Synopsis : With so many swarms lost by beekeepers, why are there relatively few feral colonies? Do they die from starvation, depredation or disease? What kills feral colonies?
Introduction
It can take a long time to understand complex natural phenomena. When you take into account geographic and seasonal variation you often end up with an explanation littered with more caveats than actual answers.
For example … do honey bees compete to the detriment of native solitary bees?
During May in an environment with limitless yellow acres of oil seed rape … probably not, but during early spring in an arable area with limited hedgerows … almost certainly.
OSR and threatening clouds
Sometimes the explanation may seem obvious, but isn’t. Bumble bees restrict themselves to field margins whereas honey bees venture hundred of metres into the middle of a field of OSR. Not only are there huge amounts of pollen and nectar available, but the different species exploit it in different areas of the field.
By many accounts, it’s been a very ‘swarmy’ season. The BBKA’s swarm line was swamped 2. Many beekeepers ran out of equipment (and no doubt patience) hiving swarms lost by beelosers with poor swarm control.
With ~250,000 colonies in the UK I wouldn’t be surprised if there were 50-100,000 lost swarms and casts.
That being the case, why aren’t there more feral honey bees?
Synopsis : How promising is the “world’s first vaccine for honey bees”? Separating hype from hope, good news from bad news, and with a bonus discussion of trans-generational immune priming and beemageddon.
Introduction
Bad news sells newspapers. A survey of two decades of news preferences by the Pew Research Centre showed that the most-read stories were those that could be classified as either war, weather, disaster, money or crime.
’If it bleeds, it leads’ as they say.
And combinations – like crooks making huge profits from pandemics – ensure top billing.
Enough! This isn’t a politics blog … let’s move on.
That survey was ~15 years ago, but it’s equally true today. However, these days additional topics sometimes force their way into the buffet of gloom that make up the headlines. Royalty is one, particularly with the tabloids, though sometimes these could equally well be classified under ‘war, weather, disaster, money or crime’1.
Weather … we’ve been having some
More recently, climate change and environmental apocalypse have started headlining. Unfortunately for journalists, the measurables are often rather esoteric. Kilotons of greenhouse gases or atmospheric CO2 levels of over 400 ppm mean little to the layman, or most journalists.
But cute, furry, hard working bees do … particularly if there’s no mention of stings 😉 .
So, the impact of climate change or the environmental apocalypse on bees often gets top billing … and not just any bees, honey bees.
Everyone knows what a honey bee is, and almost everyone loves honey.
Beemageddon
All of which means that some of these stories are couched in terms of the potential for beemageddon. And because honey bees are ‘threatened’ 2 and familiar, related stories about honeybees also tend to get wide coverage.
Royalty, death and bees? BINGO … we have a winner!
One of these – the bee vaccine – looks like it could be good news.
Of course, the need for the vaccine means there’s some bad news to fully justify the story (don’t forget that impending beemageddon).
The world’s first bee vaccine sounds good doesn’t it?
Let’s have a look at some of the claims and the technology behind it.
Vaccines
What is a vaccine?
In the dim and distant past the word vaccine originated from the Latin for ‘cow’ (vacca). The link to vaccines is of course Edward Jenner who made a smallpox vaccine derived from the related cowpox virus.
In 1798, in an experiment that would shred all current ethical regulations, Jenner inoculated James Phipps with cowpox and, six weeks later, challenged him with pustular material from a smallpox case. Not only did Phipps survive, but he developed no smallpox symptoms either.
A vaccine is therefore something derived from an infectious agent that, when administered (inoculated), provides protection (immunity) from subsequent infection (challenge) by the same or a closely related infectious agent.
As an aside, Jenner could perhaps claim to have made the world’s first vaccine … despite the fact that a Dorset farmer, Benjamin Jesty, had done the same thing two decades earlier. In addition, variolation, usually involving administering dried smallpox material from a mild case, had been used prophylactically to prevent smallpox for hundreds of years.
Claiming originality is a tricky business … and something I’ll return to.
In mammals (like James Phipps) vaccines work by primarily stimulating a cell- and protein-based immune response. Cells are ‘primed’ to recognise a pathogen. Should subsequent infection occur, the cells and proteins, which have a molecular memory, are reactivated, amplified and subsequently destroy the invading pathogen.
Similar immune systems have proven so effective that evolution has created lots of them … many of which bear little immediate similarity to the one mammals (and most vertebrates) have. But there are similarities; many also have a ‘memory’ that can be reactivated should subsequent exposure occur.
And, scientists are starting to understand immunity in honey bees, and how to exploit it.
Bees, flies, RNA and, er, dunno
The most detailed studies of insect immunity have been done with fruit flies (Drosophila) as they are, by some distance, the best understood insects. The primary immune system in flies is not protein based, but instead uses nucleic acids. Immunity involves things that are called interfering ribonucleic acids which, understandably, are conveniently abbreviated to RNAi.
And honey bees also have and RNAi-based immune system, and it is increasingly well understood. Actually, it’s so well understood that we can stimulate it with experimental treatments against Israeli Acute Paralysis Virus and Deformed wing virus or even Varroa.
‘Experimental’ in this case means ”works, sort of, but not as well as we want … or need”.
But the world’s first bee vaccine that I’m going to discuss this week is not RNAi-based. It uses a completely different immunity system termed trans-generational immune priming, which is also conveniently abbreviated to TgIP (or TGIP in some studies 7 ).
And the thing about TgIP is that we have almost no idea as to how it works.
Just like the press article (“New vaccine to prevent beemageddon”) there’s both good news and bad news resulting from our cluelessness about TgIP.
The good news is that I can focus on the results rather than the mechanism, so making this post precisely 6430 words shorter than it would otherwise be.
The bad news is that by focusing on the results and some of the subsequent claims, the balance between the hope and hype in the title of this post gets shifted a bit 🙁 .
Sorry.
The discovery of TgIP in honey bees
The Tg (trans-generational) in the TgIP reflects the fact that:
‘ … maternal immune experience has been demonstrated to be transmitted to progeny and may therefore have a positive impact on offspring resistance and survival’ (Hernandez Lopez et al., 2014).
Essentially that means that if the mother is inoculated, the ‘children’ inherit some of the immunity.
Although the mechanisms are usually poorly understood – and may well not be the same in all species – TgIP has been demonstrated in vertebrates and invertebrates, including amongst the latter, bumble bees (Sadd et al., 2005), beetles and butterflies (Tidbury et al., 2010; Freitak et al., 2014).
The first study I’m aware of on honey bees was conducted in the University of Graz, Austria (Hernandez Lopez et al., 2014). In this study they demonstrated that queens immunised with the causative agent of American Foulbrood (AFB) subsequently produced larvae that were at least partially resistant to subsequent AFB disease.
American foulbrood
American foulbrood is a bacterial disease of honey bees caused by Paenibacillus larvae. The name, foulbrood, reflects the smell of diseased larvae in the hive. It is a brood disease, caused by the ingestion of bacterial spores by very young larvae. The spores are effectively metabolically inert, heat resistant forms of the bacteria, that can survive for decades and germinate when ingested by a larva.
Adult bees are resistant to infection, but are the vectors that transmit the spores between larvae in the hive, and between hives while drifting and robbing.
AFB outbreaks are dealt with by destruction of the colony and in many countries it is a notifiable disease.
Inoculating queens by injection
Hernandez Lopez and colleagues heat-killed (90°C for 10 minutes) a vegetative 8 culture of Paenibacillus larvae and injected mated queens with the resulting ‘soup’ of proteins. They subsequently returned the queens to their nucleus colonies and, at an unspecified time later, removed day old larvae to plastic dishes in an incubator and fed them an artificial diet containing infectious P. larvae spores.
Then it was simply a case of counting the corpses …
Like all proper experiments this one was controlled in a variety of ways. To determine whether any benefit observed was due to inoculation of the queen with the heat-killed bacterial soup they injected a similar number of queens with an inert buffer solution. They repeated the study a year later and used two different strains of P. larvae spores for the challenge.
Finally, they tested the colonies both before and after inoculating the queens. This was an important control. Queens were unrelated and open mated and this control was needed to demonstrate whether there was any inherent differences in susceptibility to AFB, for example reflecting genetic differences between larvae.
For brevity, I’ll only show one set of the results.
Counting the corpses
Results from these type of studies can be presented as dull-as-dishwater numerical tables, or visually-rewarding ‘kill curves’. More properly these are called Kaplan-Meier curves. These plot time (horizontal) against the proportion of test subjects that exhibit – typically – disease or survival (vertical).
The resulting stepped curves therefore start at 100% (sometimes – as here – represented as 1) and drop over time as the corpses pile up. The stepped curves plot the cumulative body count.
Kaplan-Meier plots of larval survival a) before queen vaccination, b) after queen vaccination (11-2 & 11-3)
The black line indicates larval losses due to experimental handling. These control larvae were not challenged with AFB. As you can see, about 5-10% of larvae die off during the experiment and it’s nothing to do with AFB.
The graph on the left (a) shows larval survival after AFB challenge before the queens were inoculated. There’s no statistical difference between the coloured lines indicating that all are equally susceptible to AFB infection.
On the right are the kill curves Kaplan-Meier curves after inoculation of queens with the control buffer (line 11-1) or with the heat-killed P. larvae bacterial soup (lines 11-2 and 11-3). Clearly fewer larvae die over the time course of the experiment from nucs headed by inoculated queens.
Remember, these are cumulative survival curves – each line is derived from 96 to 192 individual challenged larvae.
Overall 65% of challenged larvae from buffer-inoculated (11-1) queens succumbed, whereas only 39% died after challenge if the queen had received the P. larvae ’soup’ inoculation.
Therefore this demonstration of TgIP in honey bees accounts for a reduction in larval mortality of ~26%.
You won’t feel a thing
Whilst broadly encouraging, there are a couple of issues with the Hernandez Lopez study that limit its application or potential usefulness.
The first is the level of protection seen. The dose of spores administered to the larvae was small, and potentially much smaller than one naturally experienced by larvae doing in-hive infection.
How good would the protection be with a dose 10, 100 or 1000 times as large? This can be tested, and presumably white-coated boffins with ample foreheads are busy doing this as I write.
The second is that the queens were inoculated with the P. larvae ‘soup’ by direct injection. This involves chilling the queen on ice for several minutes, injecting her using a sterile syringe, warming her up and then returning her to the colony.
Inevitably a few queens are lost during this process and – at least with workers – there are some issues with longevity for bees that have been cold-anaesthetised (though I can’t remember seeing any data on queen longevity following this procedure).
Injecting queens is practical if you want a few dozen, but it’s a non-starter if you’re producing thousands or need tens of thousands.
For those sorts of numbers you need to feed the queen with the vaccine … which, since mated queens don’t feed themselves, means caging the queen with a few workers and providing a food source laced with the vaccine.
A recent attempt to induce TgIP against European foulbrood (EFB) by feeding the queen with inactivated Melissococcus plutonius (the bacteria that causes EFB) was unsuccessful (Ory et al., 2022).
Perhaps oral induction of TgIP is a non-starter?
A glimmer of hope
However, towards the end of 2022, the University of Graz group published a study demonstrating promising evidence for TgIP using orally administered Paenibacillus larvae (Dickel et al., 2022) and this is the basis for the world’s first bee vaccine.
The paper was published in Frontiers in Veterinary Science and is relatively light on data.
This isn’t unusual for a scientific publication supporting a commercial – or planned commercial – product. The focus is on safety and demonstrating some level of efficacy, rather than understanding the underlying mechanism.
Or for that matter providing too many details that could undermine its potential commercial success, or the attractiveness of the company to future investment.
Bacterin = ’soup’
The vaccine preparation was commercially prepared by the company involved in the study (Dalan Animal Health) and there are no details of how it was prepared or what it contains. It could just be a heat-inactivated bacterial soup, or it might be supplemented with all sorts of weird and wonderful ingredients like unobtanium or virgin unicorn tears.
If you ask them it would probably be a case of ”I could tell you, but then I’d have to kill you”9.
The authors use the term bacterin (you won’t find this word defined in the OED … though unobtainium is in there). If you’re reading the Dickel paper just remember to translate bacterin to soup.
Let them eat cake bacterin
Caged queens, with attendant workers, were fed soup bacterin added to a corn syrup/sugar mix for 8 days and then used to requeen 5 frame nucs 10.
After at least 18 days, day-old larvae were harvested from the nucs, transferred to the incubator and challenged with a stock preparation of AFB spores in larval food. Larvae were subsequently fed AFB-free larval food and monitored for a further 8 days of development.
The experiment was repeated 3 times in two different study sites. In the interests of providing the bare minimum number of results (!) the authors simply plot the proportion of larvae derived from placebo- or bacterin-fed queens that died over the 8 day period.
Larval AFB challenge studies after oral vaccination of queens (see text for details)
Unfortunately, the axis labelling on the graph is almost too small to read in the original let alone the image above.
This figure shows three repeats. Larvae from bacterin- and placebo-fed queens are in light or dark shading respectively. For each repeat, paired bars on the right are the AFB-challenged larvae.
Note that the bacterin-fed larvae are shorter bars i.e. fewer died.
Overall, ~50-60% of larvae from placebo-fed queens succumbed to AFB, a figure that was reduced by 28-30% following prior vaccination of the queens with the bacterin.
‘By’not‘to’ 28-30%.
The results were statistically significant but perhaps less good than you’d hope for.
An approved vaccine for AFB …
Well, to be pedantic, the approval that has been issued is a conditional licence by the USDA Animal and Plant Health Inspection Service. There’s a PDF with very few details on their woefully slow website . The key quote is:
Conditionally licensed products are required to be pure and safe, and have a reasonable expectation of efficacy.
There may be additional unpublished studies used to support the licensing application … I don’t know.
However, based on the published work what has been approved is:
a proprietary product containing inactivated Paenibacillus larvae11
that reduces a ~50% lethal challenge of AFB spores by ~30%
and that has never been used outside a Petri dish in the laboratory
Clearly that’s some way from an AFB vaccine that’s going to revolutionise bee health and beekeeping (to say nothing of averting the impending beemageddon).
It might, but there’s a long way to go yet … to see just how far let’s briefly return to the villain of the piece, Paenibacillus larvae, and consider its life cycle.
The biology of Paenibacillus larvae
The only known host of Paenibacillus larvae is the honey bee (see Ebeling et al., 2016). Larvae are infected by ingesting spores of P. larvae supplied in brood food from workers in the colony. Exposure and infection during the first 36 hours after hatching is inevitably fatal.
Spores germinate in the midgut lumen, the bacteria proliferate massively, breach the midgut epithelium and reach the haemocoel. By now the larvae are dead. However, the bacteria continue to proliferate, literally ’turning the larval biomass into bacterial biomass’ (a quote from Ebeling et al., 2016).
By this time the bacteria are starting to starve and so sporulate, eventually drying down in the cell to form a scale containing millions of infectious spores.
How infectious?
Very.
The dose-mortality relationship depends upon the age of the larvae. The standard way to express infectiousness is the dose required to infect or kill 50% of the test subjects, abbreviated to ID50 or LD50 respectively 12. Studies dating back to the 1960’s reported that the LD50 for 0-6 hour larvae was ~200 spores and for 18-24 hour larvae was ~2000 spores (Hoage and Rothenbuhler, 1966).
However, supplementary information in the Hernandez-Lopez paper reports an LD50 in first instar larvae (<24 hours) of only ~20 spores, and this was the dose used as a challenge in their study.
Whether the LD50 is 20 or 200 spores is probably academic … a single dried scale contains millions of spores.
Hope or hype?
A bit of both.
Hope because a 30% reduction in larval infection is better than none at all.
Hype because there’s no evidence this provides colony-level protection in field-realistic situations.
The LD50 quantification studies show that very small numbers of spores can result in infection. An LD50 of ~20 spores in naive larvae results in 50% of them becoming infected, but perhaps ingesting just 5 spores could result in 5% of larvae becoming infected. 13.
If the larvae originated from a vaccinated queen the level needed to infect should be higher.
But would it be high enough?
I’ve no idea.
I don’t know how many spores are transmitted when an exposed worker feeds a larva and I’m not sure anyone does.
The scale of the problem
However, I do have an idea of the levels of spores in honey and hive debris – both of which are likely to be related to spore counts carried by nurse bees – from a recent paper (Kusar et al., 2021).
Honey from asymptomatic hives (no overt disease) in an apiary where other hives had AFB contained ~100 spores/g. The honey from symptomatic hives in the apiary contained 104 to 106 spores/g … 100 to 10,000 times as much.
Hive debris was much worse.
In hives with disease the debris contained 109 spores/g (that’s 1 billion for those unfamiliar with scientific notation). Asymptomatic hives averaged ~105 spores/g but covered a very wide range (0 to ~1010 spores/g).
That’s a lot of spores.
How many spores might foragers pick up and potentially transfer when drifting or robbing nearby hives?
Perhaps there are some studies of this … the assays are available and it’s information that is needed to determine whether vaccinating queen bees is likely to be beneficial in preventing the transmission of AFB.
I hope it works. I also hope that the hype helped raise some VC or investment money to fund the expensive and extensive field trials that will be needed to show that it works well enough.
In my view, only then will it qualify as the world’s first honey bee vaccine.
Note to Facebook users/followers
If you are one of the few hundred that rely on Facebook to get announcements of new posts please instead follow me on Instagram or Twitter or even Mastodon (or subscribe for email notifications – right margin). It is likely that the automagic notifications to Facebook will stop in the next few weeks and I don’t use Facebook as I find it a bit overwhelming shambolic 😉
References
Dickel, F., Bos, N.M.P., Hughes, H., Martín-Hernández, R., Higes, M., Kleiser, A., and Freitak, D. (2022) The oral vaccination with Paenibacillus larvae bacterin can decrease susceptibility to American Foulbrood infection in honey bees—A safety and efficacy study. Frontiers in Veterinary Science 9 https://www.frontiersin.org/articles/10.3389/fvets.2022.946237.
Ebeling, J., Knispel, H., Hertlein, G., Fünfhaus, A., and Genersch, E. (2016) Biology of Paenibacillus larvae, a deadly pathogen of honey bee larvae. Appl Microbiol Biotechnol 100: 7387–7395 https://doi.org/10.1007/s00253-016-7716-0.
Freitak, D., Schmidtberg, H., Dickel, F., Lochnit, G., Vogel, H., and Vilcinskas, A. (2014) The maternal transfer of bacteria can mediate trans-generational immune priming in insects. Virulence 5: 547–554 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4063815/.
Hernández López, J., Schuehly, W., Crailsheim, K., and Riessberger-Gallé, U. (2014) Trans-generational immune priming in honeybees. Proceedings of the Royal Society B: Biological Sciences 281: 20140454 https://royalsocietypublishing.org/doi/10.1098/rspb.2014.0454.
Hoage, T.R., and Rothenbuhler, W.C. (1966) Larval Honey Bee Response to Various Doses of Bacillus larvae Spores1. Journal of Economic Entomology 59: 42–45 https://doi.org/10.1093/jee/59.1.42.
Kušar, D., Papić, B., Zajc, U., Zdovc, I., Golob, M., Žvokelj, L., et al. (2021) Novel TaqMan PCR Assay for the Quantification of Paenibacillus larvae Spores in Bee-Related Samples. Insects 12: 1034 https://www.mdpi.com/2075-4450/12/11/1034.
Ory, F., Duchemin, V., Kilchenmann, V., Charrière, J.-D., Dainat, B., and Dietemann, V. (2022) Lack of evidence for trans-generational immune priming against the honey bee pathogen Melissococcus plutonius. PLOS ONE 17: e0268142 https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0268142.
Tidbury, H.J., Pedersen, A.B., and Boots, M. (2010) Within and transgenerational immune priming in an insect to a DNA virus. Proceedings of the Royal Society B: Biological Sciences 278: 871–876 https://royalsocietypublishing.org/doi/10.1098/rspb.2010.1517.
Synopsis : Does repeated oxalic acid vaporisation of colonies rearing brood work sufficiently well? Is it as useful a strategy as many beekeepers claim?
Introduction
Oxalic acid is a simple chemical. A dicarboxylic acid that forms a white crystalline solid which dissolves readily in water to form a colourless solution. It was originally extracted from wood-sorrels, plants of the genus Oxalis, hence the name. In addition to the wood-sorrels it is present in a wide range of other plants including rhubarb leaves (0.5% oxalic acid 1 ), the berries and sap of Virginia creeper and some fruits, such as starfruit. Additionally, fungi excrete oxalic acid to increase the availability of soil nutrients.
Oxalic acid is inexpensive to produce by a variety of processes and was possibly the first synthesised natural product. About 120,000 tonnes are produced annually and it is mainly used for bleaching wood (and often sold as ‘wood bleach’) and cleaning products – including teeth. It chelates iron and so is used for rust removal and is used as a dye fixative (or mordant 2 ).
Oxalic acid and API-Bioxal … the same but different
It is also, when used properly, devastatingly effective against the ectoparasitic mite Varroa destructor.
And, even more importantly, when used properly it is extremely well-tolerated by honey bees.
Great!
Not so fast …
Unfortunately for beekeepers, some of the commercially available i.e. licensed and approved, oxalic acid-containing treatments either contain unnecessary additives and/or have limitations in their approved modes of administration that reduces their efficiency and use in real world beekeeping situations.
Oxalic acid-containing miticides and their use
A quick search of the UK’s 3 Veterinary Medicines Directorate snappily titled Product Information Database for ‘target species = bees’ and ‘active ingredient = oxalic acid’ yields three products :
Varromed (BeeVital GmbH) which is a solution containing formic acid and oxalic acid
Oxybee (DANY Bienenwohl GmbH) which is an oxalic acid solution PLUS a separate powder containing essential oils and sugar. As far as I can tell, Oxybee looks to be the same product as Dany’s BienenWohl powder and solution, which – although listed and licensed – I cannot find for sale 4 in the UK
API-Bioxal (Chemicals Laif S.P.A) which is purchased as a powder composed of 88% oxalic acid dihydrate together with silica and glucose
I’m going to largely ignore Varromed and Oxybee for the rest of this post. I’m sure they’re perfectly good products but I’ve not used either of them so cannot comment from personal experience.
Keeping your powder dry
More relevant to this post, Oxybee and Varromed are both liquids, and this post is about vaporising (aka sublimating) oxalic acid.
And vaporisation involves using the powdered form of oxalic acid.
Which neatly brings me to the methods of application of oxalic acid-containing treatments to kill mites.
I’m sure there are some weird and wonderful ones, but I’ll be limiting any comments to just three which – from my reading of the instructions – are the only ones approved (and then not for all of the products listed above) : 5
Spraying a solution onto the surface of the bee-covered frames
Dribbling or trickling a solution onto each seam of bees between the frames
Vaporisation or sublimation of powdered oxalic acid by heating it in a metal pan to convert it to a gas. This permeates the hive, settling on all the surfaces – woodwork, comb, bees – and remains active against mites for a period after administration
Broodless is best
Oxalic acid, however it is administered, does not penetrate brood cappings. Therefore all of the approved products are recommended for use when the colony is broodless.
Typically – though not exclusively – this happens in the winter, but the beekeeper can engineer it at other times of the season.
If the colony is broodless you can expect any oxalic acid-containing miticide to reduce the mite population by 90% or more. There are numerous studies that support this level of efficacy and it’s what you should be aiming for to give the colony the best start to the season.
I discussed at length how to determine whether a winter colony is broodless a fortnight ago in Broodless?
This post is a more extensive response to several comments (made to that Broodless? article) that recommended repeated vaporisation of oxalic acid at, either 4, 5 or 7 day intervals.
The idea is that this kills the phoretic mites present when the colony is first treated and the mites subsequently released as brood emerges.
How many repeats?
I’ve seen anything from two to seven recommended online.
I’ll discuss this further below, but I’d note that the very fact that there’s such variation in the recommended repeat treatments – perhaps anything from two, fours days apart to seven at weekly intervals (i.e. spanning anything from 8 days to 49 days) – suggests to me that we don’t know the optimal treatment schedule.
Which is a little weird as, a) Varroa is a globally-distributed problem for beekeepers and is more or less invariant (as is the brood cycle of the host honey bee), and b) repeated treatment regimes have been used for over 20 years.
Which brings me back to a crude comparison of vaporisation vs dribbling, or …
Sublimation vs. trickling
A hive can be sublimated with oxalic acid without opening the hive. The vaporiser alone is introduced through the hive entrance or – in the case of certain models – the vapour is squirted through a hole in the floor, brood box or eke. In contrast, trickling oxalic acid requires the removal of the crownboard.
In the video above I’m using a Sublimox vaporiser. The hive entrance is sealed with foam and the open mesh floor is covered with a tightly fitting slide-in tray. As you can see, very little vapour escapes.
Although oxalic acid is well tolerated by bees, and it has no effect upon sealed brood, a solution of oxalic acid is detrimental to open brood. Therefore, trickled oxalic acid weakens the colony – because the acidity kills some or all of the open brood – and repeated trickling of oxalic acid is likely to compound this (see Al Toufailia et al., 2015). In contrast, repeated oxalic acid vaporisations appear not to be detrimental to the colony (caveat … I’m not aware of any long-term studies of this, or for the impact on the queen).
API-Bioxal approved methods of administration
The instructions for API-Bioxal clearly state that only a single treatment by vaporisation is approved per year. The exact wording is:
Maximal dose 2.3g per hive as a single administration. One treatment per year.
In contrast, when used as a solution for trickling the instructions state:
Up to two treatments per year (winter and/or spring-summer season in brood-free colonies).
This seems nonsensical to me considering what we now know about oxalic acid – remember, API-Bioxal was licensed in the same year (2015) that Al Toufailia et al., demonstrated it was detrimental to open brood, and I’m reasonably sure this had been shown previously (but can’t currently find the reference).
But, it gets worse …
API-Bioxal contains oxalic acid with powdered silica and glucose. I presume the silica is to keep it free-running. I’m not aware that powdered silica kills mites and I’m damned certain that glucose has no miticidal activity 😉 .
Neither of these two additives – which I’ve previously called cutting agents – are there to increase the activity of the oxalic acid … and the presence of the glucose is a real problem when vaporising.
Caramel coated Sublimox vaporiser pan
When glucose is heated to 160°-230°C it caramelises (actually, this happens at 150°C 6 ), coating the inside of the vaporising pan. This needs to be cleaned out afterwards 7. The instructions state:
Cool down and clean the vaporizer after use to remove possible residue (max 6%, around 0.140 g).
However, I don’t want to focus on what I consider to be a very effective but decidedly sub-optimal product … instead I want to discuss whether repeat treatment with oxalic acid actually works when there is brood present.
Why is repeat treatment recommended?
Remember, it’s not recommended or approved by the manufacturers of API-Bioxal or the Veterinary Medicines Directorate. I really should have titled this section ’Why is repeat treatment recommended by those who advocate it?’
But that wouldn’t fit on a single line 😉 .
When you sublimate oxalic acid, the gas cools and the oxalic acid crystals settle out on every surface within the hive – the walls, the frames, the comb, the bees etc.. For this reason, I prefer to vaporise oxalic acid when the colony is not tightly clustered. I want everything to be coated with oxalic acid, and I particularly want every bee to be coated because that’s where most of the mites are.
Unless they’re in capped cells 🙁 .
And if they’re in capped cells, the only way the Varroa (released when the brood emerges) will come into contact with oxalic acid is if it remains present and active within the hive. Unfortunately, it’s unclear to me exactly how long the oxalic acid does remain active, or what accounts for a drop in its activity.
But it does drop.
If you treat a colony with brood present and count the mites that appear on the Varroa tray every day it looks something like this:
Mite drop per day before and after treatment
’Something like’ because it depends upon the phoretic mite levels and the amount and rate of brood uncapping. For example, you often see higher mite drops from 24-48 hours than 0-24 hours after treatment.
I know not why.
The drop in the first 48 hours – presumably almost all phoretic mites – can be very much higher than the drop from day three onwards 8.
The duration of activity after vaporisation
Some studies claim oxalic acid remains active for 2-3 weeks after administration. I’m a little sceptical that it’s effective for that long and my own rather crude observations of post-treatment mite drop (of brooding colonies) suggests it returns to background levels within 5-7 days.
I could rabbit on about this for paragraphs as I’ve given it a reasonable amount of thought, but fortunately the late Pete Little did the experiment and showed that:
The recommended dose for colonies with brood is three or four doses seven days apart, however I found out that this is not effective enough, and treated 7, 6, 5 4, 3, 2 days apart to find out the most effective which is 5.
It therefore makes sense that three treatments at five day intervals should be sufficient. This period comfortably covers a complete capped brood cycle (assuming there is no drone brood in the colony) which is 12 days long.
If there is drone brood present you would theoretically need four treatments at 5 day intervals to be sure of covering the 15 day capped brood cycle of drones.
But it turns out there are some additional complications to consider.
Dosage
In the UK the recommended i.e. approved, maximum dose of API-Bioxal is 2.3 g by vaporisation. Remember my comments about the other rubbish stuff API-Bioxal contains, 2.3 g of API-Bioxal actually contains a fraction over 2 g of oxalic acid dihydrate.
This is the active ingredient.
When comparing different experiments where some have used ‘plain’ oxalic acid dihydrate and others have used – or will use – API-Bioxal, it’s important to consider the amount of the active ingredient only 9 .
In the US, oxalic acid was registered as an approved treatment for Varroa in 2015. By vaporisation, the approved dosage is 1 g of oxalic acid dihydrate per brood box i.e. half that approved in the UK.
Remember also that a deep Langstroth is 5% larger (by volume) than a National brood box.
And Jennifer Berry and colleagues in the University of Georgia have recently determined whether repeated administration of vaporised oxalic acid to a colony rearing brood is an effective way of controlling and reducing Varroa infestations (Berry et al., 2021).
And the answer is … decidedly underwhelming
Here are the experimental details.
The paper doesn’t state 10when the experiment was done but they measured honey production in the treated colonies and were definitely brood rearing, so I’m assuming late summer.
Colonies were treated with 1 g / box (double Langstroth deeps) vaporised oxalic acid every five days for a total of 35 days i.e. 7 applications. Mite infestation levels (percent of workers carrying phoretic mites) were measured before and after treatment. Almost 100 colonies were used in the experiment, in three apiaries, randomly split into treated and control groups.
Let’s get the easy bit out of the way first … there was no difference in brood levels, adult bees or food stores at the end of the study. The treated hives were not disadvantaged by being treated … but they didn’t gain an advantage either 🙁 .
Mite levels after treatment normalised to pre-treatment levels (dotted line = no change)
During the experiment the percent mite infestation (PMI) levels in the untreated control colonies increased (as expected) by ~4.4. This is an average and there was quite a bit of variation, but it means that an initial mite infestation level of 4 (average) increased to 8.4 i.e. over 8 mites on every 100 adult workers in the hive.
3% is often considered the cutoff above which treatment is necessary.
Overall, the PMI of treated colonies reduced over the duration of the experiment … but only by 0.7.
From a colony health perspective this is a meaningless reduction.
Seven treatments with the recommended (in the US) dose of oxalic acid stopped the mite levels increasing, but did not reduce them.
Repeated administration of the US-approved oxalic acid dose by vaporisation does not reduce mite levels in a way that seems likely to significantly benefit the colony.
🙁
Dosage, again
I’m not sure the primary data used to justify the US approved 1 g / box dosage. Early studies by Thomas Radetzki (PDF) showed a 95% reduction in mite levels using a dose of 1.4 g. This was a large study involving ~1500 colonies and a dose of 2.8 g was not significantly more effective. I’m quoting the figures for broodless colonies 11.
The Berry results were similar to two smaller previous studies by Jamie Ellis and colleagues (Jack et al., 2020, 2021) who demonstrated that 1 g oxalic acid vaporised three times at weekly intervals was ineffective in controlling mite levels.
However Jack et al., (2021) also applied a similar treatment schedule using different doses of oxalic acid.
Data from Jack et al., 2021 using different repeat doses of oxalic acid
Ignore the intermediate values in panel A, just look at the pretreatment and ‘3 weeks’ mite infestation values.
Mite levels increased in untreated controls and decreased in all treated colonies. However, there was a clear dose response where the more oxalic acid used the greater the impact on the mite levels.
Four grams of oxalic acid reduced the mite infestation rate significantly … from ~5% to ~2% (I’ll return to this). However, the intermediate levels of oxalic acid, whilst reducing mite levels, did not do so significantly from the next closest amount of oxalic acid. For example, 1 g wasn’t significantly more effective than no treatment (as already stated), 2 g was not significantly more effective than 1 g and 4 g was not significantly more effective than 2 g.
But wait … there’s more
I’m familiar with two other studies that look at dose and/or repetition and efficacy (there are more, but this isn’t meant to be an exhaustive review, more a ”Do we know enough?” overview).
Gregoric et al., (2016) published a 12 study that appeared to use combinations of treatments in multiple apiaries. The abstract claims 97% reduction using three 1 g vaporisations, though these are spread over a 57 day period (!) stretching from mid-August to late-November. Mite drop in November following treatment was ~75% (presumably broodless) , but only 10-20% in August. Interestingly I can’t find the figure 97% anywhere in the results …
Finally, Al Toufailia et al., (2015) investigated the dose response to vaporised oxalic acid, showing an 80% reduction in infestation at 0.56 g and 93-98% who using 1.125, 2.25 and 4 g of oxalic acid. All of these studies were determined using broodless colonies.
The Al Toufailia and Jack studies – as well as the Berry study – also reported on adverse effects on the colony. With certain exceptions vaporisation was well tolerated. Some colonies went queenless. Where the queen was caged in late summer to render it broodless (Jack et al.,) some colonies subsequently failed to overwinter successfully (though, look on the bright side, mite levels were reduced 😉 ).
Don’t do that at home … I presume they impacted the production of winter bees.
confused.com
I’m not sure there’s a compelling, peer-reviewed study that definitively shows that repeat treatments of vaporised oxalic acid administered to a brood rearing colony reduces mite levels sufficiently.
Yes, the Jack et al., (2020) showed a significant reduction in the infestation rate (using 4 g three times at seven day intervals), but it was still around 2%.
In late summer, with 20-30,000 bees in the box and 6 frames of brood, that’s still ~600 mites (and potentially more in the capped brood).
In midwinter with about 10,000 workers and much smaller amounts of brood in the hive a 2% infestation rate is still 200 mites.
That’s still a lot of mites for a nearly broodless colony … I treat my colonies when broodless (and assume I’m killing ~90% of the mites present) and am disappointed if there are 45 mites on the Varroa tray. 50 mites on 10,000 workers is an infestation rate of 0.5%.
I’ve waffled on for too long.
All those advocating – or using – repeated oxalic acid vaporisation on brood rearing colonies in late autumn/winter need to think about:
dosage … 1 g is clearly too little (at a 5-7 day interval, but what if it was at a 4 day interval?), 2 g is better and 4 g is well-tolerated and certainly more effective
frequency … which I suspect is related to dosage. The goal must be to repeat sufficiently frequently that there is never a period when oxalic acid levels fall below a certain amount (and I don’t know what that amount is). 1 g on a daily basis might work well … who knows?
duration … you must cover a full capped brood cycle with the repeats
adverse effects … inevitable, but can be minimised with a rational treatment schedule
Broodless is best
It really is.
But, if your colonies are never broodless 13 then I wouldn’t be confident that repeat treatment was controlling Varroa levels sufficiently.
I have treated repeatedly with oxalic acid. In the good old days before API-Bioxal appeared. It certainly reduced Varroa levels, but not as well as my chosen Apivar does these days.
Repeated oxalic acid vaporisation is regularly proposed as the solution to Varroa but I’m certainly not confident that the data is there to support this claim.
Take care out there 😉
Notes
In a future post I’ll revisit this … I’ve got a pretty clear idea of how I’d go about demonstrating whether repeated oxalic acid treatments are effective in meaningfully reducing mite levels i.e. sufficient to protect the colony overwinter and through to the following late summer.
References
Al Toufailia, H., Scandian, L. and Ratnieks, F.L.W. (2015) ‘Towards integrated control of varroa: 2) comparing application methods and doses of oxalic acid on the mortality of phoretic Varroa destructor mites and their honey bee hosts’, Journal of Apicultural Research, 54(2), pp. 108–120. Available at: https://doi.org/10.1080/00218839.2015.1106777.
Berry, J.A. et al. (2022) ‘Assessing Repeated Oxalic Acid Vaporization in Honey Bee (Hymenoptera: Apidae) Colonies for Control of the Ectoparasitic Mite Varroa destructor’, Journal of Insect Science, 22(1), p. 15. Available at: https://doi.org/10.1093/jisesa/ieab089.
Gregorc, A. et al. (2016) ‘Integrated varroa control in honey bee (Apis mellifera carnica) colonies with or without brood’, Journal of Apicultural Research, 55(3), pp. 253–258. Available at: https://doi.org/10.1080/00218839.2016.1222700.
Jack, C.J., van Santen, E. and Ellis, J.D. (2020) ‘Evaluating the Efficacy of Oxalic Acid Vaporization and Brood Interruption in Controlling the Honey Bee Pest Varroa destructor (Acari: Varroidae)’, Journal of Economic Entomology, 113(2), pp. 582–588. Available at: https://doi.org/10.1093/jee/toz358.
Jack, C.J., van Santen, E. and Ellis, J.D. (2021) ‘Determining the dose of oxalic acid applied via vaporization needed for the control of the honey bee (Apis mellifera) pest Varroa destructor’, Journal of Apicultural Research, 60(3), pp. 414–420. Available at: https://doi.org/10.1080/00218839.2021.1877447.
Synopsis : How far do swarms move? Can estimates of environmental apiary and hive densities help determine whether “isolated, lost or ancient” bees are anything of the sort?
Introduction
A little more on feral colonies this week. It’s an interesting topic to think about as the temperature drops, the wind picks up and the trees change into their autumn finery.
A riot of autumn colour
If there are any colonies in the local woods, how did they get there and what are their chances of survival?
I discussed some answers to this last week, using the specific example of old-growth forests in Germany (Kohl et al., 2022). In those cases the reality was that the majority of colonies perished within a year – the average time they survived was only ~32 weeks.
The most likely explanation for their presence in the forest was ‘spillover’ of lost swarms from managed colonies in neighbouring farmland. My assumption – though this wasn’t covered in the paper – was that the colonies perished from either disease or starvation.
This week I want to consider the isolation – or otherwise – of ‘remote’ forests and the distance swarms travel from their origin. Inevitably this will involve some back of an envelope calculations and even outright guesstimates1, so I’ll finish on a more familiar topic (to me) by briefly considering the pathogen loads of feral colonies.
Are these feral healthy and thriving, or riddled with disease?
Beekeepers and hives …
There are about 50,000 beekeepers in the UK and they manage about 250,000 hives.
That’s two ’abouts’ in one sentence, so the guesstimates have started already. The National Bee Unit reports there are 272,000 hives in the UK (2021 figures). They call this an ‘experimental statistic’ because ’several assumptions formed part of the calculations’2. This number is up from 247,000 in 2017.
I suspect some of these assumptions include extrapolating from the numbers of beekeepers/apiaries and hives registered on the National Bee Unit’s BeeBase. In 2013 this was 29,000 beekeepers managing 126,000 colonies.
That extrapolation is needed as not all beekeepers are registered on BeeBase 3, in the same way that not all beekeepers belong to a national or local association.
I’m going to ignore our commercial cousins, the bee farmers. There are only about 400 of them and only one or two of them manage more than 1,000 colonies.
The 2013 BeeBase numbers suggest that registered beekeepers manage 126,000/29,000 = 4.3 hives each. My opening sentence to this section would indicate that the average is perhaps about 5 hives. However, if the experimental statistic is correct but beekeeper numbers are still around 50k, then it’s a little over 5.4 hives per beekeeper.
Let’s keep the maths simple … on average, beekeepers manage 5 colonies 😉 .
… and apiaries
Unfortunately, I’m not aware of any publicly available statistics on hive density, but there is at least partial information available on apiary density.
If you are registered on BeeBase, two of the things you record are the apiary location and the number of hives in each apiary. Once an apiary is registered you can determine the ‘Apiary density within 10 km’ 4.
Beebase shows the ‘density’ of apiaries within 10 km
A radius of 10 km from your registered apiary encompasses 314 km2, so it is perhaps not surprising that there can be a large number of other apiaries in the neighbourhood.
When I lived in Warwickshire my two apiaries – separated by ~5 km – had 255 and 267 apiaries within a 10 km radius. This is a busy beekeeping area, with a very active local association (my alma mater, WLBK).
Hives in the corner of a Warwickshire field (almost every field!)
I don’t know how many hives there were in the surrounding environment, but it seemed as though almost every field margin or spinney contained a little row of hives balanced on old pallets.
Convenient assumptions
On the basis that I don’t have any other information, and in the interest of getting on with the article, I’m going to assume that each apiary contains an average of 5 hives. I think this is reasonable, though I’d be interested if anyone has any real figures.
With ~260 apiaries within 10 km, each containing an average of 5 hives, it suggests the hive density was 4.1 km2.
Coincidentally 5 this is almost exactly the same figure quoted in Kohl et al., (2022) last week.
And each year a significant proportion of these hives will attempt to swarm.
Swarms
With exemplary swarm control it is possible to avoid losing any swarms.
Of course, we do our beekeeping in the real world, and the reality is that we all lose swarms sometimes.
Hopefully not many and perhaps not even every year, but swarms are lost.
When I lived in Warwickshire I never failed to attract swarms to my bait hives each season. When I lived in Fife – where there were only ~45 apiaries within 10 km 6 – I caught four swarms in a bait hive in my back garden one season, and (again) never failed to attract swarms in the time I lived there.
Although I’d like to think this reflects the care I take in preparing my bait hives, I suspect it really means that – during the swarming season – a lot of queen cells are missed and swarms are lost.
Bivouacs and scout bees
Generally, though there are exceptions, the swarming process goes something like this:
the colony starts producing queen cells
on the first good day (warm, dry, fine etc.) after the first queen cells are sealed the colony swarms
the swarm bivouacs nearby, perhaps only 10-20 metres away
scout bees survey the environment for likely new nest sites, ‘dancing’ on the surface of the bivouac to persuade other scout bees to check out promising looking locations
a quorum decision is reached by the scout bees on the ‘best’ new nest site and they lead the swarm there 7
The scout bees survey at least a 2-3 km radius around the original hive; they probably start this process before the colony swarms, continuing it once the swarm has bivouacked. Since we can interpret the waggle dance, it is possible to observe the scout bees and infer from them the approximate distance and direction to the selected nest site.
By doing this, scientists have determined how far swarms usually travel (a relatively short distance) and how far they sometimes go (a long way).
Swarming distances
Most swarms relocate just a few hundred metres from their origin. Martin Lindauer did some of the first studies on swarming distances in the mid-50’s and Thomas Seeley and Roger Morse produced strikingly similar data in 1977 (Seeley and Morse, 1977).
Most swarms only travel a short distance to a new nest site
There are a number of related studies from the early 1980’s which demonstrate that, although scout bees may survey the environment from ~300 m to over 4 km away, at least 50% of swarms move no more than 1 km from their origin.
However, they can travel much further.
In recent studies José Villa studied swarming of bees in Louisiana (Villa, 2004). He studied swarm size (weight), nest volume preference and the timing of swarming. In addition, by interpreting scout bee waggle dancing, he recorded the distance 16 swarms travelled from their origin.
In this study a marked preference for relatively ‘local’ nest sites was not seen. Four swarms travelled less than 1 km, six from 1 to 4 km, five between 4 and 7 km and one ~10 km.
With three of the swarms, two that moved <500 m from the origin and one 2.2 km away, he confirmed their location by finding the uniquely tagged queen present in the original swarm.
Although I said ’they can travel much further’ it’s worth remembering that the distance travelled was inferred from the duration of the waggle run by scout bees on the surface of the bivouacked swarm (and specifically, the predominant dances being conducted 30 minutes before the swarm left the bivouac).
That’s not quite the same as proving that swarms may travel 5-10 km, but it is certainly suggestive that they do.
Isolated woodland in a bee-filled environment
Let’s do a bit more arm waving …
Assume there’s two to three thousand hectares of old native woodland, oak, beech, sycamore etc., rather than conifers. In the absence of black woodpeckers (see last week) some of these trees will still contain hollow cavities. They will have lost boughs or been hit by lightning, the rain will have rotted the exposed heartwood and a cavity will eventually form.
Voilà … a potential nest site for bees 🙂
A wood of 2500 hectares (or is that a forest?), if circular, fills a circle of 5.6 km diameter. Of course, it’s very unlikely to be circular, but it makes the maths easier so bear with me.
Assume this wood is in the middle of good quality mixed farmland, with early season oil seed rape, hedgerows filled with hawthorn and blackberry, and ample clover polka-dotted pasture.
In other words, a good environment for honey bees.
So the local beekeepers plonk a few hives in the corners of fields, or along field margins.
Eventually, the density of these hives reaches 4 km2 (as justified above).
Cartoon of woodland (green) and surrounding farmland (blue and red)
In the diagram above the inner (green) circle is the native woodland. The surrounding blue and red rings represent the surrounding farmland, in each case the area covered by an additional 1 km radius respectively from the centre.
The woodland contains no managed colonies and is 24.6 km2. The blue ring (excluding the central wooded area) has an area of 20.7 km2 and so contains – based upon all those assumptions above – 83 managed hives. Likewise, the red ring has an area of 27 km2 and contains 108 hives.
Define ‘isolated’
As shown above, 50% of swarms move no more than a kilometre to a new nest site, but some move further … and a few may move much further.
Any of the managed hives in the blue ring might produce a swarm that could reach the forest boundary. In addition, assuming the blue ring contained few suitable nest sites – and I’ll return to this point shortly – swarms issuing from hives in the red ring might well travel further and reach the forest.
In fact, if you overlay the roundel diagram with the swarm dispersal diagram – at the same scale – from the paper by Villa (2004) you can see that swarms from a very wide area are ‘in range’ of the hollow tree-filled forest.
Woodland (green) and surrounding farmland with – at the same scale – swarming distances from Villa (2004)
The swarm dispersal diagram shows the swarms starting from a central point, so you just need to imagine the arrows are reversed.
In fact, if you assume that swarms can travel up to 7 km (only one swarm studied by Villa may have gone further, but one third travelled 4-7 km) there could be as many as 517 potentially swarming colonies ‘in range’ 8.
Therefore, as far as migrating swarms are concerned, it’s quite possible that none of the forest is ‘isolated’.
Nest sites in farmland and forests
In the Kohl et al., (2022) paper I discussed last week, the majority of the woodpecker holes used by bees were in large beech trees. The average diameter of the trees was 55 cm when measured 1.5 m above ground.
These were substantial trees.
Trees of that size are common in old growth forest … but they’re rare in farmland.
Hedging, if it hasn’t been grubbed up, contains predominantly small trees. Many small copses and spinneys have also disappeared, all to make way for combine harvesters and subsidies.
Lots of forage but not a lot of mature trees
Of course, there are large trees in farmland, they’re just a whole lot less common than they are in old native woodland.
Therefore swarms issuing from managed hives on farmland – assuming they don’t end up in one of my bait hives – are more likely to gravitate to the forest as there will be more nest sites there.
Blenheim bees
I don’t know much about the widely-publicised ‘Blenheim bees’ that I briefly introduced last week.
However, I do know that the Blenheim Estate near Oxford has about 2500 hectares of woodland, and that there are a lot of beekeepers in Oxfordshire.
That 2500 hectares, if circular (which it isn’t) and centred on Blenheim Palace, would span from Combe to Oxford Airport, and completely covers the small market town of Woodstock 9.
This is a popular area for beekeeping. The National Bee Unit’s ‘BeeBase’ informs me that there are ~200 apiaries within 10 km of Blenheim Palace. Combe to the west has ~190 apiaries within 10 km.
If these apiaries have the expected number of hives in (i.e. 4 km2, and I see no compelling reason why not … for example, the countryside is similar to Warwickshire) then there are a very large number of colonies capable of producing swarms that are well within range of the forested area.
But let’s just revisit that figure of ~200 apiaries within 10 km.
How accurate it is?
Certainly some of the apiaries will have been ‘forgotten’ and are now vacant. I bet there’s a lot of redundant data on BeeBase.
Perhaps ~200 apiaries is not a very accurate figure?
I think it is probably inaccurate … but I strongly suspect it’s an underestimate rather than an overestimate of apiary numbers in the area.
Many beekeepers are not registered on BeeBase. Only the National Bee Unit knows 10 the proportion of beekeepers/apiaries/hives missing, but I’d be amazed if it was less than 25% and not at all surprised if it was 40%.
This is probably part of the ’fiddle factor’ used to extrapolate from BeeBase registrations and hive numbers to that ’experimental statistic’ of 272,000 hives in the UK.
Occam’s razor, the law of parsimony, and ‘isolated’ feral/wild bees
Are there self-sustaining populations of honey bees in the UK?
By self-sustaining I mean not dependent upon an annual influx of swarms from nearby managed colonies. These swarms compensate for the very high winter attrition rate seen in the Kohl et al., (2022) study which is likely due to pathogens and starvation (I’m going to deal with pathogens – briefly – next).
Well, are there?
I don’t know.
Based upon registered and predicted apiary and hive numbers, and the known distances swarms migrate, I think the simplest – and therefore most likely – explanation for feral colonies in ‘isolated’ locations are recent (< 1 year) swarms from nearby managed colonies.
Even assuming the National Bee Unit’s predicted 272,000 hives are evenly distributed over the entire UK (242,000 km2) that’s still >1 hive / km2. They’re obviously not evenly distributed; many areas are unsuitable or, at best, borderline for beekeeping.
I’d like to have been able to discuss the area of old growth forests in the UK and how isolated or otherwise it is. Unfortunately, I don’t have the data … or the GIS mapping skills to interrogate it.
Therefore I’ll close instead with something I know a little more about …
Feral colonies, pathogens and genetics
How healthy are feral colonies in the UK?
There aren’t a lot of published studies. Catherine Thompson and colleagues showed that the pathogen load – including Deformed wing virus (DWV), Black queen cell virus (BQCV) and Nosema (both apis and ceranae) – were similar or higher in feral colonies than in managed colonies (Thompson et al., 2014).
Pathogen levels in feral (F) and managed (M) colonies
Levels of DWV in feral colonies were significantly higher than in managed colonies, but they were similar to the levels seen in beekeeper’s hives not treated to control Varroa infestation.
We know – though many are still bitterly reminded every year – that colonies in which mite levels are high and uncontrolled usually perish overwinter.
Catherine Thompson also studied the genetic characteristics of feral colonies and compared them to managed colonies (Thompson, C. PhD. thesis, University of Leeds, 2010). Her results show that the feral colonies she studied were very similar – and effectively indistinguishable – to managed colonies when the overall level of genetic heterozygosity was analysed. This means that these feral colonies are not a distinct genetic race of bees.
That’s not the same as showing they were genetically related to (and so originated from) nearby managed colonies … those experiments still need to be done.
Are these wild bees self-sustaining, unique and ancient?
If a colony or two of bees (or even a hundred) are found in the woods I’d suggest the following tests need to be applied to convincingly demonstrate they are a unique and self-sustaining population.
how isolated are they really? Are there managed colonies within 5-10 km that could act as a source of swarms? Geographic isolation may be due to factors other than distance, for example an island population, or an isolated valley surrounded with mountains.
is the population truly self-sustaining? Do colonies regularly survive for sufficient time to reproduce? To be self-sustaining, annual colony losses must be less than or equal to new colonies established from the same feral bees.
are the bees genetically distinct from managed colonies within 10 km or so? If they are a well-established population you would expect this.
If the population is truly isolated, reproduces sufficiently to replace annual losses and is genetically distinct, then it may well be self-sustaining.
However, if it doesn’t meet any one of these three criteria then I suspect the population is dependent upon ‘spillover’ losses of swarms from neighbouring managed colonies.
Interesting perhaps, but not surprising, not unique and certainly not ancient.
Unsurprisingly, I’m sceptical about many of the claims made for long lost and unique strains of bees living in the woods (or anywhere else for that matter).
A glimmer of hope (?) … the Arnot Forest bees
The Arnot Forest is not dissimilar in size to Blenheim estate (17 km2vs. 24 km2).
However, it is surrounded by lots more old growth forest (100+ years) and so is effectively more isolated. There are some managed colonies in the surrounding forests, but – when tested – they were genetically distinct from the Arnot Forest bees (Seeley et al., 2015). Finally, the colony survival characteristics (~1.5 years) and annual swarming of the Arnot Forest bees indicates that the population is self-sustaining. These Arnot Forest bees have adapted to live with Varroa through behavioural changes – frequent swarming, small colonies etc.
Clearly, self-sustaining populations of feral colonies can exist 11, but this is not the same as claiming that all feral populations are self-sustaining, unique or ancient.
Finally, it’s worth noting that the mechanisms that self-sustaining populations of bees have evolved to become Varroa tolerant (they are unlikely to be resistance) – small, swarmy, colonies – may make them unsuited for either beekeeping or pollination.
References
Kohl, P.L., Rutschmann, B. and Steffan-Dewenter, I. (no date) ‘Population demography of feral honeybee colonies in central European forests’, Royal Society Open Science, 9(8), p. 220565. Available at: https://doi.org/10.1098/rsos.220565.
Seeley, T.D. et al. (2015) ‘A survivor population of wild colonies of European honeybees in the northeastern United States: investigating its genetic structure’, Apidologie, 46(5), pp. 654–666. Available at: https://doi.org/10.1007/s13592-015-0355-0.
Seeley, T.D. (2017) ‘Life-history traits of wild honey bee colonies living in forests around Ithaca, NY, USA’, Apidologie, 48(6), pp. 743–754. Available at: https://doi.org/10.1007/s13592-017-0519-1.
Seeley, T.D. and Morse, R.A. (1977) ‘Dispersal Behavior of Honey Bee Swarms’, Psyche: A Journal of Entomology, 84, pp. 199–209. Available at: https://doi.org/10.1155/1977/37918.
Thompson, C. (2010) The health and status of the feral honeybee (Apis mellifera sp) and Apis mellifera mellifera population of the UK. phd. University of Leeds. Available at: https://etheses.whiterose.ac.uk/5211/ (Accessed: 19 October 2022).
Thompson, C.E. et al. (2014) ‘Parasite Pressures on Feral Honey Bees (Apis mellifera sp.)’, PLOS ONE, 9(8), p. e105164. Available at: https://doi.org/10.1371/journal.pone.0105164.
Synopsis : Honey bees were eradicated on Santa Cruz Island following the introduction of Varroa. This provides some useful lessons for beekeepers on the importance of controlling Varroa.
Introduction
Honey bees are not native to North America. They were first introduced in March 1622 at Jamestown, Virginia. The bees did well and spread west, following the settlers. They finally arrived on the west coast, in Santa Clara, California, 231 years later in 1853. Of a dozen hives ordered by Christopher Shelton, a Santa Clara botanist and rancher, only one survived the journey from New York via Panama.
Shelton barely had a chance to enjoy his bees 1 as he was unfortunately killed when the steamboat Jenny Lind exploded in mid-April 1853.
Explosion on the steamboat Jenny Lind near San Francisco, California
His bees survived 2 and three hives derived from the original stock were auctioned for $110 each. This was over 20 times the price of hives on the east coast at that time and equivalent to over $4200 today 3.
Californian Channel Islands map
Bees were in demand and they continued to spread – both as feral swarms and as farmers established apiaries to help pollination and for honey production. Having reached the California coast they were then spread to the nearby islands. Bees were transported to Santa Cruz, the largest of the eight Channel Islands near Los Angeles, in the 1880’s. They flourished, but did not spread to the other Channel Islands.
Field station, nature reserves, pigs and bees
Santa Cruz Island is 250 square kilometres in area and lies ~35 km south of Santa Barbara. It is one of the four Northern Channel islands. There is a long central valley lying approximately east-west and the rocky mountainous land reaches 740 m. It has a marine temperate climate; the average low and high temperatures are 9°C and 21°C respectively and it receives about 0.5 m of rain a year. It is a good environment for bees.
From the 1880’s to 1960’s Santa Cruz Island was farmed – primarily for wine and wool, and from the 1940’s for cattle – but, after period of university geology field trips and the establishment of a field station on the island, in 1973 it became part of the University of California’s Natural Reserve System (UC NRS).
In the late 1970’s the Stanton family sold their ranching business on the island to The Nature Conservancy who subsequently bought additional land on the eastern end of the island.
Santa Cruz Island is now jointly owned by The Nature Conservancy, National Parks Service, UC NRS and the Santa Cruz Island Foundation and much of the island is used for scientific research and education.
But what about the bees?
Good question.
As a nature reserve and research station, the presence of non-native species causes a potential problem. Why go to all the expense of managing a remote island research centre if all the same species are present as on the mainland?
The Nature Conservancy therefore initiated a programme of eradicating non-native species. It took 14 months to eliminate the feral pigs, using a combination of trapping, helicopter-based shooting and the release of sterilised radio-tagged pigs to locate the stragglers 4.
But getting rid of the bees took a bit longer …
Save the bees, or not
Why get rid of the bees? Surely they weren’t doing any harm?
The introduction of any non-native species upsets the balance (if there’s ever balance) in the ecosystem. The introduced species competes directly or indirectly with those native to the area and can lead to local extinctions.
Jonathan Rosen has described5 how honey bee swarms, through occupying tree cavities previously used for nesting, probably played a major role in the extinction of the Carolina parakeet.
Pining for the fjords … a stuffed Carolina parakeet (nailed to its perch)
Competition between honey bees and native pollinators has been well studied. It is not always detrimental, but it certainly can be. Furthermore, it is probably more likely to be detrimental in a small, isolated, island ecosystem. For example, studies showed that the presence of honey bees dramatically reduced visitation of native pollinator to manzanita blossoms on Santa Cruz Island.
As part of the larger programme of non-native plant and animal eradication on Santa Cruz Island plans were drawn up in the late 1980’s to eliminate European honey bees. The expected benefits were to:
eliminate competition with native bee species (and presumably other non-bee pollinators, though these rarely get a mention 🙁 )
reduce pollination of weed species (some of which were also non-native to Santa Cruz Island)
facilitate recovery of native plant species that were reliant on native bee pollination
provide a ‘field laboratory’ free from ‘exotic’ honey bees in which comparative studies of native pollinators would be possible
Killer bees
After the plans to eradicate Apis mellifera were approved an additional potential benefit became apparent.
There were increasing concerns about the spread of Africanised honey bees which had recently reached Santa Barbara County. Although there was reasonably compelling evidence that swarms could not cross from the mainland (e.g. none of the other Northern Channel Islands had been colonised by bees) there were concerns that the Santa Ana winds might help blow drones from the mainland.
Had these drones arrived they might mate with the non-native but nevertheless local queens resulting in the spread of the dominant genes for defensiveness and absconding. The resulting swarmy, aggressive Africanised bees would cause problems for visitors and scientists working on the island (as they have for visitors to Joshua Tree National Park).
Aerial view of Santa Cruz Island
Although the introgression of African honey bee genes was used as further justification for the eradication it’s not clear whether drones could actually cross 30-40 km of open sea 6.
As an aside, there’s a current project – the amusingly named ’Game of Drones’ – running on the Isles of Scilly investigating whether drones can cross the sea between St Agnes, Tresco, Bryher, St Mary’s and St Martin’s. These are, at most, 11 km apart (northern most tip of St Martin’s to most southerly point of St Agnes) but the individual islands are only separated by 1-2 km. I would be surprised if drones could not cross that distance (at least with a strong following wind).
Killing bees
Adrian Wenner and colleagues set about exterminating the honey bees on Santa Cruz Island (Wenner et al., 2009). The process started in 1988 and ended in 2007, and was divided into four phases:
1988-1993 – location and elimination of feral colonies
2005-2007 – confirmation of the absence of honey bees
None of this is ’beekeeping’ – actually it’s the exact opposite – so I don’t intend to dwell in much detail on the work that was conducted. However, the ’94-’97 phase includes some sobering lessons for beekeepers which are worth discussing.
By the end of phase 1 the team had identified the existence (if not the location) of at least 200 colonies and eliminated 153 of them.
Remember, none of these were managed colonies in hives. They were all feral colonies occupying natural cavities in trees or rocks etc. Each colony was found using painstaking bee lining techniques similar to those described in Thomas Seeley’s book Following the Wild Bees.
Once located, nests were destroyed with methyl chloroform and the cavity sealed to prevent it being reoccupied.
Some colonies could not be accessed; in these cases acephate-laced sucrose-honey syrup baits were used. This organophosphate has delayed toxicity for bees, allowing foragers to return to the colony which in due course dies. This approach had been partially successful in eliminating Africanised bees on the mainland (Williams et al., 1989), but baits needed to be be monitored to avoid killing the other insects they attracted.
The scientists also deployed swarm traps (aka bait hives) and destroyed any swarms that moved in.
Together these interventions reduced honey bee numbers significantly – as monitored by regular observations at pollen- or nectar-rich plants – but did not eradicate them.
Let there be mite
Heavy rains in January ’93 washed out roads on Santa Cruz Island, thereby severely limiting travel around the island. In addition, the previous removal of cattle had resulted in the near-uncontrolled growth of fennel which now formed dense, impenetrable thickets.
Bee lining became impossible and the scientists had to invent more devious strategies to eliminate the residual feral colonies.
The approach they chose involved the introduction of Varroa.
Varroa was first detected in the USA in 1987 (in Florida) and became widespread over the next 5-8 years. Up until 1994 the honey bees on Santa Cruz Island were free of the ectoparasitic mite.
It was likely that they would have remained that way … there was no beekeeping on Santa Cruz Island and the location was too remote for bees to cross from the mainland (see above).
Varroa was already known to have a devastating impact on the health of honey bee colonies (Kraus and Page, 1995). It was also known that, other than its native host Apis cerana (the Eastern honey bee), Varroa did not parasitise other bee or wasp species (Kevan et al., 1991).
These two facts – host specificity and damage inflicted – suggested that Varroa could be used for biological control (‘biocontrol’) on Santa Cruz Island.
Biological control
Biological control or biocontrol is a method of controlling pests using natural mechanisms such as predation or parasitism.
The pest could be any living thing – from animals to bacterial plant diseases – present where it’s unwanted.
On Santa Cruz Island the pest was the honey bee.
In other studies (covered in a previous post entitled More from the fungi7 ) biocontrol ofVarroa has been investigated.
Control of the pest involves the introduction or application of a biological control agent. The key requirements of the latter have already been highlighted – specificity and damage.
Biological control works well when the specificity is high and the damage is therefore tightly targeted. It can be an abject failure – or worse, it can damage the ecosystem – if the specificity is low and/or the damage is widespread.
The cane toad was introduced to Australia to control infestations of greenback cane beetle (a pest of sugar cane). Cane toads were introduced in 1935 and rapidly spread. Unfortunately, cane toads can’t jump very high and so singularly failed to control the greenback cane beetle which tends to 8 stay high up the cane stems.
Female cane toad (not jumping)
But it gets worse; cane toads have a very catholic diet and so outcompeted other amphibians. They introduced foreign diseases to the native frogs and toads and – because of the poisons secreted from their skin – harmed or killed predators that attempted to eat them.
Oops.
Vertebrates are usually poor biological control agents as they tend to be generalist feeders i.e. no specificity.
But Varroa is specific and so the damage it causes is focused. The likelihood of ecosystem damage was considered low and so the mite was introduced to the island.
Introduction of Varroa
In late 1993 Adrian Wenner caught 85 foraging bees and, to each one, added a singleVarroa mite. The bees were then released and presumably flew back to their colonies … taking the hitchhiking mite with them.
Adult mites – the dark red ones you see littering the Varroa tray after you treat with Apivar – are mated females.
Due to their incestuous lifestyle a single mite is sufficient to initiate a new infestation.
The mated adult female mite parasitises a honey bee pupa and produces a series of young; the first is male, the remainder are female. You’re probably reading this before the 9 pm watershed so I’ll leave it to your lurid imagination to work out what happens next (or you can read all the sordid details in Know your enemy).
The presence of honey bees – determined by successful swarm trapping or field observation at likely sites – was then regularly monitored over the next four years.
Swarm numbers remained largely unchanged until 1996 and then dramatically decreased.
Numbers of new swarms on Santa Cruz Island 1991 – 2005. Varroa introduction indicated.
It’s worth noting that during ’94-’96 over 70 swarms were found in natural sites or bait hives. There must have been a significant number of established colonies in 1993 to produce this number of swarms.
But, from 1997 it all stopped … only a single swarm was subsequently found, in a natural cavity in 2002.
Monitoring and confirmation of eradication
From 1998 to 2004 the scientists continued to actively monitor the island for honey bees, focusing on 19 areas rich in natural forage. Although honey bees were found – in decreasing numbers – there were too few to attempt bee lining to locate their colonies.
At the sites being monitored, bees were detected 9, 7, 4, 2 and 1 times respectively in the 5 years from 2000 to 2004. After that, despite continued monitoring, no more honey bees were detected.
The final phase of the project (’05-’07) confirmed the absence of honey bees on Santa Cruz Island.
Whilst, as a scientist, I’m a firm believer that ’absence of evidence does not mean evidence of absence’, as a beekeeper I’m well aware that if there are no scout bees, no swarms and no foragers (when I search in likely places) then there are no honey bee colonies.
Lessons for beekeepers
I wouldn’t have recounted this sorry tale – at least from a beekeeping perspective – unless I thought there were some useful lessons for beekeepers.
There are (at least) three.
The first relates to Varroa resistance, the second to Varroa transmission in the environment and the last to ‘safe’ levels of Varroa. All require some ‘arm waving guesstimates’9, but have a good grounding in other scientific studies.
Varroa resistance
There wasn’t any.
At a very conservative estimate there were at least 20 colonies remaining on Santa Cruz Island in 1995. I say ‘conservative’ because that assumes each colony generated two swarms that season (see graph above). In studies of other natural colonies only about 75% swarm annually, meaning the actual number of colonies could have been over 50.
The numbers – 20 or 50 – matter as they’re both much higher than the number of colonies most beekeepers manage (which, based upon BBKA quoted statistics, is about 5).
Whether it was 20 or 50, they were all eliminated following the introduction of 85 mites. Colonies did not become resistant to Varroa.
This all took a few years, but – inferring from the swarm numbers above – the vast majority of colonies were killed in just two years, 1994 and 1995. This timing would fit with numerous other studies of colony demise due to mites.
Wenner estimates that only 3 colonies survived until 2001.
Leaving small numbers of colonies 10 untreated with an expectation that resistance – or even tolerance (which is both more likely and not necessarily beneficial) – will arise is a futile exercise.
I’ve discussed this before … it’s a numbers game, and a handful of colonies isn’t enough.
Varroa spread
Wenner doesn’t elaborate on where the foragers were captured before he added the mites. If I was going to attempt this I’d have chosen several sites around the island to ensure as many feral colonies as possible acquired mites … let us assume that’s what he did.
However, with 85 mites piggybacking on returning workers, and somewhere between (my guesstimated) 20 to 50 colonies, I think it’s highly likely that at least some colonies received none of this ’founding’ mite population.
Yet almost all the colonies died within two years, and those that did not subsequently died with no further intervention from the scientists. We don’t know what killed off the last surviving colonies but — and I know I’m sticking my neck out here – I bet it was the mites.
This is compelling evidence for the spread of Varroa throughout the island environment, a process that occurs due to the activities of drifting and robbing.
If a neighbouring apiary to yours has mites some will end up in your hives … unless you are separated by several kilometres 11.
The transmission of mites in the environment is a very good reason to practice coordinated Varroa control.
One mite is all it takes
But, just as I’ve argued that some colonies may have received none of the founding mites, I’m equally sure that others will have acquired very small numbers of mites, perhaps just one.
And one mite is all it takes.
Without exceptional beekeeping skills, resistance in the bee population or rational Varroa control12 there is no safe level of mites in a colony.
The more you prevent mites entering the colony in the first place, and the more of those that are present you eradicate, the better it is for your bees.
Here endeth the lesson 😉
Note
It’s worth noting that island populations do offer opportunities for the development of Varroa resistant (or tolerant) traits … if you start with enough colonies. Fries et al., (2006) describes the characteristics of the 13 surviving colonies on Gotland after leaving about 180 colonies untreated for several years. I’ve mentioned this previously and will return to it again to cover some related recent studies.
References
Fries, I., Imdorf, A. and Rosenkranz, P. (2006) ‘Survival of mite infested (Varroa destructor) honey bee (Apis mellifera) colonies in a Nordic climate’, Apidologie, 37(5), pp. 564–570. Available at: https://doi.org/10.1051/apido:2006031.
Kevan, P.G., Laverty, T.M. and Denmark, H.A. (1990) ‘Association of Varroa Jacobsoni with Organisms other than Honeybees and Implications for its Dispersal’, Bee World, 71(3), pp. 119–121. Available at: https://doi.org/10.1080/0005772X.1990.11099048.
Kraus, B. and Page, R.E. (1995) ‘Effect of Varroa jacobsoni (Mesostigmata: Varroidae) on feral Apis mellifera (Hymenoptera: Apidae) in California’, Environmental Entomology, 24(6), pp. 1473–1480. Available at: https://doi.org/10.1093/ee/24.6.1473.
Wenner, A.M., Thorp, R.W., and Barthell, J.F. (2009) ‘Biological control and eradication of feral honey bee colonies on Santa Cruz Island, California: A summary’, Proceedings of the 7th California Islands Symposium, pp. 327–335. Available as a PDF.
Williams, J.L., Danka, R.G. and Rinderer, T.E. (1989) ‘Baiting system for selective abatement of undesirable honey bees’, Apidologie, 20(2), pp. 175–179. Available at: https://doi.org/10.1051/apido:19890208.
