Category Archives: Problems

Aristotle’s hairless black thieves

Aristotle not in his beesuit

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

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

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

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

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

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

Little blacks, maladie noire, schwarzsucht

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

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

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

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

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

It’s a distressing sight.

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

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

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

Emerging and re-emerging disease

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

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

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

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

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

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

Often the terms are used interchangeably.

Sporadic and rare … but increasing?

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

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

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

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

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

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

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

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

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

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

Is chronic bee paralysis disease increasing?

Yes.

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

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

Apiaries recorded with chronic bee paralysis between 2006 and 2017.

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

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

But is this disease caused by CBPV?

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

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

Or indeed, any virus?

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

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

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

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

Disease clustering

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

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

They were.

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

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

They did not.

Clustering of CBPV – spatial and temporal analysis.

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

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

Apiary-level disease risk factors

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

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

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

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

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

Bee imports does not mean disease imports

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

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

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

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

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

All publicity is good publicity …

… but not necessarily accurate publicity 🙁

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

Some more accurately than others 🙁

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

The Times

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

The Sun

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

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

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

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

The Telegraph

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

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

😉

Conclusions

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

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

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

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


Full disclosure:

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

Acknowledgements

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

Swarm prevention

Swarm prevention and control are distinct phases in the management of colonies during the next few weeks of the beekeeping season 1.

Not all beekeepers practice them and not all colonies need them.

But most should and will … respectively 😉

Swarm prevention involves strategies to delay or stop the colony from initiating events that lead to swarming.

Swarm control strategies are more direct interventions that are used to prevent the loss of a swarm.

Why do colonies swarm?

Without swarming there would be no honey bees.

Swarming is honey bee colony reproduction. Without management (e.g. splitting colonies) colony numbers would remain static. And, since bees have only been managed for a few thousand years, they must have been successfully reproducing – by swarming – for millions of years before then.

So one of the major drivers of swarming is the innate need to reproduce.

Bees also swarm if their current environment is unable to accommodate further colony expansion. Therefore, another driver of swarming is overcrowding.

And, of course, there is some overlap in these two drivers of swarming.

You can therefore expect that strong, healthy, populous colonies will probably try to swarm on an annual basis.

The mechanics of swarming

When a colony swarms about 75% of the worker bees – of all age groups – leave with the queen. They set up a temporary bivouac near the original hive and subsequently relocate to a new nest site identified by the scout bees.

The original colony is left with all the brood (eggs, larvae and sealed brood), a significantly-depleted adult bee workforce and almost 2 all of the honey stores.

What they lack is a queen.

But what the swarm also leaves behind, amongst the brood, is one – or more often several – newly developing queens. These occupy specially enlarged cells that are located vertically on the edges or face of the comb.

Queen cells ...

Queen cells …

Queen cells look distinctive and their initial appearance – before the swarm leaves – is a clear indication that the time for swarm prevention has gone and swarm control is now urgently needed 3.

This is one of the reasons why regular colony inspections are essential, particularly during mid/late Spring and early summer which is the time of the season when swarming is most likely.

Colony fate and the risks of swarming

But back to the recently swarmed colony. In a few days the new queen(s) emerges. If there’s more than one they usually fight it out to leave just one. She goes on one or more mating flights and a few days later starts laying eggs.

This colony should survive and thrive. They have time to build up strength (and collect more stores) before the end of the season. Under natural conditions 87% of swarmed colonies overwinter successfully 4.

Alternatively, the swarmed colony may swarm again (and again), each with a virgin queen and each further depleting the worker population. Colonies can swarm themselves to destruction like this.

Swarms headed by virgin queens are termed casts. I’m not sure what determines whether a swarmed colony also produces one or more casts. Colony strength is a determinant, but clearly not the only one as some casts contain little more than a cup full of bees.

Under natural conditions swarming is a very risky business. Swarm survival is less than 25% 5 – many will not collect sufficient stores to overwinter – and the survival of casts will be even lower because of their size and the risks associated with queen mating.

But ‘our’ bees don’t live under natural conditions

For beekeeping the ‘risks’ associated with swarming are somewhat different.

When a colony swarms you lose the majority of the workforce. Therefore honey production will be significantly reduced. You’re unlikely to get a surplus from the swarmed colony.

Of course, honey might not interest you but propolis and wax production are also reduced, as is the strength of the colony to provide efficient ecosystem services (pollination).

Secondly, despite swarms being one of the most captivating sights in beekeeping, not everyone appreciates them. Non-beekeepers may be scared and – extraordinary as it may seem – resent the swarm establishing a new nest in the eaves of their house.

Incoming! from The Apiarist on Vimeo.

Inevitably some beekeepers will claim they’ve never met anyone scared of bees, or swarms are always welcomed in the gardens that abut their apiary.

Unfortunately, that does not alter the reality that – to many – swarms are a nuisance, a potential threat and (to a small number of people 6 ) a very real danger.

Therefore, as beekeepers, we have a responsibility to practice both swarm prevention and control. This prevents our hobby/obsession irritating other people and means we have more bees to make delicious honey for family, friends and customers.

Overcrowding

I’ve already defined the event that separates swarm prevention from swarm control. It is the appearance of queen cells during the weekly colony inspection.

Swarm prevention involves managing the colony to delay the appearance of queen cells. Once queen cells are produced, swarm control is required 7

I’ve also defined the two major drivers of swarming – overcrowding and the need to reproduce 8.

How does a colony determine that it is overcrowded? As beekeepers, how can we monitor and prevent overcrowding?

As a colony expands during the spring the queen lays concentric rings of eggs from the centre of the brood nest. Imagine this initially as a kiwi fruit-sized ball, then an orange, then a grapefruit, until it is the size of a large football.

Brood frame

Perhaps a slightly squashed football, but you get the general idea.

Running out of storage space

It takes bees to make bees. The initial brood reared helps feed subsequent larvae and keeps the maturing brood warm.

As the season develops more sources of nectar and pollen become available. These are collected in increasing amounts by the expanding numbers of foragers.

This all needs to be stored somewhere.

One possibility is that the stores are loaded into the cells recently vacated by emerging workers within the brood nest. This is often termed “backfilling”. Sometimes you find a frame in which the central concentric rings of brood have emerged and, before the queen has had a chance to re-lay the frame with new eggs, workers have backfilled the cells with nectar (or, less frequently, pollen).

But, at the same time as the space available for the queen to lay is reducing, the colony population is increasing. Very fast. There are larger numbers of unemployed young bees. Unemployed because there are reduced amounts of brood to rear because the queen is running out of space.

Pheromones

And the increased number of workers means that the pheromones produced by the queen, in particular the queen mandibular pheromone, are effectively diluted. Studies by Mark Winston and colleagues 9 investigated the relationship between queen mandibular pheromone (an inhibitor of queen cell production) and colony congestion. In it he concluded that overcrowding inhibits the transmission of this pheromone, so favouring queen cell production.

Play cup or queen cell?

Play cup or are they planning their escape …?

The distribution of other pheromones is also reduced in overcrowded colonies. Lensky and Slabezki 10 showed that the queen rarely visited the bottom edges of comb in overcrowded colonies. Consequently, the levels of queen footprint pheromone was reduced. This pheromone is an inhibitor of queen cup production, the very earliest stages of queen cell development.

So, overcrowded colonies start to prepare queen cells … and swarm control is needed.

Make space

If the colony is overcrowded then you have to provide more space for colony expansion.

Just piling supers on top may not be sufficient, though it may temporarily ease congestion and partially help. Leaving a colony with no supers during a strong nectar flow is a surefire way to fill the brood box with nectar and trigger swarm preparation.

If the colony is backfilling the brood nest with nectar then the addition of supers is likely to encourage them to move the stores up, providing more space for the queen.

It will additionally have the beneficial effect of moving some bees ‘up’, to store and process the nectar, again reducing congestion in the brood nest.

However, you probably also need to encourage the bees to expand the brood nest by providing frames for them to draw out as comb. Essentially you’re spreading the brood nest by inserting one or two empty frames within it.

Expanding or spreading the brood nest

I routinely do this by removing the outer frames, which often contain stores, and adding new foundationless frames on one or both sides of the centre of the brood nest. Usually I would place these about three to four frames apart 13.

You can routinely replace queens by purchasing new ones, by rearing your own, or through colony manipulation during swarm control e.g. by reuniting a vertical split.

Of these, I’d strongly recommend one of the last two approaches. It’s more interesting, it’s a whole lot more satisfying and it is a lot easier than many beekeepers realise.

Locally bred queen ...

Locally bred queen …

You have the additional advantage that the queens produced in your own apiary will – by definition – be local and there is good evidence that local queens are better adapted to local conditions.

Robbing brood and making nucs

There are at least two additional, and related, ways of increasing the space available so helping swarm prevention in a rapidly expanding colony.

The first is stealing a frame of brood 14 and using it to boost a weaker colony.

Take care when doing this.

If the recipient colony is weak due to disease or a failing queen then you’re just wasting the donated brood. However, if the colony is healthy but small it can be a good investment of resources and may help delay swarming in the donor colony as well.

More drastically, it may be possible to remove a frame (or perhaps even two) of brood and adhering bees to make up a nucleus colony. In my experience, a strong donor colony can almost always be used to produce a nuc without compromising honey production, and with the added benefit of delaying swarm preparations.

I’m going to write about nuc production in more detail in a few weeks as it deserves a full post of its own. It’s worth noting here that the nuc should also be provided with sufficient bees and stores to survive and you will need a queen for it (or at least a queen cell).

Do not just dump a couple of brood frames and bees into a box and expect them to rear a half-decent queen on their own.

However, if you have a queen (or mature queen cell) then splitting a nuc off a strong colony is usually a win-win solution for swarm prevention.


 

The scent of death

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

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

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

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

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

Which means there’s some housekeeping to do.

Bring out your dead

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

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

Corpses

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

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

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

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

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

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

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

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

Dead parrot

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

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

Or stunned.

Or pining for the fjords.

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

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

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

As opposed to a resting bee 4.

The scent of death

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

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

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

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

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

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

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

Odours and pongs

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

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

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

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

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

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

Cuticular hydrocarbons

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

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

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

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

Cool corpses and cuticular hydrocarbons

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

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

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

But which one?

Gas chromatography

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

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

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

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

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

Summary

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

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

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

Or they might do something else entirely.

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

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

Global warming and hive cooling

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

We’re living in a warming world.

Temperatures are rising

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

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

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

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


 

Time to deploy!

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

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

So … just like any normal season really.

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

Keep on keeping on

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

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

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

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

Mistakes will be made.

Queen cells will be missed.

Colonies will swarm 1.

Queen cells

Queen cells …

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

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

Which brings me back to swarming.

Swarmtastic

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

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

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

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

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

Let the bees do the work.

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

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

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

Not just any dark box

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

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

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

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

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

How convenient 🙂

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

Inside ...

Bait hive floor

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

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

Big swarms are better 🙂 7

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

What’s in the box?

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

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

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

Bait hive ...

Bait hive …

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

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

Lemongrass oil and cotton bud

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

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

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

No foundation for that

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

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

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

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

Bamboo foundationless frames

Bamboo foundationless frames

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

Beautiful … but equally irritating 🙂

Final touches

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

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

Foam block ...

Foam block …

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

Bait hive location and relocation

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

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

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

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

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

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

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

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

Or move grandma 😉

Lucky dip

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

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

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

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

Varroa treatment of a new swarm in a bait hive…

But they must be healthy.

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

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

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

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

What are you waiting for 😉 ?


 

Bees in the time of corona

I usually write a review of the past year and plans for the year ahead in the middle of winter. This year I reviewed 2019 and intended to write about my plans when they were a little better formulated.

Inevitably, with the coronavirus pandemic, any plans would have had to be rapidly changed. It’s now not clear what the year ahead will involve and, with the speed things are moving at, anything I write today 1 may well be redundant by publication time on Friday.

Nothing I write here should be taken as medical advice or possibly even current information. I teach emerging virus infections and have studied RNA viruses (like DWV, coronavirus also has an RNA genome but it is a fundamentally different beast) for 30 years but defer to the experts when hardcore epidemiology is being discussed.

And it’s the epidemiology, and what we’ve learned from the outbreak in Italy, that is determining the way our society is being restructured for the foreseeable future.

Talking the talk

I gave three invited seminars last week. It was good to see old friends and to meet previously online-only contacts. It was odd not to shake hands with people and to watch people seek out the unoccupied corners of the auditorium to maintain their ‘social distancing’.

All of the beekeeping associations I belong to have cancelled or postponed talks for the next few months. Of course, there are usually far fewer talks during the beekeeping season as we’re all too busy with our bees, but those that were planned are now shelved.

Not me …

I expect that forward-thinking associations will be looking at alternative ways to deliver talks for the autumn season. If they’re not, they perhaps should as there’s no certainty that the virus will not have stopped circulating in the population by then.

I already have an invitation to deliver a Skype presentation in mid/late summer (to an association in the USA) and expect that will become increasingly commonplace. Someone more entrepreneurial than me will work out a way to give seminars in which the (often outrageous 2) speaker fee is replaced by a subscription model, ensuring that the audience can watch from the comfort of their armchairs without needing to meet in a group.

There is a positive spin to put on this. My waistline will benefit from not experiencing some of the delicious homemade cakes some beekeeping associations produce to accompany tea after the talk 😉 … I’m dreaming thinking in particular of a fabulous lemon drizzle cake at Fortingall & District BKA 🙂

It will also reduce the travel involved. For everyone. It’s not unusual for me to have a 2-3 hour journey to a venue 3 and, much as I enjoy talking, the questions, the banter and the cake, driving for 2-3 hours back can be a bit wearing.

At risk populations

Everyone is getting older … but beekeepers often have a head start. In the UK the average age of bee farmers is reported to be 66 years old. In my many visits to beekeeping associations I meet a lot of amateur (backyard) beekeepers and suspect that the majority are the wrong side of 50 4.

And that’s significant as Covid-19 is a more serious infection for those over 50.

Infection outcomes are also worse for men, and the majority (perhaps 65%) of beekeepers are men. The rates of infection appear similar, but men – particularly elderly men – often have less good underlying health; they are more likely to smoke and have less effective immune responses.

Enough gloom and doom, what does this mean for beekeeping?

Mentoring

If you took a ‘beginning beekeeping‘ course this winter you may struggle to find a mentor. If you’ve been allocated one (or someone has generously volunteered) think twice about huddling over an open hive with them.

Actually, don’t huddle with them at all … the veil of a beesuit is no barrier to a virus-loaded 5μm aerosol.

Mentoring is one of the most important mechanisms of support for people starting beekeeping.  I benefitted hugely from the experienced beekeepers who generously answered all my (hundreds of) idiotic questions and helped me with frames of eggs when I’d inadvertently ‘lost’ my queen and knocked back all the queen cells.

Without mentoring, learning to keep bees is a lot more difficult. Not impossible, but certainly more challenging. Beekeeping is fundamentally a practical pastime and learning by demonstration is undoubtedly the best way to clear the initial hurdles.

But thousands before have learnt without the benefit of mentoring.

However, if you can wait, I suggest you do.

If you cannot 5, you need to find a way to compensate for the potential absence of experienced help ‘on hand’.

All of us are going to have to learn to communicate more effectively online. Camera phones are now so good that a quick snap (or video) sent via WhatsApp may well be good enough to diagnose a problem.

Get together (virtually!) with other beginners at a similar stage and compare notes. Discuss how colonies are building up, early signs of swarming and when hives are getting heavier.

Bees in the same environment tend to develop at about the same rate. If your (virtual) ‘bee buddy’ lost a swarm yesterday you should check your colonies as soon as possible.

Getting bees

Thousands of nucs, packages and queens are imported to the UK every year. I’ve no idea what will happen to the supply this season. It might be unaffected, but I suspect it will be reduced.

If you’re waiting for an “overwintered nuc” and your supplier claims now not to be able to supply one 6 all is not lost.

Under offer ...

Under offer …

Set out one or two bait hives. With isolation, movement restrictions, curfews and illness 7 it’s more than likely that some nearby colonies will be poorly managed. If you use a bait hive you can attract a swarm with almost no work and save an overworked beekeeper from having to do a cutout from the roofspace of the house the swarm would have otherwise selected.

At the very least, you can have the pleasure of watching scout bees check out the hive in the isolated comfort of your own garden.

Keeping bees

I think the last few days have shown that the future is anything but predictable. Who knows where we’ll be once the swarming season is here. You can practice swarm control with social distancing in your out apiary unless there are movement controls in place.

In that case, you cannot get there in the first place.

Let us hope that it doesn’t come to that.

What you can do is be prepared. Give the bees plenty of space when the first nectar flow starts. Two supers straight away, or three if your knowledge of local conditions suggests two may not be enough.

Clip one of the wings of the queen. This doesn’t stop the bees swarming (almost nothing does) but it does stop you losing the bees. Although I cannot be certain that queen clipping is painless – because I’m not sure that bees feel pain (evidence suggests they don’t) – I do know that clipped queens have as long and as productive lives as unclipped queens.

There she goes ...

There she goes …

Clipped queens buy you a few days grace. The colony tends to swarm when the new virgin queen emerges rather than when the queen cell was capped. That can make all the difference.

The colony swarms but the queen spirals groundwards and usually then climbs back up the hive stand, around which the swarm then clusters. Sometimes the queen returns to the hive, though it doesn’t always end well for her there in the subsequent duel with the virgin now in residence.

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

Not lost swarm

Honey sales

Selling honey is not without risk of virus transmission, in either direction. When I sell “from the door” it often involves an extended discussion about hay fever, local forage, bumble bees and the weather. All of that can still continue but both parties will have to speak a bit louder to maintain social distancing.

Selling through shops might be easier … if the shops stay open. Farmers markets, village fetes and country fairs (fayres?) are likely to all be cancelled or postponed, at least temporarily.

There’s a neighbourhood initiative here selling high quality local produce, ordered online and collected at a set date and time. Similar things are likely to be developed elsewhere as customers increasingly want to support local producers, to buy quality food and to avoid the panic buying masses fighting over toilet tissue 8 in the supermarkets.

Peter Brookes, Panic Buying, 7-3-20, The Times

An initiative like Neighbourfood might make even more sense if there was a local delivery service to reduce further the need for contact. No doubt these things exist already.

The unknown unknowns

I’ve discussed the unknown knowns previously. These are the things you know will happen during the season, you’re just not quite sure when they’ll happen. Swarming, Varroa management, winter feeding etc.

To add to the uncertainty this year we will have the unknown unknowns … things you didn’t expect and that you might not know anything about. Or have any warning about. Social distancing, quarantine, school closures and potential lockdowns all fall into this category.

Preparing for things that cannot be predicted is always tricky. All we can do is be as resilient and responsible as possible.

My beekeeping season will start in late April or early May. I’m self-sufficient for frames and foundation and can switch entirely to foundationless frames if needed. I have enough boxes, supers, nucs etc 9 to maintain my current colonies.

I’m actually planning to reduce my colony numbers which I’ll achieve by uniting weak colonies or selling off the surplus. With a bit more free time from work (and I’m working very remotely some of the time) I intend to rear some queens when the weather is good. These will be used to requeen a few tetchy colonies for research, though it’s increasingly looking like we’ll lose this field season as the labs are effectively closed.

I’m not dependent on honey sales other than to offset the costs of the hobby. If I cannot buy fondant for autumn feeding I’ll just leave the supers on and let them get on with it.

This is why we treat ...

This is why we treat …

Which leaves only the treatments for Varroa management as essential purchases … and if I cannot mail order Apivar then things have got very serious indeed 🙁 10

In the meantime, I’m planning some more science and beekeeping posts for the future. This includes one on a new collaborative study we’re involved in on chronic bee paralysis virus which, like Covid-19, is classed as causing an emerging viral disease.


Colophon

Love in the time of cholera

The title is a rather contrived pun based on the book Love in the time of cholera by the Columbian author Gabriel García Márquez. There are no other similarities between this post and the Nobel laureates work … cholera isn’t even a virus.

Cholera, which has characteristic and rather unpleasant symptoms, might be an excuse to panic buy toilet rolls.

Covid-19, which has equally characteristic and unpleasant (but totally different) symptoms, is not 😉

 

Measles, mites and anti-vaxxers

About 11,000 years ago nomadic hunter-gatherers living near the river Tigris discovered they could collect the seeds from wild grasses and, by scattering them around on the bare soil, reduce the distance they had to travel to collect more grain the following year.

This was the start of the agricultural revolution.

They couldn’t do much more than clear the ground of competing ‘weeds’ and throw out handfuls of collected seed. The plough wasn’t invented for a further 6,000 years and wouldn’t have been much use anyway as they had no means of dragging it through the baked-hard soil.

But they could grow enough grains and cereals to settle down, doing less hunting and more gathering. Some grains grew better than others, with ‘ears’ that remained intact when they were picked, making harvesting easier. The neophyte farmers preferentially selected these and, about 10,000 years ago, the first domesticated wheat was produced.

Einkorn wheat (Triticum monococcum), one of the first domesticated cereals

Since they were less nomadic and more dependent upon the annual grain harvest they took increasing care to protect it. They were helped with this by the hunting dogs domesticated from wolves several thousands years earlier. The dogs protected the crops and kept the wild animals, primarily big, cloven-hooved ungulates and the native wild sheep and goats, at a distance.

But those that got too close were trapped and were remarkably good to eat.

And since it was easier to keep animals penned up to avoid the need to actively hunt them it was inevitable that sheep and goats were eventually domesticated (~9,000 years ago) … and the nomadic hunter-gatherers became settled farmers practising recognisably mixed agriculture.

Domestication of cattle

The sheep and goats were a bit weak and scrawny. The large ungulates, the aurochs, gaur, banteng, yak and buffalo 1 had a lot more meat on them.

Inevitably, first aurochs (which are now extinct) and then other wild ungulates, were independently domesticated to produce the cattle still farmed today. This process started about 8,000 years ago.

Auroch bull (left) and modern domesticated bull (right). Auroch were big, strong (tasty) animals.

Cattle were great. Not only did they taste good, but they could be managed to produce milk and were strong enough to act as beasts of burden.

The plough was invented and crop yields improved dramatically because the grain germinated better in the cleared, tilled soil. Loosely knit families and groups started to build settled communities in the most fertile regions.

Bigger farms supported more people. Scattered dwellings coalesced and became villages.

Not everyone needed to farm the land. The higher yields (of grain and meat) allowed a division of labour. Some people could help defend the crops from marauders from neighbouring villages, some focused on weaving wool (from the sheep) into textiles while others taught the children the skills they would need as adults.

Communities got larger and villages expanded to form towns.

Zoonotic diseases

Hunter-gatherers had previously had relatively limited contact with animals 2. In contrast, the domestication of dogs, sheep, goats and cattle put humans in daily contact with animals.

Many of these animals carried diseases that were unknown in the human population. The so-called zoonotic diseases jumped species and infected humans.

There’s a direct relationship between the length of time a species has been domesticated and the number of diseases we share with it.

Domestication and shared zoonotic diseases (years, X-axis)

The emergence of new diseases requires that the pathogen has both the opportunity to jump from one species to another and that the recipient species (humans in this case) transmits the disease effectively from individual to individual.

The nomadic hunter-gatherers had been exposed to many of these diseases as well but, even if they had jumped species, their communities were too small and dispersed to support extensive human-to-human transmission.

Rinderpest and measles

Until relatively recently rinderpest was the scourge of wild and domesticated cattle across much of the globe. Rinderpest is a virus that causes a wide range of severe symptoms in cattle (and wild animals such as warthog, giraffe and antelope) including fever, nasal and eye discharges, diarrhoea and, eventually, death. In naÏve populations the case fatality rate approaches 100%.

Rinderpest outbreak in South Africa, 1896

Animals that survive infection are protected for life by the resulting immune response.

Rinderpest is closely related to canine distemper virus and measles virus. Virologically they are essentially the same virus that has evolved to be specific for humans (measles), dogs (canine distemper) or cattle (rinderpest).

Measles evolved from rinderpest, probably 1,500 to 2,000 years ago, and became a human disease.

Rinderpest was almost certainly transmitted repeatedly from cattle to humans in the 6,000 years since auroch or banteng were domesticated. However, the virus failed to establish an endemic infection in the human population as the communities were too small.

However, by about 1,500 – 2,000 years ago the largest towns had populations of ~250,000 people. Subsequent studies have demonstrated that you need a population of this size to produce enough naÏve hosts (i.e. babies) a year to maintain the disease within the population.

This is because, like rinderpest, measles induces lifelong immunity in individuals that survive infection.

Measles is a devastating disease in an unprotected community. Case fatality rates of 10-30% or higher are not unusual. It is also highly infectious, spreading very widely in the community 3. Survivors may suffer brain damage or a range of other serious sequelae.

Measles subsequently changed the course of history, being partially responsible (along with smallpox) for Cortés’ defeat of the Aztec empire in the 16th Century.

John Enders, Maurice Hilleman and Andrew Wakefield

In the late 1950’s John Enders developed an attenuated live measles vaccine. When administered it provided long-lasting protection. It was an excellent vaccine. Maurice Hilleman, in the early 1970’s combined an improved strain of the measles vaccine with vaccines for mumps and rubella to create the MMR vaccine.

Widespread use of the measles and MMR vaccines dramatically reduced the incidence of measles – in the UK from >500,000 cases a year to a few thousand.

Incidence of measles in England and Wales

If vaccine coverage of 92% of the population is achieved then the disease is eradicated from the community. This is due to so-called ‘herd immunity’ 4 in which there are insufficient naÏve individuals for the disease to be maintained in the population.

Measles cases (and deaths) continued to fall everywhere the vaccine was used.

There was a realistic possibility that the vaccines would – like rinderpest 5 – allow the global eradication of measles.

And then in 1986 Andrew Wakefield published a paper in the Lancet suggesting a causative link between the MMR vaccine and autism in children.

Subsequent studies showed that this was a deeply flawed and biased study. And totally wrong.

There is not and never was a link between autism and measles vaccination 6. But that didn’t stop a largely uncritical press and subsequently even less critical social media picking up the story and disseminating it widely.

Measles and the anti-vaccine movement

Measles vaccination rates dropped because a subset of parents refused to have their kids vaccinated with the ‘dangerous’ measles vaccine.

Several successive birth cohorts had significantly lower than optimal vaccination rates. Measles vaccine coverage dropped to 84% by 2002 in the UK, with regional levels (e.g. parts of London) being as low as 61%. By 2006, twenty years after the thoroughly discredited (and now retracted) Lancet paper vaccine rates were still hovering around the mid-80% level.

As immunisation rates dropped below the critical threshold, measles started to circulate again in the population. 56 cases in 1998 to ~450 in the first 6 months of 2006. In that year there was also the first death from measles for many years – an entirely avoidable tragedy.

In 2008 measles was again declared endemic (i.e. circulating in the population) in the UK.

Similar increases in measles, mumps and rubella were occurring across the globe in countries where these diseases were unknown for a generation due to previous widespread vaccination.

The distrust of the MMR vaccine was triggered by the Wakefield paper but is part of a much wider ‘anti-vaccination movement‘.

“Vaccines are dangerous, vaccines themselves cause disease, there are too many vaccines and the immune system is overloaded, vaccines contain preservatives (thiomersal) that are toxic, vaccines cause sterility etc.”

None of these claims stand up to even rudimentary scientific scrutiny.

All have been totally debunked by very extensive scientific analysis.

The World Health Organisation consider the anti-vaccine movement (anti-vaxxers) one of the top ten threats to global health. Vaccination levels are lower than they need to be to protect the population. Diseases – not just measles – that should be almost eradicated now kill children every year.

Where are the bees in this beekeeping blog?

Bear with me … before getting to the bees I want to move from fact (all of the above) to fantasy. The following few paragraphs (fortunately) has not happened (and to emphasise the point it is all italicised). However, it is no more illogical than the claims already being made by the anti-vaccine movement.

Childhood measles

The inexorable rise of internet misinformation and social media strengthened the anti-vaxxers beliefs further. Their claims that vaccines damage the vaccinees were so widespread and, for the uncritical, naturally suspicious or easily influenced who simply wanting to protect their kids, so persuasive that vaccine rates dropped further. They refused to consider the scientific arguments for the benefits of vaccines, and refused to acknowledge the detrimental effects diseases were having on the community.

The obvious causative link to the inevitable increase in disease rates was not missed – by both the anti-vaxxers and those promoting vaccination. However, the solutions each side chose were very different. Measles remained of particular concern as kids were now regularly dying from this once near-forgotten disease. The symptoms were very obvious and outbreaks spread like wildfire in the absence of herd-immunity 7.

The anti-vaxxers were aware that population size was a key determinant of the ability of measles to be maintained in the population. Small populations, such as those on islands or in very isolated regions, had too few new births annually to maintain measles as an endemic disease.

With the increase in remote working – enabled by the same thing (the internet) responsible for lots of the vaccine misinformation – groups of anti-vaxxers started to establish remote closed communities. Contact with the outside world was restricted, as was the size of the community itself.

A quarter of a million was the cutoff … any more than that and there was a chance that measles could get established in the unprotected population.

Small communities 8 work very well for some things, but very badly for others. Efficiencies of scale, in education, industry, farming and trade became a problem, leading to increased friction. When disease did occur in these unprotected communities it wreaked havoc. Countless numbers of people suffered devastating disease because of the lack of vaccination.

In due course this led to further fragmentation of the groups. They lived apart, leading isolated lives, flourishing in good years but struggling (or failing completely) when times were hard, or when disease was introduced. Some communities died out altogether. 

They chose not to travel because, being unvaccinated, they were susceptible to diseases that were widespread in the environment. Movement and contact between villages, hamlets and then individual farm settlements was restricted further over time.

The benefits of large communities, the division of labour, the economies and efficiencies of scale, were all lost.

They didn’t even enjoy particularly good health.

They had ‘evolved’ into subsistence farmers … again.

OK, that’s enough! Where are the bees?

Anyone who has bothered to read this far and who read Darwinian beekeeping last week will realise that this is meant to be allegorical.

The introduction of Varroa to the honey bee population resulted from the globalisation of beekeeping as an activity, and the consequent juxtaposing of Apis mellifera with Apis cerana colonies.

Without beekeepers it is unlikely that the species jump would have occurred.

Apis cerana worker

Undoubtedly once the jump had occurred transmission of mites between colonies was facilitated by beekeepers keeping colonies close together. We do this for convenience and for the delivery of effective pollination services.

The global spread of mites has been devastating for the honey bee population, for wild bees and for beekeeping.

But (like the introduction to measles in humans) it is an irreversible event.

However, it’s an irreversible event that, by use of effective miticides, can at least be partially mitigated.

Miticides do not do long-term harm to honey bees in the same way that vaccines don’t overload the immune response or introduce toxins or cause autism.

There can be short term side effects – Apiguard stinks and often stops the queen laying. Dribbled oxalic acid damages open brood.

But the colony benefits overall.

Many of the miticides now available are organic acids, acceptable in organic farming and entirely natural (even being part of our regular diet). Some of the hard chemicals used (e.g. the lipid-soluble pyrethroids in Apistan) may accumulate in comb, but I’d argue that there are more effective miticides that should be used instead (e.g. Apivar).

I’m not aware that there is any evidence that miticides ‘weaken’ colonies or individual bees. There’s no suggestion that miticide treatment makes a colony more susceptible to other diseases like the foulbroods or Nosema.

Of course, miticides are not vaccines (though vaccines are being developed) – they are used transiently and provide short to medium term protection from the ravages of the mite and the viruses it transmits.

By the time they are needed again the only bee likely to have been previously exposed is the queen. They benefit the colony and they indirectly benefit the environment. The colony remains strong and healthy, with a populous worker community available for nectar-gathering and pollination.

The much reduced mite load in the colony protects the environment. Mites cannot be spread far and wide when bees drift or through robbing. Other honey bee colonies sharing the environment therefore also benefit.

The genie is out of the bottle and will not go back

Beekeepers (inadvertently) created the Varroa problem and they will not solve it by stopping treatment. Varroa will remain in the environment, in feral colonies and in the stocks of beekeepers who choose to continue treating their colonies.

And in the many colonies of Apis mellifera still kept in the area that overlaps the natural (and currently expanding) range of Apis cerana.

Treatment-free beekeepers may be able to select colonies with partial resistance or tolerance to Varroa, but the mite will remain.

So perhaps the answer is to ban treatment altogether?

What would happen if no colonies anywhere were treated with miticides? What if all beekeepers followed the principles of Darwinian (bee-centric, bee friendly, ‘natural’) beekeeping – well-spaced colonies, allowed to swarm freely, killed off if mite levels become dangerously high – were followed?

Surely you’d end up with resistant stocks?

Yes … possibly … but at what cost?

Commercial beekeeping would stop. Honey would become even scarcer than it already is 9. Pollination contracts would be abandoned. The entire $5bn/yr Californian almond crop would fail, as would numerous other commercial agricultural crops that rely upon pollination by honey bees. There would be major shortages in the food supply chain. Less fruits, more cereals.

Pollination and honey production require strong, healthy populous colonies … and the published evidence indicates that naturally mite resistant/tolerant colonies are small, swarmy and only exist at low density in the environment.

Like the anti-vaxxers opting to live as isolated subsistence farmers again, we would lose an awful lot for the highly questionable ‘benefits’ brought by abandoning treatment.

And like the claims made by the anti-vaxxers, in my view the detrimental consequences of treating colonies with miticides are nebulous and unlikely to stand up to scientific scrutiny.

Does anyone seriously suggest we should abandon vaccination and select a resistant strain of humans that are better able to tolerate measles?


Notes

It is an inauspicious day … Friday the 13th (unlucky for some) with a global pandemic of a new zoonotic viral disease threatening millions. As I write this the UK government is gradually imposing restrictions on movement and meetings. Governments across Europe have already established draconian regional or even national movement bans. Other countries, most notably the USA and Africa, have tested so few people that the extent of Covid-19 is completely unknown, though the statistics of cases/deaths looks extremely serious.

What’s written above is allegorical … and crudely so in places. It seemed an appropriate piece for the current situation. The development of our globalised society has exposed us – and our livestock – to a range of new diseases. We cannot ‘turn the clock back’ without dissasembling what created these new opportunities for pathogens in the first place. And there are knock-on consequences if we did that many do not properly consider.

Keep washing your hands, self-isolate when (not if) necessary, practise social distancing (no handshakes) and remember that your bees are not at risk. There are no coronaviruses of honey bees.

Darwinian beekeeping

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

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

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

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

Differences

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

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

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

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

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

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

Real differences

Of course, some of the differences are very real.

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

Abelo poly hives

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

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

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

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

Darwinian beekeeping

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

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

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

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

This is presumably unnnatural beekeeping

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

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

Practical Darwinian beekeeping

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

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

Good and not so good advice

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

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

High altitude bait hive …

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

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

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

Let’s deal with them individually.

Small hives – one brood and one super

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

They’ll run out of space and swarm.

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

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

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

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

A small swarm

A small swarm … possibly riddled with mites

Thanks a lot!

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

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

Kill heavily mite infested colonies

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

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

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

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

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

They’ll procrastinate, they’ll prevaricate.

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

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

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

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

Less stress and better health

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

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

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

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

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

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

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

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

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

I’ll wrap up with two closing thoughts.

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

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


 

Which is the best … ?

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

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

Their enthusiasm is palpable 1.

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

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

Moving to higher ground ...

Moving to higher ground …

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

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

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

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

Which is the best …?

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

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

These questions reflect a couple of things:

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

Neither of these are criticisms.

All beekeepers should want the best for their bees.

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

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

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

The best smoker fuel

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

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

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

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

Fuel bucket

XYZ …

And that happens … precisely never.

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

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

Note that I said ‘some’ 😉

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

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

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

The best hive

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

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

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

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

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

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

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

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

There are some that are unsuitable.

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

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

Anthropocentrism

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

It’s what suits us as beekeepers.

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

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

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

But what’s best for the bees?

None, or any, of the above.

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

Take your pick ...

The bees do not care …

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

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

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

Oak … preferred by bees. Or not.

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

No.

Doing better …

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

We can’t ask them.

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

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

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

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

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

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

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

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

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

Egg box smoker

Smouldering egg box …

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

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

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

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

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

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

Exceptions to the above

Inevitably there are exceptions.

It wouldn’t be beekeeping without qualifications and caveats.

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

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

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

Large Dadant smoker

I know, because my happy bees told me so 🙂


 

 

Who’s the daddy?

I’ve recently discussed the importance and influence of polyandry for honey bee colonies. Briefly, polyandry – the mating of the queen with multiple (~12-18) drones – is critical for colony fitness e.g. ability to resist disease, forage efficiently or overwinter successfully.

Hyperpolyandry, for example resulting from instrumental insemination of the queen with sperm from 30+ drones, further increases colony fitness and disease resistance.

How do you measure polyandry?

Essentially, you genetically analyse the worker bees in the colony to determine the range of patrilines present. Patrilines are genetically distinct offspring fathered by different drones. Essentially they are subfamilies within the colony.

With a finite number of patrilines – which there must be, because the queen does not mate with an infinite number of drones – there will be a point at which the more workers you screen the fewer new patrilines will be detected.

Search and ye shall find – detecting rare patrilines

The more you screen, the more you are likely to have detected all the patrilines present.

However, the queen uses sperm randomly when fertilising worker eggs. This compounds the difficulty in determining the full range of different patrilines present in a population. In particular, it makes detecting very rare patrilines difficult.

For example, if 20% of workers belong to one patriline you don’t need to sample many bees to detect it. In contrast, if another patriline is represented by 0.0001% of randomly selected workers you would probably have to screen thousands to be sure of detecting it.

Consequently, rare patrilines in the honey bee worker population are very difficult to detect. Inevitably this means that the number of drones the queen mates (~12-18) with is probably an underestimate of the actual number 1.

Half-sisters and super-sisters

Worker bees are often described as ‘half sisters’ to each other. They share the same mother (the queen), but different fathers.

Actually, as you should now realise, that’s an oversimplification because – with only ~12-18 different fathers contributing to the genetics of the colony – some workers are going to be more related to each other because they share the same father and mother.

Half-sisters share the same mother but have different fathers and share about 25% of their genes.

Super-sisters share the same mother and father and so share about 75% of their genes (25% from the queen and 50% from the drone).

Super-sisters are more likely to help each other in the colony 2.

Emergency queens and nepotism

What’s the most important decision a colony makes?

If the queen is killed (or removed) the workers rear new queens under the so-called ’emergency response’. They feed selected young larvae copious amounts of Royal Jelly to rear a replacement queen.

Arguably, the most important decision the workers make is the selection of the day-old larvae to rear as new queens.

If they get it wrong the colony is doomed. If they get it right the colony will flourish 3.

But as described above, workers are more or less related to each other genetically.

To ensure the continued propagation of at least some of their genes it might be expected that the nurse bees making this selection 4 would choose larvae more closely related to themselves.

Do worker bees exhibit nepotism when rearing emergency queens?

If workers were nepotistic you’d expect the most common patrilines in the nurse/worker bee population would also predominate in the queens reared.

However, for at least 20 years evidence has been accumulating that indicates bees are not nepotistic. On the contrary, emergency queens appear to be reared from some of the rare patrilines in the colony.

A recent paper from James Withrow and David Tarpy has provided some of the best evidence for the existence of these so-called royal patrilines in honey bee colonies 5.

Royal patrilines

Evidence for these goes back to at least 1997 6, with about half a dozen publications in the intervening period. Essentially all used broadly the same approach; they genetically screened worker bees and the emergency queens they reared to determine which patrilines were present in the two groups. 

With certain caveats (size of study, number of microsatellites screened, colony numbers etc.) all concluded that colonies rear emergency queens from some of the rarest patrilines in the colony.

The recent study by Withrow and Tarpy is well explained and probably the most comprehensive, so I’ll use that to flesh out the details.

Experimental details

Six double-brood colonies were each split into a three separate colonies; a queenright single-brood colony and two five-frame nucs. The latter contained eggs and young larvae and so reared emergency queens.

Seven days later the developing emergency queens were all harvested for future analysis. One or two frames from the nucs were then exchanged with frames containing eggs and day-old larvae from the matched queenright colony.

The nucs then started rearing new queens … again.

And again … and again.

This process was repeated until the nucs failed.

In total over 500 queens were reared (to 7 days old) from these six original colonies. These queens were analysed genetically by microsatellite analysis, as were over 500 workers from colonies.

Within the 6 experimental colonies the authors identified a total of 327 patrilines (or subfamilies as Withrow and Tarpy describe them), ranging from 34-77 per colony. 108 patrilines (4-40 per colony) were exclusively detected in worker bees and 130 patrilines (5-55/colony) were exclusively detected in queens.

Cryptic “royal” subfamilies

Over 40% of queens raised per colony were produced from the patrilines exclusively detected in the queen population.

Subfamily distribution per colony.

As shown in the figure above, many queens (black bars) were reared from subfamilies (patrilines) not represented in the worker bee population (grey bars, sorted left to right by abundance).

Since there were different numbers of patrilines per colony (34-77), the bias towards the rarer patrilines is more apparent if you instead split them into tertiles (thirds) based upon worker abundance.

Are the queens predominantly reared from the most common tertile, the intermediate tertile or the rarest tertile?

Frequency distribution of subfamilies.

It’s very clear from this graph that workers select queens from the rarest patrilines within the colony.

It is therefore very clear that worker bees do not exhibit nepotism when choosing which larvae to rear emergency queen from.

Implications for our understanding of honey bee reproduction

Two points are immediately apparent:

  • there is a cryptic population of queen-biased patrilines that have largely been overlooked in genetic studies of honey bee polyandry
  • honey bee queens mate with more drones than conventional studies of worker bee patrilines indicate

Colony 5 had at least 77 distinct subfamilies (there might have been more detected had they screened more than the 94 workers and 135 queens from this colony). By extrapolation it is possible to determine that the effective queen mating frequency (me; the number of drones the queen had mated with) was ~32 if all the samples (worker and queen) were taken into account. If only the worker or queen samples were used for this calculation the effective queen mating frequency would be ~12 or ~65 respectively.

The average effective queen mating frequency over the six colonies was ~33 (total), significantly higher than the oft-quoted (including at the top of this page) me of ~12-18.

So perhaps honey bees really are hyperpolyandrous … or even extremely hyperpolyandrous as the authors suggest.

It’s worth noting in passing that routine mating frequencies over 30 are almost never quoted for honey bees 7, but that the ‘normal’ me ~12-18 is rather low when compared with other species within the genus Apis. The giant honey bee, Apis dorsata, exhibits mating frequencies of greater than 60.

Who’s the daddy?

So, when it comes to emergency queens , although we might not know precisely who the daddy is, we can be pretty certain the particular patriline selected by the workers is most likely to be one of the rare ones in the colony.

Mechanistically, what accounts for this?

Are these larvae selected solely because they are rare?

That seems unlikely, not least because it would require some sort of surveying or screening by nurse bees. Not impossible perhaps, though I’m not sure how this would be achieved.

Perhaps it is not even worker selection?

An alternative way to view it is larval competition. A better competing larvae would be fed Royal Jelly and would be much more likely to pass on her genes to the next generation.

We don’t know the answers to these questions … yet.

Or whether they’re the wrong questions entirely.

Swarming and supercedure

The colony rears a new queen under three conditions; enforced queenlessness (as described above) which induces emergency queen rearing, prior to swarming and during supersedure.

These are fundamentally different processes in terms of the larvae used for queen rearing.

During swarming and supersedure 8 the queen lays the egg in a ‘play cup’ which is subsequently engineered into a queen cell in which the new queen develops.

Play cups

However, it is known that the patrilines of queens reared during the swarming response are similar to those of workers in the same colony 9, implying that there is no overt selection by the workers (or the parental queen).

Queen rearing

Does this insight into how bees rear new queens have any implications for how beekeepers rear new queens?

There are about as many queen rearing methods as there are adult workers in a double-brood colony in late June. Many  exploit the emergency queen rearing response by a colony rendered temporarily or permanently queenless.

Beekeepers often comment on the differential ‘take’ of grafted larvae presented to queenless cell raising colonies.

Sometimes you get very good acceptance of the grafted larvae, other times less so.

Of course, we only show the ones that worked well!

3 day old QCs ...

3 day old QCs …

Differential ‘take’ is often put down to the state of the cell raising colony or the nectar flow (or the cackhandedness of the grafter, or the phase of the moon, or about 100 other things).

I have never heard of beekeepers comparing the ‘take’ of larvae originating from the cell raising colony with those from another colony. The latter are always going to be ‘rare’ if you consider the patrilines present in the cell raising colony. However, grafts taken from the same colony as used for cell raising 10 are likely to reflect the predominant patrilines.

Are these accepted less well by the nurse bees?

I suspect not … but it is testable should anyone want to try.

My expectation would be that the presentation of larvae in a vertically oriented cell bar frame would likely override any genetic selectivity by the colony. They’re desperate to raise a new queen and – thank goodness – here’s a few that might do.

Alternatively, differential acceptance is more likely to reflect use of larvae of an unsuitable age, or that have been damaged during grafting.

As I listen to the wind howling outside it seems like a very long time until I can test any of these ideas … 🙁


Colophon

Ray Winstone (as Carlin) 1979

Who’s the daddy? is British slang for who, or what, is the best. It originated in a line by Ray Winstone’s character Carlin from the 1979 film Scum. This was not a romantic comedy and I’m certainly not recommending viewing it. Nevertheless, the phrase became widely used over the subsequent couple of decades and seemed appropriate here because the colony is dependent on selecting high-quality larvae for colony survival.

Apivar (amitraz) resistance

Apivar is a widely used acaricide (a pesticide that kills mites and ticks) used to control Varroa.

The active ingredient of Apivar 1 is amitraz, a synthetic chemical discovered and developed almost 50 years ago.

Amitraz

Amitraz …

Amitraz has multiple molecular targets. I previously discussed the mechanism of action and summed it up with the words:

Essentially, amitraz binds and activates receptors that are critically important in a range of important aspects of the Varroa activity and behaviour … amitraz changes [this] behaviour and so exhibits miticidal activity. It has additional activities as well … these multiple routes of action may explain why resistance to amitraz is slow to develop.

I made the point in a subsequent post that amitraz resistance was very well documented … in cattle ticks 2 but that there was only anecdotal or incompletely documented evidence of resistance in Varroa in the USA, Argentina and Europe.

Apivar strip – fit and (don’t) forget

Amitraz has been used for mite control in honey bees for over twenty years. Considering its widespread use, the concentrations it is used at, and the relatively high replication rate of Varroa it is surprising that there has not been better evidence of resistance.

But that is no longer the case 🙁

Do you want the good news or the bad news first?

The bad news

A very recent paper 3 has clearly documented amitraz resistant Varroa in several commercial beekeeping operations in the USA.

I’ll discuss the key results of this paper first and then make some general comments on the implications for beekeepers and beekeeping.

The study had three components:

  1. Determine the sensitivity of Varroa never treated with amitraz to the chemical. This forms the baseline sensitivity against which field samples from commercial beekeepers could be tested.
  2. Screen Varroa from hives maintained by commercial beekeepers (with a multi-year history of Apivar usage) for amitraz resistance.
  3. Validate that the reduced efficacy of Apivar correlates with the observed amitraz resistance.

Essentially it involved harvesting live Varroa from colonies by a large-scale dusting with icing sugar 4. The Varroa were then tested to determine whether they showed resistance to amitraz, and the sensitivity was compared with the baseline sample of mites from colonies never treated.

Finally, an Apivar sensitivity test was conducted to determine the proportion of mites killed in a standardised assay in a set time period, again compared with the control (baseline sample).

The results of the study

You should refer to the paper for the primary data if needed.

Not all the apiaries tested yielded sufficient mites to screen for Apivar resistance. This is part of ‘the good news’ which I’ll get to shortly … but first the science.

Of those apiaries that did, Apivar resistance (determined by LC50 – the Lethal Concentration required to kill 50% of the mites) ranged from similar to that seen in the baseline samples to ~20-fold greater than the controls.

Two apiaries had an over 10-fold increase of the resistance ratio (the observed LC50 divided by the baseline LC50), with some individual colonies having high levels of Varroa infestation despite an active application of amitraz.

Apivar kills mites very quickly. Using a known number of mites trapped in a cage with a single small square of Apivar it is possible to ‘count the corpses’ and plot a kill curve over time. Sensitive mites from the control colonies were all killed within 3 hours.

Time course of Apivar efficacy in amitraz-susceptible Varroa

Using this as the baseline control it was then possible to determine the efficacy of Apivar in killing the mites (in the same 3 hour timeframe) from apiaries exhibiting resistance.

Apivar efficacy in commercial beekeeping apiaries.

Two apiaries (B and C, above) contained mites that exhibited high levels of resistance to Apivar, reflected in a low level of Apivar efficacy (above). In these apiaries, an average of less than 80% of mites were killed within the 3 hour assay.

Finally, the author demonstrated a correlation between Apivar efficacy and amitraz resistance. Unsurprising, but a necessary concluding point for the experimental data.

Within apiary variation

It was interesting that the author notes that the range of Apivar efficacy was much greater in colonies from apiaries with clear evidence of amitraz resistance.

For example, apiary B exhibited a range of Apivar efficacy in colonies from 28% to 97%, with an average (plotted above) of 68%. Whilst this is clearly an unacceptably low level, it is interesting that some of the colonies within the same apiary had mites killed at an efficacy similar or better (>90%) to apiaries A2 and A4 in the graph above.

I’ve re-plotted the primary data of Apivar efficacy vs. mite counts from individual colonies to emphasise this point.

Variation of Apivar efficacy vs mite infestation levels in individual colonies from commercial apiaries

Apiaries B and C (red markers) could be considered as ‘failing apiaries’ as the average Apivar efficacy of each was below 80% (see bar chart). Together the average mite load and Apivar efficacy for these two apiaries was 6.75 mites/100 bees and 72% respectively.

However, of the 16 colonies screened from these two apiaries (8 from each):

  • One colony had insufficient detectable mites to be included in the the full analysis.
  • Eight dropped less than 3 mites/100 bees during the sugar dusting analysis (the average over the 63 colonies screened was 5.33 mites/100 bees).
  • Four colonies exhibited ≥90% Apivar efficacy.
  • One colony from apiary B was a clear outlier, with >50 mites/100 bees ( 😯 ) and only ~28% Apivar efficacy. Inevitably this sample skews the averages …

Clearly the average figures presented in the bar chart above hides a very significant level of within-apiary variation.

Weird

I commented recently on the variation in mite levels during midwinter treatment of colonies with OA/Api-Bioxal. I attributed this – with little supporting evidence (!) – to different rates of late-season brood production. Colonies brooding late into the autumn were expected to have higher midwinter mite levels.

However, the variation seen here is different.

With the exception of that one heavily infested colony from apiary B, the mite levels in the ‘failing apiaries’ (B and C) are actually less than the average of the remainder of the study group (3.88 vs. 4.85).

What differs is the efficacy of Apivar treatment, not the resulting mite levels.

Frankly, this is a bit weird … on two counts:

  1. If Apivar treatment had been failing for a long time in apiaries B and C I would have expected much higher than average mite levels.
  2. Considering the amount of drifting and robbing that goes on between juxtaposed colonies I would have also expected Apivar-resistant mites to be very widely distributed within the ‘failing apiaries’.

Caveat on the mite counts – Apiaries in Louisiana, New York and South Dakota were analysed in this study. Louisiana apiaries were sampled in April, the others in July and August. I don’t know enough about the climate or mite-replication kinetics in these states to know how much this would have influenced the mite infestation levels (or prior or ongoing treatment regimes, which would also influence mite numbers). Unfortunately, the locations of the apiaries (A, B, C etc.) are not provided, other than the control apiary which is in Baton Rouge, LA. If the study had been done in the UK mite drops in April and August would have been wildly different depending upon the location.

Idle speculation

Apivar resistance does appear to have arisen in some of these colonies, but it does not appear to have become widely distributed within the apiary.

Why not?

I don’t actually think we have enough information to work with. The paper contains almost no additional background details – Apivar treatment history, use of other treatments, colony loss data etc.

But that won’t stop me speculating a little bit 😉

Do Apivar-resistant mites stop bees from drifting? Probably not, but it would explain why resistance was not widespread in the apiary 5.

More sensibly, perhaps Apivar resistance is detrimental in the absence of selection.

In the colonies in which resistance evolves it gives the mites a significant advantage. The ongoing infestation could encourage prolonged or repeated treatment, so selecting for yet more resistant mites. Eventually the colony succumbs to the resulting high viral load.

In other colonies, treatment is withdrawn (or forgotten … remember, we have zero information here!) and the Apivar-resistant mites are then at a disadvantage to their sisters.

This isn’t unheard of.

Apistan resistance appears to be detrimental in the absence of selection. There are some relatively straightforward molecular explanations for this type of phenotype.

You would have to assume differential colony treatments within apiaries B and C for this to be part of the explanation (and to account for drifting). Let’s hope the colony records are less shambolic than mine many beekeepers keep 😉

Until a clearer picture emerges of the management history of these colonies all we’re left with is the slightly (or very) confusing observation that Apivar resistance is a hive-specific phenomenon.

As the author states:

This colony level resolution suggests that each colony may act an island of resistance with its own distinct Varroa population. Beekeepers have reported inconsistency in amitraz treatment efficacy among colonies within an apiary and this variation seems to support those anecdotal observations.

And the good news?

I think there are two ‘encouraging’ observations in this paper (though of course I’d be happier if there was no resistance).

  1. About half of the commercial apiaries surveyed (5 of 11 that had a long history of Apivar usage) had too few mites detectable to screen for amitraz resistance. Clearly Apivar works, and often works very well indeed.
  2. Apivar resistance is not widespread in the apiaries within which it had arisen. For whatever reason, resistant mite populations appear restricted to individual colonies.

And these, in turn, have implications for practical beekeeping.

Implications for practical beekeeping

How does Apivar resistance evolve? Classically, misuse or overuse of treatments results in their eventual failure. Antibiotics are a good example of this.

I’ve been told by commercial beekeepers that some use a half dose of Apivar midseason to knock mite levels back sufficiently for the late season nectar flows. This is a typical example of misuse. It may not result in the development of resistance and it may not be a strategy used by the beefarmers managing apiaries B and C, but it is not the correct way to use Apivar.

What about overuse? Mites still dropping after 6 weeks of Apivar? Go on, slip another couple of strips in for another month or two. An (expensive) example of overuse.

Used Apivar strips

Or what about the Apivar strip found lying on the bottom of the hive at the first spring inspection? Again, overuse as there are likely to be lingering traces of Apivar present in the colony all winter 6.

So the first implication for practical beekeeping is to use Apivar correctly to help avoid the development of resistance. Don’t overdose or underdose, remove after 6-10 weeks, do not leave in over the winter.

Secondly, use alternate treatments to knock back the mite population. This is again a classic strategy to avoid selecting for resistance.

For example, use Apivar in late summer and Api-Bioxal in midwinter.

The mechanism of action of these two treatments is fundamentally different, so resistance to one will not confer resistance to the other (and there are no documented cases of oxalic acid resistance I’m aware of).

If you don’t treat midwinter (and you probably should 7) then use Apiguard one year and Apivar the next. Again, totally different mechanisms of action.

Finally, do not rely on individual colonies within an apiary being indicative of all colonies. I know some beekeepers who only conduct mite drop counts in one colony as a ‘sentinel’ 8.

If the drop is high then treatment is needed.

Or vice versa … no mites, so no treatment needed.

There’s a lot of colony to colony variation so it’s worth monitoring them all 9. And this is probably even more important with the colony level Apivar resistance reported in this paper.

Just something else to worry about … 🙁