Category Archives: Responsibility

Urbane bees

Urbane as in ‘of the city‘ as well as ‘polite and courteous‘.

Over 80% of the UK population live in towns. Although it’s unlikely that beekeepers are evenly distributed between urban and rural areas, it still means that most beekeepers (or wannabe beekeepers) probably live in towns. With the increase in the popularity of beekeeping over the last few years this inevitably means that more bees are being kept in towns than ever before.

Bees can do very well in towns

Cities have higher ambient temperatures 1 which effectively extends the season, starting earlier and finishing later in the year. These higher temperatures also provide more protection from extended cold periods during the winter.

Despite the depressingly obvious acres of grey concrete, cities can be remarkably ‘green’, with large parks and gardens in even some of the most densely populated areas. Satellite mapping analysis shows that cities like Liverpool, London and Edinburgh have 16 – 49% ‘green space’.

Many towns and cities have large numbers of well established trees, including lime and sycamore, both of which can give great honey. In addition, there are thousands of suburban gardens with a wide range of ornamental flowering plants.

As a consequence, city bees have access to a range of nectars throughout the season, helping create some strikingly good honey. There are entire businesses built around supplying honey from bees in the city – or cities – including the London Honey Company, Bermondsey Street Bees and the Sheffield Honey Company.

City rooftop bees

City rooftop bees …

But it’s not all roses … or begonias or geraniums

However, a quick look at the honey sold by ‘city’ honey companies shows that only some of it originates from, er, cities. They also sell Suffolk coastal honey, heather honey, borage honey etc. Of course, this probably – and rightly – reflects demand. There’s a wonderful range of different honey produced in the UK, so why not sell it alongside honey from the city?

Except there isn’t any honey from the city available at the moment. All gone. Neither of the two London-based companies listed above have any London honey for sale 2. Demand clearly outstrips supply.

And this is probably because supply is limited. Cities are surprisingly green, but many of the ornamental flowers favoured by gardeners are poor nectar producers and the trees are often planes, which produce no nectar for bees. With the increase in interest in beekeeping it’s been suggested that there are too many bees in cities 3.

I don’t think the data to support this conclusion is good enough (yet). Hive numbers are certainly up significantly, but perhaps not as high as some think. Whether they’re at saturation level for the forage available will require analysis over several years, taking account of the actual honey yields, the weather and accurate information on colony density.

It’s interesting to note that Fera’s Beebase report the apiary density around my local apiary in rural Fife is 1/25th that of Central London (29 vs. 710 within a 10km radius). These figures aren’t reliable or even accurate … each apiary may have very different numbers of hives and significant numbers of beekeepers (perhaps as many as 50%) aren’t even registered on Beebase. Nevertheless, it probably gives a general indication of the relative density of hives.

Being neighbourly

There are more important issues than potentially poor honey yields with urban bees. Bees aren’t domesticated 4 and they can’t really be controlled. They forage where nectar and pollen is available, they drink water when they need it, they swarm when the colony is doing well and – there’s no real way to be delicate about this – they crap wherever they want. They can also get tetchy when forage becomes limiting, during stormy weather or when poorly handled.

All of which means that your bees might cause problems for your neighbours.

Poop target ...

Poop target …

They’ll forage freely in their gardens, drink water from the bird bath or jacuzzi 5, swarm en masse and hang pendulously from the climbing frame, and they’ll defecate repeatedly on the neighbours recently waxed and polished BMW.

These are not insignificant issues and they shouldn’t be ignored.

If you’ve got bees, whatever the evidence (or lack of it), it will be your bees that sting your neighbours grandchild, poop on their Beemer and swarm onto the garden swing.

Swarm on a swing ...

Swarm on a swing …

Guilty until proven innocent.

Good urban beekeeping practice

I’ve kept bees in an urban garden and, while I can’t really advise on how you establish and maintain good relations with your neighbours 6, I can provide some beekeeping hints to make their life – and yours – a bit easier.

These are more or less in order of importance …

  1. Make sure you have access to an out apiary over three miles away. Perhaps the training apiary for your association, or a friend with a large rural garden. Arrange this in advance, not when an angry neighbour is remonstrating with you about his toddler and anaphylaxis. Seriously. Some problems are only solved by moving bees away and you might need to do this in a hurry.
  2. Put out a bait hive at the beginning of the season. You might stop a swarm from your own bees disappearing over the fence (but see 3). More importantly, another swarm from the neighbourhood might neatly hive themselves rather than ending up in the neighbours garden. Brownie points 7 for you and no blame can be attached! I’ve never failed to catch swarms with bait hives in urban or semi-urban gardens … and they weren’t mine because I always clip my queens. Which brings me to …
  3. Always clip your queens. Although clipping the wing of a queen does not stop swarming, it does stop the swarm flying off. They’ll usually end up on the hive stand or underneath the floor.
  4. Learn, and get good at, swarm prevention and control. Provide space for the colony before it’s needed, replace queens regularly, control colony expansion by taking off a nuc, conduct timely splits to control swarming and reunite to requeen. If you don’t yet know what these things are then there’s quite a bit to learn. Are you ready to keep bees in your town garden?
  5. Keep well-tempered bees and keep them well-tempered (see 8). Aggressive bees are unpleasant at the best of times. They make beekeeping a chore if you’re in the corner of a remote field. In town they’re an abomination. Requeen or move them immediately with any repeated tendency to show signs of bad behaviour.
  6. Engineer the flight lines to force bees up and away. If you situate the hive(s) in a corner facing into a fence or wall the foragers will be forced to fly up and over the obstacle, ideally well over head height. I’ve seen this done very successfully using an open-topped netting cage. My bee shed is surrounded by security fencing with 2″x6″ mesh … >95% of the foragers choose to fly over this rather than through the mesh 8.
  7. Be sensible about when you conduct your weekly inspections. Not when there’s a children’s party next door, not on the first warm, sunny day for a fortnight (when everyone is outside) and not when there’s a thunderstorm predicted and the bees are already agitated. You’ll find this is surprisingly restrictive. You’ll want to inspect your colony on the same day everyone else is enjoying the good weather. I used to keep my bees about six feet from where my neighbour parked their car to unload the shopping … I lost count of the number of times I had to abandon an inspection as they returned from Sainsburys. And they seemed to do a lot of shopping 🙁
  8. Learn to inspect your colonies well. This is perhaps the most difficult thing to achieve for a beginner. The idea is that you conduct a thorough inspection while causing the minimum disruption to the colony. ‘Thorough‘ so you’re confident about what’s happening in the colony (and so don’t need to do it too frequently). The ‘minimum disruption‘ is important so you don’t leave agitated bees flying around for ages afterwards. This is a skill and is generally only learned with lots of experience – minimal smoke, gentle handling of the frames, proper examination of each frame, no crushed bees (so no alarm pheromone) … with all this being achieved quickly.
  9. Good Varroa management. Controlling Varroa means your colonies are likely to stay strong, so they are less likely to be robbed out by the dozens of other colonies in the area. This is both responsible beekeeping and stops the sort of frenzied mobbing of bees around the hive that are likely to really worry the neighbours.

Forewarned is forearmed

As I’ve said before, the principles of beekeeping are really rather simple. It’s practice – lots of it – that is needed to acquire the necessary skills to keep bees well. I’d argue that good beekeeping is particularly important in towns because your mistakes, or the intransigence of the bees, don’t just cause you a problem. They potentially cause problems – or at least concerns – for your neighbours.

That’s neither fair or responsible.

Some of the best beekeepers I know keep quite large numbers of colonies in surprisingly small suburban gardens. Do not underestimate the skill needed to achieve this. All of them have somehow arrived at a method of beekeeping that addresses all of the points above.

But I’ve also been asked to urgently requeen double brood colonies in tiny town gardens that were so aggressive they needed a double beesuit over a fleece for protection, where the garden was off-limits and where inspections had been completely abandoned.

I hate to think of the problems this caused their neighbours … or the additional bad publicity for beekeeping in general.


Colophon

Urbane means (of a person, especially a man) courteous and refined in manner. It’s derived from Middle French urbain which meant both polite, courteous, elegant and belonging to a city. This in turn is derived from Classical Latin urbanus meaning much the same. For an article about bees in towns the word seemed remarkably appropriate, referencing both cities and the need for courteous and refined behaviour.

Of the bees … and the beekeeper 😉

About the only thing wrong with the current use of the word is that it is usually applied to males.

🙄

 

Principles and practice

There’s a high level of ‘churn’ amongst new beekeepers. Beekeeping is relatively easy and inexpensive to start. The principles of beekeeping appear straightforward. But large numbers of beginners give up after a season or two.

Here I argue that the colonies and hives some of these beginners abandon pose a threat to other beekeepers, sometimes for years …

A better appreciation of the commitment required to successfully practice the principles of beekeeping might increase the success rates of beginners, though it might also dissuade some from starting in the first place.

Save the bees, save humanity

Supermarket bees

Supermarket bees …

Bees are popular. You only need to visit the supermarket, spend time on the High Street or browse the web, to find bees or pollinators mentioned. The plight of the honey bee is extensively documented in the press. In places some of these references are little more than thinly-veiled adverts … there are any number of beers or ales that now include ‘local honey’ to support bees and beekeeping.

So, public awareness is high.

A good thing

In some ways this is a good thing. The public are aware that, for a variety of reasons, our honey bees (and other pollinators, but I’m going to restrict myself to honey bees for the remainder of this post) are facing real problems. Habitat destruction, monoculture, disease, farming practices, global warming, mobile phone masts, parasites, imports and – the current favourite – neonicotinoids, are all/solely (delete as appropriate) to blame for the problems faced by our cute little bees.

Monoculture ... beelicious ...

Monoculture … beelicious …

It’s a good thing because you might get to sell more local honey which, as a consequence, means you’ll look after your bees carefully and manage them to make more honey next year. It’s a good thing – and I’ll declare a vested interest here – because the Government is encouraged to spend money on research to discover what the real threats to honey bees are (hint, it’s probably not mobile phone masts). This money will also help develop ways to mitigate these threats in due course.

There are a lots of other reasons why it’s a good thing. People are designing bee-friendly gardens, they’re planting wild-flower meadows, they’re reducing pesticide usage and favouring biological control or other pest management techniques. Farmers are being encouraged to leave wide field margins or build beetle banks … and some might even be doing this.

Too much of a good thing?

Some people are so concerned about the plight of the honey bee they decide to do the obvious thing and buy a hive and bees for the bottom of their garden. Obvious, because they’ve increased the number of hives and they’ll be getting lots of delicious honey at the end of the summer.

Some attend a winter ‘start beekeeping’ course (or fully intend to next year, once they’ve kept bees for the current season). Some think they’ll be OK with generous offer of telephone support from the person who sold them a midsummer nuc.

Others do this without any training, without any advice and without anyone to mentor them. 

What could possibly go wrong?

These new beekeepers are certainly well-intentioned. They fully intend to help bees. They really think they’re going to help. They love the idea of their own local honey.

Unfortunately, although many might think they appreciate the basic principles of keeping bees, they know very little about the practice of beekeeping.

Principles

Actually, the principles of beekeeping are a little more complicated than buying a hive, dumping a nuc into it and harvesting the honey at the end of the season.

The bees need to be fed when there’s a dearth of nectar, or in preparation for winter. They need to be protected from pests and diseases. They need space to expand. They need to be monitored in case they’re thinking of swarming. If they are, action is needed. And all this needs to be regularly and repeatedly checked throughout the Spring and Summer.

In short, they need to be properly managed. This management is the practice of successful beekeeping.

Without proper management I’d argue that one of the biggest threats to bees and beekeeping is the unmanaged colony (or hive) lurking in the corner of a field.

Practice

It’s easy to overgeneralise here. The following paragraphs are really describing beekeepers in their first few seasons. Experienced beekeepers can modify their management practices to one that suits their bees, environment, climate and strategy. Bear with me.

Inspections need to start before colonies build up too strongly in the Spring. Queens should ideally be found and marked (and clipped in my view, but some prefer not to do this). Inspections continue at 7 day intervals until the swarming season is well and truly over.

Not 11 day intervals … not when “the weather is better than today”, not when “I get back from the  fortnight in Crete”, not when “I can be bothered” … and certainly not only when “the neighbour is angry about the swarm clustered on their garden swing”.

Inspections have to be conducted thoroughly and with a purpose. It’s not a cursory glance in the top of the box. There’s a reason you’re doing it, so do it well.

Inspections must be done even if it’s 32°C in the shade and you’re melting in your beesuit, when the bees are stroppy as the OSR has just gone over and there’s no nectar coming in, when the weather is (again) miserable and all 50,000 will be ‘at home’ (and possibly tetchy as well) and even if you think “surely they’ll be OK for another day or two?”.

They probably won’t.

Hard labour

Beekeeping is hard work. If you’re lucky and the supers are bulging full it can be backbreaking.

You have to work reasonably fast and carefully. Manage only one of these two and, for different reasons, inspections can become tiresome.

You will get stung, though not often if you’re fast and careful and if you have well-tempered bees.

It can be hot as hell in summer and you can get wet, miserable and cold at any time of the season.

Uh oh ... swarming ...

Uh oh … swarming …

It’s not only physically hard, it is also mentally hard. Not like quantum physics, but it still requires quite a bit of thought. Bees are not ‘fit and forget’.

Using a combination of observation, experience and knowledge (and perhaps a little inspired guesswork) you need to determine what’s going on in a forty litre box containing over 50,000 bees. Is there disease present? Is it one you can do anything about? Is it notifiable? Is the queen present and laying well? Is the colony thinking of swarming (hint, a dozen sealed cells is usually an indication the colony has swarmed, not that it’s thinking of swarming 😉 ). Do they have enough stores? Do they need more space?

You need to be prepared for disappointment (and have a contingency plan). Despite your best efforts the colony may swarm. An extended period of lousy summer weather prevents the new queen from getting mated properly. The colony dwindles, is too weak to defend itself and is robbed out by another colony. Any number of things can go wrong.

Bees are managed, not domesticated.

That’s the reality of beekeeping. That’s the practice that underlies the principle of just dumping a nuc of bees in a box in late April and harvesting pound after pound of golden honey in early September.

If only it were that simple!

Beeless “beekeepers”

I regularly meet people who ‘once kept bees’. I’m sure you do to. Further discussion often shows that they certainly once had bees, but that they failed to keep them.

The colony died, was robbed out, repeatedly swarmed, absconded or – much more frequently – these beekeephaders simply lost interest.

Often they aren’t actually sure what happened to the colony. Have you ever asked them?

Their initial enthusiasm was tempered a bit by the first couple of inspections. The colony was getting much bigger, much faster than their experience made them comfortable with. They got a bit frightened but wouldn’t actually admit that. They missed an inspection (or two) as they were in Crete for the family holiday. The colony swarmed. They’d read somewhere that the colony shouldn’t be disturbed for a month, so they didn’t. They remembered again three months later but were then too late for the autumn Varroa treatment. Have you got any fondant to spare? They’ll have another go next year.

Definitely.

It’s not unusual for these hives to be simply abandoned. You find them in the corners of fields or tucked up against the hedge in a large sprawling garden.

Out of sight and out of mind.

Forgotten, but not gone

Forgotten, but not gone …

The gift that keeps on giving

Sometimes the colony limps on for a season or two. More often though it expires in the winter. The hive may then be repopulated the following year by a swarm. They flourish, or more likely perish and are repopulated again. Even if mice move in for winter and wax moth trashes the comb they still attract swarms.

duunnn dunnn ...

duunnn dunnn …

There’s a dozen or more hives like this on private land I know of. Some local beekeepers visit every year or so to collect any swarms that have moved in. I can’t imagine the state of the comb … or the colonies they collect.

But (queue Jaws music … duunnn dunnn… duuuunnnn duun… duuunnnnnnnn dun dun dun dun dun dun dun dun dun dun dunnnnnnnnnnn dunnnn) these abandoned and unmanaged hives mainly provide a great opportunity for Varroa to flourish. Together with both the foul broods, Nosema and goodness knows what else.

The abandoned hives effectively act as bait hives, attracting swarms which become established feral colonies. Most will eventually be decimated by Varroa and its viral payload, but many will chuck out a swarm or two first, or drones that drift from colony to colony. Some will get robbed out as they collapse – perhaps by one of your strong colonies – leading to a huge infestation with phoretic mites carried by the returning robbers.

They’re like a 40 litre cedar version of Typhoid Mary.


† And my extensive market research suggests they are very delicious too 😉

‡ After all, there’s no time like the present to start and the sooner you buy and populate that lovely cedar hive, the faster honey bee colonies numbers will increase. But they will definitely attend the beekeeping course next winter. Absolutely!

Telephone support. Really?! Have you ever tried to give telephone advice to a new beekeeper who’s standing by an open hive, mobile clamped to their ear, desperately looking for eggs, or deciding whether the queen cells are capped or uncapped? I’ve tried … don’t bother. Grab the beesuit and get to the apiary 😉

There are others I know of and have access to. The entrances to these have miraculously become stuffed tight with grass, so preventing their repopulation. How did that happen? 😉

A poor analogy, but it makes the point. Typhoid Mary (Mary Mallon) was an Irish immigrant  New York cook in the early part of the 20th Century. She was also an asymptomatic carrier of typhoid, a bacterial infection. During the period 1900-07 she infected at least 51 people, three of whom died. Investigative epidemiology traced a series of typhoid fever outbreaks to places where Mary Mallon worked. She was named Typhoid Mary in a 1908 article in the Journal of the American Medical Association.

Mary Mallon

Mary Mallon

Mary Mallon refused to accept that she was infected, was forcibly incarcerated (quarantined) twice and eventually died after three decades of isolation. The analogy is poor because Mary Mallon appeared in good health, whereas these abandoned hives (and the bees they contain) are often pretty skanky. However, the term “like Typhoid Mary” is often used to indicate a source of repeated infection … which is spot on.

 

 

SaveSave

SaveSave

SaveSaveSaveSave

SaveSaveSaveSave

SaveSave

SaveSave

SaveSave

SaveSaveSaveSave

SaveSave

SaveSaveSaveSave

Honey and hay fever

300 jars of honey

300 jars of honey

I’m conflicted. As a beekeeper I appreciate offsetting the cost of indulging my hobby from honey sales. In a good year I get much more honey than I could ever give away to friends and family. Despite making some of my own equipment, there are the costs of purchasing (yet more) boxes, miticides, extraction equipment and winter feed. There’s also an ever-growing wishlist of things that, whilst not essential, would be very welcome. Abelo’s heated honey creamer looks very nice 😉  Bottling, labelling and then selling honey – either from the door or from local shops – provides a few quid to help … a sort of self-perpetuating process in which I transfer all that summer effort by the bees into the coffers of Thorne’s and C. Wynne Jones.

However, I regularly get asked for local honey to ‘prevent the symptoms of hay fever’. Emails or phone calls go something like this:

“My son/daughter/husband/wife suffers really badly from hay fever and I read that locally produced honey could help her symptoms” … followed by a request to confirm that what they’ve read is correct and could I sell them some honey.

As a scientist I can’t do the former and so usually fail to achieve the latter. No way to run a business perhaps, but honesty is the best policy.

Achoo!

Bless you

Bless you

Hay fever is an allergic reaction to pollen in the air. About 20% of the population have, or will develop, hay fever. I never had it as a child, but in my 30’s developed a strong reaction to some grass pollens that still makes a fortnight or so in mid/late June pretty miserable. Hive inspections with bad hay fever are really miserable.

Symptoms are characteristic – itchy eyes, sneezing and a runny nose (where does all that stuff come from?!). Anti-histamines, either prescription or over-the-counter, help prevent the allergic reaction from occurring. Usually this is sufficient to make the symptoms bearable.

Severe hay fever symptoms, where anti-histamines or corticosteroids are insufficient, can be treated by immunotherapy. Over several months, the patient is exposed sub-cutaneously or orally, to low and increasing doses of the allergen (the compound that causes the allergy) to help develop immunity. Full desensitisation takes about three years.

Honey contains pollen

Honey contains small amounts of pollen. The presence of the pollen forms the basis for lots of tricky questions in the BBKA examinations and is a feature used by food standards to discriminate between flavoured sugar syrup and real honey.

This is probably where the ‘honey prevents hay fever” stories originate. It’s this small amount of pollen that is supposed to stimulate the immune system of hay fever sufferers. A sort of DIY desensitisation course using toast or porridge to help deliver the allergen. Tasty 😉

All this seems pretty logical and straightforward. Honey contains pollen. Low doses of pollen are used to stimulate immunity that, in turn, stops hay fever from developing. Local honey prevents hay fever … I must get this printed on my labels to boost sales further.

Don’t let the facts get in the way of a good theory

Unfortunately, there are a couple of irritating facts that scupper this nice little theory. The first is  a sort of error of omission, the second is the absence of evidence supporting the theory (or, more accurately, the evidence that the theory is wrong).

Honey certainly contains pollen. At least, real honey doesMelissopalynologists – those who study the pollen in honey – can identify the genus of plants that the bees have been visiting and so may be able to deduce the geographic origin of the honey.

The key part of that last sentence is “that the bees have been visiting”. The vast majority of pollens in honey are from the flowers and trees that they visit to gather nectar. These pollens are usually large and sticky so they adhere to the passing bee and are then transferred to another plant when the bee moves on.

What’s missing are any significant quantities of pollens from wind-pollinated plants such as grasses. Studies have shown that almost all pollens that cause allergies such as hay fever are from these wind-pollinated species. It’s logical that these pollens are largely absent … since the flowers, grasses and trees that produce them are anemophilous (wind-pollinated) they don’t need to generate nectar to attract bees, so the bees don’t visit. So there’s little or none of this type of pollen in honey.

No bees legs ...

No bees legs …

Testing, testing …

So that’s the error of omission. What about scientific support, or otherwise, for the theory that local honey prevents hay fever? After all, this must be an easy (and tasty) experiment to do. Feed a group of people honey and compare their hay fever symptoms with a group fed synthetic honey (or perhaps imported pseudo-honey sold from a supermarket near you).

Researchers in Connecticut did this experiment in 2002. They published their results in a snappily-titled paper “Effect of ingestion of honey on symptoms of rhinoconjunctivitis” published in the Annals of Allergy, Asthma and Immunology.

Rhinoconjunctivitis, or perhaps more correctly, allergic rhinoconjunctivitis, is the symptoms of hay fever – the itchy eyes, sneezing and runny nose. Three groups of a dozen hay fever sufferers, pre-screened for reactivity to common wind-borne allergens, were randomly assigned to receive local ‘raw‘ honey, filtered non-local honey and honey-flavoured syrup (the placebo group). They took one tablespoon of honey, or substitute, a day and recorded their hay fever symptoms. The abstract of the paper neatly summarises the results:

Neither honey group experienced relief from their symptoms in excess of that seen in the placebo group.

… leading the authors to conclude that:

This study does not confirm the widely held belief that honey relieves the symptoms of allergic rhinoconjunctivitis.

Absence of evidence does not mean evidence of absence

So, this study does not confirm (prove) that honey prevents hay fever. What about the opposite? Can we use it as evidence that honey does not prevent hay fever symptoms?

1934 Loch Ness haox

1934 Loch Ness hoax

Tricky … as the skeptic James Randi asserted, you can’t prove a negative. I can’t prove that the Loch Ness Monster doesn’t exist. However, in the absence of convincing evidence that it does exist, I can be reasonably sure that Nessie is a 6th Century tale, embellished in the 19th Century and blatantly exploited by the 21st Century tourist industry.

Of course, lake monsters are ‘found’ worldwide, which isn’t evidence that any of them actually exist 😉

We’re getting into the messy intersection of science and philosophy here. I think it’s sufficient to say that there’s no scientific evidence that honey prevents hay fever. The Connecticut experiment was a properly controlled random study. To my mind (as a scientist) this is much more compelling evidence than any amount of anecdotal stories to the contrary.

An abbreviated version of which is what I tell potential customers who want me to confirm that buying my local honey will help alleviate their hay fever symptoms. Essentially, it won’t.

Sure, they might not get hay fever after eating my honey, but that’s almost certainly a coincidence. It’s a coincidence I’m happy to live with, but not one I’m happy to promote as a reason to buy my local honey.

Why buy local honey?

I don’t think it’s necessary to cite dubious medical benefits when encouraging people to buy local honey.

Why claim something that’s probably not true?

Far better to claim the things that are true, some of which are also clearly demonstrable:

  • It’s local, from the hedges and fields within 3 miles of the apiary. It wasn’t imported by the tonne from a location or locations unknown.
  • It’s a very high quality product – clearly to claim this you need to ensure it looks wonderful and that there are no legs or antennae lurking in the jar.
  • It hasn’t been excessively heated before jarring – all the goodness is still present, including pollen, just not the sort of pollen that will prevent hay fever.
  • The honey hasn’t been micro-filtered, pasteurised or tampered with in any way.
  • It varies during the season as the forage changes – a jar of spring OSR honey is very different  in flavour from a jar of mid-summer floral (hedgerow) honey. It’s a wonderful edible snapshot of the changing seasons.
  • Buying it supports a local cottage industry.
  • It tastes fantastic – clearly demonstrable.

The ‘taste test’ is usually the deciding factor. A couple of tester jars – clearly labelled – a limitless supply of plastic coffee stirrers and a discard pot will allow customers ample opportunity to ‘try before they buy’.

Which they surely will … 🙂


∑ Honesty is the best policy is an idiom dating back to the late 16th Century when Sir Edwin Sandys, a founder of the Virginia Company and one of the first settlers in America, stated “Our grosse conceipts, who think honestie the best policie”.

A corruption of the saying by Mark Twain “Don’t let the facts get in the way of a good story”. 

† Jean Emberlin (2009). “Grass, tree, and weed pollen”. In Kay et al. The Scientific Basis of Allergy. Allergy and Allergic Diseases. 1:942-962. John Wiley & Sons. ISBN 9781444300925

‡ This isn’t xenophobia. The UK is a net importer of honey. 95% of the honey eaten in the UK is imported – 50% of the 34,000 tonnes imported in 2012 came from China. Most honey on the supermarket shelves contains some rather vague term like Produce of EU and non-EU countries. You don’t know where it came from, and probably nor does the supermarket. There have been bans on imported honey due to it being not honey (just doctored corn syrup), or being contaminated with antibiotics.

Apistan redux†

I’ve discussed Apistan, a pyrethroid treatment for Varroa, in two recent posts. In these I explained in some detail its molecular mechanism of action. I also explained the two major problems associated with Apistan (and the related tau-fluvalinates ) – the widespread resistance of Varroa to Apistan and the residues it leaves in wax.

In this final post I’m going to revisit just how useful Apistan could be if it was used in a more rational manner. I’m going to concentrate on resistance and you’ll probably need to read the previous post on this topic to provide necessary the background. I’ll only really touch on the residues in wax at the end – I’ve already discussed how these can be minimised if you consider them an issue.

This is (another) long post. It draws together the concepts described in previous articles and links the science of Varroa control to potential strategies to benefit practical beekeeping.

How good is Apistan if Varroa are not resistant?

Apistan

Apistan

Exceptionally good. Pyrethroids are some of the most widely used pesticides. They are widely used because they are very effective. Apistan is no exception. When used to treat Varroa populations that are not already resistant it kills over 98% of the mites in the colony when used according to the manufacturers instructions. 98% … that reduces the National Bee Units’ recommended maximum mite load of 1000 to just 20.

Just how effective is emphasised by a quote from the Apidologie paper cited above. “In treated hives, worker pupae and adult bee infestations decreased from 14.2 ± 7.3% to zero and from 15.7 ± 7.3% to zero, respectively. Whereas, in the two control hives, during the first 6 weeks, the average worker pupae infestation increased from 15.9 ± 2.9% to 19.7 ± 3.5%”.

Most mite mortality occurred during the first 4 weeks of treatment and the level of Apistan present at the beginning and end of treatment remained at about 10% i.e. it should be as active at the end of the treatment period as at the beginning.

How good is Apistan in reality

Resistance was first demonstrated in 2002 and is now widespread in the UK. In a recent paper, Ratneiks and colleagues (University of Sussex) demonstrated that Apistan was significantly less effective at killing Varroa when used for a second treatment, four months after the first. In this study they showed only 33% of mites were killed at the second treatment, whereas 58% were killed in colonies treated for the ‘first time in five years’.

This isn’t rocket science … if there are some resistant mites in a population then Apistan will preferentially allow these to survive. Consequently they will make up a greater proportion of the mite population when re-treated.

Since we know the molecular basis of resistance to Apistan it would now be possible to determine – without doing the treatment and counting the corpses – what proportion of mites were resistant in a population before treatment. It would therefore be easy to determine whether treatment would be likely to work.

Equally, it would be possible to determine whether the colonies ‘not treated with Apistan for five years’ still maintained significant levels of Apistan resistant mites. As will become clear, there are studies that contradict this, and the definitive test – the presence of absence of the mutation that confers resistance – was not done in the Sussex study.

Apistan resistance and fitness costs

Mutations, such as the one that confers resistance to Apistan, can – in broad terms – exert three different effects:

  1. Beneficial – the presence of the mutation favours the organism (a fitness benefit), the mutation will be selected for and it’s presence in the population is likely to increase.
  2. Detrimental – the mutations causes a fitness cost and organisms that carry it are likely to reproduce less well, resulting in it being lost from the population.
  3. Neutral – the mutation is neither beneficial nor detrimental.

In the presence of Apistan, the Leucine to Valine mutation at residue 925 (L925V) of the voltage gated sodium channel (VGSC; please see the previous article on the molecular basis of resistance), is a beneficial mutation. Any mites that carry it will not be killed and will be able to reproduce, so increasing it’s prevalence in the population. The same reasoning applies to other Apistan resistance mutations.

The VGSC of Varroa evolved over eons in the absence of Apistan. The mutation is in a part of the protein critical for its function (that’s why Apistan binding blocks function). It’s therefore perhaps unsurprising that in the absence of Apistan selection there is evidence that the L925V mutation is detrimental. In simple terms the VGSC works less well with a Valine at position 925 than a Leucine unless Apistan is present. Where’s the data that supports this?

The influence of prior treatment on Varroa genotype

Table 1. Apistan resistance mutations in Varroa from treated and untreated colonies

Table 1. Apistan resistance mutations in Varroa from treated and untreated colonies

The table above needs a little explanation. Colonies from Henlow and Shillington were treated with Apistan and tested one month later. Colonies from Harpenden, Bishop Stortford, St. Albans and Peterborough had no history of Apistan treatment in the recent past. Unfortunately, the paper does not make clear when the last treatment was, with the exception of a sample from Harpenden which had not been treated for at least 3 years.

Varroa is diploid i.e. there are two copies of the gene for the VGSC. The S and R heading the columns SS, SR, RR, indicates whether the Apistan resistant mutation is absent (S = sensitive) or present (R=present). SR indicates that the mite was heterozygous, one resistant copy and one sensitive. Whether these mites have lower resistance than RR mites has not been determined – for the purpose of the remaining discussion I’m going to lump the SR mites with the RR mites and assume they are resistant§.

Of 279 mites tested, 40 were from Apistan-treated and 329 from -untreated colonies. Of the 40 mites from Apistan-treated colonies, all contained the mutation conferring resistance to the fluvalinate. Of the 239 mites from colonies not recently treated with Apistan, 215 were sensitive and only 25 were resistant.

This suggests that in the absence of Apistan, Varroa sensitive to the fluvalinate replicate better.

Is this a surprise?

No. Partly for the reasons explained above … the Leucine at position 925 is likely to stop the VGSC working as well. More compellingly though is the wealth of data suggesting that insecticide resistance is associated with fitness costs in a range of other insects.

Colorado beetle

Colorado beetle

For example, pyrethroid resistant Myzus persicae (peach-potato aphid) exhibit fitness effects in overwintering survival, response to aphid alarm pheromone and vulnerability to parasitoids; pyrethroid-resistant Cydia pomonella (codling moth) have reduced fecundity, body mass of instars, adult male longevity and larval development; finally, pyrethroid-resitant mutants of the snappily-named Leptinotarsa decemlineata (which you of course know as the stripy-attired Colorado beetle) have reduced fertility and fecundity.

Google will find relevant reference on all the above examples or you can refer to a concise mini-review by Kliot and Ghanim Fitness costs associated with insecticide resistance published in Pest Management Science (2012) 68:1431-37.

Before discussing implications for practical beekeeping I should add that the rate at which the loss of the L925V mutation, and other mutations associated with Apistan resistance, needs to be accurately determined. If, as looks likely, a period of 3+ years results in selection for the sensitive variant of the VGSC, it might be possible to develop rational Varroa treatments that exploit this.

Apistan resistance, rational Varroa control and practical beekeeping

For the sake of discussion, let’s accept the following statement:

  • Apistan is devastatingly effective on sensitive mite populations.
  • Apistan is much less effective (or almost completely useless) on resistant mite populations.
  • Resistance by Varroa is acquired rapidly and lost over the subsequent 2-3 years in the absence of selection.

An effective and rational Varroa control strategy would only use Apistan once every 3-4 years, alternating it with other treatments. To mitigate the transfer of Apistan-resistant mites between colonies due to drifting and robbing, or due to the movement, sale and/or relocation of hives during the season, Apistan use would have to be coordinated. This coordination would have to be both geographical and temporal. There would be no point in the Fife beekeepers using it one year if the Angus beekeepers planned to use it the following year.

“Like herding cats” I hear some mutter …

Perhaps, but the benefits would be considerable. How could it be achieved? Perhaps by restricting the sale of Apistan to certain years, in a formulation or package that meant it had to be used quickly or became inactive.

What about the residues in wax?

I’m not sure whether the level Apistan accumulates to in wax is sufficient to be a selective pressure on the mite population. Apistan strips are 10% Apistan. Nothing like that much accumulates in wax. In a recent study fluvalinate levels ranged between 2 and 200,000 parts per billion in wax (mean ~7500 ppb). However, it is a valid concern and so would necessitate a relatively simple experiment to determine the rate at which Apistan resistant mutations are lost in the presence of absence of trace levels of Apistan in comb.

Herd immunity and the responsibility of the individual

There’s a debate in human healthcare about the necessity to vaccinate individuals in a well-vaccinated population. The chance of an infectious disease spreading to the unvaccinated individual in a protected population is very slight. So, why vaccinate?

Well, what if increasing numbers decided not to vaccinate? Once protection in the population falls below a certain level there is a significant chance that an infectious disease will spread widely. We saw this in the UK after the MMR (measles, mumps and rubella) vaccine was falsely claimed to be associated with autism. Vaccination rates dropped from 90+ percent, to low 80’s and – in parts of the country – to only 60%. Unsurprisingly, measles cases increased and – tragically, for the first time in years – there were childhood deaths due to measles infection.

This may seem a million miles away from looking after our bees, but there are parallels. As beekeepers we have responsibility for our own stock. We also have responsibility to the wider community of beekeepers which – because of the way our bees forage and mingle – happily exchange pests and pathogens.

Beekeepers who do not control Varroa (and consequently virus) levels threaten the viability of their own colonies and those of other beekeepers in the area. The same applies to the foulbroods. This is why the bee inspectors try and check all colonies in the vicinity of an outbreak. This is why standstill orders are placed on apiaries where outbreaks occur.

Perhaps this sort of communal responsibility also applies to Varroa treatment using Apistan? Beekeepers who treat without demonstrating very high levels of susceptibility first in their stocks are simply selecting for resistant mites, reducing the efficacy of treatment for themselves, and others, in the future. Indiscriminate or incorrect use of Apistan has resulted in widespread resistance, thereby compromising Varroa control for all beekeepers.

The coordination and control, geographically and temporally, of Apistan usage would benefit beekeeping and beekeepers.

And … it would also benefit those who chose never to treat with Apistan. Treated colonies in the one year in three Apistan was used would have very low mite levels. Fewer mites would be transferred from these colonies by drifting or robbing … what’s not to like?


 Redux, as in the literary term meaning brought back or restored, derived from the Latin reducere (to bring back).

 This is one compelling reason why Apistan strips should not be left in the colony longer than is recommended. It kills the susceptible mites within the first month or so. After that it effectively selects for resistant mites, allowing them to replicate.

 With apologies to any population biologists who were reading this and have now given up in horror.

§ And I’ll save discussion of the influence of the incestuous lifestyle of Varroa and Varroa levels on the ratio of homozygotes to heterozygotes at different stages of the season for a later post. It’s a fascinating and at the same time rather sordid tale …

 Or 4 or 5 – this would need to be determined empirically.

Apistan resistance

Apistan

Apistan

In an earlier article I discussed what Apistan is – a pyrethroid miticide – and the consequences of using it. These include decimation of the mite population if it is susceptible, coupled with the accumulation of long lasting residues in wax. These residues may adversely effect queen and drone development. I also discussed ways to avoid build-up of Apistan residues in comb.

The key phrase in the paragraph above is ‘if it is susceptible’. Unfortunately, resistance to Apistan and the related tau-fluvalinates develops very quickly. To understand why we’ll need to look in a little more detail at how Apistan and other pyrethroids work.

How does Apistan work?

Apistan, like other pyrethroids, works by blocking the activity of voltage gated sodium channels (VGSC) resulting in paralysis because the axonal membrane cannot repolarise.

What on earth does that mean?

Action potential

Action potential

Nerve transmissions – like the signal from the Varroa brain to tell the Varroa legs to move – travel along axons. These are usually very long thin cells. In the adjacent image the ‘brain’ is on the left and the leg muscles on the ‘right’. The nerve impulse (the moving arrow) travels down the axon ‘driven’ by a change in polarity (charge) across the membrane of the axon. In the resting state, when there is no impulse, this is positively charged on the outside and negatively charged on the inside. Sodium – remember the ‘S’ in the acronym VGSC – is positively charged and crosses the membrane (out to in) via a small pore or hole as the impulse passes. This makes the inside of the axon transiently positive. The pore or hole is the VGSC.

Top view of a VGSC

Top view of a VGSC

The VGSC is a transmembrane protein. It actually crosses the membrane multiple times and assembles to form a very narrow channel through which the sodium passes. The cartoon on the right shows the top view of a VGSC, looking “down” the pore into the inside of the axon. The blue bits can move to open or close the pore, allowing sodium to traverse – or not – the membrane into the axon. Apistan binds to the transmembrane protein and prevents the pore from closing. As a consequence, sodium continues to pass from the outside to the inside of the axon, the nerve cannot repolarise and no further impulses can be transmitted. As a consequence, Apistan paralyses the Varroa.

But I don’t suppose many beekeepers will feel much sympathy for the mite 😉

Why isn’t the beekeeper paralysed as well?

Nerve impulses in Varroa and humans are transmitted in essentially the same way. We also have VGSC’s that operate in a similar manner. Why doesn’t Apistan also paralyse careless beekeepers? More generally, why are pyrethroids the most widely used insecticides, available in all garden centres and supermarkets?

Two factors are at work here. The first is the specificity of binding. The VGSC is a protein. Proteins are made from building blocks termed amino acids. The precise sequence, or order, of amino acids is usually critical for protein function. However, two proteins with a similar function can exhibit differences in the amino acid sequence. Although the human and mite VGSC have a similar function they have a different amino acid sequence. Apistan binds much better to the mite VGSC than the human VGSC (this also explains why bees aren’t also paralysed by Apistan … the miticide is specific for the mite VGSC and binds poorly to the honey bee VGSC). In addition, many mammalian species have a number of detoxifying enzymes which deactivate pyrethroids, rendering them ineffective. Together, this explains the specificity of Apistan and other pyrethroids, and the low level of toxicity to humans.

So now you know how Apistan works we can address the much more important question …

Does Apistan work?

Unfortunately, usually not. Since the late-1990’s there have been a large number of publications of Apistan- or fluvalinate-resistant mites from many countries, including the USA (1998, 2002), Israel (2000), UK (2002), Spain (2006), Korea (2009) and Poland (2012). The National Bee Unit used to report Varroa resistance test results by geographic region in England and Wales. Resistance was first reported in mites from Cornwall and Devon (in 2001 and 2002). By 2006 resistance was very widely distributed throughout England. By then approximately a third of all mite samples tested were resistant. The number of tests conducted (or at least reported) then dwindled and there have been none reported since 2010. Not no resistance … no tests. Presumably it’s no longer worth reporting as resistance is so widespread.

The most up-to-date map on the distribution of Apistan resistance I could find is in the NBU booklet on Managing Varroa [PDF; page 28 of the 2015 edition], though the data presented is from 2009.

However, bee equipment suppliers continue to sell Apistan (even Vita, the manufacturer, states that resistance is widespread) and beekeepers continue to use it. Many do so without first testing whether the mite population in their colonies is sensitive to the miticide. How should this be done?

Testing for resistance

Vita suggest two tests. Their first (the “rule of thumb test”) is deeply flawed in my view. It suggests simply looking for a drop of 100’s of mites in the first 24 hours after treatment starts as indicative of a sensitive population.

This isn’t good enough. What if there were thousands of mites present? Perhaps 20% of the population are sensitive, with the remainder resistant. 20% of 5000 mites is 1000 … so you might expect a drop of 100-200 (the majority of the phoretic population) within the first 24 hours. Some might consider this drop indicates a sensitive population … it doesn’t.

It’s not sufficient to count the corpses … you need to know how many mites were unaffected by the treatment.

The second Vita-recommended test is a cut-down version of the “Beltsville” pyrethroid resistance test which is fully described in an NBU pamphlet (PDF). This is much more thorough. Essentially this treats ~300 bees with Apistan, counts the mites that are killed in 24 hours and then counts the unaffected mites remaining on the bees. It’s only by knowing the total number of mites at the start and by determining the percentage of mites sensitive that you can be sure that the treatment is effective.

What is the molecular basis of resistance?

We’re almost there … specific pyrethroids, like Apistan, bind to specific parts of the VGSC. The VGSC is a protein made up of a long connecting chain of amino acids. The binding of the pyrethroid requires an interaction with a small number of specific amino acids in the VGSC. If these particular amino acids change – through mutation for example – then the pyrethroid will no longer bind. If the pyrethroid does not bind the VGSC can open and close again, so the axon repolarises and the mite is not paralysed. The mite is resistant and can then go on to rear lots more resistant baby mites … which, in due course, transfer the viruses that kill your bees.

And that’s exactly what happens.

Leucine

Leucine

A single mutation that causes a substitution of amino acid number 925 in the Varroa VGSC, which is usually a leucine, to either a valine, a methionine or an isoleucine, is sufficient to prevent Apistan and other tau-fluvalinates from binding. At least 98% of mites resistant to Apistan have one of these substitutions. Apistan resistant mites with substitutions at position 925 have been found in the UK, eastern Europe and several sites in South-Eastern USA. It wouldn’t be surprising if the remaining ~2% of resistant mites had a mutation at one of the other amino acids involved in pyrethroid binding. Further studies will confirm this (there are alternative mechanisms that cause resistance, but the one described here is the most frequently seen).

Why aren’t all Varroa mites resistant to tau-fluvalinates?

Apistan resistance has clearly been demonstrated for the last two decades. Resistance is easy to acquire and selection – in the presence of the pyrethroid – is effectively absolute. Without the necessary mutation the mites die, with the mutation they survive.

Bees – and the phoretic mites that are associated with them – are moved around the place all the time, by migratory beekeepers, by importers and through robbing and drifting between colonies.

Why therefore aren’t all Varroa mites now resistant to Apistan and other tau-fluvalinates?

The answer to that is interesting and suggests strategies that could make Apistan an effective treatment again … but I’ll save that for another time.


Only transiently as the charge is reversed shortly afterwards by a similar, though not identical,  mechanism that does not use the VGSC. However, life is simply too short to describe this bit as it’s not needed to understand pyrethroid – or Apistan – activity and resistance.

 The incestuous life cycle of the Varroa mite is important here. This post is already too long to fully elaborate on this but the size of the mite population relative to available open brood (and whether you get single or multiple occupancy of cells) will likely influence the proportion of resistant, partially resistant and sensitive mites in a population.

Credits – the action potential GIF was created by Laurentaylorj from Wikipedia.