Category Archives: Diseases

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 ūüôĀ

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% ¬Ī 9.9% more sealed cells) than the loss observed in the reverse exchange (-8.0% ¬Ī 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 ūüôā


 

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 ‚ÄúIf the bee disappears from the surface of the earth, man would have no more than four years to live‚ÄĚ 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 Marjom√§ki 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 ūüėČ

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 Рother than it being appreciably more work Рto 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 Рsmall, swarmy colonies Рthat 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 Рthough not necessarily accurate Рcalculator 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 ūüėČ 7

Of course, many beekeepers have used MAQS without problems.

So, what other strategies are available?

Oxalic acid Api-Bioxal

Many beekeepers these days Рif you read the online forums Рwould 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‚Äôt 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 ūüėČ

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 Varroa, Nosema, 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 Рbut is not restricted to Рpreventing 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


 

Convenience or laziness?

It’s cold and dark and all is quiet in the apiary. Hives appear somnolent. Colonies are clustered 1 and, other than the odd corpse or two on the landing board, I’ve not seen a bee for at least a fortnight.

The apiary in winter ...

The apiary in winter …

Based upon previous experience I suspect colonies are – or very soon will be – broodless. I usually reckon that the first extended (2-3 weeks) period of cold weather 2 in the winter is the most likely time for the colony to be broodless.

In 2016/17 this was the first week in December.

In 2017/18 it was just a day or two later.

In both instances, when the hives were checked, they had no brood.

What’s all this about being broodless?

If a colony is broodless there are no capped cells in which the Varroa mite can ‘hide’. As a consequence¬†it’s an¬†ideal time to apply a miticide like a trickled solution of Api-Bioxal 3.

There are very good reasons why a midwinter OA treatment is necessary, particularly if you treated early enough in the autumn to protect the overwintering workers from the ravages of Deformed Wing Virus (DWV). High DWV levels reduce the lifespan of bees and contribute to many (possibly most) winter colony losses. I’ve even suggested here that “isolation starvation” might actually be due to Varroa-transmitted viral disease.

Time of treatment and mite numbers

Time of treatment and mite numbers

Early autumn treatment protects the winter bees but also leaves the long autumn for the residual mites to continue replicating.

And there will be residual mites. No treatment is 100% effective.

So, paradoxically, if you treated early enough in the autumn to really help protect the winter bees, your mite levels will be higher at the end of the year.

Which also means they’ll be higher at the beginning of next year.

Not a good start to the 2019 season ūüôĀ

Convenience or laziness?

Many beekeepers, for convenience, laziness or historical precedent, choose to apply the winter OA treatment between Christmas and New Year. I suspect that this is often too late. If the queen starts laying again around the winter solstice there will be sealed brood – and therefore unreachable Varroa – by the end of the month.

I’d prefer to have a cold and damp afternoon in the apiary slaughtering¬†Varroa now¬†than the convenience of treating them less effectively¬†during the Christmas holiday period.

The latter might be more convenient … the office will be closed, I’ll be replete with turkey and sprouts and it will be a good excuse to ‘escape’ visiting relatives and yet more mince pies 4.

But is it the best time for your bees?

We have the technology

We have a couple of hives with Arnia hive monitors fitted 5. These have a temperature probe inserted into the brood nest. Brood rearing temperature is around 34¬įC. Here is a trace of one colony over the last month.

Arnia hive monitor temperature

Arnia hive monitor temperature

The colony temperature was pretty stable (around 33-35¬įC) until about the 19th of November and has dropped about 10¬įC since then. Although I’ve not opened the colony I think that this is additional evidence that the colony is broodless 6.

Beekeeping by numbers

Keeping bees properly involves being aware of the seasons, the available forage and the state of the colony. This varies from month to month and year to year 7.

You can’t mechanically (‘by the numbers’) add supers on the 5th of May and harvest honey on the 15th of June. Sure, it might work some years, but is it the¬†best time to do it?

Similarly, you can’t¬†optimally treat a colony for Varroa¬†on the 30th of December¬†unless the climatic conditions and state of the colony coincide to make that the best time to treat.

It might be, but I suspect that generally it’s a bit late if there is a brood break.

If you’re going to the trouble of preparing the OA treatment, donning the beesuit and disturbing the colony you might as well do it at the right time for the bees.

I’ll be treating in between the predicted sleet showers and sunny periods this weekend.

Time to treat

Time to treat

Isn’t evolution a wonderful thing? This post started with a working title of¬†Know your enemy”¬†and was on a different topic altogether. I’ll save that for next week.


STOP PRESS

The above was written at the beginning of the week. Now the weekend is closer it’s clear the weather is going to be cold with heavy snow predicted. Unless the forecast is wrong (and how often does that happen?!) I’ll hold off treating until a) it’s over 5¬įC, and b) the roads are safe.

Botulism

Do not feed to infants

Do not feed to infants

I was recently asked, Why can’t you give young babies honey?

You can.

But just because you can doesn’t mean you should.

And on this point the NHS guidelines are very clear. You should not give honey to babies under 12 months of age because there is a risk that they might get botulism.

Bacteria, toxins and Botox

Botulism is a serious, sometimes fatal, disease caused by infection with a bacterium called Clostridium botulinum. As it grows, C. botulinum produces neurotoxins which cause a flaccid (floppy) paralysis and can result in respiratory failure. About 5-10% of cases are fatal, but infections thankfully very are rare.

Symptoms include fatigue, weakness, blurred vision and difficulty speaking and swallowing. The paralysis is ‘descending’, generally starting in the head and neck, then moving to the shoulders, arms, chest and lower limbs.

Botulinum toxin

Botulinum toxin

Unusually for a bacterial infection there is no fever. This reflects the fact that there’s probably only limited bacterial growth (which typically induces fever) and the potent neurotoxicity of the botulinum toxin.¬†This toxin stops the release of the neurotransmitter acetylcholine from the nerve endings, thereby causing paralysis.

Botulinum toxin is one of the most acutely lethal toxins known. The lethal dose depends upon the route of administration, but is between 1.3 and 13 ng/kg 1.

Remember, botulinum toxin is the active ingredient in Botox.

No thanks. I’ll stick with the wrinkles ūüėČ

Botulism cases in the UK/Europe

Botulism is a notifiable disease. Consequently, we have good data on the incidence of botulism in the UK and Europe. In 2014 there were 91 confirmed cases in the EU, with 14 cases reported in the UK between 2010 and 2014. Other than injecting drug users, a significant proportion of the cases are in infants – see below.

C. botulinum is widespread in the environment and infection usually occurs by ingestion of improperly prepared food e.g. undercooked or improperly canned foods, in which the bacteria survives.

Clostridium botulinum

Clostridium botulinum

The bacteria grows in the absence of oxygen¬†and produces the toxin during growth. Although the toxin is heat-inactivated if properly cooked (over 85¬įC), the bacterium also produces heat-resistant¬†spores during growth. These spores can withstand temperatures over 100¬įC for long periods and usually require both high temperatures and pressures to inactivate them.

As a consequence of this the spores are also very widespread in the environment … cue¬†the¬†Jaws soundtrack … just waiting to encounter the correct conditions to germinate and initiate a new round of bacterial growth (and toxin production).

Botulism cases in children

About a third of all cases of botulism are in the 0-4 age group. I’ve been unable to find a more detailed breakdown by age, but there have been 19 cases of infant (children less than 12 months old) botulism in the UK since 1978.

In many cases of infant botulism the source of the spores is unknown. However, other than well-documented cases of contaminated milk powder, honey is the only food regarded as a significant risk factor. About 60% of cases of infant botulism are in babies with a history of honey consumption 2 and, in several cases, epidemiological follow-up has confirmed that honey was the source of the infection.

Treatment is not with antibiotics as it’s the toxin that causes the symptoms, not the bacteria. Instead patients are treated with immunoglobulin (antibodies) specific for the toxin. These inactivate toxicity fast and recovery is usually complete, but can be protracted.

C. botulinum spores in honey

Oxygen inhibits the growth of C. botulinum. So do acidic conditions. Honey is acidic, with a pH of about 3.9, which is too low for the bacterium to grow. However, the spores remain viable at low  pH. It is this contamination of honey with C. botulinum spores that poses a risk for infants.

It is possible to microbiologically examine honey for contamination with C. botulinum spores. When this has been done, 6-10% of honey samples tested were contaminated, with contamination levels estimated at 5 to 80 spores per gram of honey. The infectious dose for a human is estimated at 10-100 spores 3.

So … much less than one teaspoon of contaminated honey.

Despite this, there is no requirement for honey to carry a label warning that it should not be fed to infants. Instead, the Food Standards Agency recommend honey carries a warning that it is unsuitable for children under one year of age.

Why is infant botulism so rare?

If up to 10% of honey is contaminated with C. botulinum spores, why are there not many more cases of botulism in infants? After all, European paediatricians have even been known  to recommend honey Рa long-standing traditional solution Рas a means of soothing crying babies4.

The intestine of the developing baby is full of bacteria – the so-called commensal microbiota – all competing to get established and to lead a long, happy and healthy association with their human host. The spores of¬†C. botulinum have to germinate and establish an infection in the face of this competition and, usually, they fail. A likely possibility is that infant botulism only occurs in babies in which the commensal microbiota have not properly developed … either because they are so young, because broad-spectrum antibiotic use has prevented the development of the microbiota or for a pre-existing genetic condition.


 

Survival of the fattest

Winter bees have high levels of vitellogenin, a glycolipoprotein 1, deposited in their fat bodies which act as a food reservoir for the long winter.

These fat winter bees are essential for the successful overwintering of the colony.

Last week I discussed the major points that need attention for overwintering i.e. strong, healthy colonies with ample food in a weathertight hive.

This week I want to explore the relationship between colony strength, health – specifically with regard to Varroa and deformed wing virus (DWV) – and isolation starvation.

Isolation starvation describes the phenomenon where a small colony of tightly clustered honey bees gets isolated from the honey stores laid down in autumn, resulting – typically during protracted cold periods – in the colony starving to death.

Isolation starvation ...

Isolation starvation …

It’s both a pathetic and distressing sight. Bees, with their heads crammed into the bottom of cells searching for food, dying from starvation when literally inches away from capped stores.

Deaths and births

In temperate climates the winter is characterised by low temperatures and little or no forage for the bees. The queen usually stops laying sometime in autumn and starts again around the turn of the year. During the intervening period she may lay intermittently, but generally in limited amounts.

The fat bodied winter bees that are reared in late summer and early autumn are long-lived (about 6 months) and are responsible for getting the colony through the winter. They protect the queen, thermoregulate the hive and they help rear the brood raised in the autumn and through the winter.

In their absence – or if there are just too few of them – the colony will perish.

Winter bees do not all live for 6 months. The usual figure quoted is ~175 days 2. Some live shorter lives, some longer … up to 9 months under certain conditions.

Importantly, in studies I’ve discussed at length previously, high levels of DWV¬†reduces the lifespan of winter bees. We know this because, in¬†Varroa-infested colonies, researchers 3¬†have shown that the winter bees die off faster 4.

Live fast, die young

Winter bees with high levels of DWV don’t really live fast … but they do die young. In the studies above the average lifespan of winter bees was reduced by 20% in the colonies that died overwinter.

There are a couple of important things to note here. Dainat and colleagues were not looking at bees in the presence or absence of Varroa, or in the presence or absence of high or low levels of DWV. They simply looked at hives that succumbed in the winter or that survived, then measured DWV and¬†Varroa levels. It’s a subtle but important difference. Their surviving colonies still had¬†Varroa and DWV.

From analysis of hives that died or survived, and having marked known numbers of bees in late summer, they could determine the life expectancy of workers – in their surviving colonies it was ~88 days, in those that died it was ~71 days.

Healthy colonies

The gradual death of bees through the winter coupled with the reduced lifespan of winter bees with high levels of DWV explains why colonies need to be strong and healthy.

The following graphs are based upon modelled data 5, but show the influence of colony size and winter bee lifespan.

The first graph – the least important – simply shows the lifespan of bees. The graph plots the number of bees (on the vertical axis) in a population that die at a particular time (on the horizontal axis) after the start of the experiment. The blue bees have a longer average lifespan than the red bees 6.

Lifespan of winter bees

Lifespan of winter bees

In the following graphs remember that the blue bees are healthy, with low levels of Varroa and Рconsequently Рlow levels of DWV. The red bees are unhealthy and have high levels of Varroa and DWV.

Using this lifespan data we can look at the influence on the total number of winter bees in a colony (on the vertical axis) over time (horizontal). Imagine that the horizontal axis is the long, dark, wet and cold months of winter. Starting in early September and running through until late March.

Brrrr ūüôĀ

Winter bee numbers in healthy (blue) and unhealthy (red) colonies

Winter bee numbers in healthy (blue) and unhealthy (red) colonies

It is clear, and of course entirely predictable, that the numbers of bees in the healthy (blue) colony are higher than those in the unhealthy colony at each time point. If the average lifespan is reduced (by disease) more bees will have died by a particular time point when compared with a healthy colony at the same timepoint.

Finally, consider that the shaded section of the graph represents the lower limit of bee numbers for viability. If the number of bees in the colony drops into this region the colony will perish.

Simplistically – and in reality – starting with similar numbers of bees a healthy colony will survive longer than an unhealthy colony.

Strong colonies

Using a similar approach we can also look at the influence of the average lifespan of winter bees on the survival of strong or weak colonies.

The following graph shows the numbers of bees in the colony over time for a strong colony (solid line) and a weak colony (dashed line) where worker bee lifespan is identical 7.

Winter bee numbers in strong and weak colonies.

Winter bee numbers in large (strong) and small (weak) colonies with the same average lifespan.

The shaded section of the graph again represents colony oblivion.

Large (strong) colonies take longer to drop below the threshold for viability and so – all other things being equal – will survive longer 8.

Mix’n’match

A strong colony with high levels of Varroa and DWV might actually survive less well than a weak but healthy colony.

Strong unhealthy colonies might survive less well than weak healthy colonies.

Large unhealthy colonies might survive less well than small healthy colonies.

In this graph the weak but healthy colony drops below the ‘viability threshold’ after the strong but unhealthy colony¬†9.

Winter bees and brood rearing

This is modelled data, but it makes the point clearly. Large and/or healthy colonies retain more of the all-important winter bees and so survive longer.

Simples.

The differences might not appear marked.¬†However, for convenience 10 I’ve omitted the influence of winter bee numbers on the ability of the colony to rear brood.

If there are more winter bees, the colony is able to thermoregulate the hive better. It’s therefore able to keep any brood present warm. It’s therefore able to rear more brood.

As a consequence, the differences in bee numbers between the large or small, or the healthy and unhealthy, colonies will be much more striking.

Critically 11 the strength of the colony coming out of the winter is often the rate-limiting determinant for spring build-up to exploit early season nectar flows. Weak colonies develop less well.

Isolation starvation

Finally, returning to that pathetic little cluster of starving bees in the image at the top of the page. What is the relationship between colony health, strength and isolation starvation?

It’s now time to dust off my weak-to-non-existent Powerpoint skills …

Isolation starvation schematic

Isolation starvation schematic

Again, it’s straightforward. A large (strong) overwintering colony (A above) only has to move a short distance to access stores in midwinter. In contrast, a small (weak) overwintering colony has to move much further.

Consequently, small colonies become isolated from their stores during long, cold periods when the colony is clustered.

Prediction

Many beekeepers will be familiar with isolation starvation of overwintering colonies.

Most would explain this in terms of “very cold weather and the cluster was unable to reach its stores”.

Some would explain this in terms of¬†“the colony was far too small to reach the stores when¬†clustered”.

Very few would explain this in terms of¬†“the Varroa and DWV levels were too high because of poor disease management last autumn. Inevitably most of my winter bees died off early in the winter,¬†leaving a very small cluster of bees that were unable to reach the stores..

I suspect the real cause of isolation starvation is probably disease … specifically poor management of¬†Varroa levels and consequently high levels of DWV in the colony.


Colophon

Herbert Spencer

Herbert Spencer

Another post, another poor pun in the title. Survival of the fittest encapsulates the Darwinian evolutionary principle that the form of an organism that survives is the one able to leave the most copies of itself in future generations. Darwin didn’t actually use the term until the 5th edition (1869) of his book¬†On the origin of the species. Instead, the phrase was first used by Herbert Spencer in 1864 after reading Darwin’s book. Whilst ‘survival of the fittest’ suggests natural selection, Spencer was also a proponent of the inheritance of acquired characteristics, Lamarckism.

They think it’s all over!

We’re gently but inexorably segueing¬†into early autumn after an excellent beekeeping season. The rosebay willow herb is almost over, the farmers are busy taking in the harvest and colonies are – or should be – crowded with under-occupied workers.

Rosebay willow herb

Rosebay willow herb

Drones are being ejected, wasps are persistently looking for access and there’s a long winter – or at least non-beekeeping period – ahead.

There’s a poignancy now in being in the apiary conducting the last few inspections of the season. Only a few short weeks ago, during late May and early June, the apiary was a scene of frenetic productivity … or complete turmoil, depending upon your level of organisation or competence.

Now there’s little activity as there’s not much forage available.

Colonies are busy doing nothing.

The most important time of the season

But that doesn’t mean that there’s nothing to do.

Rather, I’d argue that late August and early September is probably the¬†most important¬†period during the beekeeping year.

However well or badly the season progressed, this is the time that colonies have to be prepared for the coming winter. With good preparation, colonies will come through the winter well. They’ll build up strongly in spring and be ready to exploit the early season nectar flows.

In Fife, this is about 8 months away ūüôĀ

This explains the poignancy.

There are some colonies inspected last weekend that probably won’t get properly opened again until mid/late April 2019. Queens I saw for the first time in August won’t get marked or clipped until next spring 1.

Au revoir!

Spot the queen ...

Spot the queen …

To survive the winter and build up well in the spring the colony has few requirements. But they are important. A lack of attention now can result in the loss of the colony later.

To appreciate their needs it’s important to understand what the colony does during the winter.

Suspended animation

Honey bees don’t hibernate in winter. In cold weather (under ~7¬įC) they cluster tightly to conserve energy and protect the queen and any brood in the colony.

At higher temperatures the cluster breaks but they largely remain within the hive. After all, there’s little or no forage available, so they use their honey and pollen stores.

The fat-bodied overwintering bees that are reared in autumn have a very different physiology to the ephemeral summer workers. The latter have a life-expectancy of 5-6 weeks whereas overwintering bees can live for many months 2.

But they’re not immortal.

Throughout the winter there’s a slow and steady attrition of these workers. As they die off the clustered colony gradually reduces in volume, shrinking from the size of a medicine ball, to a football, to a grapefruit … you get the picture.

Some brood rearing does occur. The queen often stops laying after the summer nectar flows stop 3 and laying might be sporadic through the autumn, dependent upon weather and forage availability.

Late summer brood frame from a nuc ...

Late summer brood frame from a nuc …

However, by the turn of the year she starts laying again. At a much reduced level to her maximum rate, but laying nevertheless and, with sufficient workers in the colony and as forage become available, this rate will increase.

The amount of brood reared during the winter period (late autumn to early spring) isn’t enough to make up for the losses that occur through attrition. This explains why colonies are much smaller in the spring than the early autumn.

Strong, healthy, well-provisioned and weathertight

Knowing what’s happening in the colony during the winter makes the requirements that must be met understandable.

  • Strong colonies start the winter with ample bees. Assuming the same attrition rate, a larger colony will get through the winter stronger than a smaller one. There will be more workers available to ‘reach’ stores (I’ll deal with this in the next week or two) and keep the queen and brood warm. Hence there will be more foragers to exploit the early crocus, snowdrop and willow.
  • Healthy colonies will have a lower attrition rate. The overwintering workers will live longer. High levels of deformed wing virus (DWV) are known to shorten the life of winter bees. To minimise the levels of DWV you¬†must reduce the levels of¬†Varroa in the colony. Critically, you must protect the overwintering bees from¬†Varroa exposure. Treat too late in the season and they will already be heavily infected …
  • Well-provisioned colonies have more than enough stores to survive the winter. The clustered colony will have to move relatively short distances to access the stores. As a beekeeper, you won’t have to constantly meddle with the colony, lifting the lid and crownboard to add additional stores in midwinter.
  • Weathertight¬†colonies will be protected from draughts and damp 4.The hive must be weathertight and, preferably, not situated in a frost pocket or damp location 5.

Winter preparation

Once the honey supers are off all activities in the apiary are focused on ensuring that these four requirements for successful overwintering are achieved in a timely manner.

Clearing bees from wet supers ...

Clearing bees from wet supers …

Weak colonies are united with strong colonies. At this stage in the season – other than disease – the main reason a colony is likely to be weak is because the queen isn’t up to the job. If she’s not now, what chance has the colony got over the winter or early spring? 6

Varroa treatment is started as early as reasonably possible with the intention of protecting the overwintering bees from the ravages of DWV. This means¬†now, not early October. Use an appropriate treatment and use it correctly. Apiguard, oxalic acid (Api-Bioxal), Apivar¬†etc. … all have been discussed extensively here previously. All are equivalently effective if used correctly.

All colonies get at least one block (12.5kg) of bakers fondant, opened like a book and slapped (gently!) on the tops of the frames. An eke or an empty super provides the ‘headspace’ for the fondant block.¬†All of the¬†Varroa treatments listed above are compatible with this type of feeding simultaneously 7.

Hopefully, hives are already weathertight and secure. Other than strapping them to the hive stands to survive winter gales there’s little to do.

They think it’s all over!?

It is … almost ūüôā


Colophon

They think it’s all over! is a quote by Kenneth Wolstenholme made in the closing stages of the 1966 World Cup final. Some fans had spilled onto the pitch just before Geoff Hurst scored the the last goal of the match (England beat West Germany 4-2 after extra time), which Wolstenholme announced with “It is now, it’s four!”. This was the only World Cup final England have reached, whereas Germany have won four.

As Gary Lineker says “Football is a simple game; 22 men chase a ball for 90 minutes and at the end, the Germans win.”