Category Archives: Miscellaneous

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 🙂


 

Matchstick miscellany

White propolis

What is propolis for?

Why, when you go to open a hive that you’ve not visited for some time, is the crownboard invariably stuck down with propolis?

Are the bees trying to stop you looking in? Do they think a thin bead of propolis is defence against a well-aimed hive tool?

Of course not.

What they are doing is sealing up every tiny nook and cranny, every gap and interstice.

You might think the crownboard is a snug fit.

The bees don’t.

Even the brand new, smooth, flat plastic interface between an Abelo crownboard and brood box get glued together within days.

Every fissure through which wasps 1 could gain access or heat could escape or water enter or whatever is gummed shut with a liberal helping of propolis.

Propolis is of course also antibacterial and has a host of other great properties, but for the purpose of this post I’m restricting myself to its use as a sort of “No Nonsense Decorators Caulk” of the bee world 2.

Mind the gap

Additional evidence that bees really do ‘mind the gap’ is easy to find if you use crownboards with holes in them.

Not the great gaping opening(s) designed to accommodate a porter bee escape (I’ll return to these shortly), but instead something like the ventilated disks in the grossly over-engineered Abelo poly crownboards.

Abelo poly National crownboard ...

Abelo poly National crownboard …

Here’s a brand new one, just out of the packing, with all the little fiddly ventilated plastic disks and poly plugs to cover them.

And this is what one of those ventilated holes looks like after a few weeks use …

Exhibit A … ventilated hole in an Abelo crownboard

And the same thing applies to wire mesh screens when I use split boards as crownboards (because I’ve run out … even of the 25p polythene ones).

Split board

Split board …

Which end up looking like this …

Exhibit B … are you getting the message?

Matchsticks … don’t try this at home

I’m an increasingly irregular visitor and even less frequent contributor to the online beekeeping discussion forums. On one 3 there’s a perennial discussion thread around this time of year concerning matchsticks.

Matchless matches

Essentially the discussion starts with a question or comment on the need for matchsticks as spacers to separate the crownboard from the brood box during the winter.

You’ll find this advice in many beekeeping books going back more than half a century and you’ll hear it in many ‘Start beekeeping’ winter courses … often taught by beekeepers who learned their beekeeping half a century ago.

In many cases the online forum discussion is started by a recommendation in the monthly BBKA 4 newsletter, or another online forum or Facebook group (again often BBKA-based).

The subsequent ‘discussion’ is generally nothing of the sort. The advice is (in my view rightly) criticised but as much or more effort goes into bashing the BBKA as evidencing why the advice is wrong.

I’m not here to bash the BBKA and I’ve already provided the unequivocal evidence why it’s wrong.

Much better use …

If you provide a narrow space or gap over the top of the colony they will try and seal the gap closed with propolis.

So don’t.

If you want to use matchsticks in the winter … build a model of Notre Dame instead. The bees will appreciate it more.

What are the bees telling you?

The speed with which bees seal up gaps and crevices tells you that that they ‘prefer’ not to have have these types of spaces overhead.

I’m using the word ‘prefer’ here in place of some convoluted justification around evolutionary selection of traits that benefit the long-term survival of the colony and maintenance/transmission of the genes in the environment.

They seal the gaps because to not do so, over eons, is detrimental to Apis mellifera. Not necessarily to that colony per se, but to the species.

Whether they do it to reduce robbing, to stop draughts or rain entering or to prevent the loss of warm air is, in many ways, irrelevant.

Do beekeepers really know better than millions of years of evolution?

No.

The “I always used matchsticks and my bees do well” justification

Is so deeply flawed it barely deserves contradicting.

But since I’m here, I will.

Bees have a fantastic ability to survive and even flourish despite the most cackhanded fumbling by beekeepers 5.

Just because your bees overwintered successfully with a gaping void in the crownboard does not mean they need that gaping void to survive 6.

Observe what the bees do and apply it to your beekeeping.

But what about crownboards with a big hole in for a porter bee escape? The bees don’t block those with propolis.

No, they don’t. But that’s still not justification to leave a void above the cluster. Bees seal gaps smaller than ‘bee space’ (say 8-9 mm) with propolis.

Perhaps they don’t seal up these large holes in the crownboard because the ‘triggers’ that make them seal smaller gaps aren’t present.

As an aside, I wonder if they deploy guard bees to defend these large holes above the cluster? 7

But back to the matchsticks; these create a gap significantly less than 8mm and the bees clearly demonstrate – each and every time you crack open the crownboard – that this is far from optimal.

I’m not going to get into the chimney effect, lost heat, holes in trees, water ingress, draughts etc.

Whether it’s a good idea to ventilate the winter cluster, to get rid of excess humidity or anything else, the evidence is compelling 8the bees would rather you didn’t.

Winter preparation miscellany

The two propolis-adorned crownboard pictures above were taken during an apiary visit in mid-October. I was opening hives for the final time this year. It was 12-13°C and bees were flying, bringing back pollen I presumed was largely from the ivy flowering nearby.

They fancied that fondant

Most had finished their final half block of fondant. The empty wrapper, eke and QE 9 were removed.

Others still had fondant left. In this case I bodily lifted off the QE, fondant and eke/super to give me access to the brood box.

Unfinished fondant

If you feed fondant above a QE you can balance it on an eke or empty super, so avoiding crushing the hundreds of bees clustered underneath the fondant 10

And the reason I needed access to the brood box was to recover the Apivar strips.

If the strip is fixed near the top of the frame this takes just seconds and a small amount of dexterity with a suitable hive tool.

The strips also have a small hole top and centre allowing them to be hung between frames on a matchstick.

But I don’t have matchsticks in the apiary 😉 so instead use the spike to fix them in the comb.

Apivar strips should not be left in for longer than the approved treatment period (6 – 10 weeks; these went in on the 28th of August, so are being removed after 7 weeks). This is important to avoid the reduced levels of amitraz in the ageing strips selecting for Apivar-resistant mites.

The few colonies I checked more thoroughly had little or no brood. All boxes were reassuringly heavy.

I saw a single drone amongst the dozen or so colonies I opened. Not long for this world I fear.

Since there was still pollen coming in I delayed fitting mouseguards to the colonies that need them.

I’ll deal with that once the frosts start 11.

Not long now 🙁


 

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.

Cabinet reshuffle

Don’t worry, this isn’t a post about the totally dysfunctional state of British politics at the moment 1.

Once the honey supers are removed there’s seemingly little to do in the apiary. There is a temptation to catch up on all those other jobs postponed because I was “just off to the bees”.

Well, maybe temptation is a bit strong. After all, like all good procrastinators, I can usually find an excuse to postpone until next week something that could be left until at least tomorrow.

However, as I said last week, preparations for winter are very important and should not be delayed.

I covered feeding and the all-important late summer mite treatments in that post. Here I’m going to briefly discuss the various late season hive rearrangements that might be needed.

Clearing additional supers

I use very simple clearer boards to get the bees out of my supers. However, there are a couple of instances when not all the supers end up being removed:

  1. If some frames are empty or fail the ‘shake test’ I’ll rearrange these into the bottom super 2. I then clear the bees down into the bottom super and leave it for the bees.
  2. If the colony is really strong and is unlikely to fit into the brood box(es) I’ll often add a super above the queen excluder to clear the bees down into. Sometimes the bees will add a few dribbles of nectar to this … not enough to ever extract, and I’d prefer they put it in the brood box instead.

In both these situations I’ll want to remove the additional super before winter. I don’t want the bees to have a cold empty space above their heads.

Feed & clear together

I usually do this at the same time that I feed the bees.

I rearrange the boxes so that the ‘leftover’ super is above a crownboard on top of the super that is providing the headspace to accommodate the fondant blocks.

Since access to this top super is through a small hole the bees consider it is ‘outside’ the hive and so empty the remaining nectar and bring it down to the brood box 3.

If there are sealed stores in any of these super frames I bruise 4 the cappings with a hive tool and they’ll then move the stores down.

Substandard colonies

A very good piece of advice to all beekeepers is to “take your winter losses in the autumn”. This means assess colonies in the late summer/early autumn and get rid of those that are weak or substandard 5.

Substandard might mean those with a poor temper.

This is the colony which you put up with all season (despite their yobbo tendencies) because you believe that aggressive bees are productive bees’.

Were they?

Was that one half-filled super of partially-capped honey really worth the grief they gave you all summer?

Unless substandard (not just aggression … running, following, insufficiently frugal in winter etc.) colonies are replaced the overall standard of your bees will never improve.

I’ll discuss how to ‘remove’ them in a few paragraphs.

It’s probably a reasonable estimate to suggest that the ‘best’ third of your colonies should be used to rear more queens and the ‘worst’ third should be re-queened with these 6.

Over time 7 the quality will improve.

Of course, a substandard colony might well make it through the winter perfectly successfully. The same cannot be said for weak colonies.

TLC or tough love?

At the end of the summer colonies should be strong. If they are not then there is probably something wrong. A poorly mated queen, an old and failing queen, disease?

The exception might be a recently requeened colony or a new 5 frame nuc.

Everynuc

Everynuc …

Colonies that are weak at this stage of the season for no obvious reason need attention. Without it they are likely to succumb during the winter. And they’ll do this after you’ve gone to the trouble and expense of feeding and treating them … 8

There are essentially two choices:

  1. Mollycoddle them and hope they pick up. Boosting them with a frame or two of emerging brood may help (but make sure you don’t weaken the donor colony significantly). Moving them from a full hive to a nuc – preferably poly to provide better insulation – may also be beneficial. In a nuc they have less dead space to heat. An analogous strategy is to fill the space in the brood box with ‘fat dummies‘ or – low-tech but just as effective – a big wodge of bubble wrap with a standard dummy board to hold it in place.
  2. Sacrifice the queen from the weak hive and unite them with a strong colony.

Sentimentalism

Of the two I’d almost always recommend uniting colonies.

It’s less work. There’s no potentially wasted outlay on food and miticides. Most importantly, it’s much more likely to result in a strong colony the following spring.

However, we all get attached to our bees. It’s not unusual to give a fading favourite old queen ‘one more chance’ in the hope that next year will be her last hurrah.

Uniting notes

I’ve covered uniting before and so will only add some additional notes here …

Uniting a nuc with a full colony

Uniting a nuc with a full colony …

  • You cannot generate a strong colony by uniting two weak colonies. They’re weak for a reason. Whether they’re weak for the same or different reasons uniting them is unlikely to help.
  • Never unite a colony with signs of disease. All you do is jeopardise the healthy colony.
  • Find the queen and permanently remove her from the weak or poor quality (substandard) colony.
  • If you can’t find the queen unite them with a queen excluder between the colonies. In my limited experience (I usually manage to find the unwanted queen) the bees usually do away with a failing queen when offered a better one, but best to check in a week or so.
  • I generally move the de-queened colony and put it on top of the strong queenright colony.
  • Unite over newspaper and don’t interfere with the hive for at least another week.
  • You can unite one strong colony and two weak colonies simultaneously.
  • Uniting and feeding at the same time is possible.
  • You can unite and treat with a miticide like Amitraz simultaneously. You will have to make a judgement call on whether both boxes need miticide treatment, depending on the strength of the weak colony.
  • If you’re uniting a strong substandard colony and a strong good colony you will need to use an amount of miticide appropriate for a double brood colony (four strips in the case of Amitraz).
Successful uniting ...

Successful uniting …

Season of mists and mellow fruitfulness

The goal of all of the above is to go into autumn with strong, healthy, well-fed colonies that will survive the winter and build up strongly again in the spring.

A very small or weak colony 9 in autumn may survive, but it’s unlikely to flourish the following spring.

“It takes bees to make bees.”

And a weak colony in spring lacks bees, so cannot build up fast.

In contrast, an overwintered strong colony can often yield a nuc in May the following year. You’ve regained your colony numbers, but have a new, young queen in one hive with most of the season ahead for her to prove her worth.

I’ve merged three topics here – clearing supers, stock improvement and getting rid of weak colonies before winter – because all involve some sort of hive manipulation in the early autumn. I usually complete this in late September or early October, with the intention of overwintering strong colonies in single brood boxes packed with bees and stores.


Colophon

The heading of the final paragraph is the opening line of To Autumn by John Keats (1795-1821). Keats wrote To Autumn exactly two hundred years ago (September 1819, his last poem) while gradually succumbing to tuberculosis. Despite this, and his doomed relationship with Fanny Brawne, the poem is not about sadness at the end of summer but instead revels in the ripeness and bounteousness of the season.

Of course, all beekeepers know that the first stanza of To Autumn closes with a reference to bees.

Season of mists and mellow fruitfulness,
  Close bosom-friend of the maturing sun;
Conspiring with him how to load and bless
  With fruit the vines that round the thatch-eves run;
To bend with apples the moss’d cottage-trees,
  And fill all fruit with ripeness to the core;
    To swell the gourd, and plump the hazel shells
  With a sweet kernel; to set budding more,
And still more, later flowers for the bees,
Until they think warm days will never cease,
    For summer has o’er-brimm’d their clammy cells.

 

The flow must go on

Except it doesn’t 🙁

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

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

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

Long-lived bees

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

Seasonal production of sealed brood in Aberdeen, Scotland.

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

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

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

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

The purpose of winter preparations is threefold:

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

I’ll deal with these in reverse order.

Varroa and viruses

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

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

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

Worker bee with DWV symptoms

Worker bee with DWV symptoms

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

But they’re not necessarily healthy …

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

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

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

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

Protecting winter bees

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

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

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

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

Time of treatment and mite numbers

Time of treatment and mite numbers

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

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

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

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

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

Treat with what?

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

Amitraz strip placed in the hive.

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

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

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

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

Feed ’em up

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

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

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

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

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

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

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

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

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

Fancy fondant

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

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

Meaning containers to clean and store.

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

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

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

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

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

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

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

Don’t bother.

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

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

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

Project Fear?


Colophon

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

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

Women without men

The title of the post last week was The end is nigh which, looking at the fate of drones this week, was prophetic.

Shallow depth of field

Watch your back mate … !

After the ‘June gap’ ended queens started laying again with gusto. However, there are differences in the pattern of egg laying when compared to the late spring and early summer.

Inspections in mid/late August 1 show clear signs of colonies making preparations for the winter ahead.

For at least a month the amount of drone brood in colonies has been reducing (though the proportions do not change dramatically). As drones emerge the cells are being back-filled with nectar.

Seasonal production of sealed brood in Aberdeen, Scotland.

The data in the graph above was collected over 50 years ago 2. It remains equally valid today with the usual caveats about year-to-year variation, the influence of latitude and local climate.

Drones are valuable …

Drones are vital to the health of the colony.

Honey bees are polyandrous, meaning the queen mates with multiple males so increasing the genetic diversity of the resulting workers.

There are well documented associations between colony fitness and polyandry, including improvements in population growth, weight gain (foraging efficiency) and disease resistance.

The average number of drones mating with a queen is probably somewhere between 12 and 15 under real world conditions. However studies have shown that hyperpolyandry further enhances the benefits of polyandry. Instrumentally inseminated queens “mated” with 30 or 60 drones show greater numbers of brood per bee and reduced levels of Varroa infestation.

Why don’t queens always mate with 30-60 drones then?

Presumably this is a balance between access, predation and availability of drones. For example, more mating would likely necessitate a longer visit to a drone congregation area so increasing the chance of predation.

In addition, increasing the numbers of matings might necessitate increasing the number of drones available for mating 3.

… and expensive

But there’s a cost to increasing the numbers of drones.

Colonies already invest a huge amount in drone rearing. If you consider that this investment is for colony reproduction it is possible to make comparisons with the investment made in workers for reproduction i.e. the swarm that represents the reproductive unit of the colony.

Comparison of the numbers of workers or drones alone is insufficient. As the graph above shows, workers clearly outnumber drones. Remember that drones are significantly bigger than workers. In addition, some workers are not part of the ‘reproductive unit’ (the swarm).

A better comparison is between the dry weight of workers in a swarm and the drones produced by a colony during the season.

It’s worth noting that these comparisons must be made on colonies that make as many drones as they want. Many beekeepers artificially reduce the drone population by only providing worker foundation or culling drone brood (which I will return to later).

In natural colonies the dry weight of workers and drones involved in colony reproduction is just about 1:1 4.

Smaller numbers of drones are produced, but they are individually larger, live a bit longer and need to be fed through this entire period. That is a big investment.

Your days are numbered

And it’s an investment that is no longer needed once the swarming season is over. All those extra mouths that need feeding are a drain on the colony.

Even though the majority of beekeepers see the occasional drone in an overwintering colony, the vast majority of drones are ejected from the hive in late summer or early autumn.

About now in Fife.

In the video above you can see two drones being harassed and evicted. One flies off, the second drops to the ground.

As do many others.

There’s a small, sad pile of dead and dying drones outside the hive entrance at this time of the season. All perfectly normal and not something to worry about 5.

Drones are big, strong bees. These evictions are only possible because the workers have stopped feeding them and they are starved and consequently weakened.

A drone’s life … going out with a bang … or a whimper.

An expense that should be afforded

Some of the original data on colony sex ratios (and absolute numbers) comes from work conducted by Delia Allen in the early 1960’s.

Other colonies in these studies were treated to minimise the numbers of drones reared. Perhaps unexpectedly these colonies did not use the resources (pollen, nectar, bee bread, nurse bee time etc) to rear more worker bees.

In fact, drone-free or low-drone colonies produced more bees overall, a greater weight of bees overall and collected a bit more honey. This strongly suggests that colonies prevented from rearing drones are not able to operate at their maximum potential.

This has interesting implications for our understanding of how resources are divided between drone and worker brood production. It’s obviously not a single ‘pot’ divided according to the numbers of mouths to feed. Rather it suggests that there are independent ‘pots’ dedicated to drone or worker production.

Late season mating and preparations for winter

The summer honey is off and safely in buckets. Colonies are light and a bit lethargic. With little forage about (a bit of balsam and some fireweed perhaps) colonies now need some TLC to prepare them for the winter.

If there’s any reason to delay feeding it’s important that colonies are not allowed to starve. We had a week of bad weather in mid-August. One or two colonies became dangerously light and were given a kilogram of fondant to tide them over until the supers were off all colonies and feeding and treating could begin. I’ll deal with these important activities next week.

In the meantime there are still sufficient drones about to mate with late season queens. The artificial swarm from strong colony in the bee shed was left with a charged, sealed queen cell.

Going by the amount of pollen going in and the fanning workers at the entrance – see the slo-mo movie above – the queen is now mated and the colony will build up sufficiently to overwinter successfully.


Colophon

Men without Women

Men without women was the title of Ernest Hemingway’s second published collection of short stories. They are written in the characteristically pared back, slightly macho and bleak style that Hemingway was famous for.

Many of these stories have a rather unsatisfactory ending.

Not unlike the fate of many of the drones in our colonies.

Women without men is obviously a reworking of the Hemingway title which seemed appropriate considering the gender-balance of colonies going into the winter.

If I’d been restricted to writing using the title Men without Women I’d probably have discussed the wasps that plague our picnics and hives at this time of the year. These are largely males, indulging in an orgy of late-season carbohydrate bingeing.

It doesn’t do them any good … they perish and the hibernating overwintering mated queens single-handedly start a new colony the following spring.

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.