Talk by Dr Giles Budge of the National Bee Unit

On Tuesday 11th Feb 2014, Oxford’s  Cafe Scientifique held a talk on honeybee health by Dr Giles Budge, Research Coordinator of the National Bee Unit (NBU). I found out about it only on the afternoon of the same day and was fortunate to be able to attend – there were about 6 other beekeepers present and 30-40 members of the public.

I note here the key points in brief: Dr Budge started with a soft introduction by discussing the products of the hive. He talked about honey, of course, but also pollen, propolis, and wax, which he described as a fat (I’d never thought of it like that). He pointed out that honeybees are generalist pollinators – not the best for many plants, but excellent from an economic point of view. 90% of crops don’t need pollinators but these would make a dull diet, all the tasty things do. After laying out some background like this for non beekeepers, he began getting more technical.

Pests, disease and colony numbers

Dr Budge started by noting that Britain imports 14,000 queens or colonies every year, which presents a significant biosecurity issue – not just varroa, but disease.

Varroa mite as experienced by a bee

Varroa mite on a human-sized bee or bee-sized human

  • He passed around vials of alcohol with various mites, beetles and hornets in them so people could see what the threats being discussed actually looked like. He also had a model of a varroa mite scaled up to show how it would appear if we were bee-size – as modelled in the photo.
  • He mentioned that varroa mites have a chemical “cloaking” ability so their smell matches that of their host hive.
  • Many years ago, UK winter colony losses were 5 – 10%. Last year it was 29.4% ! This is thought mainly due to varroa spreading viruses, although there is a growing recognition of other causes like pesticides increasing bee vulnerability to pathogens like nosema.
  • But, it was also acknowledged that colony loss can be due to the beekeepers too – for example, in 2008 a lot of colonies died when many beekeepers harvested significant amounts of honey stores at the usual time, then there was an unusual dearth of nectar and the colonies starved because many beeks didn’t realise they needed to feed the colonies two months earlier than usual.
  • A lot of beekeepers stopped keeping bees when varroa made things difficult. This can cloud the statistics of colony decline in the UK due to parasites – the number has decreased, but several thousand of those are due to people leaving the craft and not promoting splits/new hives, etc.

Feral colonies

Britain had a large reservoir of these up to 1992, but with the introduction of varroa these declined. There is no good data on numbers before this because no one thought to monitor something that wasn’t a problem.

  • Unlike some I have heard, Dr Budge does not deny the existence of some thriving feral colonies. “In fact, when we want to check some things, we need to cut one of these feral colonies open to confirm it” he says (i.e. these are the ‘control’ for some types of experiment).
  • Dr Budge has a PhD student looking at the genetics of these colonies, who finds their genetics seems the same as in managed colonies. So in his view, ferals are (now) just escaped domestic hybrids.
  • This was a surprise to me (though I suppose genes flow both ways) but I would assert that it does not invalidate the argument that unmanaged feral colonies survive because they have “survivor” abilities, whether through genetics or epigenetics or behaviour (grooming etc).

Varroa resistance

I asked about attitudes to using natural selection to get varroa resistant bees.

  • He replied that no one doubts you can breed for varroa resistant bees. But, because you will initially lose most of your colonies by this “live and let die” strategy, it is not acceptable to large scale beekeepers.
  • He suggested I look up the varroa resistant bees bred by the USDA lab at Baton Rouge. This strain is established as resistant to varroa. The problem is, beekeepers require other traits – honey production, calm nature etc – and this strain was poor at all those, so not many people wanted them! (I’ve been unable to find documents detailing such problems with Baton Rouge bees, though there are many adverts from breeders selling the bees, and of course they aren’t going to emphasize problems.)
  • Another problem is that the desirable varroa resistance trait can be wiped out in one mating with another strain’s drone, derailing several years’ work. (I don’t think this argument holds water as many beekeepers just buy queens, see here for a map of US apiaries selling Varroa resistant queens).
  • He chided me for having an untreated hive with a varroa drop of 30 mites / day as it can spread them to neighbours’ hives (my other hive is 1/day, both are untreated). But in my previous experience when I used to treat, the hive always had significant varroa drop at certain times, and of course my neighbours’ hives are not varroa free, despite their treatment. Also, after the talk another beekeeper told me “well I treat my hives, and one has a drop of 150/day, I think it robbed a failing hive and carried a huge varroa load back”.  The reason one of my colonies has a drop of 30/day is that last year I stopped treating it with miticides, which were simply reducing numbers of the parasite but not significantly enough imo, and changed to non-treatment so the bees learn varroa-managing behaviour instead – this is how the other hive I have arrived at its very minimal varroa levels. So my ultimate aim is to host colonies of varroa resistant bees through non treatment and natural selection, which I have seen other low-intervention beekeepers achieve. I believe this will provide a more successful route than continually treating them, which wasn’t solving the problem, and it will improve the local genetics and thus ultimately benefit my neighbours’ bees too. (I would be grateful if any other beekeepers following a varroa resistant path added their comments here.)

Bee reclassification to domestic animals

The reclassification is under discussion at European level but may not happen.

  • If it does, the immediate implication would be that member states would have to set up a register of beekeepers.
  • Any beekeepers who did not register would be liable to fines, and so would the state.
  • Dr Budge was dubious this reclassification, if it did happen, would help control parasites: the NBU currently has about 66% of beekeepers on its voluntary register BeeBase (that 66% is his educated guess). BeeBase is used to warn beeks of disease outbreaks.
  • New Zealand tried compulsory registration, thought they had 100%, and then realised that 10-15% of beeks were hiding when varroa spread through the country incredibly rapidly despite controls being put in place.

The National Bee Unit

  • The NBU is not part of DEFRA (he was keen to emphasise this), it is an arm’s length agency, part of FERA, so it can give unbiased advice.
  • However FERA, and half of the NBU, are about to be sold. Dr Budge, when asked to clarify which bits, were to be sold/retained said it was too complex to go into in this meeting.
  • The NBU may launch a breeding training program called SmartBees. Or may not, as the project’s funding is now under review.

More cool bee facts

  • A starving bee colony, despite being vegetarian, as a survival strategy, will sometimes eat its very young larvae and feed them to the oldest larvae, who need protein and have the best chance of survival. Bees are, after all, descended from wasps!
  • Britain and Europe generally have a big gene pool of bees and no danger of inbreeding (which can contribute to colony failure), so we lack one of the pressures seen in the USA, where Colony Collapse is endemic. In the USA, imports of bees are highly restricted and most people get their queens from just a few breeders, so the lines are becoming very inbred. The USA is beginning to import bee sperm.
  • A new varroa treatment has been launched, called the Bee Gym. This is basically a scratching post. No academic studies of its effectiveness have been released yet. Personally, I would be wary of this: people have tried using queen excluders for the same purpose, but they found that they gradually damage wings.

The talk was generally excellent and informative, and I am grateful to Dr Budge for his presentation and Cafe Scientifique for hosting it. An audio recording of Dr Budge’s talk may be made available in the future via the hosts, Cafe Scientifique – if so, I will edit this post to include a link here.

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3 Responses to Talk by Dr Giles Budge of the National Bee Unit

  1. simplebees says:

    I was lucky enough to be the only natural beekeeper invited to Fera (near York) last Thursday to hear Giles Budge and others talking about bee diseases – mainly EFB and varroa vectored viruses. Fera are doing some fascinating and very detailed research. However, I was disappointed that the emphasis is on control of disease by humans rather than the control of disease by the bees themselves -ie how do we find ways to allow the bees to come into balance with their commensals and general hangers-on . That said, scientists are a naturally curious bunch and when one mentions to a professor of virology that there are treatment free bees out there that do not succumb to varroa viruses, his interest is aroused and he asks for one’s contact details.

    Here is a summary:

    Gene studies show that there are at least 15 different strains of EFB in the UK. One of these is (currently) isolated to a single location on the coast in Norfolk and originates from Poland!

    Of the 15 strains, there is a huge divergence in the effect of the bacterium on infected bee larvae. In laboratory trials, the least aggressive strain leads to death in about 8% of infected larvae. The most aggressive strain leads to the death of around 88% of infected larvae. The the other strains fall at roughly equal intervals between these two. Although it wasn’t stated as such, one can see that identification of the strain of an EFB outbreak could potentially lead to different strategies for dealing with aggressive and non-aggressive strains.

    Modelling EFB outbreaks suggests that local habitat and environmental factors are of key importance in determining whether an area is a persistent hot spot. For example, deciduous woodland encourages EFB, whereas rich grassland discourages it. Mountains discourage EFB but altitude away from mountainous areas has no effect or may even encourage it. Colony proximity is also an important factor (more so than beekeeper movement it seemed). Reflecting these factors, the south east of England is the area most affected by EFB, with central southern England next. Wales and Scotland have generally low EFB incidence.

    There were a couple of interesting points on the role that drones might play in spreading EFB (or not). First, drones can carry high loads of EFB. Exactly where on the body (external or internal) such loads are carried was not entirely clear. Nether is there any information as to whether this means that drones can carry EFB from hive to hive. Second, however, drones will feed both workers and other drones with syrup under laboratory conditions. Whether they do this in the field has not been studied but this gives rise at least to the possibility that drones could transfer infection to other bees/hives.

    On the role of infected comb, polished brood cells awaiting an egg have been found to be completely free of EFB bacteria, as have the eggs laid therein. No mention was made of the infectivity of the nurse bees that do the cleaning!

    The varroa section of the day concentrated on viruses, of which the most important by far was said to be DWV. It seems that DWV in the UK consists of 4 or 5 different strains. All trigger an immune response in infected pupae but one seems to overwhelm the defences of the pupa and causes major disruption, especially to growth genes (hox genes) that results in stunted growth, string wings, impaired physiology, shortened lifespan etc. About a week after infection, pupae infected with this strain show a viral load that is 10,000 times higher than the other strains. Not surprisingly, the conclusion was that this is the only strain that matters in terms of bee health!

    The presenter was pretty convinced that Varroa itself acts as a passive carrier of DWV. The aggressive strain does not preferentially multiple in the mite.

    Evidence was presented suggesting that DWV and Nosema ceranae can both spread from honeybees to Bombus spp at least to some degree (depending on honey bee density and infection level). Some other viruses seem to spread in the the opposite direction, from Bombus spp to Apis. Also questions were raised as to whether N ceranae actually originates from Bombus, spreading into Apis and then back again. Imported Bombus spp used for pollination were said to be nowhere near as disease-free as they are meant to be.



  2. Tim Evans says:

    Paul & Gareth, thanks for this (I’m catching up on a rainy day).
    Paul: “the argument that unmanaged feral colonies survive because they have “survivor” abilities, whether through genetics or epigenetics or behaviour (grooming etc).”
    – maybe the survival characteristic is that they are unmanaged? Uninterrupted control of temperature & chemistry; choosing cavities for themselves.
    If so, it might be possible to detect an effect in low-intervention hives designed to imitate the cavities bees choose. My old regional inspector, now retired, thought Warres gave a better varroa survival rate. Shame the NBU’s not researching that (are they?) .

    Tim, Hackney


  3. Paul says:

    Tim, thanks for that feedback… you know: it occurred to me the other day, maybe varroa are evolving too, because parasites which are too successful wipe out their hosts. I wonder if the breeding rates of European varroa are lower than the original ones which parasitise apis cerana in Asia?


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