Category Archives: Diseases

Polyandry and colony fitness

Honey bees are polyandrous. The queen mates with multiple drones during her mating flight(s). Consequently, her daughters are of mixed paternity.

In naturally mated queens there is a relationship between the number of patrilines (genetically distinct offspring fathered by different drones) and the ‘fitness’ of a colony.

Colony fitness

A ‘fit’ colony is one that demonstrates one or more desirable traits (those that benefit the colony … and potentially the beekeeper) such as better population growth, weight gain, resistance to pathogens or survival.

If you analyse the molecular genotype of the worker offspring you can determine which patriline they belong to. If you genotype enough workers you start to see the same patrilines appearing again and again. The more patrilines, the more drones the queen mated with 1.

Shallow depth of field

One of many …

Naturally mated queens mate with ~13 drones. Depending upon the study a range from as low as 1 to as high as 40 (and exceptionally into the high 50’s) has been demonstrated, though different studies all tend to produce an average in the low- to mid-teens.

There is a well-established link between polyandry and colony fitness 2. Essentially, the more genetically diverse a colony i.e. the larger the number of patrilines, the fitter that colony is.

The benefits of polyandry

Why should colonies with increased genetic diversity be fitter?

There are a number of hypotheses that attempt to explain why intracolonial genetic diversity is beneficial. These include the increased behavioural repertoire of the worker bees, a reduced production of diploid drones (which would otherwise be produced due to the single-locus sex determination system) and an increased resistance to a wide range of parasites and pathogens 3.

Parasites and pathogens are an extremely effective evolutionary selective pressure. Several studies from David Tarpy and Thomas Seeley have shown that increased polyandry results in better resistance to chalkbrood and American foulbrood.

But what about Varroa? It’s a new pathogen (evolutionarily speaking) to honey bees and there is evidence that the resistance mechanisms observed are genetically determined 4.

Does polyandry contribute to Varroa resistance? 

Would increased polyandry result in improved resistance to mites?

Limits of polyandry and natural resistance

Why is the average number of drone matings in the low teens?

If polyandry is beneficial – and there’s no doubt it is – then surely more patrilines (hyperpolyandry) would be even more beneficial?

How could this be tested?

Naturally mated queens only very rarely exhibit 30+ drone matings. Not only are these colonies hard to find, but they are so rare that doing any sort of statistical analysis of the improved (or otherwise) fitness is probably a non-starter.

Perhaps there’s an alternative way to approach the question? Rather than look at individual colonies within a mixed population, why not study the overall level of polyandry within a population that demonstrates resistance?

For example, do queens that head colonies of untreated feral bees that exhibit a demonstrated enhanced resistance to Varroa, the most important pathogen of honey bees, exhibit higher levels of polyandry?

Two relatively recent scientific papers have tackled these questions. Both have produced clear answers.

Drones : if more is better, is lots more better still?

Yes.

Keith Delaplane and colleagues used instrumental insemination (II) of virgin queens to produce queens ‘mated’ with 15, 30 or 60 drones. Sperm was collected from 1, 2 or 4 drones from 15 donor colonies, mixed thoroughly and used for queen insemination.

Full-sized colonies were requeened with the II queens and left for 6 weeks 5 after which sampling started. Over a two seasons a total of 37 colonies (with 11, 13 and 13 colonies respectively headed by queens ‘mated’ with 15, 30 and 60 drones) were tested at approximately monthly intervals.

Testing involved visual analysis of colony strength 6 and comb construction. Mite levels were measured using standard alcohol wash of ~300 bees at mid- or late-summer timepoints.

Brood frame with a good laying pattern

The results of this study are commendably brief … just 8 lines of text and two tables. I’ll summarise them in just a couple of sentences.

Colonies headed by queens ‘mated’ with 30 or 60 drones produced significantly more brood than the colony headed by the queen ‘mated’ with only 15 drones. Conversely, significantly more colonies headed by queens mated with only 15 drones had a higher level of mite infestation 7.

Natural Varroa resistance and polyandry

One of the best studied populations of feral bees co-existing with Varroa are those in the Arnot Forest in New York State. These are the bees Thomas Seeley and colleagues study.

These colonies live in natural holes in trees at low density through the forest. The colonies are small and they swarm frequently. Their spatial distribution, size and swarminess (is that a word?) are all evolutionary traits that enable resistance, or at least tolerance, to Varroa and the pathogenic viruses the mite transmits.

I’ve discussed Seeley’s studies of the importance of colony size and swarming previously. I don’t think I’ve discussed his work on spatial separation of colonies, but I have described related studies by Delaplane and colleagues.

Essentially, by being well-separated, mite transmission between colonies (e.g. during robbing) is minimised. Similarly, by existing as small colonies that swarm frequently Iwith concomitant brood breaks) the mite population is maintained at a manageable level.

Marked queen surrounded by a retinue of workers.

Her majesty …

Do the Arnot Forest Varroa-resistant 8 bees exhibit especially high levels of polyandry, suggesting that this contributes their survival?

No.

Seeley and colleagues determined the number of patrilines in 10 Arnot Forest colonies using the same type of genotyping analysis described earlier. They compared these results to a similar analysis of 20 managed honey bee colonies located nearby.

On average, Arnot Forest queens had mated with ~18 drones (17.8 ± 9.8) each. In contrast, queens in managed colonies in two nearby apiaries had mated with ~16 and ~21 drones. These figures are not statistically different from each other or from the natural mating frequencies reported for honey bees in other studies.

Hyperpolyandry and colony fitness

The first of the studies confirms and extends earlier work demonstrating the polyandry (and in this instance hyperpolyandry i.e. at an even greater level than seen normally) increases colony fitness – at least in terms of colony strength and Varroa resistance.

Delaplane and colleagues hypothesise that the increased mite resistance in hyperpolyandrous (30 or 60 drones) colonies may be explained by either:

  • the importance of extremely rare alleles (gene variants), which would only be present in colonies in which the queen had mated with a very large number of drones.
  • the presence of beneficial non-additive interactions between genetically-determined traits e.g. grooming and hygienic behaviour and reduced mite reproduction.

Neither of which are mutually exclusive and both fit at least some of the extant data on natural mite resistance. Discriminating between these two hypotheses and teasing apart the variables will not be straightforward.

Absence of hyperpolyandry in naturally mite-resistant colonies

At first glance, the absence of the hyperpolyandry in the mite-resistant Arnot Forest bees studied by Thomas Seeley and colleagues appears to contradict the studies using the instrumentally inseminated queens.

The Arnot Forest bees exhibit the same level of polyandry as nearby managed colonies, and for that matter, as colonies studied elsewhere. They are mite-resistant but the queen has not mated with an increased number of drones.

In other studies 9, naturally mated colonies exhibiting different levels of polyandry (within the normal range) showed no correlation between Varroa levels and queen mating frequency.

Perhaps it’s surprising that the Arnot Forest queens hadn’t mated with fewer drones considering the extreme separation of the colonies (when compared with managed colonies). The colony density within the Forest is approximately one per square kilometre.

However, at least during the peak swarming and mating period in the season, drone availability is rarely limiting.

This is because drones are not evenly spread in the environment. Instead, they accumulate in drone congregation areas (DCA) to which the queen flies for mating.

What limits polyandry?

Polyandry is beneficial and, apparently, hyperpolyandry is more beneficial. However, queens mate with 10 – 20 drones, rather than 50 or more. Why is this?

Queen mating is a risky business. The queen has to fly to the DCA, mate with multiple drones and then return to the hive. She may make one or several mating flights.

I’ve discussed how far drones and queens fly to reach the DCA previously. Most drones fly less than 3 miles and 90% of matings occur within about 5 miles of the virgin queen’s hive. The queen probably flies further to the DCA.

All the time she is travelling to and from the DCA, and all the time she is present within it mating, she’s potentially at risk from hungry house martins, swallows, bee eaters (!) or from thunderstorms.

Or simply from getting lost.

Additionally, a number of honey bee pathogens are transmitted between drones and queens during mating. Hyperpolyandrous queens 10 are therefore at risk from these sexually transmitted diseases 11.

It’s therefore likely that the level of polyandry observed in honey bees has evolved as a consequence of the beneficial pressures polyandry brings balanced by the risks associated with mating multiple times.

Practical beekeeping

Although the two studies described here don’t have an immediate relevance to day-to-day practical beekeeping, it’s worth remembering that poor queen mating is regularly blamed for queen failures e.g. queens that develop into drone layers during the winter.

I’m going to write about drones later this year so for the moment will just make these points:

  • drone production is maximised to generate sexually mature drones for the swarming season
  • after eclosion, drones need to mature before being able to mate
  • drones live about 30 days and their sperm volume, though not necessarily viability, decreases as they age

Together this means that late in the season – perhaps late July or early August (though this will vary depending upon location) – the number of drones will decrease.

More significantly, the drones will be ageing.

In turn this means that late-mated queens may not mate with as many drones, or that the matings may not result in insemination.

Most beekeepers will be aware of queens that apparently ‘run out of sperm’ and become drone layers.

However, there may be less obvious problems with late-mated queens. I’m not aware of any studies on seasonality of queen mating and polyandry. However, I would not be at all surprised if they exhibited a reduced level of polyandry.

And, as described above, these colonies are likely to exhibit reduced fitness.

Something else to consider when deciding whether to unite a colony late in the season or hope the last of your virgin queens mates successfully …


 

Questions & Answers

One of the challenging things about beekeeping is that the season can be both confusing and entertaining in equal measure.

It’s entertaining because it’s always a little bit different from the seasons that have preceded it. The environment changes. There’s an early spring, or late frosts, a drought, a monsoon or the local farmer changes from one strain of OSR to another.

Sometimes you get all of those in a single season … or month.

Mainly dry ...

Mainly dry …

But not only does the environment change, so do your bees. Inevitably your queens will be replaced over the years. In turn, they influence the performance of the colony. Your virgins fly off to the drone congregation areas where they mate with the ‘bad boys’ from colonies run by a nearby beekeeper with much thicker gloves and a fleece under his beesuit 🙁

Mayhem ensues. Inspections get a whole lot less fun. Quickly.

Or you collect a swarm headed by a fecund queen who busies herself producing calm, prolific, frugal and productive workers.

The colony gets bigger. And bigger. It shows no signs of swarming.

As you add the fourth super you feel like you’ve really cracked this beekeeping lark.

Sorted 🙂

But these things also make beekeeping incredibly confusing to the newcomer.

If you take a calendar-centric view there is no right answer to ‘When will the colony swarm?’ or ‘Is this the right time to treat for mites?’ or ‘Should I remove the supers now?’.

And many beginners do have a calendar-based viewpoint. It’s so much easier to prepare if you’re told that swarming starts in the third week of May and the supers should be removed at the end of August.

Not only is that easier to understand, but the telltale signs that the bees produce aren’t – for a beginner – very good at telling tales.

The first half-hidden charged queen cell, a reduced laying rate, the reduction in loaded returning foragers etc.

Play cup or queen cell?

Play cup or are they planning their escape …?

But, for me, at least half of the enjoyment is deciphering these signs and working out what the colony is doing, or going to do.

And therefore, what I should be doing.

Questions and answers

Most of this is observation, interspersed with a bit of record keeping and sprinkled with some ‘best guesses’.

If you keep asking the (right) questions you will slowly but surely start finding the answers.

Are they running out of space, making more play cups, and slimming the queen down for the great escape?

But many of these things are too subtle for beginners overwhelmed by the difficulty in just finding the queen amongst 38,789 of her daughters.

Inevitably this means that beginners – quite rightly – ask other beekeepers lots of questions.

I did.

I still do.

And in this increasingly connected world, some of those questions take the form of internet searches.

And some of these questions pop up as search terms on this site.

Mites

Willie Wonka meme

Many of these queries are about mite management:

  • best time to treat for varroa in honey bees?
  • should bees be treated for mites in spring?
  • use apiguard in june?
  • oxalic acid to treat varroa can i do it this week?
  • when to treat bees with oxalic acid in arkansas?

Very specific questions, very calendar-centric. There are hundreds more queries like these 1.

A correct answer requires an understanding of the biology of the mite and an appreciation of the state of the hive.

Neither necessarily involves the calendar. Both can be acquired with a little homework and good observation. However, the very fact that ~25% of queries are about mite management emphasises that many struggle with this aspect of beekeeping.

I remain convinced that the biggest challenge new beekeepers face is how to effectively manage mites. Without proper mite management your colonies will perish.

If you lose your colonies every winter you soon get disheartened.

The easiest way to properly control mite numbers is with chemicals.

It’s what I do.

Returning a marked and clipped queen

However, it’s not the only way.

Excellent beekeeping, selective rearing of mite-tolerant colonies (or of attenuated viruses!) and yet more excellent beekeeping – coupled with a favourable environment – may mean you can keep colonies without chemical intervention, and without excessive losses 2.

All beginners lack the necessary experience to achieve this. Most lack the ability to learn the skills quickly enough to save their colonies and the majority probably live in areas that are unsuitable.

Most importantly, many beginners aren’t resilient enough to ‘learn the hard way’. They believe the (largely incorrect) statements about the evils of treatment, they want their bees to be ‘healthy and happy’ 3, they like the sound of the term biodynamic 4 … but they cannot cope with losing their stocks every single winter through disease and starvation.

So they give up.

Learn to keep bees … then learn (again, using the years of knowledge already accumulated) to keep them without chemical intervention if you want. Not the other way round.

Read all you can – here and elsewhere – but remember that nothing is as valuable as time spent observing your bees.

Technical queries

These are the sorts of questions that probably can be easily answered 5.

Remembering of course that there are usually at least two correct answers for every question, and any number of incorrect ones.

  1. honey warming cabinet plans
  2. how long does it take bees to chew through newspaper?
  3. what is the chance of a queen being left in my hive when i have just lost a huge swarm?
  4. alighting board angle
  5. where and how to set up bait hives?

My honey warming cabinet is one of the most useful things I’ve built for my beekeeping and the pages that first describe it, the plans and its use, remain some of the most popular on this site.

The answer to Q2 obviously depends upon how many sheets of newspaper are involved.

I think we all know the answer to Q3 and it’s not going to make the questioner happy 😉

It’s very rare that you can provide an absolute definitive answer in beekeeping. However, after many years of exhaustive, well-controlled and independently verified trials I have unequivocally shown that the answer to Q4 is 47.7°.

47.7° precisely

Not more, not less.

Remembering of course that a landing (alighting) board isn’t actually needed at all 😉

Tom Seeley has done the definitive studies on bait hives (Q5). He clearly describes the ‘where’. My recommendations are rather more pragmatic. It’s easier to monitor and move bait hives if they’re not 5 metres above the ground.

Miscellaneous or just weird

And then there are lots of queries that are simply amusing typos, nonsensical or just odd. My favourites this year are:

  1. maxant crank mechanism
  2. langtorthe eke
  3. how to wear rigger boots?

I’ve no idea how the first of these landed up on the apiarist.org as it’s a term I’ve never used. The middle query (Q2) is a typical typo. It’s an obvious one, but it constantly amazes me how good fuzzy matching algorithms are these days.

Q3 is about beekeeping footwear. My last pair of rigger boots were abandoned years ago when the lining fell apart and they eventually turned my feet to a bloody pulp.

How to wear them?

I wore mine while hobbling. It’s not something I’d recommend.

I now wear Muck boots – specifically the now discontinued Edgewater II short boots – which are lightweight, very comfortable and fully waterproof. No steel toe cap, but I never drop full supers.

Oops ...

Oops …

Well, almost never.

Questions and comments

Not all questions originate in internet searches. Many come via the comments sections at the end of most posts. Most of these are both welcomed and useful; they allow me to clarify things that I’d presented confusingly, or they provide an opportunity to expand on parts of the post.

The numbers of comments have increased significantly this year.

More words and more comments

This increase probably reflects the increased readership (and page accesses) of the site.

Alternatively it might mean the writing is getting worse as the comment numbers correlate with the increased length of posts 🙁

I try and answer as many comments/questions as I can. Many make very salient points and I’m very grateful for those who take the time to comment, either to correct me, to seek clarification or to provide their own insight on the topic.

I ignore those that are dogmatically stupid or just plain wrong. My prerogative. There’s enough bad advice on the internet without propagating more.

I apologise to those who comment via Facebook or Twitter. I almost exclusively use both for promoting posts made here 6. Both generate a lot of traffic to this site but I simply don’t have time (or interest) to use them interactively.

If you want to contact me do so via the comments section or the, aptly named, contact form.

More Readers’ Questions

Which, in a rather circuitous way, brings me to the Readers’ Questions Answered column in the BBKA News. I was asked to tackle these a few months ago and January and February are already written 7.

BBKA News Readers’ Questions Answered proofs

The BBKA News is the monthly newsletter of the British Beekeepers Association. It has a circulation of ~25,000. Each year a different victim expert mug contributor prepares the answers. I’m taking over from Bob Smith, NDB from Medway BKA who did an excellent job and will be a hard act to follow. Some of the previous contributors have been anonymous which might have been a sensible option, but it’s too late for me now.

My family joke that I’m now an agony aunt for beekeepers.

I discussed this with Calum, a regular contributor to the comments section of these pages, who provided (as usual) some very sage advice, including “Bees put up with a lot of sh1t from beekeepers”. I don’t think the BBKA will want to use that as my strapline but it certainly sums things up pretty accurately.

Happy New Year … may your queens be well mated, your mite numbers low, your supers heavy and may your prime swarms be in my bait hives  🙂


 

Rinse and repeat

Midwinter mite treatment is no substitute for a properly applied late summer treatment that protects your all important winter bees. However, you also need to control mites in the winter or there is a good chance their numbers will reach damaging levels the following season 1.

Mid September

Late summer treatment and no winter treatment – mite levels in red.

OA (oxalic acid-containing) treatments are the ones to use in midwinter (e.g. Api-Bioxal). These can be trickled in syrup onto each seam of bees or they can be vaporised (sublimated), effectively coating everything in the hive with a very fine dusting of crystals.

Trickling damages open brood whereas sublimation is exceedingly well-tolerated by the colony.

If you are certain the colony is broodless then trickling is faster 2 and – because you don’t need power or any more PPE 3 than a pair of gloves – much easier.

If the ambient temperature is consistently below ~6°C and I know the colony is broodless I usually trickle. If the temperature is higher and/or I’m uncertain about whether there is brood present I usually vaporise.

I watch the weather and treat after the first prolonged cold spell of the winter.

Experience over the last few years suggests this is when colonies are most likely to be broodless.

Most likely is not the same as certain 🙁

Count the corpses

After treating I closely monitor the mite drop over several days. I use white Correx Varroa trays that slide underneath the open mesh of my kewl floors.

Easy counting ...

Easy counting …

I don’t count the mites every day, but I do try and count the day after treatment and 2-4 days later. I record the mite drop per hive and, over time, look for two things:

  1. The cumulative mite drop. This indicates the original infestation level of the hive. Usually it’s in the range 10-75 mites (total) for my colonies in midwinter, but – as you’ll see – it can be much higher.
  2. The speed with which the daily mite drop falls to a low single-digit average. OA treatment is very effective at killing phoretic mites. If there’s a continuing high level of mite drop it suggests that more are getting exposed over time.

In my experience, vaporised OA often results in a greater mite drop 24-48 hours post-treatment rather than in the first 24 hours 4. After that I expect (hope) the daily mite drop tails off very quickly.

Vaporised OA remains effective in the hive for several days. Randy Oliver reports studies by Radetzki who claims it remains effective for up to three weeks. I think this is an overestimate but I’m sure it continues working well for four to five days.

OA, whether vaporised or trickled, on broodless colonies is 90-95% effective i.e. if there were 100 mites in the colony you should expect as few as 5 remain after treatment.

Four to five days after the initial treatment I eyeball the numbers across all the hives in an apiary and look at the profile of the mite drop.

Mite drop profiles

I couldn’t think of a better term for this. Essentially, it’s the shape of a graph of mites dropped per day after treatment.

I don’t usually draw the graph – I have a life – but I do look carefully at the numbers.

Here are a couple of sketched graphs showing what I mean. Days are on the horizontal (X) axis, dead mites per day are on the vertical (Y) axis. Treatment applied on day 0. No count (yet) on day 6.

Mite drop profile – this is what you want

In the graph above there are high(er) levels of dropped mites on the first day or two after treatment, but levels thereafter drop to a basal level of perhaps 1-4 mites per day.

Each time I count the mites I clean the Varroa tray (the rinse in the title of the post).

Assuming the day 5 mite drop is very low, the profile above is what I’m looking for. It shows that treatment has worked and no repeat is necessary.

The profile below is much less promising 5.

Mite drop profile – this suggests additional treatment is needed

In this graph (above) the mite drop remains high every day after treatment. Sometimes they even increase over time.

If you assume treatment is equally effective – say 90%+ – on the five days after treatment 6 this must mean that there are mites being killed on days 4 and 5 that were not exposed to treatment on the earlier days.

How can this be?

The most likely explanation is that the colony had some sealed brood that has emerged in the days following treatment, exposing previously ‘hidden’ mites to the miticide.

It’s good that they’ve perished, but are there more hiding? How do you tell?

Enough of my hand drawn idealised graphs with no real numbers … what about some actual data?

Real world data

The graph below shows data for seven colonies in a single apiary. All were treated with Apivar in late summer. All were treated with a vaporised oxalic acid-containing treatment on the 28th of November. 

Mite drop profiles – real world data

I counted the mite drops on the 29th (T+1), the 2nd (T+4) and 3rd (T+5). The figures for 30th to the 2nd were averaged, which is why the bars are all the same height.

  • Colonies 3 and 6 had very low mite levels. Though not the lowest in the apiary 🙂
  • Colonies 2 and 7 had pretty good mite drop profiles, with low single-digit numbers on day T+5. None of these four colonies (2, 3, 6, 7) need treating again.
  • Colonies 1 and 5 have high mite levels 7 and – despite the pretty good levels on T+5 in colony 1 – were both re-treated.
  • Colony 4 was also treated again as the profile was flat and I suspected they had low levels of mites but were rearing brood..

And repeat

Note: The instructions for Api-Bioxal specifically state that the maximal dose of 2.3g/hive should be made in a single administrations with only one treatment per yearPrior to the VMD licensing and approval of Api-Bioxal there was effectively tacit approval for beekeepers to use unadulterated oxalic acid by trickling or vaporisation, without any particular limitations on frequency of usage.

It’s worth stressing that you should not repeat oxalic acid trickling 8.

Here is some real data for repeat treatments of another colony in the same apiary.

Repeat treatment for brood-rearing colony

The average mite drop per day over the first 5 days was ~60. This justified an additional treatment. Over the next 6 days 9 the average drop was ~20. I considered a third application was needed after which the mite drop per day was in the low single digits.

And again

Repeated treatment is needed if there is sealed brood in the colony.

The likelihood is that two additional treatments will be required.

Why two?

Here’s a reminder of the development cycle of the Varroa mite in developing worker or drone brood.

Repeated oxalic acid vaporisation treatment regime.

Worker brood occupies capped cells for 12 days (days 10 – 21 of development, shown above). Vaporised oxalic acid-containing treatments show a drop in efficacy after 4-5 days 10.

Therefore, to cover a complete cycle of capped brood, you need 3 x 5 day treatments to be sure no mites emerge without them being greeted with a lethal dose of something really, really unpleasant 😉

There should be no drone brood in your winter hives 11 but, if there was, 3 x 5 day treatments should just be enough to cover the complete cycle of capped drone brood as well. However, a fourth treatment might be needed.

Note (again): The instructions for Api-Bioxal specifically state that the maximal dose of 2.3g/hive should be made in a single administrations with only one treatment per year

Not all hives are equal

There are 15 hives in the apiary containing the bee shed. Colony 1 had just about the highest mite levels. However, as shown in one of the graphs above, adjacent colonies can have markedly different mite levels.

There is no clear correlation between mite drop after treatment and colony size. Colony 1 is a double brood monster, but the others in the bee shed are all single brood 10 and 11 frame Nationals 12.

Some colonies need repeated treatment, others did not.

To maximise efficient treatment and minimise unnecessary miticide usage it is necessary to monitor all the colonies.

It’s also worth noting that monitoring only a single hive in an apiary may be misleading; compare colonies 1 and 6 above in the graph of real data from the bee shed.

This monitoring takes just a few minutes. I usually do it after work. In the bee shed this is easy as I now have LED lighting and it’s nice and dry.

Easy conditions to count mites

In my out apiaries I have to do it by headtorch … under an umbrella if it’s raining 🙁

Checking mite drop by torchlight

That’s the last job of the winter completed … time now to review the season just gone and plan for next year.


Colophon

Rinse and repeat

Rinse and repeat is a truncation of instructions often found on the side of shampoo bottles – Lather, rinse and repeat. Other than potentially resulting in an endless loop of hair washing, it also means that a process is (or needs to be) repeated.

In The Plagiarist by Benjamin Cheever, a marketing executive becomes an industry legend by adding one word – REPEAT – to shampoo bottles. He doubles sales overnight.

For Varroa treatment the instructions should be amended to Repeat if necessary … and note again the instructions on Api-Bioxal which, at the time of writing, is the only oxalic-acid containing VMD approved miticide that can be administered by vaporisation.

 

More local bee goodness?

Before the wind-down to the end of the year and the inevitable review of the season I thought I’d write a final post apparently supporting the benefits of local bees. This is based on a recently published paper from the USA 1 that tests whether local bees perform better than non-local stocks.

However, in my view the study is incomplete and – whilst broadly supportive – needs further work before it can really be seen as an example of better performing local bees. I suspect there’s actually a different explanation for their results … that also demonstrates the benefits of local bees.

This is a follow-up to a post three weeks ago that provided evidence that:

  1. Colonies derived from different geographic regions show physiological adaptations (presumably reflecting underlying genetic differences) that seem pretty logical e.g. bees from Saskatchewan express more proteins involved in heat production, whereas Hawaiian bees show higher levels of protein turnover (which would make sense if they had evolved locally to have high metabolic rates).
  2. In a study by Büchler, European colonies survived better overwinter in their local environment; a fact subsequently attributed to the colonies being stronger going into the winter. In turn, this agrees with a recent study that clearly demonstrates the correlation between overwintering success and colony strength.

I suggest re-reading 2 that post as I’m going to try and avoid too much repetition here.

Strong colonies

Strong colonies overwinter better and – if you’re interested in that sort of thing – are much more likely to generate a profit for your honey sales.

So how can you ensure strong colonies at the end of the season?

What influences colony strength?

One thing is colony health. A healthy colony is much more likely to be a strong colony.

In the ambitious 600-colony Büchler study in Europe they didn’t do any disease management. The colonies were monitored over ~2.5 years during which time 84% of colonies perished, at least half due to the ravages of Varroa.

Clearly this is not sustainable beekeeping and doesn’t properly reflect standard beekeeping practices.

Study details

The recent Burnham study makes a nice comparison to the Büchler study.

It was conducted in New York State using 40 balanced 3 colonies requeened in late May.

Queens were sourced from California (~4000 km west) or Vermont (~200km east in the neighbouring state, and therefore considered ‘local’) and colonies were assigned queens randomly.

Unlike some previous studies the authors did not evidence the genetic differences between queens.

A local queen

A local queen

However, the queens looked dissimilar and the stocks were sourced from colonies established in California or Vermont for at least 10-15 generations. I think we can be reasonably confident that the queens were sufficiently distinct to be relevant for the tests being conducted.

Colonies were maintained using standard beekeeping practices, Varroa levels were managed using formic acid (MAQS for European readers) and the colony weight and productivity (frames of bees) was quantified, as was the pathogen load.

In contrast to the Büchler study, Burnham and colleagues only followed colonies over one beekeeping summer season. This was not a test of overwintering survival, but mid-season development.

Results

The take-home message is that colonies headed by the ‘local’ Vermont queens did better. The colonies got heavier faster and brood levels built up better.

Bigger, faster, stronger …

It’s notable that colony weight built up before any brood would have emerged from the new queen (upper panel) and that brood level in colonies headed by the local queen recovered much better after formic acid treatment (arrow in lower panel).

Nosema levels

However, Nosema levels were significantly different (above) as were the levels of Israeli Acute Paralysis Virus (IAPV; below).

Virus loads (DWV, BQCV and IAPV)

There were no significant differences in the Varroa loads before or after treatment (not shown), or in the levels of DWV or Black Queen Cell Virus (BQCV).

Taken together – bigger, heavier, stronger colonies and lower pathogen loads (at least of some pathogens) – seems good evidence to support the contention that local bees are beneficial.

The benefits are precisely what you want for good overwintering – strong, healthy colonies.

That’s a slam-dunk then?

Case proven?

No.

IAPV is a virus rarely detected in the UK. It causes persistent and systemic infections in honey bees and can be found in every caste (drones, workers, queens) and at every stage of the life cycle.

As IAPV is detectable in eggs and larvae – neither of which are Varroa-exposed – it is assumed to be vertically transmitted from the queen. IAPV is also found in the ovaries of the queen, which is additional evidence for vertical transmission.

At the first timepoint (12 days post requeening) the levels of IAPV are different between the two colony types, but not significantly so. However, by 40 days (T2) the levels are very different. At this later timepoint all the bees in the colony will be have come from the introduced queen.

The authors explain the differences in IAPV levels in terms of local bees being more resistant to ‘local’ pathogens … in much the same way that Pizarro’s 168 conquistadors, being more resistant to smallpox, defeated the might of the Inca Empire with the help of the virus diseases they inadvertently introduced to Peru.

I suspect there’s another explanation.

Perhaps the Californian queens were IAPV infected from the outset?

If this was the case they could introduce a new and virulent strain of IAPV to the research colonies and – over time – the levels would increase as more and more workers in the colony were derived from the new queen. IAPV is present in ~20% of US colonies so it seems perfectly reasonable to suggest it might have been largely absent from the Vermont queens and the test colonies, but present in the queens introduced from California.

How should they have tested that?

The obvious thing to do would be to characterise the IAPV present in the colony. IAPV shows geographic variation across the USA. If the predominant virus was of Californian origin it would suggest it was brought in with the queen. This is a relatively easy test to conduct … a sort of 23andme to determine bee virus provenance.

Alternatively, though less conclusively, you could do the experiment the other way round … ship Vermont queens to California and compare their performance with colonies headed by Californian queens on their own territory. If the Californian queens again performed less well it undermines the ‘local bees do better’ argument and suggests another explanation should be sought.

Nosema is sexually transmitted but it is not vertically transmitted, so the same arguments cannot be made there. Why the Nosema levels drop so convincingly in colonies headed by the local queens is unclear. Nosema was present at the start of the study and was lost over time in the stronger colonies headed by the local queens.

One possibility of course is that the stronger colonies were better fed – more workers, more foragers, more pollen, more nectar. Improved diet leads to a more active and effective immune system and an increased ability to combat pathogens. Simplistic certainly, but it is known that diet influences pathogen resistance and colony performance.

So what does this paper show?

I suspect it doesn’t directly show what the authors claim (in the title) … that local queens head colonies with lower pathogen levels.

This largely reflects the lack of proper or complete controls. However, it does not mean that local bees are not better.

More than anything I think this paper demonstrates the impact queen quality has on colony performance.

Perhaps the Vermont-sourced queens were just better queens. Local certainly (on a USA scale definition of the word local), but not better because they were local, just better because they were better.

However, if my interpretation of the source of the IAPV is correct i.e. introduced from the Californian queens, I think the paper indirectly demonstrates one of the most compelling reasons why local bees are preferable.

If they’re local – your apiary, your neighbours, someone in your association – there is little chance they will be bringing with them some unwanted baggage in the form of an undetected exotic pathogen.

Or a more virulent strain of one already circulating relatively benignly.

Extensive bee movements, whether of queens, packages or full colonies, risks spreading parasites and pathogens.

There is compelling evidence that hosts and pathogens co-evolve to reduce the pathogenicity of the interaction. Naive hosts are always more susceptible to introduced pathogens, or novel strains of pre-existing pathogens. After all, look what happened to the Peruvian Inca when they met the measles- and smallpox-ridden conquistadors.

So, when thinking about the claims being made by bee importers (or, for that matter, strong advocates of local bee breeding), it’s worth considering all of the factors at play – queen quality per se, genetic adaptation of the queen to the local environment and the potential for the introduction of novel pathogens with introduced non-local stock.

And that’s before you also consider the benefits to your beekeeping of being self-sufficient and not reliant on others to produce your stocks.

I never said it was simple 😉


 

Spotty brood ≠ failing queen

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

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

We need a reminder of what we’re missing.

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

Brood frame with a good laying pattern

This is a sight welcomed by all beekeepers.

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

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

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

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

What are these lines of empty cells?

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

That'll do nicely

That’ll do nicely …

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

I don’t know why.

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

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

Good laying pattern ...

Good laying pattern …

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

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

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

What are all these empty cells?

But sometimes a brood frame looks very different.

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

Patchy brood pattern

Patchy brood & QC’s …

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

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

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

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

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

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

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

Right?

Perhaps, perhaps not …

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

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

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

If you are squeamish look away now.

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

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

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

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

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

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

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

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

Hmmm … puzzling.

Colony-level variables

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

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

Again, no statistical differences.

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

And vice versa …

Queen exchange studies

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

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

Changes in sealed brood pattern after queen exchange

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

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

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

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

Matched and mismatched workers

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

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

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

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

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

But it might be worth thinking twice about this …

Insufficient storage space

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

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

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

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

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

In which case, definitely keep her 🙂


 

Virus resistant bees?

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

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

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

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

IAPV

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

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

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

To a virologist they are a fascinating group of viruses.

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

Schematic of the RNA genome of Israeli Acute Paralysis Virus

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

Phylogenetic relationships between picorna-like viruses

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

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

IAPV resistance

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

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

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

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

And now for the crunch experiment …

Virus challenge

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

Only 2% survived.

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

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

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

If it is correct.

Subsequent studies

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

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

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

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

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

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

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

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

Unfinished business

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

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

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

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

Where next?

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

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

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

Monoculture ... beelicious ...

Monoculture … beelicious …

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

What’s new?

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

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


 

Magic mushrooms not magic bullets

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

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

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

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

‘shrooms

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

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

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

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

Fungi and viruses

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

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

Shrooms

Mushroom

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

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

Have you?

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

Not just any viruses

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

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

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

Not just any ‘shrooms

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

Hoof fungus … and not a honey bee in sight.

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

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

Results

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

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

Nevertheless, reductions there were.

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

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

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

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

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

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

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

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

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

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

Hope or hype?

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

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

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

Questions

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

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

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

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

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

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


Colophon

Magic!

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

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

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

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

Leave and let die

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

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

DWV symptoms

DWV symptoms

The principle is straightforward. It goes something like this:

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

A crude oversimplification?

Yes, I don’t deny it.

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

But won’t.

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

But I’ll start with a simple question …

How many colonies have you got?

One? (in which case, get another)

Two?

Ten?

One hundred?

Eight-two thousand? 3

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

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

This is why we treat ...

This is why we treat …

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

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

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

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

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

Where ‘likely to be’ means will be.

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

It could be you … but it’s unlikely

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

And so on.

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

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

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

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

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

Apologies. Let’s not go there.

Let’s cut to the chase …

Comparison of treated vs untreated colonies over 3 years

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

Amitraz

Amitraz …

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

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

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

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

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

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

Treatment and seasonal variation

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

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

The fourth group were the untreated controls.

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

The apiary in winter ...

The apiary in winter …

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

Results …

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

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

Out, damn'd mite ...

Out, damn’d mite …

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

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

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

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

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

… and some additional observations

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

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

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

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

Evolution …

March of Progress

Evolution …

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

Does this start to sound familiar?

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

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

Lots of colonies.

Actually, almost all of them.

… takes time

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

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

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

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

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

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

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

Almost all the colonies died.

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


 

Midseason mite management

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

Pupa (blue) and mite (red) numbers

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

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

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

And you know what mites mean

Mites in midseason

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

What circumstances?

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

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

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

How do you identify midseason mite problems?

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

Out, damn'd mite ...

Out, damn’d mite …

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

And vice versa.

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

Overt disease

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

High levels of DWV

High levels of DWV …

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

Treatment options

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

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

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

The combination of these two factors is the issue.

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

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

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

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

MAQS

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

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

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

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

Of course, many beekeepers have used MAQS without problems.

So, what other strategies are available?

Oxalic acid Api-Bioxal

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

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

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

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

Varroa counts

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

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

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

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

What do you mean by compatible?

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

That is about as definitive as possible.

Another one for the extractor ...

Another one for the extractor …

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

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

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

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

Absence of evidence is not evidence of absence

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

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

One day 14.

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

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

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

Frankly, without this information we’re just guessing.

Why risk it?

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

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

Do I know what this tastes like? 15

No, and I’d prefer not to find out.

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

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

What are the options?

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

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

Quite possibly.

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

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

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

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

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

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


 

Responsibilities

In draughty church halls the length and breadth of the country potential apiarists are just starting their “Beginning beekeeping” courses run by local associations. The content of these courses varies a bit but usually contains (in no particular order):

  • The Beekeeping Year
  • The hive and/or beekeeping equipment
  • The life cycle of the honey bee
  • Colony inspections
  • Pests and diseases
  • Swarm prevention and control
  • Products of the hive

I’ve seen these courses from both sides. I took one before I started beekeeping and I’ve subsequently taught on them.

Although I’m not convinced the seven topics above are the optimal way to cover the basics of beekeeping (perhaps that’s something for a future post?), I am a strong supporter of the need to educate new beekeepers.

Theory and practice

You can learn some of the theoretical aspects of beekeeping on dark winter evenings. In my experience a liberal supply of tea and digestives hugely helps this learning process 😉

However, beekeeping is essentially a practical subject and any responsible association will offer apiary-based training sessions once the season starts. A good association will run these throughout the season, enabling beginners to experience all aspects of the beekeeping year.

Trainee beekeepers

Trainee beekeepers

If they don’t, they should (both run them and run them through the season).

The reason is simple … ‘hands on’ with the bees is a much better way of appreciating some of the most important characteristics of the colony. It’s strength and temperament, the rate at which it’s developing, the levels of stores etc.

But all this takes time. A couple of early-season apiary sessions might be held on cool evenings in failing light, or dodging Spring weekend showers. This means that ‘hive time’ is often restricted and beginners only get a small snapshot of the beekeeping season.

Curb your enthusiasm

Inevitably, many new beekeepers are desperate to get their own bees as soon as possible. After all, the season has started and there are kilograms of nectar out there waiting to be collected and converted into delicious honey for friends and family.

Demand for overwintered nucs is very high (usually significantly outstripping supply, meaning a considerable price premium) and a purchased colony, which should be strong and building up fast, becomes the property of someone who potentially has yet to see an open hive.

The seasonal nature of the hobby and the way we train beginners creates a very steep learning curve for new beekeepers 1. Almost as soon as they’re out of the classroom (or draughty church hall) they’re faced with the start of their first swarm season.

Queen cells ...

Queen cells …

Their inevitable – and completely understandable – enthusiasm to start practical beekeeping reaches a crescendo at a time when they are singularly poorly equipped to manage the colony 2.

What’s missing?

The emphasis on the theory and practical aspects of beekeeping is understandable. There’s a lot to learn in a relatively short time.

However, this focus on the practicalities often overlooks emphasising the responsibilities of beekeepers.

In the frenetic early-season enthusiasm to ‘become a beekeeper’ these might seem unimportant, superfluous or entirely obvious.

But they’re not.

Oil seed rape (OSR) ...

Oil seed rape (OSR) …

Later in the season the colony can become bad tempered, unmanageably large or ignored. Some or all of these happen with new (and not-so-new) beekeepers. The OSR goes over and colonies get stroppy, April’s 5-frame nuc “explodes” to occupy a towering double brood monstrosity or a new-found enthusiasm for dahlias or crown green bowls becomes all-consuming.

Bees? What bees? Have you seen my dahlias?

Bees? What bees? Have you seen my dahlias?

This is when the responsibilities of beekeepers become really important.

What are the responsibilities of beekeepers?

As I see it, as beekeepers we have responsibilities to:

  • The general public
  • Other beekeepers
  • The bees 3

As I stated above, these might seem entirely obvious. However, every year new beekeepers start with the best of intentions but some have a near-total lack of awareness of what these responsibilities are (or mean).

The general public

The combination of calm bees, careful handling and appropriate protective clothing means that bees essentially pose no risk to the beekeeper.

However, strange as it may seem to a beekeeper, some people are terrified of bees (mellisophobics). Others, due to adverse allergic reactions (anaphylactic shock), may have their lives endangered by bee stings. Finally – and thankfully by far the largest group – are the remainder of the public who should never feel bothered or threatened by our bees, whether we consider this a rational response or not.

What does this mean in terms of practical beekeeping? I think it can be distilled to just three points:

  1. Keep calm bees
  2. Keep bees and the public well-separated
  3. Restrict beekeeping activities to times when the public are not inconvenienced

The first point is sensible, whether or not there’s anyone else around. It makes beekeeping a much more relaxing and rewarding experience.

The second point involves either keeping bees in unfrequented locations (infinitely preferable) or ensuring that bees are forced to fly up and away from the hives (by suitable screening) and well-away from passers-by.

The final point is the most inconvenient, but also the most important. If there are members of the public around who might be bothered by your bees – walkers strolling across the field towards your apiary, kids playing in the garden next door – don’t open the hives.

My apiaries have generally been in large rural gardens, private farmland and very well screened. I’ve also kept bees in urban environments, with no problems from the neighbours. However, I have always maintained out apiaries to move my bees to should they exhibit poor temper. Additionally, I’d only conduct inspections when the adjacent gardens were empty … meaning inspections were often carried out in sub-optimal weather or late in the evening.

Finally, while many beekeepers consider the sight of a swarm is one of the truly great sights of beekeeping, this isn’t a sentiment shared by most non-beekeepers.

Swarm on a swing ... not ideal if it's in the next door garden

Swarm on a swing … not ideal if it’s in the next door garden

Keep non-swarmy bees, clip the queen and keep a bait hive prepared to lure any swarms that do emerge.

Other beekeepers

The responsibilities beekeepers have to other beekeepers are probably restricted to:

  1. Courtesy
  2. Disease

The first is straightforward. Don’t do things that negatively impact other beekeepers 4. For example, don’t plonk two dozen hives over the fence from an established apiary, unless you’ve first discussed it with the beekeeper and you’re both happy that the local forage is sufficient.

And, of course, don’t steal hives or colonies 5.

Disease is perhaps less obvious and more insidious. The health of your bees influences the health of other colonies in the area. Over short distances bees drift from one hive to another. Over much longer distances strong colonies can rob weaker colonies.

All these bee exchanges also move the parasites and diseases they carry between hives. This includes VarroaNosema, a panoply of pathogenic viruses and European and American foulbrood.

Of these, the foulbroods are statutory notifiable diseases and beekeepers are legally required to report suspected diseased colonies under the Bee Diseases and Pests Control Order 2006 (and amendments). Responsible beekeepers will register their apiaries on the National Bee Unit’s Beebase so they are notified of local outbreaks, and so the bee inspectors can check their colonies if there is a nearby outbreak.

National Bee Unit Beebase

National Bee Unit Beebase

Whilst not notifiable, the remaining parasites and pathogens are also best avoided … and certainly should not be foisted upon other local beekeepers.

If your colony is weak, disease-riddled and poorly managed it may get robbed-out by other local strong colonies. In doing so, your bees will transfer (some of) the pathogen load to the stronger colony.

That is irresponsible beekeeping.

US beekeepers use the term ‘mite bomb’ to refer to an unmanaged, Varroa-riddled, collapsing colony that introduces significantly higher mite levels to local strong colonies as it’s robbed. This is more extreme, but not dissimilar, to beekeepers that treat with miticides far too late in the season. Their colonies retain high mite levels and can spread them to nearby hives. One way to avoid this is to coordinately treat mites in the same geographic area.

The bees

Bees may or may not be classified as livestock. The standard definition 6 of “domestic animals kept on a farm for use or profit; esp. cattle, sheep, and pigs” is perhaps a little restrictive 7 so lets accept for the moment that they are livestock.

If you keep livestock you usually need to register them and vaccinate them, and you always need to look after their health, feed and transport them properly and generally take responsibility for them.

If you don’t look after their welfare you may be prosecuted.

Of course, bees are invertebrates, not mammals or animals with backbones. Legally invertebrates are not usually considered as animals in the Animal Welfare Act 2006 8 which defines the law on animal welfare.

But all these definitions are a distraction.

In my view, if you keep bees you have a responsibility to look after them properly.

Even if this isn’t a legal requirement, its a moral responsibility.

This responsibility to your bees includes – but is not restricted to – preventing and treating them for disease when appropriate and ensuring they have sufficient stores going into winter (and during periods with no nectar).

If you can’t do this perhaps take up crown green bowls instead.

Blimey, this is all getting a bit heavy isn’t it?

Bees are not ‘fit and forget’.

Actually, they’re quite the opposite.

Proper management means that there are certain things that must be done at a particular time. This includes treating for mites at the end of the summer honey season, feeding the colony up for winter and swarm prevention and control.

If you work abroad for April and May or if you holiday on the Maldives for six weeks every autumn you’re unlikely to become a successful beekeeper.

Powder blue surgeonfish, Maldives

Bees? What bees? They’ll be OK …

And you’re certainly unlikely to be a responsible beekeeper.

You might start with bees, but you’re unlikely to keep them …

What prompted this post? A combination of things … cabin fever and online discussion forum posts from beekeepers puzzling why their colonies all died (no mite treatment, ever) or starved (no feeding before winter) or hadn’t been inspected in the last 15 months (“I’ve been busy”).

It’s going to be a long winter … 9