In fact, many of the most problematic viruses (for bees or beekeepers [measles, the common cold, influenza, yellow fever, dengue, ebola]) are RNA viruses.

RNA viruses evolve rapidly. They exhibit a number of features that mean they can evade or subvert the immune responses of the host, they can acquire mutations that help them switch from one host to another and they rapidly evolve resistance to antiviral drugs.

To a virologist they are a fascinating group of viruses.

IAPV isn’t a particularly unusual RNA virus. It is a so-called dicistrovirus 5 meaning that there are two (di) regions of the genetic material that are expressed (cistrons) as proteins. One region makes the structural proteins that form the virus particle, the other makes the proteins that allow the virus to replicate.

Schematic of the RNA genome of Israeli Acute Paralysis Virus

There are many insect dicistroviruses. These include very close relatives of IAPV that infect bees such as Acute Bee Paralysis Virus (ABPV) and Kashmir Bee Virus (KBV). They are very distant relatives of DWV and, in humans, poliovirus; all belong to the picorna-like viruses (pico meaning small, rna meaning, er, RNA i.e. small RNA containing viruses … I warned you about the Latin).

Phylogenetic relationships between picorna-like viruses

Like DWV, IAPV-infected bees can exhibit symptoms (shivering, paralysis … characteristic of nerve function or neurological impairment in the case of IAPV) or may be asymptomatic. The virus probably usually causes a persistent infection in the honey bee and is transmitted both horizontally and vertically:

  • horizontal transmission – between bees via feeding, direct contact or vector mediated by Varroa (not all of these routes have necessarily been confirmed).
  • vertical transmission – via eggs or sperm to progeny.

IAPV resistance

An interesting feature of IAPV is that some colonies are reported to be resistant to the virus. This is stated in an interesting paper by Eyal Maori 6 but, disappointingly, is not cited.

At the same time these studies were being conducted there was a lot of interest in genetic exchange between pathogens and hosts (e.g. where genetic material from the pathogen gets incorporated into the host) and an increasing awareness of the importance of a process called RNA interference (RNAi) in host resistance to pathogens 7.

Maori and colleagues screened the honey bee genome for the presence of IAPV sequences (i.e. a host-acquired pathogen sequence) using the polymerase chain reaction 8. About 30% of the bees tested contained IAPV sequences derived from the region of the genome that makes the structural proteins of the virus. Other regions of the virus were not detected.

Two additional important observations were made. Firstly, the IAPV sequences appeared to be integrated into a number of location of the DNA of the honey bee (remember IAPV is an RNA virus, so this requires some chemical modifications to be described shortly). Secondly, the IAPV sequences were expressed as RNA. This is significant because RNA is an intermediate in the production of RNAi (with apologies to the biologists who are reading this for the oversimplification and to the non-scientists for some of this gobbledegook. Bear with me.).

And now for the crunch experiment …

Virus challenge

Maori and team injected 300 white eyed honey bee pupae that lacked the integrated IAPV sequence with virus.

Only 2% survived.

They went on to inoculate a further 80 pupae selected at random. Thirteen of these survived (16%) and emerged as healthy-looking adults. The 67 corpses all showed evidence of virus replication and lacked the integrated IAPV sequence in the bee genome.

In contrast, the 13 survivors all contained integrated IAPV sequences but showed no evidence for replication of the virus.

This is of profound importance to our understanding of the resistance of honey bees to pathogens … and in the longer term for the selection or generation of virus-resistant bees.

If it is correct.

Subsequent studies

It’s of such profound importance that it’s extraordinary that there have been no subsequent follow-up papers (at least to my knowledge).

What there have been are number of outstanding but indirectly related studies that have demonstrated a potential mechanism for the integration of RNA sequences into a DNA genome.  We also now have a much improved understanding of how such integrated sequences could confer resistance to the host of the pathogen.

Perhaps the best of these follow-up studies is one by Carla Saleh 9 on the molecular mechanisms that underlie the integration of viral RNA sequences into the host DNA genome. This study also demonstrates how an acute virus infection of insects is converted to a persistent infection.

One of the big problems with the Maori study is explaining how RNA gets integrated. RNA and DNA are chemically similar but different. You can’t just join one to the other.

Saleh showed the an enzyme called an endogenous reverse transcriptase (an enzyme that converts RNA to DNA) was required. In the fruit fly virus model system she worked with she showed that this enzyme was made by a genetic element within the fruit fly genome (hence endogenous) called a retrotransposon.

Importantly, Saleh also showed that the integrated virus sequences acted as the source for interfering RNAs (RNAi) which then suppressed the replication of the virus.

The study by Saleh and colleagues is extremely elegant and explains much of the earlier work on integration of RNA pathogen sequences into the host genome.

However, it leaves a number of questions unanswered about the bits of IAPV that Maori claim are associated with virus resistance in honey bees.

Unfinished business

The Saleh study is really compelling science. Perhaps the same process operates in honey bees?

This is where issues start to appear. The honey bee genome has now been sequenced. Perplexingly (if the Maori study is correct) it contains few transposons and no active retrotransposons.

Without a source of the reverse transcriptase enzyme there’s no way for the RNA to be converted to DNA and integrated into the host genome.

The second major issue is that there are conflicting reports of the presence of viral sequences integrated in the honey bee genome. The assembled sequence 10 appears to contain no virus sequences but there are conference reports of sequences for IAPV, DWV and KBV using a PCR-based method similar to that used by Maori.

Where next?

There’s a lot to like about the Maori study on naturally transgenic bees (a phrase they used in the conclusion to their paper).

It explains the reported IAPV resistance of some bees/colonies (though this needs better documentation). It implicates a molecular mechanism which has subsequently been demonstrated to operate in a number of different insects and host/pathogen systems.

It’s also a result that as a beekeeper and a virologist I’d also like to think offers hope for the future in terms honey bee resistance to the pathogens that can blight our colonies.

Monoculture ... beelicious ...

Monoculture … beelicious …

However, the absence of some key controls in the Maori study, the lack of any real follow-up papers on their really striking observation and the contradictions with some of the genomic studies on honey bees is a problem.

What’s new?

Eyal Maori has a very recent paper (PDF) on RNAi transmission in honey bees. It was in part prompted by the second of the IAPV studies I want to discuss that arose after IAPV was implicated as a possible cause of CCD. That study, to be covered in a future post, demonstrates field-scale analysis of RNAi-based suppression of IAPV.

It is important for two reasons. It shows a potential route to combat virus infections and, indirectly, it emphasises the importance of continuing to properly control Varroa (and hence virus) levels for the foreseeable future.


 

Magic mushrooms not magic bullets

Bees are very newsworthy. Barely a week goes by without the BBC and other news outlets discussing the catastrophic global decline in bee numbers and the impending Beemaggedon.

These articles are usually accompanied by reference to Colony Collapse Disorder (CCD) and the apocryphal quote attributed to Albert Einstein “If the bee disappears from the surface of the earth, man would have no more than four years to live” 1.

They also generally illustrate news about honey bees with pictures of bumble bees … and conveniently overlook the global increase in honey bee colonies over the last 50 years.

Never let the truth get in the way of a good story 2

‘shrooms

And the story is particularly newsworthy if it includes the opportunity for a series of entirely predictable (but nevertheless amusing) puns involving mushrooms or fungi 3.

And for me, it is even better if it involves viruses.

It was inevitable I’d therefore finally get round to reading a recent collaborative paper 4 from Paul Stamets, Walter Sheppard, Jay Evans and colleagues. Evans is from the USDA-ARS Beltsville bee labs, Sheppard is an entomologist from Washington State University and Stamets is a really fun guy 5, an acknowledged mushroom expert and enthusiast, award-winning author 6 and advocate of mushrooms as a cure for … just about anything. Stamets is the founder and owner of Fungi Perfecti, a company promoting the cultivation of high-quality gourmet and medicinal mushrooms.

An an aside, you can get a good idea of Stamets’ views and all-encompassing passion for ‘shrooms by watching his YouTube video on the Stoned Ape [hypothesis] and Fungal Intelligence.

Fungi and viruses

It has been shown that extracts of fungi can have antiviral activity 7, though the underlying molecular mechanism largely remains a mystery (for a good overview have a look at this recent review in Frontiers in Microbiology by Varpu Marjomäki and colleagues). I’m not aware of any commercial antivirals derived from fungi 8 and none that I’m aware of are in clinical trials for human use.

Stamets cites his own observations of honey bees foraging on mycelia (the above-ground fruiting body we call ‘mushrooms’) and speculates that this may be to gain nutritional or medicinal benefit.

Shrooms

Mushroom

This seems entirely reasonable. After all, bees collect tree resins to make propolis, the antimicrobial activity of which may contribute to maintaining the health of the hive.

I’ve not seen bees foraging on fungi, but that certainly doesn’t mean they don’t.

Have you?

Whatever … these observations prompted the authors to investigate whether mushroom extracts had any activity against honey bee viruses.

Not just any viruses

Specifically they tested mushroom extracts against deformed wing virus (DWV) and Lake Sinai Virus (LSV).

DWV is transmitted by Varroa and is globally the most important viral pathogen of honey bees. It probably accounts for the majority of overwintering colony losses due to a reduction in longevity of the fat bodied overwintering bees.

LSV was first identified in 2010 and appears to be widespread, at least in the USA. It has also been detected in Europe and is a distant relative of chronic bee paralysis virus. It has yet to be unequivocally associated with disease in honey bees.

Not just any ‘shrooms

Mycelial extracts were prepared from four species of fungi. As a lapsed fly fisherman I was interested to see that one of those chosen was Fomes fomentarius, the hoof fungus which grows on dead and dying birch trees. This fungus, sliced thinly, is the primary ingredient of Amadou which is used for drying artificial flies 9.

Hoof fungus … and not a honey bee in sight.

Mycelial extract preparation took many weeks and generated a solution of ethanol, aqueous and solvent soluble mycelial compounds together with potentially contaminating unused constituents from the growth substrate. This was administered in thin (i.e. 1:1 w/v) sugar syrup.

Don’t just try hacking a lump off the tree and placing it under the crownboard 😉

Results

In laboratory trials all the fungal extracts reduced the level of DWV or LSV in caged honey bees by statistically significant amounts.

Unfortunately (at least for the layman trying to comprehend the paper) the reductions quoted are n-fold lower, based upon an assay called a quantitative reverse transcription polymerase chain reaction. Phew! It might have been preferable – other than it being appreciably more work – to present absolute reductions in the virus levels.

Nevertheless, reductions there were.

Encouragingly they were generally dose-dependent i.e. the more “treatment” added the greater the reduction. A 1% extract of hoof fungus in thin syrup reduced DWV levels by over 800-fold. Against LSV the greatest reductions (~500-fold) were seen with a different extract. In many cases the fold change observed were much more conservative i.e. less activity (though still statistically significant).

A) Normalised DWV and LSV levels in individual bees. B) Activity of mushroom extracts against LSV.

These lab studies encouraged the authors to conduct field trials. Five frame nucleus colonies were fed 3 litres of a 1% solution of one of the two most active extracts. Virus levels were quantified 12 days later. Control colonies were fed thin syrup only.

These field trials were a bit less convincing. Firstly, colonies fed syrup alone exhibited 2- to 80-fold reduction in DWV and LSV levels respectively. Against DWV the fungal mycelial extracts reduced the level of the virus ~40-fold and ~80-fold better than syrup alone. LSV levels were more dramatically reduced by any of the treatments tested; ~80-fold by syrup alone and ~90-fold or ~45,000-fold better than the syrup control by the two mycelial extracts.

Or is it any ‘shrooms … or ‘shrooms at all?

It’s worth emphasising that syrup-alone is not the correct control for use in these studies. As stated earlier the mycelial extract likely also contained constituents from the fungal growth media (sterilised birch sawdust).

The authors were aware of this and also tested extracts prepared from uninoculated birch sawdust. This definitely contained endogenous fungal contamination as they identified nucleic acid from ‘multiple species’ of fungi in the sterilised sawdust, the majority from three commonly birch-associated fungi (none of which were the original four species tested).

The authors are a little coy about the effect this birch sawdust extract had on virus levels other than to say “extracts from non-inoculated fungal growth substrate also showed some activity against DWV and LSV”. In lab studies it appears as though ‘some activity’ is between 8- and 120-fold reduction.

Without some additional controls I don’t think we can be certain that the compound(s) responsible for reducing the viral levels is even derived from the mushroom mycelium, whether the endogenous ones present in the sawdust, or those grown on the sawdust.

For example, perhaps the active compound is a constituent of birch sawdust that leaches out at low levels (e.g. during the extraction process) but that is a released in large amounts when fungi grow on the substrate?

Hope or hype?

Readers with good memories may recollect articles from fifteen years ago about fungi with activity against Varroa. In that case the fungus was Metarhizium anisopliae. There are still groups working on this type of biological control for mites but it’s probably fair to say that Metarhizium has not lived up to its early promise 10.

A lot more work is needed before we’ll know whether mushroom extracts have any specific activity against honey bee viruses. There are lots of unanswered questions and it will take years to have a commercial product for use by beekeepers.

Don’t get rid of your stocks of oxalic acid or Apivar yet!

Questions

What are the active ingredient(s) and mode of action?

Do the extracts actually have any activity against the viruses per se, or do they instead boost the immune response of the bee and make it better to resist infection or clear established infections?

How specific are the extracts? Do they have activity against other RNA viruses of honey bees? What about Nosema? Or the foulbroods? If they boost immune responses you’d expect a broad range of activities against bee pathogens.

You’d also expect that bees would have evolved to actively forage on mushroom fruiting bodies and so be a common sight in late summer/early autumn.

Are they toxic to bees in the longer term? Are they toxic for humans? Fomes formentarius is considered “inedible, with a slightly fruity smell and acrid taste”. Delicious!

Finally, is the reduction in virus levels observed in field studies sufficient to have a measurable positive influence on colony health? It’s worth remembering that Apivar treatment reduces mite levels by 95% and virus levels by about 99.9999%.


Colophon

Magic!

Magic mushroom is a generic term used to refer to a polyphyletic group of fungi that contain any of various psychedelic compounds, including psilocybin, psilocin, and baeocystin. Talk to Frank to find out more about the effects and dangers of magic mushrooms. The de facto standard guide for the identification of magic mushrooms is Psilocybin Mushrooms of the World by … you guessed it, Paul Stamets.

The term magic mushroom was first used in Life magazine in 1957.

A magic bullet is a highly specific drug or compound which kills a microbial pathogen without harming the host organism. The term (in German, Zauberkugel) was first used by Nobel laureate Paul Ehrlich in 1900. Ehrlich discovered/developed the first magic bullet, Salvarsan or Arsphenamine, an organoarsenic compound that is effective in the treatment of syphilis.

Mycelial extracts of fungi are not (yet at least) a magic bullet for use in the control of honey bee viruses.

Teaching in the bee shed

An observant beekeeper never stops learning. How the colony responds to changes in forage and weather, how swarm preparations are made, how the colony regulates the local environment of the hive etc.

Sometimes the learning is simple reinforcement of things you should know anyway.

Or knew, but forgot. Possibly more than once.

If you forget the dummy board they will build brace comb in the gap 🙁

There’s nothing wrong with learning by reinforcement though some beekeepers never seem to get the message that knocking back swarm cells is not an effective method of swarm control 😉

Learning from bees and beekeeping

More generally, bees (and their management) make a very good subject for education purposes. Depending upon the level taught they provide practical examples for:

  • Biology – (almost too numerous to mention) pollination, caste structure, the superorganism, disease and disease management, behaviour
  • Chemistry – pheromones, sugars, fermentation, forensic analysis
  • Geography and communication – the waggle dance, land use, agriculture
  • Economics – division of labour (so much more interesting than Adam Smith and pin making), international trade
  • Engineering and/or woodwork – bee space, hive construction, comb building, the catenary arch

There are of course numerous other examples, not forgetting actual vocational training in beekeeping.

This is offered by the Scottish Qualifications Authority in a level 5 National Progression Award in Beekeeping and I’ve received some enquiries recently about using a bee shed for teaching beekeeping.

Shed life

For our research we’ve built and used two large sheds to accommodate 5 to 7 colonies. The primary reason for housing colonies in a shed is to provide some protection to the bees and the beekeeper/scientist when harvesting brood for experiments.

On a balmy summer day there’s no need for this protection … the colonies are foraging strongly, well behaved and good tempered.

But in mid-March or mid-November, on a cool, breezy day with continuous light rain it’s pretty grim working with colonies outdoors. Similarly – like yesterday – intermittent thunderstorms and heavy rain are not good conditions to be hunched over a strong colony searching for a suitable patch containing 200 two day old larvae.

Despite the soaking you get the colonies are still very exposed and you risk chilling brood … to say nothing of the effect it has on their temper.

Or yours.

Bee shed inspections

Here’s a photo from late yesterday afternoon while I worked with three colonies in the bee shed. The Met Office had issued “yellow warnings” of thunderstorms and slow moving heavy rain showers that were predicted to drift in from the coast all afternoon.

All of which was surprisingly accurate.

Bee shed inspections in the rain

For a research facility this is a great setup. The adverse weather doesn’t seem to affect the colonies to anything like the same degree as those exposed to the elements. Here’s a queenless colony opened minutes before the photo above was taken …

Open colony in the bee shed

Inside the shed the bees were calmly going about their business. I could spend time on each frame and wasn’t bombarded with angry bees irritated that the rain was pouring in through their roof.

Even an inexperienced or nervous beekeeper would have felt unthreatened, despite the poor conditions outside.

So surely this would be an ideal environment to teach some of the practical skills of beekeeping?

Seeing and understanding

Practical beekeeping involves a lot of observation.

Is the queen present? Is there brood in all stages? Are there signs of disease?

All of these things need both good eyesight and good illumination. The former is generally an attribute of the young but can be corrected or augmented in the old.

But even 20:20 vision is of little use if there is not enough light to see by.

The current bee shed is 16′ x 8′. It is illuminated by the equivalent of seven 120W bulbs, one situated ‘over the shoulder’ of a beekeeper inspecting each of the seven hives.

On a bright day the contrast with the light coming in through the windows makes it difficult to see eggs. On a dull day the bulbs only provide sufficient light to see eggs in freshly drawn comb. In older or used frames – at least with my not-so-young eyesight – it usually involves a trip to the door of the shed (unless it is raining).

It may be possible to increase the artificial lighting using LED panels but whether this would be sufficient (or affordable) is unclear.

Access

Observation also requires access. The layout of my bee shed has the hives in a row along one wall. The frames are all arranged ‘warm way’ and the hives are easily worked from behind.

Hives in the bee shed

Inevitably this means that the best view is from directly behind the hive. If the shed was used as a training/teaching environment there’s no opportunity to stand beside the hive (as you would around a colony in a field), so necessitating the circulation of students within a rather limited space to get a better view.

A wider shed would improve things, but it’s still far from ideal and I think it would be impractical for groups of any size.

And remember, you’re periodically walking to and from the door with frames …

Kippered

If you refer back to the first photograph in this post you can see a smoker standing right outside the door of the shed.

If you use or need a smoker to inspect the colonies (and I appreciate this isn’t always necessary, or that there are alternative solutions) then it doesn’t take long to realise that the smoker must be kept outside the shed.

Even with the door open air circulation is limited and the shed quickly fills with smoke.

If you’ve mastered the art of lighting a properly fuelled efficient smoker the wisp of smoke curling gently up from the nozzle soon reduces visibility and nearly asphyxiates those in the shed.

Which brings us back to access again.

Inspections involve shuttling to and from the door with frames or the smoker, all of which is more difficult if the shed is full of students.

Or bees … which is why the queen excluder is standing outside the shed as well. I usually remove this, check it for the queen and then stand it outside out of the way.

Broiled

In mid-March or November the shed is a great place to work. The sheltered environment consistently keeps the temperature a little above ambient.

Colonies seem to develop sooner and rear brood later into the autumn 1.

But in direct sunlight the shed can rapidly become unbearably warm.

Phew!

All the hives have open mesh floors and I’ve not had any problems with colonies being unable to properly regulate their temperature.

The same cannot be said of the beekeeper.

Working for any period at temperatures in the low thirties (Centigrade) is unpleasant. Under these conditions the shed singularly fails to keep the beekeeper dry … though it’s sweat not rain that accumulates in my boots on days like this.

Bee shelters

For one or two users a bee shed makes a lot of sense if you:

  • live in an area with high rainfall (or that is very windy and exposed) and/or conditions where hives would benefit from protection in winter
  • need to inspect or work with colonies at fixed times and days
  • want the convenience of equipment storage, space for grafting and somewhere quiet to sit listening to the combined hum of the bees in the hives and Test Match Special 😉

But for teaching groups of students there may be better solutions.

In continental Europe 2 bee houses and bee shelters are far more common than they are in the UK.

I’ve previously posted a couple of articles on German bee houses – both basic and deluxe. The former include a range of simple shelters, open on one or more sides.

A bee shelter

Something more like this, with fewer hives allowing access on three sides and a roof – perhaps glazed or corrugated clear sheeting to maximise the light – to keep the rain off, might provide many of the benefits of a bee shed with few of the drawbacks.


 

Leave and let die

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

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

DWV symptoms

DWV symptoms

The principle is straightforward. It goes something like this:

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

A crude oversimplification?

Yes, I don’t deny it.

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

But won’t.

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

But I’ll start with a simple question …

How many colonies have you got?

One? (in which case, get another)

Two?

Ten?

One hundred?

Eight-two thousand? 3

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

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

This is why we treat ...

This is why we treat …

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

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

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

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

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

Where ‘likely to be’ means will be.

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

It could be you … but it’s unlikely

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

And so on.

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

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

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

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

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

Apologies. Let’s not go there.

Let’s cut to the chase …

Comparison of treated vs untreated colonies over 3 years

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

Amitraz

Amitraz …

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

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

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

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

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

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

Treatment and seasonal variation

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

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

The fourth group were the untreated controls.

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

The apiary in winter ...

The apiary in winter …

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

Results …

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

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

Out, damn'd mite ...

Out, damn’d mite …

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

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

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

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

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

… and some additional observations

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

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

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

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

Evolution …

March of Progress

Evolution …

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

Does this start to sound familiar?

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

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

Lots of colonies.

Actually, almost all of them.

… takes time

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

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

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

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

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

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

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

Almost all the colonies died.

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


 

Natural vs. artificial swarms

I’ve now covered four of the most frequently used swarm control strategies. These are:

  • Pagden’s artificial swarm – the horizontal splitting of the colony
  • The vertical split – an equipment-frugal variant of the above involving a vertical separation of the colony
  • The nucleus method – in which the queen is removed with sufficient workers to make up a small (nuc) colony, leaving the original colony to rear another queen
  • The Demaree method – which, at its simplest, relocates the queen from the brood and associated nurse bees, but does not physically split the colony

If conducted correctly all should prevent loss of a swarm. However, the individual methods – even the first three which involve the physical separation of the bees in the hive – are not the same.

In addition, these swarm control methods do not recapitulate the separation of bees that occurs when a hive naturally swarms.

The purpose of this post is to contrast the original and new colony composition of the split-based methods of swarm control (i.e. Pagden and vertical) with natural swarms.

Temporal polyethism

I introduced this term when discussing the honey bee colony as a superorganism. It means that adult worker bees have different roles depending upon their age. For the first two and a bit weeks they have duties inside the hive such as cell cleaning, brood rearing and wax production.

They then transition through a period of being guard bees before becoming foragers, flying from the hive and collecting water, nectar and pollen.

For convenience I’ll refer to these two groups of bees as young, nurse or hive bees and flying bees.

Vertical and horizontal splits

The classic Pagden artificial swarm and the vertical split are fundamentally the same process.

If unsealed queen cells are found during a colony inspection the queen, with a frame of emerging brood, is moved to a new box. This box is placed on the site of the original hive.

The remaining bees and brood are moved, either to one side in the case of the Pagden or on top of the queen-containing box (separated by a split board) in a vertical split.

Split board ...

Split board …

Critically, the new box with the brood and bees is provided with a new hive entrance, located off to one side or on the opposite side of the original hive 1.

Flying home

Over the following day or two the flying bees leave the relocated brood box with the new entrance and return to the queen-containing brood box in the original location.

As a consequence of their excellent homing navigational skill, the hive manipulation results in the separation of the bees into two populations:

  1. The flying bees i.e. those over ~3 weeks of age that had orientated to the original hive location, which are now located with the queen.
  2. The nurse bees i.e. those less than 3 weeks old, which remain in the relocated brood box, together with the brood in all stages (eggs, larvae and pupae).
Artificial swarm separation of the colony

Artificial swarm separation of the colony

How does the artificial swarm compare with the age distribution of bees in a real swarm?

Real swarms

I’ve previously discussed prime swarms and casts. The former contain a mated queen. In contrast, casts are produced from very strong colonies after the prime swarm has left. Casts are headed by a virgin queen. These are sometimes called after swarms and are usually smaller than prime swarms.

What about the workers in the swarm? What might be expected?

Perhaps they’re primarily the older flying bees? After all, these are the bees that have finished their hive duties and are now routinely foraging outside the hive. It’s the natural place for them.

Swarm of bees

Swarm of bees

Alternatively, remember that swarms have no ‘homing’ instinct for a day or two after emerging. They can be readily moved and you can safely ignore the less than three feet or more than three miles rule. Perhaps this means that they’re primarily young bees that have yet to go on their orientation flights?

Real experiments and contradictory results

Enough speculation … how do you determine this experimentally?

There have been numerous studies of the age distribution of bees in natural swarms. However, the data tends to be rather contradictory though the methods used are often broadly similar.

How do you determine the age composition of workers in a swarm?

Essentially you ‘spike’ the colony with a set number of marked bees of a known age over about 8 weeks. This is easy to do, but tedious.

Workers are allowed to emerge in an incubator. On the day of emergence (0 days old) they are marked with a colour that distinguishes them from older or younger bees. Every three days 100 identically marked i.e. same age, bees are added to the study hive(s). Over the period May to July this will accumulate red, then yellow, then blue, then mauve, then cyan, then pink etc. cohorts of workers, each representing a known age class.

It must be a nightmare spotting the queen in these hives 😉

The colony is allowed to swarm, the swarm collected and the number of bees of the different age cohorts in the swarm counted.

I missed a step out there. Have you ever tried counting the bees in a swarm? It’s much easier if they don’t move.

1002, 1003, 1004, 1005, er, where was I? Damn!

1002, 1003, 1004, 1005, er, where was I? Damn!

Perhaps it’s best that I missed that step out 🙁

What you end up with is a count of the total number of bees in the swarm and the numbers of bees of each 3 day cohort over the last several weeks. You can therefore determine the age distribution of the workers in the swarm.

Is it as simple as that?

I’ve actually oversimplified things a bit. There’s a possibility that different age cohorts of bees die within the hive at different rates, perhaps depending upon forage availability or weather or something else.

Think about it. Assume there was a dearth of nectar in late May and the blue and red labelled cohorts added during that period were underfed and died prematurely.

If there were very low numbers of blue and red bees in the swarm you might assume that these ages were ‘left behind’ by the swarm … when actually they weren’t able to swarm at all.

The real question is therefore whether the age distribution of bees in the swarm is similar to that in the parental hive.

OK, OK … is it?

No.

Swarms do contain bees of all ages.

However there are significantly more young bees and many fewer old bees than would be expected from the age distribution of workers in the parental colony.

Age distribution of bees in swarms

Age distribution of bees in swarms

The o and e in the graph above represents the position of the observed and expected median age class for the expected distributions. So, in swarm C the observed median age is ~10 days old, whereas the originating hive median age was ~19 days.

The graph above comes from a 1998 study by David Gilley 2 and supports earlier work 3 by Colin Butler 4 which is often cited as one of the definitive studies on the ages of bees in a swarm.

Additional considerations

Is it surprising that young bees predominate in natural swarms?

Swarms usually emerge from the hive late morning or early afternoon on warm, sunny days. In fact, at exactly the time most older bees aren’t in the hive anyway because they’re out and about foraging.

Remember also that swarming is a precarious activity for the colony. Most swarms do not survive 5. Natural selection will have resulted in swarm populations that maximise their chance of survival.

Once bees start foraging their life expectancy is pretty short. It has been estimated that they experience about 10% mortality per day. If only old bees left in the swarm with the queen the newly established colony would very rapidly dwindle in size, perhaps before significant numbers of new brood emerged (which takes 21 days from the first egg being laid). This would likely limit the chances of survival of the new colony.

What has this got to do with artificial swarms?

As beekeepers (or at least as responsible beekeepers) we spend May and June rushing about like headless chickens trying to control swarming in our bees.

Many of us achieve this using a variety of methods which are generically referred to as artificial swarms. I suspect that many beekeepers think that the artificiality is because of our interventions.

Where have all my young girls gone?

Where have all my young girls gone?

It is … but it’s worth remembering that the artificial swarms we generate are very different in composition to natural swarms. Our artificial swarms predominantly leave the older bees associating with the queen, with the young bees remaining with the brood.

These old bees have to draw new comb and rear the new brood. These are activities they last did weeks ago (a long time in the life of a bee).

Final thoughts

There are artificial swarm control methods that were developed to better replicate the age distribution of bees in a natural swarm. One example of these is use of a Taranov board. I’ll cover this in a future post.

It’s also worth noting that the bees of different ages in a natural swarm have different roles even before they occupy a new location. The older bees form a mantle around the bivouacked swarm that protects it from inclement weather (amongst other things) and the oldest bees are the scouts responsible for finding a new nest site.

Again, both topics for another post … I’ve got bait hives to set out 🙂


 

Superorganism potential

The term superorganism can be used to refer to a colony of honey bees. The term gained prominence in the mid/late noughties having been reintroduced by the world-renowned myrmecologist 1 E.O. Wilson.

Bees, like ants (myrmex, “ant”, from the Greek μύρμηξ), are social insects in which there are divisions of labour. Different individuals within the colony perform different tasks. Some of these roles are defined by the castes in the colony – queen, worker and drone in a colony of honey bees for example – and some are defined by physiological differences between individual members of the same caste.

The term superorganism describes the entirety of the colony and is defined as a group or association of organisms which behaves in some respect like a single organism.

Essentially, a superorganism has characteristics and behaviours that the individuals within the colony – due to caste or physiological specialisation – do not exhibit.

The superorganism operates as a unified entity, collectively working together to maintain and reproduce the colony.

Division of labour and temporal polyethism

Drones and queens have relatively straightforward roles in the colony. Drones, like teenage boys, lounge around eating and thinking about sex. The queens are egg-laying machines.

An egg laying machine

An egg laying machine

Although there’s undoubtedly work involved in laying your bodyweight in eggs at the height of the season, the real work in the colony is – appropriately – done by the workers.

Worker bees exhibit temporal polyethism i.e. they display different patterns of behaviour depending upon their age. They have a maturational schedule in which they sequentially undertake age-correlated roles in the colony:

  • Young bees work in the hive in a series of roles starting with cell cleaning (days 1-2), nursing developing larvae (nurse bees; days 3-11) and wax production (days 12-17).
  • After two to three weeks the workers undergo significant physiological changes (weight loss, changes in immune function, reduced stress resistance) which prepare them for a productive life outside the hive. During this period the bees transition through a period when they act as guard bees.
  • Older bees (the ‘flying’ bees) perform a range of foraging activities including water carrying, pollen collection and nectar gathering.

And then they die in the field 🙁

Behavioural plasticity

This behavioural maturation is controlled by a so-called negative feedback loop between vitellogenin (Vg 2) and juvenile hormone (JH).

Nurse bees have high Vg levels which are reduced at the transition to foraging. Conversely JH levels increase with the onset of foraging (I know this sounds counterintuitive). These changes are responsible for a range of physiological changes in the worker bee.

Behavioural maturation in worker bees

Behavioural maturation in worker bees

But it’s not as simple as that. High Vg levels can block JH synthesis, so delaying maturation and foraging. Similarly, JH may reciprocally inhibit Vg synthesis and induce early foraging.

Clearly that last couple of sentences indicates that worker maturation is not an invariant process. It doesn’t always occur after 2-3 weeks.

In fact, the maturation or ageing process in honey bees is a very interesting phenomenon.

Ageing exhibits seasonal variability and remarkable plasticity.

Nurse bees can survive for at least 130 days and overwintering bees may survive up to 280 days. Clearly ageing in bees is a remarkably variable process. Overwintering bees ‘mature’ into either nurse bees or foragers. Presumably this has evolved as an effective mechanism of allowing spring colony build up (by having sufficient bees for the different roles) once environmental conditions improve.

In addition, there is another striking feature of the maturation process of honey bees.

Under certain social environmental conditions maturation is reversible.

This reversible maturation can be demonstrated by removing the nurse bees from the hive. Under these conditions some of the younger foragers revert, both behaviourally and physiologically, to nursing tasks. JH levels drop and Vg levels increase.

Old foragers are unable to undergo this rejuvenation.

Reversible maturation in worker bees

Reversible maturation in worker bees

Which finally and in a round the houses way gets me to the subject I meant to cover in the first place this week …

Brood and the superorganism

The honey bee colony superorganism not only contains a queen, workers and drones. It also contains brood. In the following text I’ll use the term brood as a collective noun meaning all the eggs, unsealed larvae and sealed pupae in the colony (unless otherwise specified).

Is the brood a component of the superorganism?

It certainly is.

Laying workers ...

Laying workers …

Remember previous discussion of laying workers. These are workers that lay unfertilised eggs which develop into drones. Egg laying by workers is suppressed by pheromones produced from unsealed brood 3. Therefore brood does influence the behaviour of the colony 4.

If the complete colony – brood, workers, drones and a queen – is a superorganism, which components of the colony, individually or together, have the potential to form the superorganism?

And why should this matter?

Swarming and the superorganism

During swarming, either naturally during colony reproduction, or during manipulation by the beekeeper, the ‘superorganism’ is broken up.

During natural swarming the (old) mated queen leaves the colony with 60-75% of the workers to establish a new colony. By the time the swarm leaves, the original colony – which has all the eggs, larvae and brood (obviously) – is usually already well on the way to rearing a new queen. The (new) virgin queen emerges, gets mated, and the colony has successfully reproduced.

Many of the colony manipulation methods that are used to prevent the loss of natural swarms exploit the potential of the components in the colony to form a complete new colony.

Most ‘artificial swarms’ work by breaking the colony – the superorganism – into two parts:

  1. The queen and the ‘flying’ bees. Even young bees can fly, so the term ‘flying’ bees refers to the older bees from the colony that have matured sufficiently to leave the hive.
  2. The nurse bees and all the brood.
Swarms, splits and superorganisms

Swarms, splits and superorganisms

These two parts both have the potential to create a new colony.

The queen and the flying bees that form the swarm (or the queenright part of an artificial swarm) occupy a new site (or hive 5), draw comb in which the queen lays, the larvae are fed 6, pupate and emerge. At the same time, foragers collect the necessary nectar and pollen to maintain the new colony.

The swarmed colony (i.e. the queenless part of an artificial swarm) contains ample stores and the nurse bees. What they don’t have is a queen. But they do have eggs and young larvae. The nurse bees select and feed one or more of these young larvae with copious amounts of Royal Jelly. A few days later a virgin queen emerges, matures, mates and returns to the colony to start laying eggs.

Sealed queen cell ...

Sealed queen cell …

Therefore both natural and artificial swarms exploit the potential in both parts of the original colony to eventually reproduce the colony.

No potential

Not all components of the colony have the potential to give rise to a new colony or superorganism. A solitary queen doesn’t even have the ability to feed herself properly, let alone double up for egg laying and nursing larvae duties.

This comes as a surprise to some people. If you frequent any of the online discussion forums you’ll sometime see questions posted like this:

What sort of hive do I need to buy to put a queen bee in to make honey?

Followed by some polite, or not so polite, responses saying that there’s a little bit more to beekeeping than that 7.

The ‘flying’ bees alone, in the absence of a queen, also have no potential. They can lay eggs (as laying workers, see above), but since the eggs are unfertilised the colony will be doomed. It’s not unusual for a queen from an artificial swarm (or from a cast) to fail to return from a mating flight, so condemning the workers in the hive to oblivion.

Swarms and behavioural plasticity

The classic artificial swarm involves moving the nurse bees and the brood to a new site, leaving the queen and the flying bees in the original location.

You do this so that the flying bees that have orientated to the position of the original hive – whether out in the field actively foraging or in the moved hive – eventually return and so become separated from the nurse bees and the brood.

In doing this you remove the urge to swarm and you weaken the queenless hive.

The majority of those flying bees are foragers.

And this is where behavioural plasticity is essential. remember that the artificial swarm predominantly contains foragers, not the nurse bees needed to feed developing larvae.

Some of these foragers undergo rejuvenation to produce wax or to become nurse bees. These build new comb and, in a few days, feed larvae that have hatched from the eggs laid by the queen.

This behavioural plasticity contributes to the potential of the artificial swarm to produce a new colony or superorganism.

A small swarm ...

A small swarm …

Do the same processes happen in natural swarms?

That requires a discussion of the worker composition of swarms which is not straightforward and will have to wait for another day 😉