Category Archives: Varroa

Midwinter, no; mites, yes

There’s a certain irony that the more conscientious you are in protecting your winter bees from the ravages of Varroa in late summer, the more necessary it is to apply a miticide in the winter.

Winter bees are the ones that are in your hives now 1.

They have a very different physiology to the midsummer foragers that fill your supers with nectar. Winter bees have low levels of juvenile hormone and high levels of vitellogenin. They are long-lived – up to 8 months – and they form an efficient thermoregulating cluster when the external temperature plummets.

Winter bees production

In the temperate northern hemisphere, winter bees are reared from late summer/early autumn onwards. The combination of reductions in the photoperiod (day length), temperature and forage availability triggers changes in brood and forager pheromones.

Factors that influence winter bee production

Together these induce the production of winter bees.

For more details see Overwintering honey bees: biology and management by Döke et al., (2010).

Day length reduces predictably as summer changes to autumn. In contrast, temperature and forage availability (which itself is influenced by temperature and rainfall … and day length) are much more variable (so less predictable).

All of which means that you cannot be sure when the winter bees are produced.

If there’s an “Indian summer“, with warm temperatures stretching into late October, the bees will be out working the ivy and rearing good amounts of brood late into the year. The busy foragers and high(er) levels of brood pheromone will then delay the production of winter bees.

Conversely, low temperatures and early frosts reduce foraging and brood production, so bringing forward winter bee production.

It’s an inexact science.

You cannot be sure when the winter bees will be produced, but you can be sure that they will be reared.

Protect your winter bees

And if they are being reared, you must protect them from Varroa and the viral payload it delivers to developing pupae. Most important of these viruses is deformed wing virus (DWV).

Worker bee with DWV symptoms

Worker bee with DWV symptoms

Aside from “doing what it says on the tin” i.e. causing wing deformities and other developmental defects in some brood, DWV also reduces the longevity of winter bees.

And that’s a problem.

If they die sooner than they should they cannot help in thermoregulating the winter cluster.

And that results in the cluster having to work harder to keep warm as it gets smaller … and smaller … and smaller …

Until it’s so small it cannot reach its food reserves (isolation starvation) or freezes to death 2.

So, to protect your winter bees, you need to treat with an appropriate miticide in late summer. This reduces the mite load in the hive by up to 95% and so gives the winter bees a very good chance of leading a long and happy life 😉

Time of treatment and mite numbers

Time of treatment and mite numbers

I discussed this in excruciating detail in 2016 in a post titled When to treat?.

The figure above was taken from that post and is described more fully there. The arrow indicates when winter bees are produced and the variously coloured solid lines indicate mite numbers when treated in mid-July to mid-November.

The earlier you treat (indicated by the sudden drop in the mite count) the lower the peak mite numbers when the winter bees are being reared.

Note that the mite numbers indicated on the right hand vertical axis are not ‘real’ figures. They depend on the number present at the start of the year. In the figure above I “primed” the in silico modelled colony with just 20 mites. This will become very important in a few paragraphs.

Late season brood rearing

Compare the blue line (mid-August treatment) with the cyan line 3 (mid-October treatment) in the figure above.

The mid-October treatment really hammers the mite number down and they remain low until the end of the year 4.

The reason the mite numbers remain low after a mid-October treatment is that there is little or no brood being reared in the colony during this period.

Mites need brood, and specifically sealed brood, to reproduce on.

In the absence of brood the mites ‘colony surf‘, riding around as phoretic mites on nurse bees (or any bees if there aren’t the nurse bees they prefer).

And that late season brood rearing is the reason the end-of-year mite number for the colony treated in mid-August (the blue line) remains significantly higher.

Mites that survive the miticide in August simply carry on with their sordid little destructive lives, infesting the ample brood available (which could even include some highly mite-attractive and productive drone brood) and reproducing busily.

So, the earlier you treat, the more mites remain in the hive at the end of the year.

Weird, but true.

Early season brood rearing

The winter bees don’t ‘just’ get the colony through the winter.

As the day length increases and the temperature rises the colony starts rearing brood again. Depending upon your latitude it might never stop, but the rate at which it rears brood certainly increases in early spring.

Or, more correctly, in mid- to late-winter.

And it’s the winter bees that do this brood rearing. As Grozinger and colleagues state Once brood rearing re-initiates in late winter/early spring, the division of labor resumes among overwintered worker bees.”

Some winter bees revert to nurse bee activity, to rear the next generation of bees.

And this is another reason why strong colonies overwinter better … not because they (also) survive the cold better 5, but because there are more bees available to take on these brood rearing activities.

Strong, healthy colonies build up better in early spring.

Colonies that are weak in spring and stagger through the first few months of the year, never getting close to swarming, are of little use for honey production, more likely to get robbed out and may not build up enough for the following winter.

Midwinter mite treatments

Which brings us back to the need for miticide treatment in midwinter.

The BEEHAVE modelled colony shown in the graph above was ‘primed’ at the beginning of the season with 20 mites. These reproduced and generated almost 800 mites over the next 10-11 months.

What do you think would happen if you start the year with 200 mites, rather than 20?

Like the 200 remaining at the year end when you treat in mid-August?

Lots of mites … probably approaching 8000 … that’s almost as many mites as bees by the end of the season.

So, one reason to treat in the middle of winter is to reduce mite levels later in the season. The smaller the number you start with, the less you have later.

Vapour leaks out ...

Vaporisation … oxalic acid vapour leaks out …

But at the beginning of the season these elevated levels of mites could cause problems. High levels of mites and low levels of brood is not a good mix.

There’s the potential for those tiny patches of brood to become mite-infested very early in the season … this helps the mites but hinders the bees.

Logically, the more mites present at the start of brood rearing, the more likely it is that colony build up will be retarded.

So that’s two reasons to treat with miticides – usually an oxalic-acid containing treatment – in midwinter.

Midwinter? Or earlier?

When does the colony start brood rearing again in earnest?

This is important as the ‘midwinter’ treatment should be timed for a period before this when the colony is broodless. This is to ensure that all the mites are phoretic and ‘easy to reach’ with a well-timed dribble of Api-Bioxal.

In studies over 30 years ago Seeley and Visscher demonstrated that colonies have to start brood rearing in midwinter to build up enough to have the opportunity to swarm in late spring. These were colonies in cold climates, but the conditions – and season length – aren’t dramatically different to much of the UK.

Low temperatures regularly extend into January or February. The temperature is also variable year on year. It therefore seems (to me) that the most likely trigger for new brood rearing is increasing day length 6.

The apiary in winter ...

The apiary in winter …

I therefore assume that colonies may well be rearing brood very soon after the winter solstice.

I’m also aware that my colonies are almost always broodless earlier in the winter … or even what is still technically late autumn.

This is from experience of both direct (opening hives) or indirect (fresh brood mappings on the Varroa tray) observation.

Hence the “Midwinter, no” title of this post.

Don’t delay

I therefore treat with a dribbled or vaporised oxalic acid-containing miticide in late November or early December. In 2016 and 2017 it was the first week in December. Last year it was a week  later because we had heavy snow.

This year it was today … the 28th of November. With another apiary destined for treatment this weekend.

If colonies are broodless there is nothing to be gained by delaying treatment until later in the winter.

Most beekeepers treat between Christmas and New Year. It’s convenient. They’re probably on holiday and it is a good excuse to escape the family/mince pies/rubbish on the TV (delete as appropriate).

But it might be too late … don’t delay.

If colonies are broodless treat them now.

If you don’t and they start rearing brood the mites will hide away and be unreachable … but their daughters and granddaughters will cause you and your bees problems later in the season.

Finally, it’s worth noting that there’s no need to coordinate winter treatments. The bees aren’t flying and the possibility of mites being transferred – through robbing or drifting – from treated to untreated colonies is minimal.


 

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 …

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.

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).

Midseason mite management

The Varroa mite and the potpourri of viruses it transmits are probably the greatest threat to our bees. The number of mites in the colony increases during the spring and summer, feeding and breeding on sealed brood.

Pupa (blue) and mite (red) numbers

In early/mid autumn mite levels reach their peak as the laying rate of the queen decreases. Consequently the number of mites per pupa increases significantly. The bees that are reared at this time of year are the overwintering workers, physiologically-adapted to get the colony through the winter.

The protection of these developing overwintering bees is critical and explains why an early autumn application of a suitable miticide is recommended … or usually essential.

And, although this might appear illogical, if you treat early enough to protect the winter bees you should also treat during a broodless period in midwinter. This is necessary because mite replication goes on into the autumn (while the colony continues to rear brood). If you omit the winter treatment the colony starts with a higher mite load the following season.

And you know what mites mean

Mites in midseason

Under certain circumstances mite levels can increase to dangerous levels 1 much earlier in the season than shown in the graph above.

What circumstances?

I can think of two major reasons 2. Firstly, if the colony starts the season with higher than desirable mite levels (this is why you treat midwinter). Secondly, if the mites are acquired by the colony from other colonies i.e. by infested bees drifting between colonies or by your bees robbing a mite infested colony.

Don’t underestimate the impact these events can have on mite levels. A strong colony robbing out a weak, heavily infested, collapsing colony can acquire dozens of mites a day.

The robbed colony may not be in your apiary. It could be a mile away across the fields in an apiary owned by a treatment-free 3 aficionado or from a pathogen-rich feral colony in the church tower.

How do you identify midseason mite problems?

You need to monitor mite levels, actively and/or passively. The latter includes periodic counts of mites that fall through an open mesh floor onto a Varroa board. The National Bee Unit has a handy – though not necessarily accurate – calculator to determine the total mite levels in the colony based on the Varroa drop.

Out, damn'd mite ...

Out, damn’d mite …

Don’t rely on the NBU calculator. A host of factors are likely to influence the natural Varroa drop. For example, if the laying rate of the queen is decreasing because there’s no nectar coming in there will be fewer larvae at the right stage to parasitise … consequently the natural drop (which originates from phoretic mites) will increase.

And vice versa.

Active monitoring includes uncapping drone brood or doing a sugar roll or alcohol wash to dislodge phoretic mites.

Overt disease

But in addition to looking for mites you should also keep a close eye on workers during routine inspections. If you see bees showing obvious signs of deformed wing virus (DWV) symptoms then you need to intervene to reduce mite levels.

High levels of DWV

High levels of DWV …

During our studies of DWV we have placed mite-free 4 colonies into a communal apiary. Infested drone cells were identified during routine uncapping within 2 weeks of our colony being introduced. Even more striking, symptomatic workers could be seen in the colony within 11 weeks.

Treatment options

Midseason mite management is more problematic than the late summer/early autumn and midwinter treatments.

Firstly, the colony will (or should) have good levels of sealed brood.

Secondly, there might be a nectar flow on and the colony is hopefully laden with supers.

The combination of these two factors is the issue.

If there is brood in the colony the majority (up to 90%) of mites will be hiding under the protective cappings feasting on sealed pupae.

Of course, exactly the same situation prevails in late summer/early autumn. This is why the majority of approved treatments – Apistan (don’t), Apivar, Apiguard etc. – need to be used for at least 4-6 weeks. This covers multiple brood cycles, so ensuring that the capped Varroa are released and (hopefully) slaughtered.

Which brings us to the second problem. All of those named treatments should not be used when there is a flow on or when there are supers on the hive. This is to avoid tainting (contaminating) the honey.

And, if you think about it, there’s unlikely to be a 4-6 week window between early May and late August during which there is not a nectar flow.

MAQS

The only high-efficacy miticide approved for use when supers are present is MAQS 5.

The active ingredient in MAQS is formic acid which is the only miticide capable of penetrating the cappings to kill Varroa in sealed brood 6. Because MAQS penetrates the cappings the treatment window is only 7 days long.

I have not used MAQS and so cannot comment on its use. The reason I’ve not used it is because of the problems many beekeepers have reported with queen losses or increased bee mortality. The Veterinary Medicines Directorate MAQS Summary of the product characteristics provides advice on how to avoid these problems.

Kill and cure isn’t the option I choose 😉 7

Of course, many beekeepers have used MAQS without problems.

So, what other strategies are available?

Oxalic acid Api-Bioxal

Many beekeepers these days – if you read the online forums – would recommend oxalic acid 8.

I’ve already discussed the oxalic acid-containing treatments extensively.

Importantly, these treatments only target phoretic mites, not those within capped cells.

Trickled oxalic acid is toxic to unsealed brood and so is a poor choice for a brood-rearing colony.

Varroa counts

In contrast, sublimated (vaporised) oxalic acid is tolerated well by the colony and does not harm open brood. Thomas Radetzki demonstrated it continued to be effective for about a week after administration, presumably due to its deposition on all internal surfaces of the hive. My daily mite counts of treated colonies support this conclusion.

Consequently beekeepers have empirically developed methods to treat brooding colonies multiple times with vaporised oxalic acid Api-Bioxal to kill mites released from capped cells.

The first method I’m aware of published for this was by Hivemaker on the Beekeeping Forum. There may well be earlier reports. Hivemaker recommended three or four doses at five day intervals if there is brood present.

This works well 9 but is it compatible with supers on the hive and a honey flow?

What do you mean by compatible?

The VMD Api-Bioxal Summary of product characteristics 10 specifically states “Don’t treat hives with super in position or during honey flow”.

That is about as definitive as possible.

Another one for the extractor ...

Another one for the extractor …

Some vapoholics (correctly) would argue that honey naturally contains oxalic acid. Untreated honey contains variable amounts of oxalic acid; 8-119 mg/kg in one study 11 or up to 400 mg/kg in a large sample of Italian honeys according to Franco Mutinelli 12.

It should be noted that these levels are significantly less than many vegetables.

In addition, Thomas Radetzki demonstrated that oxalic acid levels in spring honey from OA vaporised colonies (the previous autumn) were not different from those in untreated colonies. 

Therefore surely it’s OK to treat when the supers are present?

Absence of evidence is not evidence of absence

There are a few additional studies that have shown no marked rise in OA concentrations in honey post treatment. One of the problems with these studies is that the delay between treatment and honey testing is not clear and is often not stated 13.

Consider what the minimum potential delay between treatment and honey harvesting would be if it were allowed or recommended.

One day 14.

No one has (yet) tested OA concentrations in honey immediately following treatment, or the (presumable) decline in OA levels in the days, weeks and months after treatment. Is it linear over time? Does it flatline and then drop precipitously or does it drop precipitously and then remain at a very low (background) level?

Oxalic acid levels over time post treatment … it’s anyones guess

How does temperature influence this? What about colony strength and activity?

Frankly, without this information we’re just guessing.

Why risk it?

I try and produce the very best quality honey possible for friends, family and customers.

The last thing I would want to risk is inadvertently producing OA-contaminated honey.

Do I know what this tastes like? 15

No, and I’d prefer not to find out.

Formic acid and thymol have been shown to taint honey and my contention is that thorough studies to properly test this have yet to be conducted for oxalic acid.

Until they are – and unless they are statistically compelling – I will not treat colonies with supers present … and I think those that recommend you do are unwise.

What are the options?

Other than MAQS there are no treatments suitable for use when the honey supers are on. If there’s a good nectar flow and a mite-infested colony you have to make a judgement call.

Will the colony be seriously damaged if you delay treatment further?

Quite possibly.

Which is more valuable 16, the honey or the bees?

One option is to treat, hopefully save the colony and feed the honey back to the bees for winter (nothing wrong with this approach … make sure you label the supers clearly!).

Another approach might be to clear then remove the supers to another colony, then treat the original one.

However, if you choose to delay treatment consider the other colonies in your own or neighbouring apiaries. They are at risk as well.

Finally, prevention is better than cure. Timely application of an effective treatment in late summer and midwinter should be sufficient, particularly if all colonies in a geographic area are coordinately treated to minimise the impact of robbing and drifting.

I’ve got two more articles planned on midseason mite management for when the colony is broodless, or can be engineered to be broodless 17.


 

Bait hive guide

Spring this year is developing well. Even here on the chilly east coast of Scotland colonies are looking good and flying strongly when the sun is out. Large amounts of pollen are being taken in and there’s every sign that the hives are queenright and rearing lots of brood 1.

It’s too soon 2 to open the colonies but it’s not too soon to be thinking about the consequences of the inevitable continued expansion over the next few weeks.

Most healthy colonies will make preparations to swarm, often between late April and mid-June. The timing varies depending upon a host of factors including colony strength, climate, weather, forage, build up and beekeeper interventions.

Swarm prevention and control

You, like all responsible beekeepers, will use appropriate swarm prevention methods. Supers added early, ensure the brood box has space for laying etc.

In due course, once the colony gets bigger and stronger, you’ll notice queen cells and immediately deploy your chosen swarm control method e.g. the classic Pagden artificial swarm, the nucleus method I described last week, Demaree, vertical splits or – if you’re feeling ambitious – a Taranov board 3.

Which will of course be totally successful 😉

But just in case it isn’t …

… and just in case the beekeeper a couple of fields away is forgetful, unobservant, clumsy, on holiday, in prison or has some other half-baked excuse, be prepared for swarms.

As an aside, other than just walking around the fields, you can easily find hives near you by searching on Google maps and you can get an idea of the local beekeeper density 4 using the National Bee Unit’s Beebase.

You might think you know all the local beekeepers through your association, but it’s surprising the number who just ‘do their own thing’.

Swarms

This isn’t the place to discuss swarms in much detail. Here’s a quick reminder:

  1. The colony ‘decides’ to swarm and starts to make queen cells.
  2. Almost certainly, scout bees start to check out likely sites the swarm could occupy in the future 5.
  3. The swarm leaves the hive on the first calm, warm, sunny day, usually early in the afternoon, once the queen cells are capped. The prime swarm contains the mated, laying queen and about 75% of the worker bees 6.
  4. The swarm gathers around the queen and sets up a bivouac hanging from a convenient spot (tree, gatepost, bush, fence etc.) near to the hive. They rarely move more than 50 metres. It’s worth emphasising here that the spot they choose is convenient to the bees, but may be at the top of a 60 foot cypress. It may not be particularly convenient for the beekeeper 😉
  5. Scout bees continue to check out likely final sites to establish the new colony, returning to the swarm and ‘persuading’ other scouts (by doing a version of the waggle dance) so that, finally, a consensus is reached. This consensus is essentially based upon the suitability of the sites being surveyed.
  6. The scout bees lead the swarm to the new location, they move in and establish a new colony.

If you’re lucky you will be able to recapture the swarm if the spot they choose for their bivouac is within reach, not above a stream, in a huge thorny bush or on an electricity pylon.

A small swarm ...

A small swarm …

I say ‘recapture’ because, since the bivouac is usually near the issuing hive, it’s probably come from one of your own hives (unless you are snooping around your neighbouring apiaries 7).

But what if you miss the bivouacked swarm? Or if your neighbour misses it?

Those bees are going to look for a suitable location to set up home.

If you provide a suitable location, you can get them to hive themselves without the grief of falling off a ladder, toppling into a stream, getting lacerated with thorns or electrocution

This is where the bait hive comes in. Leave a couple in suitable locations and you can lure your own and other swarms to them.

Freebees 🙂

What do scouts look for?

The scout bees look for the following:

  1. A dark empty void with a volume of about 40 litres.
  2. Ideally located reasonably high up.
  3. A solid floor.
  4. A small entrance of about 10cm2, at the bottom of the void, ideally south facing.
  5. Something that ‘smells’ of bees.

What I’ve just described is … a used beehive 8.

More specifically, it’s a single National brood box (or two stacked supers) with a solid floor and a roof, containing one old dark frame of drawn comb pushed up against the back wall.

No stores, no pollen 9, just a manky old dark comb. The sort of thing you should be turning into firelighters.

That’s all you need.

However, you can improve things by giving the bees somewhere to start drawing comb and siting the hive in a location that makes your beekeeping easier.

Des Res

The first thing swarms do when they move in is start drawing comb. You can populate the bait hive with a few foundationless frames so they’ve got somewhere to start.

Bait hive ...

Bait hive …

In my view foundationless frames are much better than frames with foundation for bait hives. The scout bees measure the size of the void by flying around randomly inside 10. If you have sheets of foundation they’ll crash into it frequently, effectively giving them the impression that the void is smaller than it really is. And therefore making it less attractive to the scouts.

You can improve the smell of the hive by adding a little lemongrass oil to the top bar of one of the frames. Don’t overdo it. A drop or two every 7-10 days is more than ample.

If you do use foundationless frames make sure the hive is level. If you don’t the comb will be drawn at an angle to the frames which makes everything harder work later in the season. Your smartphone probably contains a spirit level function that makes levelling the bait hive very easy.

Location

But not if it’s above head height, or you’re teetering on top of a ladder …

It was Tom Seeley who worked out most things about scout bees and swarms (see his excellent book Honeybee Democracy). This included the observations that they favoured bait hives situated high up.

Believe me, it’s a whole lot easier if the bait hive is on a standard hive stand. It’s easier to level, it’s easier to check and it’s easier – in due course – to retrieve.

Bait hive

Bait hive

I’ve previously discussed how far swarms prefer to move from their original hive. Contrary to popular opinion (and perhaps illogically) they tend to prefer to move shorter distances i.e. 20m >> 200m >> 400m. However, there are also studies that show swarms moving a kilometre or more.

Don’t get hung up on this detail. Stick out a bait hive or two and, if there are swarming colonies in range, they’ll find it.

I always leave a bait hive in my apiaries and one or two in odd corners of the garden. In the last few years I’ve never failed to attract swarms to the bait hives, and know for certain that some have moved in from over a mile away as the bee flies (thanks Emma 😉 ).

Mites and swarms

Assuming you don’t have the luxury of living in Varroa-free areas of the UK (or anywhere in Australia) then the incoming swarm will contain mites. Studies have shown that ~35% of the mite population of a colony leaves with the swarm.

But, for about the first week after the swarm sets up home in your bait hive, what’s missing from the new arrivals is sealed brood. Therefore the mites are all phoretic.

Do not delay. Treat the swarm with an appropriate miticide to knock back the mite population by ~95%. An oxalic acid-containing treatment is ideal. Single dose, relatively inexpensive, easy to administer (trickled or vaporised) and well tolerated by the bees.

Varroa treatment ...

Varroa treatment …

You have eight days from the swarm arriving to there being sealed brood in the colony

Far better to slaughter the mites now. In a few months their numbers will have increased exponentially and the majority will be in capped cells and more difficult to treat.


 

Hanging around

I’ve recently discussed the misnamed ‘phoretic’ phase in the life cycle of Varroa destructor. Here we’ll briefly explore some features of this important, but non-reproductive, phase. It’s important because, as I’ll show, it influences subsequent mite reproduction.

I won’t rehash the life cycle of Varroa in detail as I’ve covered it previouslyVarroa is an ectoparasite of honey bees. It reproduces in capped cells, feeding on the developing pupa. A mated female mite enters the cell a few hours before capping and she and her incestuously mated daughters are released when the bee emerges.

The longer pupal development takes, the more progeny mites are produced, so Varroa has evolved to preferentially infest drone brood.

A smorgasbord of viruses

As an ectoparasite of honey bees, Varroa is responsible for the transmission of a smorgasbord of pathogenic viruses to the developing pupa. Subsequent virus replication, particularly by the aptly-named deformed wing virus, can result in developmental deformities.

Worker bee with DWV symptoms

Worker bee with DWV symptoms

Emerging workers with deformities are rapidly ejected from the hive. Other infested workers, with high viral levels, have reduced longevity. This is probably what accounts for the majority of overwintering colony losses. It may also explain so-called ‘isolation starvation‘.

The ‘phoretic’ phase

Mites outside capped cells are termed ‘phoretic’ mites. Recent studies have indicated that these mites are feeding on the workers to which they are attached. The same studies have shaken the long-held assumption that Varroa feeds on haemolymph 1 by rather neatly demonstrating that it is the fat body tissue of the bee that is the plat du jour.

The duration of the ‘phoretic’ phase is dependent upon the state of the colony. Since it is defined as the phase in which mites are not associated with developing pupae, in a broodless colony all the mites are ‘phoretic’. Under these circumstances mites remain ‘phoretic’ until either brood is produced, or they fall (or are groomed) off and drop through the open mesh floor.

The duration of the ‘phoretic’ phase

In colonies with ample brood the ‘phoretic’ phase is, on average, 6 days in length. The range often quoted is 4 – 11 days. The absolute figure must depend upon a number of factors. These include the chance of a mite encountering a late-stage larva. This is presumably influenced by the amount of suitable-aged brood in the colony and – because there is a division of labour in the hive – the type of bee upon which the mite is riding around the colony on.

For the purpose of this post we’ll consider bees of three ages – newly emerged, nurse bees and foragers. Newly emerged bees (days 1-2 post emergence) clean cells and nurse bees (days 3-11) feed developing larvae. Older bees are involved in wax production (days 12-17) and foraging (>18 days until death).

Logic would dictate that mites would ‘choose’ 2 to associate with bees that bring them into contact with developing larvae of the right age to infest.

Do they?

Hanging around with nurses

Xie et al., (2016)3 assembled artificial colonies containing equal numbers of new bees, nurse bees and foragers, all suitably marked so their age was known. These colonies were provided with a queen, open brood and stores. At the start of the experiment the colonies had 1500 bees and low Varroa levels.

The scientists then introduced 200 ‘phoretic’ mites from another colony 4 and left the colonies for 48 hours. They then age-sorted the bees and harvested all the ‘phoretic’ mites by washing them off in alcohol.

'Phoretic' mites prefer nurse bees

‘Phoretic’ mites prefer nurse bees

On average, ~16% of the nurse bees had ‘phoretic’ mites attached. In contrast, only ~10% of the foragers and ~5% of the new bees had mites. These studies involved seven individual experiments, in two countries and two separate years, using a different source colony for the mites. The statistics are significant.

So mites prefer nurse bees.

Is this ‘simply’ 5 because the nurse bees are more likely to bring the mite into close proximity with a suitably-aged larvae?

Or does associating with, and presumably feeding on, nurse bees have other benefits for the mite?

Mite fecundity and fitness

Fecundity is the reproductive productiveness 6 of an organism.

We’ve obliquely tackled this subject recently. Using an in vitro artificial ‘feed packet’ system, Ramsey and colleagues demonstrated that mites fed on the fat body of bees laid more eggs i.e. they had higher fecundity.

Xie et al., also tested fecundity of ‘phoretic’ mites from newly emerged bees, nurse bees and foragers. They did this by manually harvesting mites after a 3 day ‘phoretic’ phase, adding them to a pre-pupa and then counting the number of progeny female mites 9 days later.

Mite fecundity and fitness

Mite fecundity and fitness

‘Phoretic’ mites from nurse bees exhibited higher fecundity (more female offspring), higher fitness (more mature female offspring) and lower infertility (female mites that did not generate offspring).

So evolution has elegantly resulted in ‘phoretic’ mites associating with the right type of bee to bring them close to developing larvae (upon which they reproduce) and made them better able to reproduce once they get there.

Why do Varroa mites prefer nurse bees?

This is the title of the Xie et al., paper.

Xie et al., sort of answer the question they posed in the title. What they don’t do is explain why ‘phoretic’ mites on nurse bees are more fecund. However, the recent Ramsey paper suggests that this may be because nurse bees have a larger fat body and higher levels of vitellogenin.

If they’re better fed perhaps they produce more viable offspring? 7.

Another known unknown (semiochemicals)

How do mites detect the differences between new, nurse and older bees?

Perhaps they ‘smell’ different?

Mites preferentially infest drone brood because it produces a range of methyl and ethyl esters of straight-chain fatty acids, in particular methyl palmitate.

Similarly, the preference for nurse bees might be explained by their production of another semiochemicals 8. If we could identify this semiochemical it might be possible to create a ‘sponge’ soaked in it that attracted all the mites in the colony.

A bit simplistic, but you get the idea.

In reality, it’s likely that nurse bees are identified by the relative strengths of a range of semiochemicals produced by bees of different ages.

In reality it’s also likely that dropping a ‘sponge’ soaked in eau de nurse bee into the colony could unbalance all sorts of other events in the hive … 🙁

I told you it wasn’t simple.


Rattus norvegicus

Rattus norvegicus

Hanging Around is the fifth track on Rattus norvegicus, the 1977 debut album of one of the finest rock/punk bands of all time, The Stranglers. The album also includes the incomparable Peaches and (Get a) Grip (On yourself), both of which were released as singles.

No more heroes from the same year, but a different album, is also a classic by the same band.

You had to be there … I was 😉

 

 

Pedantically not phoresy

The life cycle of the ectoparasitic mite Varroa destructor essentially consists of two stages. The first is within the capped cell, where reproduction takes place. The second occurs outside the capped cell when the recently-mated female progeny mites matures while riding around the colony attached to a nurse bee.

Almost without exception this second stage is termed the phoretic phase.

It isn’t.

Phoresy

Phoretic is an adjective of the word phoresy. Phoresy is derived from the French phorésie which, in turn, has its etymological origins in the Ancient Greek word φορησις.

And φορησις means being carried.

Which partly explains why the correct definition of the word phoresy is:

An association between two organisms in which one is carried on the body of the other, without being a parasite [OED]

Phoresy has been in use for about a century, with the word phoretic first being recorded in the Annals of the Entomological Society of America (25:79) in 1932:

It is possible, as suggested by Banks (1915), that such young mites are phoretic, being carried about from place to place on the host’s surfaces.

And, no, they weren’t discussing Varroa.

“Without being a parasite”

These are the critical words in the dictionary definition of phoresy which makes the use of the word phoretic incorrect when referring to mites on nurse bees.

Because mites on nurse bees are feeding – or at least a significant proportion 1 of them are.

They are therefore being parasitic and so shouldn’t be described as phoretic.

Om, nom, nom 2

Last week I discussed the recent Samual Ramsey paper presenting studies supporting the feasting of Varroa on the fat body of bees.

In the study they harvested bees from a heavily mite-infested hive and recorded the location on the bee to which the mite was attached.

The majority were attached to the left underside of the abdomen. More specifically, the mite was wedged underneath the third abdominal tergite 3.

What were they doing there? Hiding?

Yes … but let’s have a closer look.

Ramsey and colleagues removed some of the mites and used a scanning electron microscope to examine the attachment point on the bee. Underneath the tergite there is a soft membrane. The imprint of the body of the mite was clearly visible on the membrane.

Varroa feeding location on adult bee

Scanning EM of Varroa feeding location on adult bee

The footpads of the mite were left attached to the membrane (left image, white arrows), straddling an obvious wound where the mouthparts had pierced the membrane (black arrow). Between them, the inverted W shape is presumably the imprint of the lower carapace of the mite.

The close-up image on the right even shows grooves at the wound site consistent with the mouthparts of the mite.

These mites were feeding.

Extraoral digestion

Varroa belongs to the order (a level of classification) Mesostigmata. Most mesostigmatids feed using a process termed extraoral digestion.

Extraoral digestion has also been termed ‘solid-to-liquid’ feeding. It involves the injection of potent hydrolytic enzymes which digest solid tissue, converting it to a semi-solid that can be easily ingested. It can reduce the time needed to feed and it increases the nutrient density of the consumed food.

If Varroa fed on haemolymph it wouldn’t need to use extraoral digestion. Instead it would need all sorts of adaptations to a high volume, low nutrient diet. Varroa doesn’t have these. It has a simple tube-like gut parts of which lack enzymatic activity … implying that digestion occurs elsewhere.

A picture is worth a thousand words

Do the images of feeding mites support the use of extraoral digestion?

EM cross-section of Varroa feeding

EM cross-section of Varroa feeding

The image above 4 shows the cross-section of a Varroa (V), wedged under the tergite (Te), feeding through a hole (arrow in the enlargement on the right) in the membrane (M). The fat body (FB) is immediately underneath the membrane. The scale bar is incorrectly labelled 5.

A close-up of the wound site shows further evidence for extraoral digestion.

Feeding wound at higher magnification

Feeding wound at higher magnification

Beneath the wound site (C, arrow) are remnants of fat body cells (white arrow) and bacteria (black arrow; of two types, shown in D). A closer look still at the remnants of the fat body (E and F) shows cell nuclear debris (blue arrows) and lipid droplets (red arrows).

These images are entirely consistent with extraoral digestion of fat body tissue by feeding Varroa. The presence of bacteria near the wound suggests that bacterial infection may result from Varroa feeding, possibly further contributing to disease in bees.

So, pedantically it’s not phoresy

So-called phoretic mites, unless they’re on the thorax or head of the bee, are not really phoretic. They are being carried about, but they are also likely feeding. By definition that excludes them from being phoretic.

Instead they are ectoparasites of adult bees.

What are the chances that beekeepers will stop using the term phoretic?

Slim to none I’d predict 6.

And, of course, it doesn’t really matter what the correct term for them is.

What’s more important is that beekeepers remember that it’s at this stage that mites are susceptible to all miticides.

The June gap

But it’s also worth thinking about the potential impact of brood breaks.

During brood breaks all the mites in the colony must be ‘phoretic’.

Generally, the majority of the mites in a hive are in capped cells. Depending upon the stage of the season, the egg-laying rate of the queen and other factors, up to 90% of the mites are associated with developing pupae.

But as the laying rate dwindles more and more mites are released from cells and become ‘phoretic’, unable to find a suitable late-stage larva to infest.

And which bees do the mites associate with?

Nurse bees primarily, for reasons I’ll discuss in the future. But – spoiler alert – one of the reasons is likely to be that they have a larger fat body.

So, a mid-season brood break (e.g. the ‘June gap’) is likely to result in lots more nurse bees becoming both the carriers and the dinner of the mite population.

Some or many of the nurse bee cohort may perish, perhaps from damage to the fat body or from the viruses acquired from the mite. However, bees exhibit phenotypic plasticity, meaning that older bees can revert to being nurse bees when the queen starts laying again.

Late season brood breaks

In late summer mite levels are usually at their highest in the hive. A brood break occurring now will release a very large number of mites to parasitise the adult bee population.

Presumably these mites select the bees best able to support them 7.

And which bees are these? The nurse bees of course. But it’s also worth remembering that there are key physiological similarities between nurse bees and winter bees. Both have low levels of juvenile hormone and high levels of vitellogenin (stored in the fat body).

So I’d bet that the ‘phoretic’ mites during a late season brood break would also preferentially associate with any early-produced winter bees.

Furthermore, once the queen starts laying again – perhaps in early/mid-autumn – the winter bees being produced would be subjected to the double-whammy of high levels of mite infestation and potential damage from ‘phoretic’ mites.

Practical considerations

More work is required to model or actually measure the impact of late season brood breaks, high levels of ‘phoretic’ mites, nurse bee numbers and winter bee development.

Compare two colonies of a similar size with a similar mite load, treated at the same time in early autumn with an appropriate miticide. If one of them experienced a late summer brood break (pre-treatment) and consequent high levels of ‘phoretic’ mites, does this reduce the chances of the colony surviving overwinter?

Who knows? Lots and lots of variables …

Fundamentally, it remains important to treat colonies early enough to protect the winter bee population. You’ve heard this from me before and you’ll hear it again.

However, it’s something to think about and I can see ways in which it might influence the strategy and timing of mite control used. I’ll return to this sometime in the future.


 

Chewin’ the fat

A little over a year ago reports started to circulate of a study showing that Varroa feed on the fat body of bees rather than on haemolymph.

Having worked in Glasgow through the early noughties the title of this post was a no-brainer and an outline draft was written in December 2017. However, the peer-reviewed paper wasn’t published until last month, so it’s only now we’ve got the chance to judge the study and consider its implications.

Varroa feed on hameolymph, right?

Historically this was the accepted dogma. However, the experimental data supporting this conclusion – based upon labelling bees with radioactive isotopes and seeing what the mites acquired after feeding – was really not definitive. The experiments had been done in the 1970’s and the specificity of the labelling was a bit dubious. In addition, during the intervening period scientists had determined that, unlike vertebrate blood which is rich in cells and nutrients 1, haemolymph has little of either and is actually a pretty lousy food source.

In addition, and somewhat more circumstantially, Varroa control using chemotherapeutics fed to bees (and subsequently taken up by the mite during feeding) had been relatively disappointing.

Perhaps these chemicals weren’t getting to the right tissues of the bee?

Perhaps Varroa don’t feed on haemolymph after all?

The Ramsey study

This new study reports three independent experiments that, together, indicate that Varroa actually feed on the fat body of bees, rather than on haemolymph. The paper is so-called ‘open access’, so anyone can access it and therefore I’ll just provide a synopsis of the important bits.

The questions Samual Ramsey and colleagues attempted to answer were:

  1. Where on the bee do mites feed? Is it primarily or exclusively near the fat body?
  2. When Varroa feeds, what host tissues are ingested?
  3. What sort of diet is required to maintain Varroa and allow their reproduction in vitro2.

Location, location, location

The authors counted phoretic mites on 104 bees. Over 95% of them were located on the underside of the body, predominantly on the left side of the bee, under the tergite or sternite3 on the third metasomal segment (i.e. the second visible segment of the abdomen).

Mite location on nurse bees

Mite location on nurse bees

This position is consistent with feeding on the fat body tissues which are most abundant under the inner ventral surface of the metasoma.

Seeing red

Bees were fed with Nile red, a lipophilic fluorescent stain that preferentially accumulates in the fat body. They co-fed bees with uranine, a differently coloured fluorophore that accumulates in the haemolymph. They then allowed mites to feed on the fluorescently labelled bees and subsequently photographed the mites under fluorescent light.

The rationale here was straightforward. If the mites fed on the fat body they would stain red due to taking up the Nile red stain.

Mites visualised after feeding on fluorescently labelled bees

Mites visualised after feeding on fluorescently labelled bees

Which they did.

It was notable that the red stain predominantly accumulated in the rectum and gut of the mite (image O above). The authors conducted all sorts of controls to confirm that the stains actually stained what they were supposed to – you can view these in the paper.

Babies!

In the final part of the study the authors maintained mites in vitro (in an incubator), feeding them on a diet containing increasing amounts of fat body or haemolymph. These are tricky experiments and in some way the least satisfactory part of the study.

Two results suggest that fat body was beneficial or essential to the mites. Firstly, only mites that had 50% or more fat body in the diet survived for 7 days. Secondly, there was a dose response to the amount of fat body in the diet and fecundity. Mites on a 100% fat body diet exhibited 40% fecundity, the highest level observed in the study.

What can we conclude from the Ramsey study

Of the three experiments presented, the Nile red fat body stain uptake by mites is reasonably compelling.

The feeding position study is essentially correlative, but there could be other interpretations of the data. For example, that location on the bee might be the least accessible to a ‘grooming’ bee. Perhaps it’s a survival mechanism?

Survival and fecundity in in vitro studies wasn’t great. However, in defence of the authors, fecundity of mites under natural conditions can be as low as 40% and is not higher than 80%. Not all mites have baby mites. Thankfully.

Only 20% of the mites survived one week under in vitro conditions, even on a 100% fat body diet. In contrast, mites fed haemolymph alone died within 48 hours. This poor level of survival was surprising and suggests other essential components of the diet were probably missing.

Other published studies have shown reasonable survival of Varroa for at least 3 days, with at least one report of mites surviving on flowers for up to 7 days. I’m also aware that other laboratories can maintain mites in vitro for longer than 7 days without using any honey bee-derived components in the diet.

Hang on … what is the fat body anyway?

The fat body is multi-functional. It has been compared to the vertebrate liver and adipose tissue. It acts as a major organ for nutrient storage, energy metabolism and detoxification of things like pesticides.

Vitellogenin made by and stored in the fat body reduces oxidative stress and is associated with extending the longevity of overwintering bees. The fat body also has critical roles in metamorphosis.

So, not only multi-functional, but also very important.

Significance of the results … is this a game changer?

This paper has been discussed online as a ‘game changer’. That’s probably a bit strong. Whilst the fluorescent stain uptake study is reasonably convincing it must be remembered that it was conducted on adult bees.

Do mites on pupae also feast on the fat body?

This will have to be determined in the future. It’s a more difficult experiment of course.

The other two studies, and a number of additional small observations I’ve not discussed here, are certainly supportive, but not alone hugely convincing. The in vitro study in particular will be interesting to compare with (currently unpublished) studies from other laboratories that do not use honey bee fat bodies in their mite feeding and maintenance diet.

Practical matters

Does it matter what part of the bee the mite feeds on?

Clearly it does for the mite, but what about the beekeeper?

I think this study is significant for the beekeeper for two reasons – the first will only be relevant if and when lipophilic miticides are developed, the second matters right now.

  1. Strategies are being developed to add highly specific miticides to the diet of bees which are then delivered to Varroa when the mite feeds. To date, these have been rather underwhelming in their performance. If Ramsey is right, modification of these miticides to make them lipophilic (like the Nile red fluorphore) will concentrate them in precisely the right place to ensure the mites get a lethal dose.
  2. A key product of the fat body is vitellogenin. The long-lived overwintering bees have high levels of vitellogenin. Mites feeding on, and depleting, the fat body would be expected to result in reduced vitellogenin levels in the bee 4. This would explain why high Varroa levels are associated with reduced longevity of winter bees and consequently increased overwintering colony losses.

The most important take home message

To prevent mites that feed on fat bodies from damaging vitellogenin production miticides have to be used early enough to protect the winter bees.

In the paper Ramsey makes the statement:

Simple reduction of mite loads late in the season to decrease the overwinter parasite load may not be enough, as it still allows for the mites to damage tissue critical to the process of overwintering …

Instead …

A treatment schedule that includes treatment in late summer or early fall before mites can significantly damage fat body in developing winter bees would likely be more effective.

Which is precisely the point I’ve made previously about treating early enough to protect winter bees.

What the Ramsey paper adds is the piece of the jigsaw possibly explaining why late summer treatment is so important.


Colophon

Chewin’ the Fat was a four-series Scottish comedy sketch show. It was broadcast from 1999 to 2002, with further Hogmanay specials until 2005. The show had a recurring cast of characters and sketches including The Big ManThe Banter BoysThe Lighthouse KeepersBallistic Bob and Taysiders in Space.

Gonna no' dae that

Gonna no’ dae that – The Lighthouse Keepers

Chewin’ the Fat was filmed in and around Glasgow (where I worked at the time) and the characters parodied a range of local ‘types’ … pretentious Kelvinsiders, Glaswegian gangsters, narcissistic golfers, The man from Kilmacolm, and shellsuit-wearing, chain-smoking, hard-drinking Glaswegian neds.

It was a bit rude and definitely an acquired taste. Without subtitles, some of the scenes would probably have been unintelligible south of the border.