Tag Archives: anti-vaxxers

Darwinian beekeeping

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

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

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

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

Differences

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

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

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

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

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

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

Real differences

Of course, some of the differences are very real.

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

Abelo poly hives

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

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

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

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

Darwinian beekeeping

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

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

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

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

This is presumably unnnatural beekeeping

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

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

Practical Darwinian beekeeping

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

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

Good and not so good advice

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

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

High altitude bait hive …

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

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

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

Let’s deal with them individually.

Small hives – one brood and one super

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

They’ll run out of space and swarm.

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

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

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

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

A small swarm

A small swarm … possibly riddled with mites

Thanks a lot!

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

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

Kill heavily mite infested colonies

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

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

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

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

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

They’ll procrastinate, they’ll prevaricate.

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

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

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

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

Less stress and better health

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

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

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

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

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

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

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

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

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

I’ll wrap up with two closing thoughts.

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

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

 

Vaccinating bees

Brace yourselves. There’s some heavyweight science this week.

I’m going to discuss a very recent publication 1 on vaccinating bees against parasites and pathogens.

The paper involves a whole swathe of general concepts many readers will have some familiarity with – vaccines, immunity, infections, parasites, the gut microbiota 2 – which, because the paper is about bees, bear little recognisable relationship in the details.

And the devil is in the detail.

The paper appears to offer considerable promise … but I’ll return to that later.

To start with, let’s begin with measles.

Measles

Measles is a virus. It is highly contagious – typically being transmitted by coughing or sneezing – and causes a characteristic rash. Complications associated with measles infections – pneumonias, encephalitis and other respiratory and neurological conditions – are responsible for a case fatality rate of ~0.3% in the USA, or up to 30% in populations that are malnourished or have high levels of immune dysfunction.

Sixteenth century Aztec drawing of a measles victim

In 1980, 2.6 million people globally died of measles. That’s about five people (mainly kids) a minute 3.

By 2014 this figure had dropped to 73,000 due to a global vaccination campaign.

The measles vaccine is excellent. It is an attenuated (weakened) strain of the virus that is injected. When it replicates it produces all of the measles virus proteins. These are not naturally found in the human body, so the vaccinee 4 recognises them as foreign and produces an immune response that eventually stops the vaccine growing.

The really important thing about the immune response is that it lasts i.e. it has a memory. If the vaccinated individual is exposed to a virulent strain of measles in the future the immune response ‘wakes up’ and stops the virus replicating.

This immune response is effectively lifelong.

One important component of the immune response are antibodies. These are proteins that specifically recognise the measles virus, bind to it and lead to its destruction.

If you’ve been vaccinated (or have survived a previous infection) and subsequently get infected your body produces lots of antibodies which destroy the incoming strain of the measles virus, so protecting you (but this immune response is very specific … the response to measles does not protect you from poliomyelitis or coronavirus or mumps.).

OK, enough about measles 5.

Bees don’t have antibodies

The point about the stuff on measles was to introduce the principles of a protective immune response.

It has several characteristic features, including:

  • highly specific
  • destruction of the incoming pathogen
  • longevity (memory)

In humans, all of the above are provided by antibodies 6.

Bees don’t have antibodies, but they do have an immune response which has all of the characteristic features listed above.

The immune response of bees uses nucleic acids 7 which are common chemical molecules found in the bodies of all living things. Specifically bees use ribonucleic acid (RNA) that interferes with the nucleic acids of invading pathogens.

RNAi

To make ribonucleic acid (RNA) that interferes easier to say it is abbreviated to RNAi 8.

RNA is made up of individual building blocks called nucleotides. There are four nucleotides, with names abbreviated to A, C, G and U. These join together in long strands e.g. ACGUUGUGCAG … the order (or sequence) of which has all sorts of important biological functions we don’t need to worry about for the purposes of vaccinating bees.

Pairs of nucleotides in different strands have the ability to bind together – A binds to U, G binds to C or U. Individually, these bonds are weak. When lots occur close together they are much stronger and therefore very specific.

For example, the sequence ACGUUGUGCAG binds very well to UGCGACGCGUU. In contrast, it binds very much less well to CGUUAGCAUUG (just count the vertical bars which indicate each of the weak bonds between the nucleotides in the two strands. The left hand pair bind tightly, those on the right do not).

                         ACGUUGUGCAG          ACGUUGUGCAG
                         |||||||||||           || | | 
                         UGCGACGCGUU          CGUUAGCAUUG

Finally, these short RNAs interfere when they bind very well to their target sequence.

What does that mean?

In the cartoon above, imagine the text in red represents the RNAi and the text in blue represents part of the RNA genome of deformed wing virus (DWV), the most significant viral pathogen of honey bees 9.

The specific binding of RNAi to its target sequence recruits enzymes that result in either the destruction of the target, or the impairment of its functionality.

RNAi binding to DWV results in the inactivation and eventual destruction of the virus genome.

Virus replication is therefore stopped.

This is a ‘good thing’.

“Foreign”

Before we get on to vaccinating bees I have one final thing to explain.

How does the bee ‘know’ it is infected with DWV (or a similar viral pathogen) and how is the RNAi actually made?

OK, that’s two things, but they’re actually closely related to each other.

I said earlier that our bodies recognise the proteins that the measles virus (or vaccine) produces as ‘foreign’ i.e. something not normally present in the body. It turns out that many organisms – including bees – have evolved specific ways of detecting double stranded RNA as a ‘foreign’ entity.

Double stranded RNA (dsRNA) is made when RNA viruses replicate, but it is never normally present in the cells of a healthy bee. Therefore if the bee detects dsRNA it ‘knows’ it is infected and it induces an immune response … specifically an RNAi-mediated immune response.

The dsRNA is recognised by a protein called Dicer which cuts up the double stranded RNA into smaller duplex RNAi molecules, one of the pair of these then associates with additional proteins (including Argonaute; Ago 10) to form the RNA induced silencing complex (RISC).

RISC, which includes the RNAi, binds to the specific target e.g. the genome of other DWV viruses, and chops it up and destroys it.

The mechanism of RNAi-mediated silencing

Finally, because RNAi is a small molecule it can easily move from cell to cell. So RNAi made in one cell can move to regions of the bee some distance away.

Phew … OK, that’s the end of the whistle-stop introduction to RNAi and insect immunity 11.

Vaccinating bees

It’s been known for some time that you can directly introduce RNAi into bees and reduce the levels of some of the viruses present.

Frankly the data on DWV has not been great, but there are reasonably compelling studies of reductions in Israeli Acute Paralysis Virus (IAPV) levels and even field trails showing benefits at the colony level.

In these studies you either inject individual bees with RNAi, or you feed them large amounts of sugar syrup containing huge amounts (in value) of RNAi.

Neither of these routes is practically or financially viable.

Injecting individual bees takes a very long time 12. You need to anaesthetise the bee with CO2 or by chilling it on ice. It’s pretty tough on the bee and not all survive the anaesthetic or the injection. You need good lighting, good eyesight and a very small needle. It’s obviously a non-starter.

What about feeding? Syrup feeding is incompatible with honey production. It’s also a rather inefficient way to deliver RNAi. RNA is a very sensitive molecule. It is easily damaged. If it has to sit around in syrup for a few days, get collected by the bee, stored in the honey stomach, regurgitated and passed to another bee etc. there’s a risk it will be inactivated.

And it’s very expensive to produce …

The gut microbiota

Which in a really roundabout way brings us to this recent study by Leonard et al., published at the end of January in the prestigious journal Science

Leonard et al., (2020) Science 367, 573-576

In this study, the authors have modified a harmless bacterium normally present in the honey bee gut so that it produces double stranded RNA specific for DWV. This bacterium, specifically called Snodgrassella alvi, is a present in the gut of all bees. It is a core member of the gut microbiota, the bacterial population present in the honey bee gut.

The concept is relatively simple, but the science is pretty cool.

The bacterium sits around in the honey bee gut producing DWV-specific RNAi. If the bee gets infected – through feeding or injection, for example by Varroa – the RNAi (which has diffused around the body of the bee) is ready and waiting to ‘silence’, through RNA interference, the replicating DWV genome.

The bee remains healthy and happy 13.

But there’s more … Snodgrassella alvi is presumably passed from bee to bee during feeding (of larvae or adult workers). Therefore the RNAi-expressing version should naturally spread through a colony, protecting all the bees. In addition, because it is present throughout the life of the bee, a genetically engineered form of the bacterium should provide the longevity that is characteristic of a protective immune response.

So, does it work?

The paper includes lots of introductory studies. These include:

  • demonstrating that engineered Snodgrassella alvi – which for pretty obvious reasons I’ll abbreviate to S. alvi for the rest of this post – colonises the bee gut and could be spread from bee to bee.
  • the introduced bacterium produces double strand RNA (dsRNA) precursors of the RNAi response.
  • that dsRNA produced in the bee gut spreads to other areas of the bee body.
  • and that the presence of dsRNA upregulates components of the immune response.
  • the demonstration that it was possible to control host gene expression using this dsRNA 14.

I’m going to return to some of these points in a future post (this one is already too long) as there are both promising and disturbing features buried within the data.

Let’s cut to the chase …

Symbiont-produced RNAi can improve honey bee survival after viral injection.

Seven day old adult worker bees were fed with S. alvi expressing RNAi to DWV or to an irrelevant target (GFP). Seven days later some were injected with DWV (solid lines in the graph above), others were injected with buffer alone (dashed lines).

In the 10 days after injection about 25% of the bees injected with buffer died. This reflects the ageing of the bees and the attrition rate due to handling in the laboratory.

About 75% of the bees ‘vaccinated’ with S. alvi expressing GFP RNAi or no RNAi died after DWV challenge over the 10 day period.

In contrast, only ~60% of the S. alvi bees expressing DWV-specific RNAi died. This is a relatively small difference, but – because the experiment was conducted with lots of bees – is statistically significant.

Killing mites

The results presented above are promising but the authors also explored the logical extension of this work.

If the RNAi produced by the engineered S. alvi becomes widely distributed in the honey bee, perhaps it also could also taken up when Varroa feeds on the bee?

In which case, if you engineered S. alvi to produce Varroa-specific RNAi’s, perhaps this would help kill mites.

Symbiont-produced RNAi kills Varroa mites feeding on honey bees

It does.

Using a similar ‘vaccination’ schedule as above, only ~25% mites exposed to bees carrying S. alvi expressing Varroa-specific RNAs’s survived 10 days, whereas 50% of mites survived when feeding on bees carrying non-specific engineered strains of S. alvi.

Again, this is encouraging.

Only encouraging?

Yes, at the moment, only encouraging.

Don’t get me wrong, this is pretty fancy technology and the results represent a lot of very laborious and elegant experiments.

At 2100 words this post is already too long … so here are a few things to think about which help justify my qualified enthusiasm for the paper.

  1. Although I didn’t show the data, transmission of engineered S. alvi between bees was rather inefficient. Over 5 days, only 33% of naive co-housed bees demonstrated infection with the modified symbiont. Why might this be an issue? Alternatively, is transmission between adult bees important? When might it be important to not transmit between adult bees?
  2. None of the experiments included any virus quantification. Did the bees that didn’t die after DWV injection challenge have lower DWV levels? If not, why not? What is the mechanism of protection?
  3. Actually, there were some virus quantification studies buried in the Supplementary data. In these the authors showed that virus levels were lower in all bees carrying engineered S. alvi, even those expressing the GFP negative control RNAi. This suggests a non-specific up-regulation of the immune response.
  4. All the challenge experiments were done with 7 day old worker bees. Are these the bees we really need to protect from DWV? Why didn’t they do any studies with larvae and pupae? These are much easier to handle and very much easier to inoculate. And very much more relevant in terms of virus-mediated colony losses.
  5. What other species sharing the environment with honey bees carries S. alvi? Why should this matter? Snodgrassella is a gut symbiont of honey bees and lives in the ileum. Is it present in honey bee faeces?

I’ll post a follow-up in the next few weeks to discuss some of these in further detail.

Congratulations to those of you who have got this far … don’t get rid of your Apivar and oxalic acid stocks just yet 😉