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Tinkerer Larry Clamp put together a very nice set up illustrated instructions for building mite washer cups, and is generously sharing them. Thanks, Larry!
The thin black screen from package bee cages (or some older veils) is easier to work with than hardware cloth, and
Depending upon the type of plastic cup, some expensive glues intended for plastics may work (I found that the alcohol may eventually work under the silicone). Brion Dunbar tells me that he’s had good luck with 3M ScotchWeld High Performance Industrial Plastic Adhesive 4693H.
Beekeeper Nick Kingan let me know that there’s a nice livestock syringe available from Tractor Supply that can be adjusted to dispense 5 mL per squeeze. I find the squeezing of this sort of syringe to be tiring to my hand if I’m treating a large number of hives, but it may be handy for those with just a few hives, since it helps to dispense the correct dose.
Update 20 Sept 2017
There are YouTubes being circulated recommending using a heat fogger to apply oxalic acid. Retired chemist Dick Cryberg, who is a very sharp guy whose observations I deeply respect, posted the following to Bee-L:
I tried fogging with 10% oxalic acid dissolved in water. I fogged ten five over five deep nucs once a week with 0.6 g of oxalic acid
dihydrate for each five deep for eight consecutive weeks this summer. I had ten nucs untreated side by side for controls. The single highest
after treatment mite count was from a treated nuc determined by alcohol wash at 3%. I saw exactly zero evidence that I killed any significant number of mites. Overall the treated hives and controls had equivalent mite counts. All were at 0 to a bit over 1% mites at the start. I dosed as high as 2g/ five deep nuc and showed no adverse effects other than a few burned bees that hit the fogger screen. Fogging ran from mid June
to late July. All were treated earlier in the spring to drive mite counts to about zero with apivar. The slow build up by early August is because I run Minnesota Hygienic queens which do a fair job of containing mite populations.I was pretty careful in the experiment. I spent several hours fooling with the fogger to figure out how to deliver a consistent dose. I had to drill a hole in the top of the handle and push down the trigger fully down with a screw driver after each shot to get consistent volume each time. I also had to pull the trigger as fast as possible to get consistent volumes. I showed, by capturing and analyzing the fog that oxalic was surviving the fogging experience at least partly intact. My capture was under 100% and analysis showed a recovery of 60% so I feel was I was not
decomposing enough to matter.I also waited 20 seconds between trigger pulls to allow full heat recovery in the coil. Even then a lot of what came out the spout was liquid that ended up on the bottom of the nuc. I found the process tedious and not really all that fast at over three minutes per nuc each treatment.I have seen the you tube vids and seen much discussion on fogging. I am the first, as far as I can tell, to ever do before and after mite counts and include controls of any type. At this point I view all such claims as pure snake oil of the usual value that snake oil typically has but am open to being proven wrong. I am a bit leary of firing alcohol due to flammability althou no one has reported a fire issue. [I would expect a fog of alcohol in air to be highly explosive, but I don’t have a heat fogger with which to test. If any reader has tested this, please let me know]
Also, oxalic acid will react very rapidly with alcohol make the ester and the ester will very rapidly decarboxylate at temps as low as 100 deg C to ethyl formate which is not going to kill mites. If you are going to fog ethanol solutions you probably need to make fresh solution just prior to fogging to avoid the inevitable ester formation that is going to happen on storage even at room temp. This chemistry is not a problem in water solution but needs to be considered in alcohol or particularly glycerin which some are using.
Update 18 March 2017
When OA dribbling package bees (or perhaps any bees), I’ve received a report from a good source that the bees tolerate the dribble better if they are full of nectar or sugar syrup–presumably because they are then less prone to imbibe the OA syrup.
Update 24 Jan 2017
There has been lots of response to my article on OA/gly in ABJ (soon to be posted to this website). I’m in communication with EPA to get this application method approved.
In response to questions about adverse effects on queens:
The evidence that I’ve seen to date indicate that vaporization does not have serious effects on the queen. On the other hand, there are indications that repeated dribble may.
In our operation, we don’t notice any effect on queens from spring treatment of nucs, or from one-time fall treatment of colonies with dribble (but we haven’t run controlled trials to compare rates of winter queen failure).
My GUESS is that repeated exposure to HIGH concentrations of OA likely is stressful to queens (for example, when applying vapor at 5-day intervals to obtain good efficacy in colonies with brood). Worker turnover in colonies is rapid in summer, so adverse effects on workers from cumulative exposure may not be as noticeable as with queens. Colonies thrive during warm weather under chronic exposure via OA/glycerin, but a beekeeper in Chile says that use during damp winter weather can result in wing burn off in queens.
Take home–we don’t yet know enough to give a definitive answer.
Update 16 June 2016
I recently received an email from a Northeastern beekeeper, Erik Donley, about his experience with applying oxalic vapor to newly-hived package bees. Excerpts follow:
* I installed 10 x 3LB packages (from OHB) in single deep hives. (April 17th) All but one hive had fully drawn out comb. (The 1 was starting with 1 drawn comb and 9 bare foundations)
* On the 8th day after installation I administered the OA treatment. I vaporized approx .75g (between 1/4 and 1/8 teaspoon) of OA into each single deep hive. (I felt that was a reasonable dose given a full 2 deep hive takes roughy 2g)
* I checked the hives 4 days after and everything seemed fine. All continued to have laying queens with solid brood patterns, there were no issues with absconding, or mutiny vs the queen.
* Since installation, the hives have moved to multiple locations across Northern Minnesota and Wisconsin and have been exposed to a variety of difficult weather conditions. (We had snow and freezing temperatures in late May). Thus the robustness of each hive has been slightly weather dependent, but it appears so far they are not populated with Mites.
Erik is planning to follow up with late summer caging of the queen, followed by another formic vaporization–I will post his results. Note: keep in mind that repeating treatments without rotation, will tend to breed for resistant mites. Better to rotate treatments (such as with thymol). Erik questioned me on this:
A reference from X said that due to the mode of action of OA, it is impossible for mites to gain resistance to it.
The above is a good example of someone talking out of their [hat]. No one even knows for sure what the mode of action of OA is against varroa, nor how it is absorbed. And no matter, I can assure you that some mites will be more resistant than others, which implies that some degree of resistance is possible. Remember, there is only a small margin of safety between the dose that kills mites, and the dose that kills bees. That means that varroa only needs to develop a slight degree of resistance until OA is as toxic to the bees as it is to the mites. Rotate treatments!
My friend Rob Stone (Pierce Beekeeping) recently treated treated a number of packages of bees for sale by spraying a total of 30mL of “weak” solution divided over the four sides of the package cages, and was happy with the results.
Original post
Following the lead of many other countries, EPA has finally approved its legal use for control of varroa. My sons and I have been using oxalic dribble for 15 years with great success. We really like the dribble method due to its low cost, ease of use, safety to the applicator, minimal adverse effects to the colony, and its high efficacy against varroa if applied correctly. Here are some tips:
Application
The typical dosage of oxalic dribble is 5 mL (1 tsp) per “seam” of bees between the frames. Solution spilled on the top bars doesn’t count. I suggest applying it carefully in order to best distribute it throughout the hive.
Although some researchers caution about applying more than 50 mL per colony, we routinely treat every seam of bees, even if it takes close to 100 mL total (we may get away with this because our broodless period in the California foothills is very short).
For application to only a few hives, use a teaspoon or 60 mL syringe (from any feed store).
Dribble being applied with a 60 mL syringe.
For commercial use, we use a garden sprayer set to a gentle stream, calibrated by the use of a graduated cylinder, to dispense 5 mL per second (1 seam of bees per second, less than 20 seconds per hive).
Calibrating the output of the stream to 5 mL per second. Tip: maintain a large reservoir of air above the liquid–this will reduce the amount of fluctuation in the flow. With practice, it is easy to eyeball the correct stream.
In fall, we treat the bees in both brood chambers. If the cluster is mainly in the lower box, we tip the upper box back and apply the oxalic from below. If the cluster is mainly in the upper box, we take off the lid and dribble each box from above.
I’m applying the fall treatment while Eric tips back the upper box. We often work in three’s, with two cracking and one squirting.
Treatment windows
You’ll get the highest efficacy against varroa if oxalic dribble is applied when there is no sealed brood present. This opportunity occurs as a result of natural or induced brood breaks.
In temperate regions, natural brood breaks typically occur in November through early December.
Alternatively, you can induce a brood break by making shook swarms, or by caging the queen for 14 days, as shown below.
By caging the queen for 14 days, you can create a 2-day window in which there is no sealed brood in which varroa can hide. Note that this window occurs starting about 6 days after you release the queen.
Package bees:Aliano and Ellis, in their very well done preliminary investigation into treating package bees with oxalic, found that the spray application of 3 mL of 2.8% (w:w) of oxalic acid in sugar syrup per 1000 bees resulted in very high varroa kill, with minimal bee kill. Since there are roughly 3500 bees per lb, that works out to:
21 mL of 2.8% OA syrup per 2-lb package,
31.5 mL per 3-lb package, or
42 mL per 4-lb package.
The 2.8% solution is roughly the same as the “weak” formula at Treatment Table. The authors note, however, that their results were preliminary, and I haven’t seen any follow-up research. If you do treat some packages, please let me know the results!
Alternatively, although you could directly treat bees in a package, I’d suggest installing them normally, and then treating them in the hive between Days 5 and 7 after installation. The timing is due to the fact that even if the queen starts laying eggs the day after installation, it wouldn’t be until Day 9 that the first brood would be of suitable age for mite invasion. Oxalic dribble kills mites for roughly 3 days after application. Thus, if you dribble the recently-installed package on Day 6, the full effect of the treatment will have taken place prior to the first opportunity for the mites to hide in the brood.
You can also use this method with shook swarms, or for any divide made without brood.
Nucs: Starting nucs with queen cells in spring presents a great opportunity for controlling varroa by dribbling on Day 19. We’ve now used this method on thousands of nucs, and really like it for getting a “clean start” each spring.
Figure 1. The theory behind the early treatment of nucs—it’s all about timing! There is a brief window of opportunity from Day 19 to Day 21 after make up in which every mite in the nuc is forced out of the safety of the sealed brood. A short-term treatment applied at that precise time could result in a very effective kill of the now-exposed mites!
An even simpler method is to make “walkaway splits”–that is, splitting a hive (into two or more splits) and allowing the queenless split to raise a new queen (although I do not particularly recommend this method, since it depends upon the splits raising emergency queens, plus the splits go without any new brood production for at least 24 days, during which laying workers may develop). The key is to make up the split containing the old queen without any sealed brood (so that all the mites are exposed to treatment). Leave this split on the parent stand to pick up the field force. Into the other (queenless) split(s), place all the sealed brood (any open brood is also fine), along with most of the bees (since all the field bees will fly back to the parent stand). Treat the split with the old queen on the day you make the split(s). Treat the queenless splits on any day from Day 21 through Day 30.
Summer treatment
Oxalic dribble is not as effective when colonies contain brood (as during spring or summer), but colonies at that time do appear to tolerate stronger or repeated doses due to the rapid turnover of the adult population at that time of year.
I don’t have data on efficacy, but I’ve treated colonies once a week for three consecutive weeks in late summer without noticing adverse effects (although we prefer thymol or formic acid at that time of year).
Use common sense when handling oxalic acid crystals. Wear glasses in case of a mishap—you don’t want to get it into your eyes! Wear latex or nitrile gloves to remind you not to rub your eyes.
Weigh the oxalic acid crystals carefully–they cannot be accurately measured by volume (such as by teaspoon measurement).
Note: The wood bleach shown above is not approved for use in bee hives. The only forms of oxalic acid approved for application as a miticide are those registered with the EPA. It is not legal to apply any OA that does not have a label approving it for application for control of varroa.
Oxalic acid is a relatively strong acid, and is more dangerous to handle than lemon juice or vinegar. You should wear the recommended protective clothing, gloves, and eye protection.
Based upon my extensive experience with handling OA, wearing safety glasses is the most important, since you definitely don’t want to get it into your eyes!
The label is the law. That said, I find the recommended glove thickness to be excessive. I’ve found that it’s not big deal when I’ve gotten either the crystals or solution on my skin for a few minutes, and that it can be easily washed off with water. We always keep a jug of neutralizing solution on hand — 10 heaping tablespoons of baking soda dissolved in a gallon of water (the necessary concentration experimentally determined by me). This solution will immediately neutralize any OA (or formic acid) on your skin, protective gear, hive tool, and smoker.
I do not recommend this, but if I suspect that there is some oxalic syrup on my skin after washing up, I taste my skin with my tongue (OA solution tastes like strong lemonade) just to be sure. This may seem foolhardy, but I can get a dose of up to a full gram of OA in a serving of spinach.
If your water is hard (contains calcium), use distilled water instead (calcium will cause some of the oxalic acid to precipitate as white calcium oxalate).
We prefer to first completely dissolve the crystals in hot water, and then add the sugar.
Oxalic acid in a sugar solution will eventually form HMF [[a]], which is somewhat toxic to bees. It’s unlikely that enough will be formed under normal use to harm the bees, but you should not use a solution that has begun to turn brown. Oxalic syrup can be stored for many months if kept refrigerated [[b]].
[a] Hydroxymethylfurfural, non toxic to humans; commonly found in cooked jams and jellies.
[b] Prandin, L, et al (2001) A scientific note on long-term stability of a home-made oxalic acid water sugar solution for controlling varroosis. Apidologie 32: 451–452. Open access.
Seasonal demographics of a colony headed by a vigorous young queen, shed wintered in Manitoba. Each band of color represents the proportion of bees in each 12-day age class at any time point. Red (0-12 days of age) through green (61-72 days) age cohorts represent short-lived “summer bees,” which rarely live longer than two months. The blue and violet age classes are the long-lived “winter” (diutinus) bees that hold down the fort when there is no incoming pollen (and thus little recruitment). The dotted line represents the number of cells of brood. The numbers along the x axis represent the average age of all bees in the hive at any time point.
I recently had the pleasure of meeting Idaho beekeeper Randy Geile, who has come up with a clever home-built modification of Langstroth hives that allows those who are wheelchair bound to practice beekeeping. View his video here.
Beekeepers are known for being of curious and experimental minds. Since factors affecting beekeeping are continually changing, new unanswered questions are bound to arise; the beekeeper “citizen scientist” can often answer them himself by performing a well-designed experiment, and then share those results to the benefit of everyone. But for the results of any experiment to be meaningful, it is important that the experiment follow certain scientific principles. I’ve written up a sheet of tips for the citizen scientist. You can download it at:
I’ve also put together a Powerpoint presentation on “how to do” bee research (for both beekeepers and academics). I’ve posted the slides, without my voice over (the presentation takes an hour and a half), at:
For grad students and other researchers, as well as interested beekeepers, I’ve also put together a list (Word doc) of applied research questions that are screaming for someone to answer!
Sorry for the low resolution of this snip of this Powerpoint slide that I created for a presentation. I’ve color coded the ellipses and arrows. Red is the pesticide active ingredient. Blue is the initial mode of exposure. Orange are the ages/temporal tasks of the bees involved. Green are the contaminated foods or combs.
Note how colony organization is set up to avoid exposing the queen and brood to toxins (whether natural or manmade). Note the special case (the pollen hogs at the lower right) in which newly emerged workers and drones get killed by planting dust.
In my area, our apiaries need to be protected from black bears. Over the years, I’ve developed a simple and effective electric fence design. You can download a pdf of plans and photos here: Bear Fence PDF (updated 11 June 2023).
Please don’t parrot misinformation–learn the actual facts!
Introduction
“GMOs” are a hot topic these days, due mainly to the media attention given to a few advocacy groups, as opposed to those who actually understand the science involved in the development of genetically-modified plants. I find this unfortunate, since the future of many species on this planet depends upon whether our expanding human population continues to convert critical wildlife habitat into farmland, and additionally whether the agricultural practices on that land include water diversion, the addition of fossil-fuel-generated nitrates, and the use of synthetic pesticides.
The main cause of the extinction of species is habitat conversion. The only realistic way to arrest such conversion is to grow food and fiber more efficiently on existing farmland. One tool for doing so is the genetic engineering of domesticated plants. Genetic engineering, coupled with conventional plant breeding, holds the promise of providing us with plants that are more drought resistant, that use less synthetic fertilizer, are more resistant to diseases, that require fewer pesticides, are more productive per acre, and that provide more nutrients (such as vitamins and omega-3 fatty acids).
As with any technology, we must thoroughly investigate and regulate any negative environmental consequences. Unfortunately, the shrill fear mongering by certain anti-GMO advocates has dominated public sentiment. I’m putting together this page to expose the reader to the other side of the story. I’ve compiled a few good reads for those who want to approach the subject with an open mind, and learn the actual facts of the matter.
Of note, there is a growing body of environmentalists (myself included) who are looking at the Big Picture, and calling for a halt in the demonization of GMOs. Some of them, such as Mark Lynas, have been brave enough to publicly admit that they have changed their minds on the subject. Another environmentalist whom I admire is one of the original founders of Greenpeace itself, Dr. Patrick Moore. Greenpeace (whose activism I normally support) has taken the lead in trying to stop the planting of genetically engineered crops in Third World countries. Dr. Moore has broken with Greenpeace and now campaigns to help save millions of children from blindness and disease with the introduction of genetically engineered Golden Rice Allow Golden Rice.
These scientists bring forth the point that activists from wealthy countries, by demonizing genetically engineered crops, are causing great harm to the poor, and contributing to greater environmental damage The Cost of Delaying Approval of Golden Rice.
Suggested reading
Update Sept 2014: Two UC Davis scientists did some “ground truthing” on GMOs by reviewing the data on the largest consumers of GM crops–U.S. livestock. My thinking is that if GE food had any negative effects on health, we would certainly see it in the billions of animals raised on diets consisting of GE corn, soy, and sugar beet.
The bottom line is that, contrary to the claims of some activists, livestock productivity and health appears to have consistently improved concurrent with the adoption of GE feedstocks. Some snips from the paper:
Numerous experimental studies have consistently revealed that the performance and health of GE-fed animals are comparable with those fed isogenic non-GE crop lines. UnitedStates animal agriculture produces over 9 billion food producing animals annually, and more than 95% of these animals consume feed containing GE ingredients.
These field data sets, representing over 100billion animals following the introduction of GE crops,did not reveal unfavorable or perturbed trends in livestockhealth and productivity. No study has revealed anydifferences in the nutritional profile of animal productsderived from GE-fed animals. Because DNA and proteinare normal components of the diet that are digested, thereare no detectable or reliably quantifiable traces of GEcomponents in milk, meat, and eggs following consumption of GE feed.
And then there’s the claim that GMO crops are devastating to poor farmers in India. A recent study by an independent German team puts the lie to that notion. They concluded that:
Bt cotton adoption has caused sizeable socioeconomic benefits for smallholder farm households in India. The technology has increased cotton yields and profits by 24% and 50%, respectively… Countrywide, this technology is now used on 90% of the cotton area. On average, household living standard increased by 18% among Bt adopters. Most of these adopting households are relatively poor. Hence, Bt cotton contributes to positive economic and social development.
Ottoline Leyser, in a recent article in PLoS, points out common misconceptions about the genetic engineering of crops and calls for us to avoid the conflation of unrelated issues: read article.
****
“The world is a broken place,” says Laurie Zolth, professor of bioethics at Northwestern University. She says our responsibility, and obligation, is to fix it. The key is to create a transparent framework that allows scientific experimentation to flourish—one that both governmental regulators and nongovernmental organizations can use to pursue projects that are good and sustainable and just, she says.
We must not only focus on the solutions to problems, but also stay very aware of ethical considerations, as well as any direct, indirect, or possible consequences of unforeseen effects.
Drew Endy, assistant professor of bioengineering at Stanford University, imagines a world in which “humanity figures out how to reinvent the manufacturing of the things we need, so that we can do it in partnership with nature. Not to replace nature, but to dance better with it.”
From Draxler, B (2013) Synthetic Biology: Life as we grow it. Discover Oct 2013 47-52.
Another useful website is one by Jon Entine. I’ll be the first to state that Jon’s writing seems to be more about objectively defending agribusiness practices rather than in criticizing them. But his accurate writing is a good balance to the fear mongering by the anti’s: http://www.geneticliteracyproject.org
Every day over a thousand children go blind; each year over a million children die; and every decade the numbers stack higher — all due to vitamin A deficiency.
The solution, according to Greenpeace and others, is an increase in vitamin A supplements and capsules — dispensed through programs that cost tens of millions or are impractical for the world’s poor. And yet, despite the deaths of millions of children, a solution, in the form of GM golden rice, waits at the doorstep of impoverished nations across Asia and Africa.
Syngenta’s role is often cited by critics as a clear sign that poor rice farmers will be lured in by golden rice promises and then fall victim to the greed of the biotech industry, but the claims don’t hold up to scrutiny. Peter Singer, professor of bioethics at Princeton University, writing at Project Syndicate: “… the company has stated that it is not planning to commercialize it. Low-income farmers will own their seeds and be able to retain seed from their harvests. Indeed, Syngenta has given the right to sublicense the rice to a nonprofit organization called the Golden Rice Humanitarian Board. The board, which includes the two co-inventors, has the right to provide the rice to public research institutions and low-income farmers in developing countries for humanitarian use, as long as it does not charge more for it than the price for ordinary rice seeds.
“The irony is that glyphosate-resistant crops are grown commercially on millions of hectares of land, whereas golden rice (which has not been shown to pose any risk at all to human health of the environment) still cannot be released.”
/
Brian Hanley, writing at International Policy Digest, brooks no tolerance for Greenpeace’s tactics: “With Greenpeace activists screaming to poor farmers that golden rice will kill their children, it’s going to be a long, tough slog for golden rice. However, I think this is going to backfire on Greenpeace and other NGO’s. Organizations like Greenpeace that misrepresent the facts while claiming righteousness are not exactly earning accolades. Greenpeace has put itself in that position with this campaign against golden rice. Greenpeace abused the IRB process in order to stop ongoing harm (blindness, disfigurement, death from disease) from being treated. Greenpeace’s Western born activists are terribly disconnected from the deadly harm that vitamin A deficiency does to the poor. It is not just obvious symptoms of extreme deficiency. Childhood diseases take far more lives when vitamin A is low.”
Golden rice opponents choose their own version of science and want to block genuine sustenance from reaching millions of people in the most remote corners of the planet, but history will prove them wrong. Professor Singer sums it up well: “In some environmental circles, blanket opposition to GMOs is like taking a loyalty oath – dissidents are regarded as traitors in league with the evil biotech industry. It is time to move beyond such a narrowly ideological stance. Some GMOs may have a useful role to play in public health, and others in fighting the challenge of growing food in an era of climate change. We should consider the merits of each genetically modified plant on a case-by-case basis.”
The backstory provides an intriguing look at how the anti-GMO industry and sycophant journalists work—and the consequences of flogging single studies to score ideological points.”
In the last installment of this article I explored the limiting factors of the honey bee realized niche prior to the influence of humans. So let’s now look at how the populating of Europe by modern humans affected the honey bee.
Setting The Stage: The Origins Of The Players
Let’s first set the stage. The time frame of interest runs from about 10,000 years ago through about 400 years ago. This period spans the time from the last “ice age” (technically, the glacial period; during which it was too cold for bees to inhabit the area), covers the invasion and colonization of the warming continent by both bees and modern humans, and ends with when humans started transporting the honey bee across oceans.
Apis mellifera
The honey bee evolved long prior to the time frame of interest. Recent research [1] suggests that the genus Apis originally developed in Europe, and then spread into Asia (where it evolved into several different species), into North America (where it later went extinct), and into Africa (via Spain/Morocco). It was in Africa that the species Apis mellifera evolved, and then later migrated back into Europe and the Middle East, branching in various ecological habitats (realized niches) into locally-adapted subspecies.
Then came a prolonged Ice Age, during which there were periods of cold and dry glaciation interspersed by periods of warming (as we are currently enjoying). During the cold periods, ice covered northern Europe, and honey bees were forced to follow suitable habitat southward, retreating into warmer “refugia.” During the warm (and wetter) periods, ice retreated and Europe could temporarily revegetate, allowing honey bees to expand their ranges back again northward. The current races of bees in Europe recolonized the region from such refugia as the climate warmed about 10,000 years ago [2]. I’ve shown the distribution of the named races (subspecies) of Apis mellifera in the map below (Fig. 1). The satellite image shows the differences in climate and vegetation in the various regions. Of note is that the first “keeping” of bees appears to have begun in the Fertile Crescent of the Middle East with A. m. jemenitica and syriaca.
Figure 1. Subspecies of Apis mellifera in Europe and the Mediterranean region. Our domesticated stocks in the U.S. primarily derive from the temperate-adapted ligustica (Italian), carnica (Carniolan), and perhaps caucasica. The feral population of bees in the U.S. also contains the mellifera (German dark) lineage [[i]]. Map by the author; satellite image from Google Earth; subspecies distribution from various sources [[ii]].
[ii] The classification of these races is rather arbitrary, and under debate by taxonomists, but gives a general idea. There are also discrete breeding populations within each of the subspecies. See:
Radloff, SE, and HR Hepburn (1998) The matter of sampling distance and confidence levels in the subspecific classification of honeybees, Apis mellifera L. Apidologie 29: 491-501. Open access.
Al-Ghamdi, AA, et al (2013) Geographical distribution and population variation of Apis mellifera jemenitica Ruttner. Journal of Apicultural Research 52(3): 124-133. Open access.
Practical application: each subspecies of honey bee is adapted to a specific habitat and climate. The “best” bee for any region is that which has already undergone countless generations of adaptation. Although the Italian bee is very popular among many beekeepers, it is certainly not the best adapted bee for non Mediterranean [5] conditions.
Homo sapiens
At the end of the last glacial period, modern humans also moved up into Europe from Africa, displacing the cold-adapted Neanderthals (as did the bees, modern humans also evolved into different races in the region). These hunter-gatherer human populations were at first not dense enough to exert an appreciable impact on the honey bee. This changed with the advent of pastoralism and agriculture—initially slash and burn, then later improved by the invention of the plow. The adoption of agricultural practices facilitated the niche of Homo sapiens—by greatly increasing the carrying capacity of the habitat (mainly by the farming of grain)–thus allowing the human population to begin its exponential growth (to be later limited by epidemics of infectious diseases).
Practical application: as we shall see, the factors of migration, locally-adapted races, displacement of existing populations, the farming of grain, and epidemics of infectious diseases will greatly affect the honey bee over the ensuing years.
Early Changes In The Honey Bee Niche Due To Humans
O.K., now that I’ve set the stage, let’s take a look at how the early expansion of humanity into the native range of the honey bee affected the limiting factors of the bee’s niche (I will cover more recent impacts later). Allow me to address each of the limiting factors that I’ve previously covered, in turn.
Limiting factor: The weather
Weather is the day-to-day expression of climate. For hundreds of thousands of years, the climate of Europe oscillated between periods of cold/dry and warmer/wetter, which of course greatly affected the local weather. The fundamental niche of the honey bee is limited by cold and prolonged winters, by extreme summer heat, and by lack of water and nectar-producing plants (especially forbs—herbaceous flowering plants other than grasses). For thousands of years at a time, parts of Europe simply did not provide conditions that met the requirements of the bees’ fundamental niche, causing the extirpation of local populations or entire species. Keep in mind that any species has “edges” to its range, past which the species is stressed, or cannot successfully live. Slight changes in weather at the edges can temporarily make that habitat unsuitable for bee survival.
Practical application: for example, cold, wet summers in England may not allow bees to store enough honey to make it through the winter. Ditto for drought-prone California. And an unusually severe northern winter will challenge colonies of Italian bees.
We humans have little ability, other than by fervent rain dancing, of changing tomorrow’s weather; however, we do have the ability to change the climate on a local basis, and likely even at the global scale. Climate then may affect the weather.
The burgeoning human population in Europe and the Mediterranean started grazing herds of domesticated mammals and cutting down the forests [6]. This loss of the shading forest cover likely resulted in the warming of central Europe, and the desertification of the Mediterranean region [7]. Such deforestation likely favored bees in central Europe (due to creating better conditions for forbs), but created drier (and less favorable) microclimates in the Mediterranean.
The Human Deforestation Of Europe
Let’s look at the vegetation of Europe at the beginning of this period of time (Fig. 2):
Figure 2. The vegetation of Europe around 4,500 years ago, just before the main agricultural and deforestation phase by humanity in the region [[i]].
Note the extensive forest cover in the natural range of the honey bee in Europe and the Mediterranean at this time in geological history. Not shown is the range of the honey bee in the moister areas of the Middle East and northern Africa, which were also densely forested. Adams [9], by reviewing data on fossils of pollen, tracked the destruction of these forests by humans over the course of a few thousand years (accelerated about 3000 years ago by the invention of the iron axe and saw). The deforestation of the habitat brought about major changes in two limiting factors of the niche of the honey bee—the abundance of forage, and the availability of nest cavities.
Limiting factor: Carrying capacity of the habitat
Although some trees provide pollen in the spring, and a few, nectar, dense forest is not prime honey bee habitat, since the tree canopy shades out flowering low-growing forbs and shrubs. It was only in natural meadows and openings of such forest that there would have been suitable forage for bees over most of the season. However, such ancient trees would have furnished abundant nest cavities.
When humans invaded those areas, they practiced slash and burn agriculture, clearing the forests for pasture or crops, or cutting trees for structures, monuments, shipbuilding, or charcoal. These forests were largely devastated by the end of the Roman Empire. Although we abhor such devastation of virgin forests today, it was likely of benefit to the honey bee, as it allowed sunlight to hit the ground, favoring the growth of bee-friendly forage plants in the pastures and cropland (remember, herbicides had not yet been invented) (Fig. 3).
Figure 3. When I’m asked to give presentations to local groups interested in gardening for the benefit of pollinators, I like to open with this slide to illustrate a point–that by cutting down pine trees (which are of no value to honey bees), one allows sunlight to hit the understory of flowering plants. Since we have suppressed natural wildfires in California, formerly open land is being reclaimed by dense pine and oak forests. Such change has been detailed for my county at [[i]].
[i] Walker, PA, et al (2003) Landscape changes in Nevada County reflect social and ecological transitions. California Agriculture 57(4): 115-121.v
Thus, by clearing the forests (by approximately 75% in central Europe), humans improved (facilitated) one aspect of the realized niche of the honey bee, since such clearing favored the growth of a greater abundance of forage plants. But there was a flip side to this.
Limiting factor: Predation
Humans (by virtue of possessing a sweet tooth, climbing ability, and wood-cutting tools) are a formidable predator of the bee. This may well be one of the reasons that the Savannah Bee (Apis mellifera scutellata) so fiercely protect their nests (their long exposure to human predation would have selected for those colonies which were able to successfully deter human honey hunters).
Hunter-gatherers do not waste energy on hunting prey that does not give a positive return on investment. It takes a considerable investment in energy, pain, and risk of life and limb to harvest the combs from a small-entranced cavity high in a hollow tree (this may be one reason that European bees prefer to nest high in trees [11]. It was only once humans had their bellies full of grain that they had the luxury of satisfying their sweet tooth by making serious efforts to attack well-defended colonies high above ground.
As the human population became more dense, the pressure of predation on the honey bee would have increased greatly, favoring the survival of bees that possessed three traits—cryptic and inaccessible nesting, vigorous defense of that nest, and frequent swarming so that colony reproduction was greater than the loss due to human predation.
Limiting factor: Nesting cavities
The clearing of ancient forests affected another parameter of the honey bee niche. The falling of each hollow bee tree eliminated one available nest cavity. As hollow trees became rarer and rarer (and tended to remain rare in regrown managed forests), there would have been fewer and fewer places for honey bees to nest. The few remaining “bee trees” would have been targeted by honey hunters, who, with the use of steel axes and saws found it easier to simply fall a tree than to climb it. Each of these destructive predations by humans eliminated yet another increasingly rare nest cavity.
So by this time point in history, two major factors of the realized niche of honey bee had been altered by humans—there would have been more herbaceous and shrub forage available, but fewer nest sites. And such change created opportunity for humans to adapt from being honey hunters to honey farmers.
Adaptation And Change In Business
On two occasions in recent years, speakers [12] have suggested at conferences that those of us in the bee business read the motivational booklet Who Moved My Cheese? [13]. I recently did so. It’s a cute little parable that can be read in minutes, but summarizes important lessons in recognizing business opportunities and adapting to changes in business niches. Two of these lessons are to:
Anticipate and Monitor Change, and then
Adapt To Change Quickly
Like it or not, things change. Niches, whether ecological or in business, change continually. Those who adapt may enjoy success; those who don’t, go extinct. Both the honey bee and their keepers have learned to exploit various realized niches, and those niches change over the years. As I mentioned before, both bees and humans are highly adaptive species. Honey bees adapt by the process of genetic (and epigenetic) trial and error that we call evolution. Human beekeepers, generally blessed with larger brains, have the capacity to recognize upcoming changes in their niche, and the associated pitfalls and business opportunities.
However, human nature is such that many will waste their time lamenting about how difficult or impossible change is, rather than quickly adapting. On the other hand, those who are innovative and cognizant of business opportunities consistently make money.
Let me state emphatically that I do not consider myself to be any sort of great beekeeper or business guru. But what I have noticed over the years are inherent differences in the business attitudes of those beekeepers who always seem to be complaining, compared to those who are able to afford shiny new trucks. Throughout this article I will return to adaptations in the business of keeping bees made by successful beekeepers. So let’s return to the change in the niche of traditional honey hunters in the homeland of the European honey bee.
The Creation Of A Niche For Bee-keeping
Honey hunters would have put themselves out of business once they cut down all the hollow trees. That situation created a novel business opportunity, since there would now exist an insufficient number of natural nest sites for the number of colonies that could be supported by the local forage. All that a human entrepreneur needed to do would be to facilitatethe bees’ realized ecological niche by supplying them with what had now become the major limiting factor—the lack of suitable nest cavities. And voilà, as the business niche of honey hunting dwindled, those skilled at plundering bee trees could adapt to become…bee-keepers! This supplying of nest cavities would have been especially successful in the Fertile Crescent once it lost its forests, and would also have allowed bee-keepers to expand the honey bee’s range into arid areas naturally lacking trees or rock cavities.
This beekeeper in Yemen supplies his bees with nest cavities in a landscape lacking such naturally. Honey from Yemen fetches a high price—over $100 per pound by mail order [[i]]. The growing popularity of beekeeping in Yemen today suggests that the beekeepers there may soon reach the carrying capacity of the land [[ii]]. Photo by Gillian Duncan [[iii]].
The honey bee, when kept as livestock, exhibited a trait that made them highly desirable to peasant farmers—a colony’s ability to exploit floral resources over an area of at least 30 square miles (80 km2) [17]. This trait meant that the bee-keeper could exploit the production from land which he did not own (as beekeepers typically continue to do to this day).
Practical application: early “beekeepers” needed only to provide artificial nest cavities in areas where natural cavities had become scarce. The bees otherwise took care of themselves—foraging far and wide, and voluntarily returning home with the goods.
The practice of bee-keeping appears to have began in the Middle East, and then spread to other regions [18]. Early beekeepers, depending upon materials at hand, created all sorts of nest cavities (hives), such as horizontal or vertical hollow logs, clay pots or tubes, or straw skeps [19]. Horizontal hives were the norm in desert and Mediterranean climes; log gums, vertical hives, and skeps were often used in northerly (cold winter) regions. Once humans controlled the nest sites of the honey bee, thus began…
The Domestication Of The Honey Bee
Domestication: adaptation to intimate association with human beings.
Primitive beekeeping was not much different from predatory honey hunting, other than the hunters providing homes for their eventual prey within which to store the precious honey. So long as early bee-keepers practiced destructive harvesting (killing the colony in order to consume both brood and honey combs), little selective breeding would likely take place, due to the temptation to harvest the the most productive hives.
Clever beekeepers in the Mediterranean region (especially in the clay-rich Fertile Crescent) got around this problem by using horizontal clay tubes as hives, with the entrances to the front, and a removable plug in the back. Since bees tend to store honey away from the entrance, these beekeepers could harvest honey from the rear with a minimum of stinging by smoking the bees off the honey combs, without disturbing the broodnest. What a concept! Instead of killing the colony, one could “milk” it. (These tube hives were especially amenable to this practice, prior to the invention of movable frame hives. However, nondestructive harvest methods were also invented by “forest” and skep beekeepers [20] in northern regions).
The next thing they learned was how to propagate new colonies by transferring combs of brood and scoops of bees to new hives. They even learned how to transfer queen cells and virgin queens.
Practical application: this control of the queens meant that these beekeepers could then practice selective breeding, the foundation of the process of domesticating a species. I’m surprised by how few modern day beekeepers in this country selectively breed their own locally-adapted stock (since these “primitive” beekeepers were doing it 3000 years ago!).
Domestication is a sort of symbiotic mutualism, in which both the humans and the selected animals benefit. Beekeepers would certainly select for propagation those colonies that were most productive and amenable to being worked. Milner [21] explains:
The gentle behaviour of the major races of honey bee may be due, of course, to selection for this quality over many generations; even the “skep” beekeepers of former days would, no doubt, tend to destroy the worst tempered bees and retain the gentler colonies.
Not only would beekeepers select from local stock, but even import more desirable stock. Three thousand years ago, in the ancient city of Tel Rehov in Israel, commercial beekeeping was practiced [22] using a gentle, productive strain of bees imported from Turkey!
Limiting factor: Competition for food
Let’s suppose that beekeepers have now increased the available supply of skeps, gums, or Langstroth hives until the bee population is no longer limited by the number of nesting sites, but by something else? And now we get to the meat of the issue—competition for food resources. There is a limit to the number of colonies of bees that any area, no matter how rich in flowering plants, can support. That limit is called the carrying capacity of the landscape, and is commonly used to calculate how many livestock a pasture can support.
Beekeepers in my neck of the woods would no more brag about how much honey they made in a particular location than would a fisherman brag about the location of his favorite fishing hole. Should one do so, he’d likely find hundreds of new hives sitting on top of him the next season. This would be a perfect example of Garret Hardin’s influential concept of The Tragedy of the Commons [23], in which he points out that it may be to the individual herder’s benefit to add yet one more head of livestock to the common pasture, but to the herder community’s detriment once the addition of another animal exceeds the carrying capacity of the land (beekeepers today in some jurisdictions have wisely (and self-protectively) mitigated this inherent and inevitable problem by limiting commercial apiaries to registered locations, typically no closer than two miles apart) (Fig. 4).
Figure 4. The Tragedy of the Commons exemplified. Locations of registered apiaries (blue dots) in North Dakota [[i]]. I added a 2½-mile-radius red circle in the center to indicate the area covered by the typical foraging range of a colony. Clearly, the forage areas of many of these locations overlap.
And what sort of carrying capacities will various landscape types support? Studies have found natural colony densities of from 1–25 per square mile (the lesser density typical in temperate forests; the higher density in tropical areas, esp. with Africanized bees) [25]. Beekeepers of managed hives generally limit their apiary sizes so as not to exceed the carrying capacity of the land to produce a surplus honey crop.
Practical application: for example, in good forage areas of Montana and the Dakotas, beekeepers try to keep commercial apiaries a minimum of 2 miles apart. If such apiaries were placed on a 2-mi grid, that would allow 4 sq. mi. of forage area per apiary. Even at a high stocking rate of 48 hives per apiary, the stocking density would be only 12 managed hives per sq. mi. (6/mi2 at 24 hives per yard).
How does the density of managed hives in the European bee’s native range compare? Eva Crane cites records of hive density in Hungary in the late 1700’s of 30 to 460 per square mile! In the European Union today, in which beekeepers in some areas are complaining of poor colony performance, there are some 15 million reported managed hives, which works out to nearly 9 hives per square mile (perhaps exceeding the natural carrying capacity of the land).
By comparison, in the U.S. (which contains roughly the same percentage of arable land) the average density is only about 1 hive per square mile. Of course, average density over a continent does not reflect the actual hive loading of any particular area. Especially in the U.S., hives tend to be moved around, as opposed to the often stationary apiaries in Europe, and during summer, over half of all hives are located in only six states, accounting for only 16% of the U.S. land mass. However, even in those six states, the density of hives only starts to approach that of Europe as a whole!
Practical application: The Tragedy of the Commons definitely applies to beekeeping, since bees can’t be fenced in. I was driven out of a very good area in Nevada by beekeepers who moved in thousands of hives to the extent that I could hit another apiary with a thrown stone from any of my long-time locations. California has also reached that point in many areas, as beekeepers step on each others’ toes looking for any favorable place to place hives.
When I hear of all the bee problems in Europe, I wonder as to how much beekeepers there have contributed to the problem by overstocking hives on the available pasture. I’ll return later to the impact of modern agricultural practices upon the carrying capacity of agricultural land for bees.
Limiting factor: Reproductive success rate
In the absence of natural nest cavities, the survival of the honey bee depended in many areas upon the provision of such nest sites by humans, in the form of some sort of managed “hives.” And that fact gave beekeepers control over the reproductive success of any particular colony. By choosing which colonies were allowed to reproduce, beekeepers would rather quickly have been able to domesticate the bee by providing nest cavities only to those most amendable to husbandry. It would only have been in the scattered relict forests that wild, unmanaged populations of bees would have been able to survive. And this finally brings us to what I suspect is a major factor negatively affecting honey bees today:
The Price Of Domestication
Are honey bees truly a domesticated animal? And if so, how has that favored or hurt them? I’m out of space for now, but it gets more interesting…
A Note And Acknowledgements
Although I’ve spent considerable time in researching this article, my interpretation of the evidence is largely speculative. If anyone can add to this subject, please let me know.
As always, I am greatly indebted to my colleague Peter Borst, without whose research assistance I could not write these articles. And I cannot express how much I grateful I am for the words of appreciation from beekeepers worldwide, as well as their donations that support my research, writing, and website maintenance.
Citations and Footnotes
1 Ulrich Kotthoff, U, et al (2013) Greater past disparity and diversity hints at ancient migrations of European honey bee lineages into Africa and Asia. Journal of Biogeography 40: 1832–1838. Open access.
2 Adams, J (n.d.) Europe during the last 150,000 years. http://www.esd.ornl.gov/projects/qen/nercEUROPE.htmlThis is a fascinating compilation of information and maps on the changes in climate and vegetation of Europe over time.
Ruttner, F (1988)Biogeography and taxonomy of honeybees. Springer-Verlag.
Miguel, I (2007) Gene flow within the M evolutionary lineage of Apis mellifera: role of the Pyrenees, isolation by distance and post-glacial re-colonization routes in the western Europe. Apidologie 38: 141–155. Open access.
Franck, P, et al (1998) The origin of West European subspecies of honeybees (Apis mellifera): New insights from microsatellite and mitochondrial data. Evolution 52(4): 1119-1134. Open access.
4 The classification of these races is rather arbitrary, and under debate by taxonomists, but gives a general idea. There are also discrete breeding populations within each of the subspecies. See:
Radloff, SE, and HR Hepburn (1998) The matter of sampling distance and confidence levels in the subspecific classification of honeybees, Apis mellifera L. Apidologie 29: 491-501. Open access.
Al-Ghamdi, AA, et al (2013) Geographical distribution and population variation of Apis mellifera jemenitica Ruttner. Journal of Apicultural Research 52(3): 124-133. Open access.
17 Beekman, M and F Ratnieks (2000) Long-range foraging by the honey-bee, Apis mellifera. Functional Ecology 14(4): 490–496.
18I’ve taken much of this historical information from Crane, Eva (1999) The World History of Beekeeping and Honey Hunting. Taylor and Francis Group.
19 I highly recommend the book The Quest for the Perfect Hive by Gene Kritsky (2010) Oxford University Press.
20 “Forest beekeeping” was practiced in Northern Europe, whereby beekeepers, would cut a recloseable door to a hollow high in a tree, allowing for repeated harvest without killing the colony.
21 Milner, A (2008) An introduction to understanding honeybees, their origins, evolution and diversity. http://www.bibba.com/origins_milner.phpThis is an excellent review of the domesticated races of the honey bee, and a well-thought plea for the breeding of locally-adapted stocks. See also:
22 Mazar, A and N Panitz-Cohen (2007) It is the land of honey: Beekeeping at Tel Rehov. Published in Near Eastern Archaeology 70(4): 202-219. Open access.
Bloch, G, et al (2010) Industrial apiculture in the Jordan Valley during Biblical times with Anatolian bees. PNAS 107(25): 11240-11244. Open access.
25 Ratnieks, FLW, et al (1991) The natural nest and nest density of the Africanized honey bee (Hymenoptera, Apidae) near Tapachula, Chiapas, Mexico. Can. Entomol. 123: 353-359.
Baum, KA, et al (2005) Spatial and Temporal Distribution and Nest Site Characteristics of Feral Honey Bee (Hymenoptera: Apidae) Colonies in a Coastal Prairie Landscape. Environmental Entomology 34(3):610-618.
Taber, S, III (1979) A population of feral honey bee colonies. Am. Bee J.ABJ 119: 842-847.
Some readers may wonder why I am spending so much time on the issue of pesticides, since to many (if not most) beekeepers, pesticides are a non issue. In answer, the main reason is that the public (and our lawmakers) are being hammered by the twin messages that the honey bee is on the verge of extinction, and that the reason is pesticides. In my writings, I’m attempting to address the validity of both of those claims. Let’s start with the first.
Reality Checks
Honey bees have clearly (and deservedly) become one of today’s most charismatic environmental poster children, and as such are a useful bioindicator that our human activities are having a negative impact upon pollinators, and wildlife in general.
But I also feel that we take care to not overstate or exaggerate our case. One of my greatest concerns is that beekeepers are allowing the media to scare the public with all the hue and cry of an impending bee-pocalypse (and that it is due to a certain type of pesticide). Our complicity in this message (as we enjoy the luxury of basking in the warmth of all the public support) may backfire on us one of these days—putting us into the position of the little boy who cried wolf. Some in the media are starting to notice that the facts don’t support the claim that bees are disappearing (Fig. 1).
Figure 1. It’s true that it’s more difficult to keep bees healthy these days, but it doesn’t look like bee-pocalypse is imminent (as evidenced by this recently-published chart). Whenever honey and pollination prices are high enough to make beekeeping profitable, resourceful beekeepers somehow manage to recover their colony losses [[i]]. Chart courtesy Shawn Regan [[ii]].
In the rest of the world, the number of managed hives has actually been increasing [3]. And as far as claims that pesticides are driving bees to extinction, Hannah Nordhaus, the author of the excellent book The Beekeeper’s Lament writes:
Reflexively blaming pesticides for all of the honey bee’s problems may in fact slow the search for solutions. Honey bees have enough to do without having to serve as our exoskeletal canaries in a coalmine. Dying bees have become symbols of environmental sin, of faceless corporations out to ransack nature. Such is the story environmental journalism tells all too often. But it’s not always the story that best helps us understand how we live in this world of nearly seven billion hungry people, or how we might square our ecological concerns and commitments with that reality. By engaging in simplistic and sometimes misleading environmental narratives — by exaggerating the stakes and brushing over the inconvenient facts that stand in the way of foregone conclusions — we do our field, and our subjects, a disservice [4].
Further reading: for a detailed and sober analysis of the factors that affect managed bee populations, I highly recommend the review by Drs. vanEngelsdorp and Meixner [5].
The reality is that it is not the honey bee that is being driven to extinction—it is instead the commercial beekeeper who is finding that his traditional business model is becoming less profitable due to today’s greater degree of colony losses and the decreasing availability of good summer forage.
The question is, to what extent are pesticides involved in those problems?
The Two Worlds Of Beekeeping
There are two very different worlds of beekeeping—small scale (hobbyists, who constitute the vast majority of beekeepers by number) and large scale (commercialized professionals, who manage the vast majority of hives), with a small continuum of sideliners bridging the gap.
Hobby beekeeping is currently enjoying a bubble of resurgence, but in the Big Picture in the U.S., hobbyists manage an insignificant number of hives. And those small-scale beekeepers tend to keep their hives close to home, largely avoiding serious exposure to pesticides. But that’s not to say that small-scale beekeepers are immune to pesticide kills; I’ve heard of several this season, and what with all the spraying for West Nile virus and the citrus psyllid, we can expect more of the same. And since there are far more small-scale beekeepers to put pressure on regulators and legislators, I feel that it is a good idea for them to be informed about pesticide issues.
Large-scale beekeepers, on the other hand, typically run migratory operations—moving their hives to almond pollination, and then to other agricultural areas (it’s problematic to keep apiaries of hundreds of hives in the suburbs). The fate of those bees (and their keepers) is largely determined by agricultural land use practices and their degree of exposure to agricultural pesticides.
It is some of those large-scale beekeepers for whom extinction is a valid concern. The reason (as with any other enterprise) is financial—they can only survive so long unless their businesses continue to be profitable [6]. In recent years, they’ve had two things going for them—sky-high honey prices and elevated pollination fees. But all is not rosy—there are reasons for those prices going up; these days it’s simply more costly to produce honey or to provide bees for pollination.
Today’s breathtakingly-high high almond rental rates typically don’t even cover operating costs—even if most of one’s colonies make it through the winter! Today’s 30% average winter loss rate is bleeding profitability from many operations. Not only does the beekeeper need to rebuild his numbers after almonds, but to stay in the black he must also make additional income from paid pollinations or a decent honey crop. And that may no longer be as easy as it used to be for various reasons:
Formerly bee-friendly farmland has been turned into agri-deserts devoid of any bee forage.
Honey producers on field crops (such as alfalfa, sunflowers, or cotton) get hammered time and again by pesticide spraying, sometimes watching whole yards of colonies dwindle or go queenless weeks afterwards.
Paid summer pollination contracts (such as for vine crops) may leave colonies in poor shape for the winter, due to the heavy stocking, the lack of nutritious pollen, and the exposure to multiple pesticides.
These days, the sad fact is that many good beekeepers are barely keeping their heads above water. So the beekeeper’s lament continues—varroa, high winter mortality, and lack of good forage are driving a number of operations into the red.
Practical application: although the “extinction of the honey bee” makes for a good rallying cry, the real concern is the possible extinction of the migratory beekeeper who supplies necessary pollination services to agriculture. So far, the almond industry has been economically propping up the bee industry, but I’m not sure how long that arrangement will be sustainable.
Pestcides And Bee-pocalypse
For some beekeepers, “bee-pocalypse” has already occurred. New York beekeeper Jim Doan, whose case I detailed in a previous article [7], sadly gave it up this year. Here is a beekeeper whose apiaries had been in the same locations for many years without noticeable pesticide problems, but who apparently suffered from devastating spray or dust kills this season and last, as evidenced by piles of fresh dead bees in front of his hives in spring.
Residue analysis of those dead bees clearly showed that they had been exposed to several pesticides, but none of the detects were at levels that would be expected to cause such carnage—so we don’t even know which pesticides or practices to point the finger at! To my scientific mind, this is very frustrating—that our “system” was not able to identify the cause of Jim’s bee kills, to change anything to keep them from recurring, nor compensate an innocent beekeeper for the loss of his livestock and livelihood.
As unlucky as Jim has been, his case is not necessarily the norm. Overall, the issue of environmental toxins is improving. In my own lifetime I’ve seen us clean up our pollution of the air and water, cease atmospheric testing of nuclear weapons, ban DDT, fluorocarbons, and PCB’s, phase out the worst pesticides, and raise the general environmental consciousness. Humans still inflict far too damaging an environmental footprint on Earth, but we are moving in the right direction, and should give ourselves some credit for that!
There is no doubt that pesticides are often involved in bee health issues, but can we blame them for all our problems? That question is best answered by considering the health of those colonies that are not exposed to pesticides:
A Comparison To Some “Control Groups”
There are plenty of beekeepers in non agricultural areas whose apiaries are not exposed to pesticides to any extent. Those hives serve as a “control group,” whose health we can compare to those colonies that do have to deal with pesticides.
For instance, in my own operation of about a thousand hives, their only exposure to pesticides is to the fungicides in the almond orchards (from which they don’t appear to suffer to any serious extent). I haven’t used synthetic miticides in over a decade, rotate my combs, and rarely feed syrup.
Yet, I’ve experienced CCD firsthand, see more queenlessness, unsuccessful supersedure, and experience somewhat higher winter losses than in the old days (meaning before varroa). I hear the same from many others in the pesticide-free control group. The simple fact is that these days it requires better husbandry to maintain productive colonies. Yet we in the “control group” can hardly blame pesticides to be the cause.
And then there are the stationary “treatment free” beekeepers in the middle of intense agriculture who suffer no higher colony loss rates than the norm, despite their apiaries being surrounded by corn and soy [8]. How the heck do we reconcile their success to the problems that the commercial guys experience in the same areas?
Do they owe their success to keeping fewer hives in a yard? To keeping locally-adapted survivor stock? To their placement within flight range of patches of undisturbed forage? To the fact that they don’t move to multiple crops? Or is it because they aren’t contaminating their combs with miticides? Believe me, if I knew the answer, I’d tell you!
As (the very successful) beekeeper Dave Mendes observes, colonies just seem to be more “fragile” these days. It’s no surprise then that the addition of toxins of any sort can help to tip a colony over. The Ericksons [9] put it this way:
Pesticides and their residues in the hive stress bees as do other factors such as weather extremes, food shortages, pests, predators, and disease. Conversely, stress induced by other factors undoubtedly has a significant impact on the level of damage that a pesticide inflicts on a colony.
Note that the above words were written prior to our colonies having to deal with varroa, the varroa-vectored viruses, Nosema ceranae, our evolving brood diseases, GMO’s, neonicotinoids, or Roundup Ready corn.
The Four Horsemen And The Tip Point
Colony growth is a function of the recruitment rate via successful broodrearing vs. the attrition rate of workers due to age, disease, the altruistic departure of sick bees, or the loss of foragers in the field. When recruitment exceeds attrition, colonies grow; when attrition exceeds recruitment, the colony population shrinks. Environmental factors, including toxins, can shift the tip point for colony growth (Fig. 2).
Figure 2. Any colony with a good laying queen has the potential to grow rapidly—the greater the rate of recruitment (successful broodrearing), the steeper the slope of the growth curve. In the real world, such potential growth is often held back by the lack of nutritious pollen, or by the stresses of toxins, chilling, or pathogens (especially the mite-associated viruses, nosema, or EFB). Any of those can strongly shift the tip point, slowing, or even reversing, the rate of colony growth.
In the last decade, something appears to have shifted that tip point—colonies today seem to more readily go into a downhill spiral and queens no longer hold up as well. Could it be due to pesticides?
Could Pesticides Cause Colony Mortality And CCD?
Of course they could! In 2010, after closely observing the progression of experimentally-induced CCD with my collaborator Dr. Eric Mussen, I published the flow chart below (Fig. 3) to detail the interactions and feedback loops involved in the step-by-step collapse of a colony [10]. At the time, I fully intended to further elaborate upon the contribution of toxins, but didn’t get around to it until now.
Figure 3. The positive feedback loops that can lead to colony dwindling and/or sudden depopulation. I’ve since observed this process take place in sick colonies time and again.
In the above chart, I called out toxins (which would include pesticides) as one of the “Four Horsemen of Bee Apocolypse” (the four factors at top left). Below I’ve indicated in red those points at which toxins may exacerbate the downhill process (Fig. 4).
Figure 4. Note that toxins can exert lethal or sublethal effects (red bubbles) at every step in the process of colony dwindling or collapse. Pesticides may in some cases be the prime cause of colony mortality; more frequently they might be “contributory factors,” especially due the prolonged sublethal effects of residues in the beebread or wax.
Please note that in these charts I’m referring to toxins generically, not specifically to manmade pesticides. Such toxins would include natural plant allelochemicals, industrial pollutants, metals such as arsenic or selenium in soil and dust, fungal and bacterial toxins (which may be altered in beebread by the presence of pesticide residues), beekeeper-applied varroacides, HMF in overheated corn syrup, all in addition to any agricultural pesticides. In the words of ecotoxicologist Dr. Helen Thompson, we must pay attention tothe totaltoxinload of the hive, plus any interactions between those chemicals, as well as other contributory factors [11]—a sentiment also echoed by the Fraziers at Penn State [12]. So, back to our original question: Can toxins, including synthetic pesticides, cause colony morbidity or mortality?
Verdict #1: clearly, synthetic pesticides and varroacides may constitute the most serious toxin load for managed bees in agricultural areas, and have the potential kill a colony outright, or to exacerbate positive feedback loops that can result in dwindling, poor overwintering, or collapse.
But does any pesticide specifically cause CCD—“the disappearance of most, if not all, of the adult honey bees in a colony, leaving behind honey and brood but no dead bee bodies” [13] (and no sign of brood diseases or varroa-induced DWV collapse).
Analysis: The most direct way to answer that question is to see whether we can fulfill Koch’s third postulate [14]: can we experimentally create the symptoms of CCD by treating a healthy hive with the pesticide in question?
Verdict #2: to the best of my knowledge, no one has yet duplicated the symptoms of CCD by treating a colony with any pesticide (the most obvious difference being that there are generally plenty of dead bees present in the case of pesticide toxicity). This is notably true for the neonicotinoids, for which any number of researchers have attempted to duplicate CCD symptoms by continually feeding colonies neonic-tainted syrup or pollen.
Hold on—drop those stones! I am not saying that pesticides cannot contributeto CCD or colony morbidity or mortality in general—my chart above clearly illustrates that they have the potential to do so. Yet even those beekeepers who manage to completely avoid pesticides may still experience sudden colony depopulations, dwindling, or excessive winter losses due to some combination the Four Horseman (as in the perfect storm detailed at [15]).
I feel that it is a serious error for us to try to link CCD to pesticides. Pesticides have always been an issue to beekeepers, but CCD-like events have historically come and gone (as in Disappearing Disease—read the description at [16]). Pesticides will remain an issue long after the term “CCD” is forgotten.
Bottom line: Despite the fact that the evidence at hand does not support the case that CCD is directly caused by any pesticide, that fact certainly does not mean that we should ignore pesticide issues. If anything, we beekeepers ourselves have helped to make pesticides even more of an issue these days.
Short Memories
There is a popular myth going around that pesticides only started to become an issue to honey bee colony survival in 2007. In fact, the sublethal effects of pesticides were well known to beekeepers and researchers long before then. If we review the older literature [17], we find that it was already well known that contaminated pollen was a more serious issue to colony health than the in-field kill of foragers. We knew that colonies might collect such tainted pollen from miles away, that dusts were worse than sprays, that young bees may be more susceptible than older bees, and that temperature and humidity had a great deal to do with pesticide toxicity. Pesticide issues were actually far worse in the 1960’s and ‘70’s than they are today, and have generally improved since then (not to say that some new issues haven’t arisen).
On the other hand, the overall contamination of combs with pesticides has increased in recent years due to the direct contribution by we beekeepers ourselves. In virtually any residue analysis of beebread or beeswax these days in any country with varroa, the most prevalent toxins are the beekeeper-applied varroacides [18]–you may wish to refer back to my chart of the “toxicological eras of honey bee evolution [19].
So one question is, To what degree we have shifted the tip point of colony health by contaminating our brood combs with miticides? Let’s explore the broodnest…
The Heart Of The Hive – The Nursery
The insidious, long-term effects of total toxin load (including pesticide and varroacide residues) would be from those that made it into the heart of the hive—the critical stored beebread and the wax of the brood combs (Fig. 5). Note: Dr. David Fischer of Bayer brings to my attention that in the case of imidacloprid, the results of his testing indicates that bees in the hive are more affected by residues in the nectar than by those in the pollen.
Figure 5. Long after a pesticide-sprayed field force has been replaced by newly-recruited foragers, the colony may still need to deal with the lingering effects of pesticide residues in the combs, and especially in the all-important stores of beebread. It is here that such persistent residues can affect colony health and buildup for many months after the initial exposure, and exactly where we should focus our attention.
Here’s some food for thought: a toxin need not actually kill a single bee to mess up a colony. There are many ways in which sublethal levels of toxins can negatively affect the colony population curve. A few examples would be:
By decreasing the survival rate of larvae (as from residues of varroacides [20, 21], or fungicides [22]) , or by increasing their development time (as effected by various pollutants, plant alleleochemicals, pesticides, or miticides).
By affecting the proper fermentation of beebread (fungicides).
By affecting the sensitive nurse bees that must digest that beebread and produce the critical jelly used to feed the brood, queen, and other workers (natural plant toxins, pollutants, or pesticides).
By affecting the normal behavioral progression of the workers. E.g., if workers initiate foraging prematurely, this greatly reduces their overall longevity, and results in severe depression of colony growth [23] (much more research is crying to be done, but many chemicals would be suspect).
By requiring bees to allocate precious resources toward the detoxification of the poisons (as per my leaky boat analogy [24]).
By increasing the virulence of varroa, nosema, or viruses (any number of pesticides and miticides have been implicated [25, 26])
By affecting normal colony homeostasis, such as thermoregulation of the brood, which is dependent upon the proper assessment of temperature, and the ability to effectively generate heat by the vibration of the wing muscles (neurotoxins would be expected to affect this ability).
By affecting the longevity of the queen, the viability of spermatozoa, or the ability of a colony to successfully supersede (coumaphos notably had this effect)
By affecting the production of, or normal communication via pheromones (which include the recognition of brood and the queen) [27] (essential oils, formic acid, other pesticides?)
By affecting foragers’ ability to communicate by dance, to navigate, to learn (a wide range of pesticides [28]), or to react properly to normal stimuli (neonics can clearly do this [29]; but similar effects could be due to any number of other pesticides).
Bottom line: the toxin load in the broodnest can greatly affect a colony in many ways, generally (but not necessarily always) negatively. The greater the total toxin load with which the colony is forced to deal, the more likely that it will suffer from the combined ill effects.
Industry’s Arguments
In order to present an objective review of pesticide issues, we should also hear Industry’s side of the argument. The industry-funded think tank OPERA [30] takes the position that:
Although, based on the facts outlined above, there does not appear to be any strong evidence that sublethal effects of pesticides play a key role as causative factors behind bee colony mortality (which is likewise supported by the fact that in several monitoring projects no correlation has been found between colony losses and pesticide exposure), sublethal effects are certainly a point where more fundamental research is needed to obtain a clearer picture of the nature of the issue.
The above statements are factually correct in that there is to date no compelling evidence that pesticides are at the root of the elevated rates of colony mortality seen in recent years, and that more fundamental research is clearly needed. But a long history of practical experience by beekeepers with the sublethal (as well as lethal) effects of pesticides leaves no doubt that pesticides certainly have the potential to cause colony health issues.
But Don’t We Already Know That It’s The Neonicotinoids?
The media have already tried and convicted the neonicotinoids as the cause of all bee problems, and it’s currently fashionable to celebrate the restrictions recently imposed on them by the European Union. But it is rational? No one has ever shown convincing evidence that neonics are linked to colony collapse; conversely, there is abundant experimental and on-the-ground evidence that the residues from seed-treated plants do not appear to cause observable harm to colonies [31].
Planting dust, soil drenches, or foliar applications are a different story, but these are generally drift or misapplication issues, hitting individual apiaries, not the bee population as a whole. Our regulators are well aware of these issues, and working to fix the problems.
Regarding the completely unacceptable bee kills due to the dust from corn seeding, of interest is a recent paper by Drs. Chris Cutler and Cynthia Scott-Dupree [32]—environmental toxicologists from Canada’s Dalhousie University—who analyzed the 110 pesticide incident reports received by Canada’s PMRA since 2007. Ranking the reports by the degree of severity of the bee kill, they found that there were over five times as many “major incidents” due to non-neonicotinoid products (including carbofuran, chlorpyrifos, coumaphos, diazinon, dimethoate, fluvalinate, formic acid, permethrin, and phosmet) as there were due to neonics, yet that these incidents are largely ignored by the press and beekeepers, who for some reason single-mindedly focus upon the neonics.
Hey, I’m as concerned about pollinators and pesticides as anyone. A recent review by Goulson [33] points out the excessive use of neonics (actually all pesticides are greatly overused), and details the many environmental questions about this class of chemicals. But here’s the thing—I can read studies all day long, but what I prefer to seek out are actual on-the-ground, real-life observations. Let me share one with you:
An “Acid Test” Of Neonic Seed Treatment
Activists are calling for a ban on clothianidin—the most common neonicotinoid seed treatment. Although honey bees appear to do just fine on seed-treated canola, their species has an advantage over solitary bees and other pollinators, due to their foraging on multiple plant species over a wide area, their social structure, and their processing of the pollen by nurse bees. So honey bees may not be the best indicator of neonic toxicity.
On the other hand, solitary bee species may be a better indicator as to whether neonic residues cause subtle adverse effects. Many solitary bees are “monovoltine,” meaning that they only raise a single generation per year. Because of this, a negative effect on any single female bee could prevent the production of the next generation. It occurred to me that the Alfalfa Leafcutter Bee (Megachile rotundata), which is used to pollinate clothianidin-treated canola (Fig. 6), would provide an excellent “acid test” of clothianidin for several reasons:
Clothianidin has been shown to be highly toxic to leafcutter bees by topical application [34]. Since neonics are typically an order of magnitude more toxic by oral exposure [35], it is reasonable to expect that the leafcutter bee would be even more susceptible to residues consumed in food.
Leafcutter bees do all their foraging within a few hundred feet of the nest [36], so those placed in the middle of a canola field would forage solely upon treated canola.
Each individual female alone forages and provisions her nest, feeding upon the contaminated pollen and nectar as her sole protein and energy sources. If the insecticide negatively affected her behavior, navigational ability, health, or longevity she would be unable to reproduce effectively.
The male bees use canola nectar as their sole energy source, and if the insecticide residues interfered with their behavior or longevity, the female bees might not get properly mated.
The larvae consume a diet consisting solely of unprocessed contaminated pollen and nectar (rather than royal jelly), and thus every item in their diet would contain verified concentrations of clothianidin (approximately 1.7 ppb in the pollen; 0.8 ppb in the nectar [37]). Note: as with honey bees, neonicotinoids are virtually nontoxic to the larvae of the leafcutter bee [38].
The female constructs her nest by cutting (with her mouthparts) leaves from the treated canola plants, which contain even higher residues of clothianidin than the pollen, thus exposing her to even more of the chemical. The larva then develops surrounded by these contaminated leaves, and the pupa overwinters in them.
Figure 6. Tents covering Alfalfa Leafcutter bee nest boxes in a canola field.
In short, the leafcutter bees would constitute the most severe test case for clothianidin exposure from a seed-treated crop. So I phoned a commercial supplier of leafcutter bees in Ontario (who declined to be named) and asked him whether he had any problems with his bees reproducing or overwintering after being set in clothianidin seed-treated canola. He said that he had been rearing them on such fields for many years and did not observe any problem. I put a good deal of faith into such unbiased field experience by a commercial bee man. You can draw your own conclusions.
So Which Pesticides Are Actually To Blame?
It’s pretty easy to diagnose an acute bee kill, what with piles of twitching bees in front of the hives (see “Signs and symptoms of bee poisoning” at [39]), and in many cases the responsible pesticide can be identified. To sidetrack briefly, remember when I mentioned a few articles back that the residues in Jim Doan’s bee kills did not indicate that the bees contained lethal doses of the chemicals? This made me strongly suspect that we can’t apply the LD50 data (in nanograms per bee) to the values obtained from actual field samples of dead bees. The recent report from Canada [40] confirms this. The highest residue level of clothianidin (from corn planting dust) found in any sample of dead bees from the entrances of a hive was 24 ppb, which works out to about a tenth of the theoretical amount necessary to kill a bee . This finding could be due to the metabolic degradation of the insecticide, but it certainly suggest that the LD50 value should be adjusted lower for samples of dead bees! I am greatly heartened that Canada is moving forward in addressing this issue of bee kills from corn planting dust [41].
Overt bee kills aside, more insidious are the residual effects due to contaminated dust, pollen, or nectar that foragers bring back into the broodnest. I’m told by beekeepers with far more experience with pesticides than I, that after exposure to certain pesticides, colony growth and production come to a standstill, sometimes for months, until the colony clears itself of residues and perhaps eventually recovers (or not). The problem is that few beekeepers (if any) can look inside a hive and diagnose which pesticide (or combination thereof) is causing the problem. He may notice spotty brood, poor buildup, winter dwindling, or queenlessness, but it is very hard to isolate the effect any particular pesticide residue, especially in today’s stew of residues in combs. But that doesn’t mean that we are completely blind…
The Evidence
Due to the rapid turnover of bees in a hive (other than the queen or “winter bees”), if a pesticide were indeed exerting a long-term effect upon colony health, then there would by necessity need to be residues of that pesticide or its degradation products persisting in the combs. With today’s testing equipment, we can detect residues to the parts per billion level, and have quite a large database of residue analyses of beebread samples, which we can perhaps use to either finger or exonerate certain pesticides suspected of being involved in colony health issues.
In a court of law, all evidence would be laid out before the court to determine whether it was substantial enough to make a case against a particular suspect. We can do something similar by reviewing two large publicly-available datasets of actual pesticide analyses of beebread from across the country—one by the Penn State team , the other by the USDA (Tables 1 and 2). I’ve condensed their data to only those pesticide detects that were found in at least 10% (Penn State) or 5% (USDA) of the samples, following this reasoning:
If a pesticide isn’t present in at least 10% of samples, then it isn’t likely to be the cause of widespread problems.
I’ve also color-coded the results as to the type of pesticide, and included the median detection level (to help us to determine whether that dose would be expected to cause colony health problems, or whether it would be insignificant).
Pesticide
Present in percent of samples*
Median detection if positive for target (ppb)
Type of pesticide
Fluvalinate
88.3
40.2
Beekeeper-applied miticide
Coumaphos
75.1
13.1
Beekeeper-applied miticide
Chlorpyrifos
43.7
4.4
Insecticide
Chlorothalonil
52.9
35
Fungicide
Pendimethalin
45.7
13.4
Herbicide
Endosulfan I
28
4.2
Insecticide
Endosulfan sulfate
26.3
2.2
Insecticide
DMPF (amitraz)
31.2
75
Beekeeper-applied miticide
Atrazine
20.3
8.9
Herbicide
Endosulfan II
20
3.8
Insecticide
Fenpropathrin
18
7
Insecticide
Azoxystrobin
15.1
10.2
Fungicide
Metolachlor
14.9
8.1
Herbicide
THPI (Captan)
14.2
227
Fungicide
Captan
12.9
103
Fungicide
Esfenvalerate
11.7
3.3
Insecticide
Carbaryl
10.9
36.7
Insecticide
Cyhalothrin
10.9
1.7
Insecticide
Table 1. The 2010 survey by the Penn State team [42], based upon (depending upon the pesticide) either 350 or 247 samples. This study (plus numerous others worldwide) clearly point out that the predominant pesticide residues in brood combs are typically those from the beekeeper-applied miticides (yellow).
Table 2. This 2012 survey by the USDA [43] echoes the previous findings—the only pesticides found in at least 10% of the samples were from either beekeeper-applied miticides or chlorpyrifos. The 99 analyzed samples came from Alabama, California, Colorado, Florida, Idaho, Indiana, New York, South Dakota, Tennessee, Texas, and Wisconsin.
Keep in mind that the above surveys screen only for 174 chosen pesticides—compare this number to the roughly 1000 pesticide active ingredients and adjuvants registered for use in California. I’ve discussed the composition of this list with USDA’s Roger Simonds, who runs the tests. It is prohibitively costly to test for every possible pesticide, so one must arbitrarily draw up a limited list of the chemicals of most concern. All are aware that this is a difficult task, since we don’t even know which toxins with which we should be most concerned!
Note that in both surveys, the most common insecticide present was chlorpyrifos– an “old school” (introduced in 1965) organophosphate neurotoxin classified as being “highly toxic” to bees, and marketed as Dursban and Lorsban. Chlorpyrifos was previously widely used by homeowners and residential pest control companies. EPA has since restricted its use due to its toxicity to wildlife and aquatic organisms, and possible links to human health issues [44]—some of the reasons that EPA favors the neonicotinoids as “reduced risk” products.
Oh Boy, Let’s Do Some Math!
But just because a pesticide is present, doesn’t necessarily mean that it is causing measureable harm. A nurse bee may consume about 10 mg of beebread per day [45], so if she consumed that amount of pollen contaminated with chlorpyrifos at 6.5 ppb, then she would have been dosed with 0.065 ng (1 nanogram = 1 billionth of a gram) of the chemical. The question then is, how much chlorpyrifos does it take to actually harm a bee?
One commonly cited figure is that the LD50 for chlorpyrifos given orally is 360 ng/bee. Compare those figures (360 ng for toxicity vs. 0.065 in the daily diet)! Even though chlorpyrifos is a disturbingly common comb contaminant, it is unlikely that the median detected concentration (alone) would be causing colony health problems (not to say that higher doses don’t hurt colonies).
But, you say, some of the neonics are even more toxic than chlorpyrifos. How about the mean 31 ppb found by the USDA in the few samples positive for imidacloprid? The typical nurse bee would consume 0.31 ng, compared to the oral LD50 of about 4-40 ng, so she’d be eating a tenth to a hundredth of the lethal dose. This would be cause for concern, tempered by the fact that a bee can easily metabolize that amount of imidacloprid a day [46]. Such consumption could legitimately be suspected of causing sublethal effects. However, keep in mind that that 31 ppb was an average, which was strongly skewed by a few samples with very high concentrations (which I’d fully expect to cause colony health problems). Plus this is not simply a matter of the average amount of contamination; one must also look at the percentage of positive detects. The Penn State team [47] puts it well:
Our residue results based on 1120 samples which include Mullin et al. (2010) and subsequently more than 230 additional samples do not support sufficient amounts and frequency of imidacloprid in pollen to broadly impact bees.
OK, so how about the varoacides fluvalinate at 40 ppb or the amitraz degradate DMPF at 100 ppb? Surprisingly, I can’t find an oral LD50 for fluvalinate, so the contact toxicity figure (200 ng/bee) will need to suffice. Those residues work out to about 1/500th expected toxicity.
Amitraz scored a bit better, with the nurse bees consuming about 0.01 ng—far below the lethal dose. But a recent study found that an oral dose of 0.2 ng of amitraz causes more than a doubling of the heart rate of a bee [48]—that’s at 1/20th of the average detect! The authors dryly state:
The above responses clearly show that the heart of the honeybee is extremely vulnerable to amitraz, which is nevertheless still used inside beehives, ostensibly to “protect” the honeybees against their main parasite, Varroa destructor.
How vulnerable? Frazier [49] observed that “Dead and dying bees collected around colonies in association with corn had only residues of 2,4-DMPF at 5,160 ppb.” Looks like perhaps the beekeeper inadvertently killed his own bees with an off-label mite treatment that may have overworked their little hearts!
And if those miticide and insecticide residue weren’t enough alone, some of the toxicity of these chemicals is additive or synergistic. The Penn State team again says it well:
[The] pyrethroids… were found in 79.4% of samples at 36-times higher amounts than the neonicotinoids, on average… The mean neonicotinoid residue was 37 ppb (scoring non-detects as 0 ppb), of which only 6.7 ppb was imidacloprid. Pyrethroids, by comparison, were present at a mean residue of 106 ppb and a frequency of 80.3% in pollen samples… Indeed, if a relative hazard to honey bees is calculated as the product of mean residue times frequency detected divided by the LD50, the hazard due to pyrethroid residues is three-times greater than that of neonicotinoids detected in pollen samples [emphasis mine].
The pyrethroids are popular because they are relatively nontoxic to humans. But they can sure kill honey bees. More so, they can cause sublethal effects, such as irreversible inhibition of olfactory learning ability [50].
Hey, we’re only getting rolling! Mussen [51] pointed out a decade ago that fungicides could kill larvae; recent research from the Tucson lab [52] and elsewhere confirm that fungicide residues can mess up the colony (we sometimes observe this in almonds). Of note is that colonies treated with some fungicides were unsuccessful at requeening themselves! And recent research by Zhu [53] found that the relative toxicity of larvae to the commonly-detected fungicide chlorothalanil was almost 40 times higher than that of chlorpyrifos. Fungicides are frequently found at high concentrations in beebread.
I cannot help from returning to the refrain that instead of limiting our concern to any single pesticide, that we should be looking at the total toxin load that the colony is forced to deal with.
And How About The “Inerts”?
The pesticide detection analyses above do not look at the “inert” adjuvants in the pesticide “formulation.” These chemicals not only help to disperse the pesticide over the waxy leaf surface, but also aid in its penetration through the insect cuticle, thus making the pesticide relatively more toxic to the bee!
Mullin and Ciarlo [54, 55] found that:
Formulations usually contain inerts at higher amounts than active ingredients, and these penetrating enhancers, surfactants and adjuvants can be more toxic on non-targets than the active ingredients. For example, we found that the miticide formulation Taktic® was four time more orally toxic to adult honey bees than the respective active ingredient amitraz. Impacts of ‘inerts’ in pollen and nectar alone or in combination with coincident pesticide residues on honey bee survival and behavior are unknown.
The researchers also found that:
Learning was [rapidly] impaired after ingestion of 20 µg of any of the four tested organosilicone adjuvants, indicating harmful effects on honey bees caused by agrochemicals previously believed to be innocuous.
One of the common adjuvants is a solvent NMP, described by BASF [56]:
NMP can be used as a solvent or co-solvent for the formulation of insecticides, fungicides, herbicides, seed treatment products and bioregulators where highly polar compounds are required. NMP is given preference over other highly polar solvents because it is exempt from the requirement of a tolerance when used as a solvent or co-solvent in pesticide formulations applied to growing crops, and it possesses a favorable toxicological and environmental profile.
The key words above are that these toxic solvents are “exempt from tolerance” [57], so they are sprayed all over crops along with the active ingredients of pesticides (including imidacloprid). Yet Zhu [58] recently reported that NMP can rapidly kill bee larvae. The authors conclude that:
Our study suggests that fungicide, the inert ingredient and pesticide interaction should be of high concern to honey bee larvae and overall colony health. None of these factors can be neglected in the pesticide risk assessment for honey bees.
Choosing To Ignore The Obvious
There is no doubt that neonics have the potential to harm bees, but the question is, do they really cause as much problem in the real world as we’ve been led to believe? This is not a matter of convincing the masses; this is an investigation of fact and evidence. For a pesticide to cause harm to a colony of bees, two necessary elements must occur:
The bees must be exposed to the pesticide. Evidence for this is best determined by chemical analysis of the pollen in the combs, since residues in the bodies of dead bees may be degraded, and because water-soluble insecticides such as the neonics are not absorbed into the wax (residues in the wax do document the history of exposure to lipophilic pesticides).
The pesticide must be present at a concentration above a trivial level.
When we take the time to determine which pesticides bees are actually found in the combs of hives, neonicotinoids are seldom present, or if detected are often at biologically irrelevant concentrations. Imidacloprid was detected in fewer than 3% of Mullin’s 350 samples, and clothianidin not at all! Similarly, there were zero detects for clothianidin in the 99 USDA samples; imidacloprid was only present in 9%. Likewise, a number of European studies have shown similar results (reviewed in [59]).
In a recent study, the Fraziers [60] looked at hives placed in cotton, corn, alfalfa, apples, pumpkins, almonds, melons, blueberries, or wild flowers, and identified the residues in collected pollen, in returning foragers, and in dead or dying bees near the hives. Again, the only neonic noted was thiamethoxam in alfalfa (in which dying bees contained residues of ten different pesticides). However, there were alarmingly high detects of fungicides, the insecticide acephate, and the metabolite of the beekeeper-applied miticide amitraz.
The latest data comes from Dr. Jeff Pettis [61], whose group determined the pesticides in bee-collected pollen from six crops: apple, blueberry, cranberry, cucumber, pumpkin, and watermelon. Of the 35 pesticides detected, beekeeper-applied miticides and ag fungicides predominated (sometimes at alarming levels), followed by common organophosphate, pyrethroid, and cyclodiene insecticides (again sometimes at alarming levels). In the 17 samples tested, residues of neonics were only found in the samples from the apple orchards, and only one was found at a biologically-relevant concentration.
So my question is why the heck are so many activists pursuing the single-minded focus upon the neonics, when the clear evidence is that neonics are not commonly found in bee-collected pollen, and if present, are generally at levels that do not appear to negatively affect colony health [62]?
There is a lot more to pesticide issues than the neonics alone, and by focusing our attention solely upon them, we ignore the often far more serious effects of other pesticides.
Blinded By Bias
During the intense focus upon neonicotinoids the past few years, we’ve learned that exposure of bees to these insecticides can result in all sorts of sublethal effects. Unfortunately, many researchers appear to be wearing blinders as to the effects of other pesticides. The resulting narrowness of these studies skews our perspective—if we only look for effects from the neonics, we don’t know how to rank the biological relevance of those effects relative to the effects of all the other toxins to which bees are exposed, generally to greater extent.
A practical complaint to researchers: if you are going to look for sublethal effects of neonics, please include positive controls of some other pesticides, so that we can learn whether the neonics are better or worse than the alternatives!
I commend one group that recently decided to take a look at the effects of a common herbicide upon the development of bee larvae [63]. The results of this straightforward and meticulous study are an eye opener!
The researchers found that exposing bee larvae to even infinitesimal amounts of the herbicide paraquat prevented them from fully developing their critical oenocyte cells (see box).
Oenocyte cells are not only involved in the production of lipids and lipoproteins, but they also appear to play a role in the constitution of external cuticle in both larvae and adults. In addition, they are involved in intermediary metabolism and synthesize hydrocarbons to waterproof cuticle or to make beeswax. Furthermore, oenocytes secrete hormones, especially those involved in larval and adult development. They are also described as the major cells expressing cytochrome P450 reductase, which is involved in detoxification of toxins [information paraphrased from the cited paper].
Exposure to even a part per trillion of paraquat suppressed the development of these extremely important cells. The authors conclude:
This study is the first which reports an effect of a pesticide at the very low concentration of 1 ng/kg, a concentration below the detection limits of the most efficient analytic methods. It shows that chemicals, including pesticides, are likely to have a potential impact at such exposure levels.
Who woulda thunk? Paraquat isn’t included in the standard screening for pesticide residues, so we don’t even know how prevalent it is in hives! The above findings should make it clear that we need to go back to the beginning if we are to understand the sublethal effects of pesticides (and adjuvants), even at perhaps undetectable levels.
We do know that here were 812,000 lbs of paraquat applied in California in 2010, as opposed to only 266,000 lbs of imidacloprid. Paraquat shows strong adverse effects upon bee larvae at a part per trillion, as compared to imidacloprid, which is so minimally toxic to bee larvae that no one has even been able to determine an LD50! So the amount of paraquat applied has far greater potential to cause problems to bees in agricultural areas (Fig. 7).
Figure 7. The herbicide paraquat appears to be harmful to bee larvae at levels as low as 1 part per trillion. Note the wide variety of crops, and the extensive areas to which it is applied.
So here we have clear scientific data from a well-designed laboratory experiment that a commonly-applied pesticide has the ability to cause immune suppression and other adverse effects in developing bees, yet these results have been virtually ignored by beekeepers and environmental groups. I just don’t understand it!
No More Safe Home To Return To
Out of their protective hive, honey bees live in a hostile world, full of predators, deadly weather, and toxic agents (both natural and manmade). But the bees of old could generally return to a “safe” home, in which the transmission of natural toxins was largely minimized by the behavior of foragers, and by the processes of the conversion of nectar to honey, and of pollen into jelly (via the digestion of beebread by nurse bees). Both of these processes help to prevent the transmission of toxins from the foragers to the queen and the brood.
With the advent manmade pesticides, bees may no longer have that “safe” home to return to. Beebread and the wax combs nowadays are often contaminated with any number of pesticides (in addition to natural plant toxins and industrial pollutants). But this is not a “new” problem:
A Historical Artifact
Even before we had the ability to detect pesticide residues in combs to the parts per billion level, pesticide analyses often found easily-detectable levels of insecticides in bee hives. As a frame of reference, I sought out a historical artifact—the residues in the beeswax that had been rendered by beekeepers and reprocessed into a sheet of “clean” foundation. I was lucky enough to find that such a sample had recently been analyzed by the Tucson Bee Lab. Dr. Diana Sammataro forwarded me the results of the analysis of an undated “very old” piece of wax foundation from the Northeast (Table 3).
THIS IS THE TABLE !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
Pesticides in an old piece of beeswax foundation.
Positive residue detect
ppb
Pendimethalin
13.1
Endrin
156
Dieldrin
160
Trifluralin
3.6
DDT p,p’
32.7
Heptachlor
35.1
Malathion
4.3
Chlorpyrifos
4.6
Dicofol
6.8
PCB’s
8190
Chlorothalonil
84.6
Table 3. We can narrow down the foundation’s date of manufacture by the residues present. Pendimethalin was first registered in 1972 (the same year that DDT was banned), and since there were no residues of fluvalinate, the foundation was clearly produced prior to the arrival of varroa around 1990. Thanks to Dr. Diana Sammataro and the Tucson Bee Lab.
Clearly, pesticide-contaminated combs are hardly a new phenomenon. In the above example, the beeswax batch used to produce the foundation came not from a single hive, but rather from the combined wax from many hives, likely from many beekeepers, and thus would represent an average sample of the degree of contamination somewhere in that 1972-1990 time frame. And that doesn’t take into account whether the raw wax came mainly from cappings (which would have been minimally contaminated), or whether it went through the common practice of being filtered through activated carbon. But any colony started on such foundation purchased from a beekeeping supply house would clearly have had to deal with at least the residues of these lipophilic toxins from the get go!
An aside: perhaps of interest is something that I noticed years ago when I switched from dipping my own wax queen cell cups to using plastic cups. My “take” rate became better and more consistent. Was that because the beeswax at the time was contaminated with residues?
The Beekeeper Contribution To Shifting The Tip Point
One thing that is “new” is that since the arrival of varroa, we’ve upped the ante—all commercial beeswax is now contaminated with residues of beekeeper-applied synthetic miticides. The three most prevalent synthetic chemicals found in combs today all get there by being applied by beekeepers for mite control.
Practical note: And although there is no reason to be concerned about the tainting of honey by the legal use of these miticides, the beekeeper/applicator should be aware that both amitraz and tau-fluvalinate make California’s list of “chemicals known to the State to cause reproductive toxicity,” and coumaphos is of concern because it is a “cholinesterase-inhibiting pesticide.” No varroacide is harmless to bees [64]—but the benefits of mite control generally (but not always) outweigh the adverse effects due to the miticide residues.
We beekeepers have clearly shifted the baseline for pesticide contamination of combs, which increases the total toxic load even before the contribution by agricultural pesticides.
Stop Right There!
Although it is a very attractive hypothesis to blame our problems on miticide or pesticide residues, let’s do a reality check. On good forage in good weather, plenty of beekeepers see their colonies thrive even on old, dark, seriously-contaminated combs; but under stressful conditions those same residues might contribute to poor colony performance or even mortality.
No study has yet found support for the hypothesis that miticide residues are the cause of our current bee problems (although one would have every reason to suspect that they may contribute). In fact, vanEngelsdorp [65] found that surprisingly, higher levels of coumaphos residues negatively correlated with colony survival. How could this be? One possible explanation is that those beekeepers who used it experienced better mite control. But there is also another intriguing possibility—hormetic effects.
Undetectable Levels And Hormesis
Is your head spinning yet? I’ve presented evidence that undetectable levels of some pesticides could harm bees, that “inert” adjuvants can do the same, and that combs are often chock full of all sorts of pesticide and varroacides residues. Criminy, it’s a wonder that bees survive at all! Or is it?
Bees have long been exposed to all sorts of natural, and recently, manmade toxins, and survived. Toxicity is a complicated subject. The only thing that separates a medicine from a poison is the dose. In general, if a pesticide has been tested upon adult and larval bees and found to have no observable adverse effects at a certain concentration, we would not expect to see adverse effects at lower concentrations. However, there are exceptions to this general rule—toxicity may vary up or down depending upon the dose [66]!
I’ve previously mentioned the term hormesis [67]— the paradoxical effect of toxins at low concentrations. The paradox is that although most chemicals are toxic at high concentrations, the majority are likely beneficial at low concentrations. For those interested in this fascinating phenomenon, I suggest Dr. Chris Cutler’s excellent and thought-provoking review [68]. It is not only possible, but actually probable that lose doses of pesticides may exert a beneficial effect upon a colony! (Don’t be ridiculous—I’m not suggesting that bees are better off for the presence of pesticides!).
Wrap Up
Toxins, whether natural or manmade, are clearly a potential issue in colony health. To what degree pesticides contribute to colony morbidity or mortality is dependent upon exposure, the dose, and a host of associated factors. Beekeepers have long noticed that their bees often do better if allowed to forage on pesticide-free land. But many beekeepers today tell me that their bees do just fine in the middle of intense agricultural areas—so this is not a black or white situation.
In recent years beekeepers themselves have greatly added to the degree of contamination of their combs. Introductions of novel pesticides and adjuvants keep changing the picture. And now we’re finding that pesticides that we formerly assumed were harmless to bees (fungicides and herbicides) may actually be quite toxic to larvae! Then there is the scary finding that undetectable levels of some pesticides might cause health issues, countered by the fascinating subject of hormesis.
I certainly do not profess to understand all this, but I have come to the following conclusions:
That bees have had to deal with toxins for a long time,
That pesticides will be with us for the foreseeable future,
That varroacides have likely added to the problem,
That pesticides can cause lethal and long-term sublethal effects in the hive, but
That many beekeepers in agricultural areas no longer consider pesticides to be a serious issue, whereas,
That colonies may go downhill after being exposed to some agricultural chemicals, or combinations thereof,
That toxicology in the hive is complex, and that there are few simple answers,
That it is unlikely that any single pesticide is to blame for our current colony health issues,
That we still have a lot to learn!
Next month I will look at the distribution of both managed colonies and of pesticide applications in the United States, and their relationship to bee health problems.
Acknowledgements
As always, I could not research these articles without the assistance of my longtime collaborator Peter Loring Borst, to whom I am greatly indebted. I also wish to thank Drs. Jim and Maryann Frazier, Chris Mullin, David Fischer, Eric Mussen, Thomas Steeger, and Roger Simonds for their generosity in taking the time to discuss pesticide issues with me.
[16] Wilson, WT and DM Menapace (1979) Disappearing disease of honey bees: A survey of the United States. ABJ March 1979: 185-186.
“Certainly with both pesticide-related and [Disappearing Disease]-caused bee losses, the adult population of a colony may be reduced rapidly to a “handful” of bees or, in some cases, the entire population may be lost.
“However, in the case of pesticide poisoning, there is usually evidence of pesticide application…the worker bees either die in the field or in or near the hive depending on the type of pesticide. When the field force is killed and they “disappear,” many dead or dying bees may be seen on the ground in the field or on the ground between the treated field and the apiary…If the foraging bees bring poison into the hive, then the nurse bees either die in the hive or at the entrance so one can see many crawling and tumbling adults and large amounts of neglected brood. Exposure to pesticides over an extended period results in very weak colonies, and some die out.
“In the case of [Disappearing Disease], the situation is quite different. The colonies frequently have gone through a period o nectar and pollen collection with active brood rearing [as in typical CCD]. Then the weather has turned unseasonably cool and damp and remained adverse for from about 3 to 14 days…During the inclement weather, the bee populations dwindle because the worker bees disappear from the hive leaving a “handful” of bees and the queen. Often these small populations recover and increase in size during hot weather and a long nectar flow or, or occasionally, the entire population absconds…”
[17] Johansen CA and DF Mayer (1990) Pollinator Protection: A Bee & Pesticide Handbook. Wicwas Press.
[21] Medici SK, Castro A, Sarlo EG, Marioli JM, Eguaras MJ (2012) The concentration effect of selected acaricides present in beeswax foundation on the survival of Apis mellifera colonies. J Apic Res 51: 164–168
[22] Eric C. Mussen, Julio E. Lopez, and Christine Y. S. Peng (2004) effects of selected fungicides on growth and development of larval honey bees, Apis mellifera L. (Hymenoptera: Apidae). Environmental Entomology 33(5):1151-1154.
[23] Frazier, J.L., M.T. Frazier, C.A. Mullin & W. Zhu – Does the reproductive ground plan hypothesis offer a mechanistic basis for understanding declining honey bee health? http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011#.UhDTZX-aucw
[27] Maisonnasse A, et al (2010) E-β-Ocimene, a volatile brood pheromone involved in social regulation in the honey bee colony (Apis mellifera). PLoS ONE 5(10): e13531. http://www.plosone.org/article/info:doi/10.1371/journal.pone.0013531 These researchers studied (E)-b-ocimene, a volatile terpene commonly produced by plants to attract predatory mites, but also a critical pheromone produced by the brood and the queen.
[34] Scott-Dupree, CD, et al (2009) Impact of currently used or potentially useful insecticides for canola agroecosystems on Bombus impatiens (Hymenoptera: Apidae), Megachile rotundata (Hymentoptera: Megachilidae), and Osmia lignaria (Hymenoptera: Megachilidae). J Econ Entomol 102(1):177-82.
[36] Hobbs, GA (1967) Domestication of Alfalfa Leaf-cutter Bees. Canada Dept. of Agriculture. Ottawa: Queen’s Printer and Controller of stationary.
[37] Dr. Jerry Bromenshenk, pers. com.
[38] Abbott, VA, et al (2008) Lethal and sublethal effects of imidacloprid on Osmia lignaria and clothianidin on Megachile rotundata (Hymenoptera: Megachilidae). J Econ Entomol 101(3):784-96.
[44] Christensen, K.; Harper, B.; Luukinen, B.; Buhl, K.; Stone, D. 2009. Chlorpyrifos Technical Fact Sheet; National Pesticide Information Center, Oregon State University Extension Services. http://npic.orst.edu/factsheets/chlorptech.pdf.
[45] Rortais, A (2005) Modes of honeybees exposure to systemic insecticides: estimated amounts of contaminated pollen and nectar consumed by different categories of bees. Apidologie 36: 71–83.
[46] Cresswell, JE, et al (2012) Differential sensitivity of honey bees and bumble bees to a dietary insecticide (imidacloprid). Zoology 115: 365– 371.
[53] Zhu, W., D. Schmehl & J. Frazier (2011) Measuring and predicting honey bee larval survival after chronic pesticide exposure http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011#.UhDTZX-aucw
[54] Mullin, C.A., J. Chen, W. Zhu, M.T. Frazier & J.L. Frazier – The formulation makes the bee poison. ABRC 2013
[55] Ciarlo TJ, Mullin CA, Frazier JL, Schmehl DR (2012) Learning impairment in honey bees caused by agricultural spray adjuvants. PLoS ONE 7(7): e40848. doi:10.1371/journal.pone.0040848
[60] Frazier, M.T., S. Ashcraft, W. Zhu & J. Frazier – Assessing the reduction of field populations in honey bee colonies pollinating nine different crops http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011#.UhDTZX-aucw
[61] Pettis, et al (2013) op. cit.
[62] A recent study confirm that the neonic residues in corn, soy, and canola pollen are at very low concentrations. Henderson, C.B. a, J.J. Bromenshenka, D.L. Fischerb. Clothianidin exposure levels from bee-collected pollen and nectar in seed-treated corn and canola plantings. ABRC 2013 http://bees.msu.edu/wp-content/uploads/2013/01/ABRC-abstracts-2013.pdf
[63] Cousin M, Silva-Zacarin E, Kretzschmar A, El Maataoui M, Brunet J-L, et al. (2013) Size changes in honey bee larvae oenocytes induced by exposure to paraquat at very low concentrations. PLoS ONE 8(5): e65693. doi:10.1371/journal.pone.0065693 http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0065693
[64] Boncristiani, H., et. al. (2011) Direct effect of acaricides on pathogen loads and gene expression levels of honey bee Apis mellifera. Journal of Insect Physiology. 58:613-620.
[65] vanEngelsdorp, D, et al () Weighing risk factors associated with bee colony collapse disorder by classification and regression tree analysis. J. Econ. Entomol. 103(5): 1517-1523. (Broken Link!) http://www.eclecticparrot.com.au/research_papers/VanEngelsdorp%202010%20Weighing%20risk%20factors%20in%20Bee%20CCD.pdf
[66] Cutler GC, Ramanaidu K, Astatkie T, and Isman MB. (2009) Green peach aphid, Myzus persicae (Hemiptera: Aphididae), reproduction during exposure to sublethal concentrations of imidacloprid and azadirachtin. Pest Manag Sci 65:205-209
First published in: American Bee Journal, March 2014
Queens for Pennies
Originally published in ABJ March 2014
Randy Oliver
ScientificBeekeeping.com
I’ve been encouraged in recent years by the number of beekeepers who appear to be successfully keeping locally-adapted stocks of bees without treatment for varroa. I am a strong supporter of their efforts, and see them as the wave of the future.
But First A Rant
Unfortunately, there is also a great deal of confusion as to what “treatment free” beekeeping really means. Allow me to use an analogy to explain:
Dairymen prefer to keep Holstein cattle. Holsteins are thin-skinned, thoroughly domesticated cattle selected solely for milk production. Their normal care requires shelter, supplemental feeding, routine vaccinations, and treatment with antibiotics. If a dairyman turned his Holsteins out on the range to fend for themselves without care, and half of them died each year, he would be accused of having committed animal neglect—“the failure to provide the basic care required for an animal to thrive.”
Yet this is exactly what thousands of recreational beekeepers do every year. Under the misconception that they are practicing “treatment free” beekeeping, they are in actuality simply neglecting their domesticated animals. The reason for this is that they are starting with commercial package bees—bees akin to Holstein cattle, in that they are bred for high brood and honey production under standard management practices (notably mite management, but also supplemental feeding or antibiotic treatment if indicated). Most commercial bee stocks should be considered as domesticated animals. There is absolutely no reason to expect that your wishful thinking will miraculously transform your newly-purchased “domesticated” bees into hardy survivor stock able to survive as wild animals without standard care and treatment.
Now don’t get me wrong, I am no more criticizing the commercial queen producers than I would criticize the dedicated breeders of Holstein cattle. The queen breeders are producing the best breeds for beekeepers willing to provide their colonies with the “standard” degree of husbandry (which includes at this time, treatment(s) of some sort for varroa). I have no problem whatsoever with that; but my crystal ball says that someday the market will dwindle for bees that require regular treatment for mites.
Do not delude yourself. Allowing domesticated package colonies to die year after year is not in any way, shape, or form a contribution to the breeding of mite-resistant stocks. There is a vast difference between breeding for survivor stock and simply allowing commercial bees to die from neglect! By introducing commercial bees year after year into an area, and then allowing those package colonies to first produce drones and then to later die from varroa, these well-meaning but misguided beekeepers screw up any evolutionary progress that the local feral populations might be making towards developing natural resistance to varroa. Not only that, but those collapsing “mite bombs” create problems for your neighbors. Referring to yourself as a bee-keeper confers upon you a responsibility to the local beekeeping community. Allowing hives to collapse from AFB or varroa makes you a disease-spreading nuisance!
Update April 15, 2014: I’ve received a great deal of positive feedback from experienced beekeepers who have been frustrated by all the well-intentioned, but sadly misguided, feel-good dreamers who don’t understand the difference between working with nature to promote varroa-resistant bee stocks, versus neglecting livestock that you have taken under your care. I like Rusty Burlew’s blog ““Let the bees be bees” Really?”
A Solution
Enough scolding. I strongly support those willing to actually practice selective breeding for treatment-free (or minimal treatment) locally-adapted stocks of bees. But let me be frank (try to stop me); if you start your hive with commercial stock, then by all means care for them as domesticated animals! If you want to go treatment free, then start with survivor stock bred to be naturally resistant to mites and viruses, such as VSH, Russian, or locally-adapted ferals. Do not kid yourself into thinking that allowing innocent domesticated bees to die a slow and ugly death is the same thing as breeding for survivor stock—“breeding” instead means the propagation of bees that don’t die [1]—the key word being propagation. And this is a frustration for many well-intentioned beginners—no one in their area is propagating survivor stock for sale. That is why I wrote this article.
To me, it is a crime against nature not to breed daughters from that fantastic survivor colony. But most beekeepers think that it is beyond their scope of ability to raise queens. Nonsense! Let me show you how to raise about 10 queens at a time for pennies apiece. This is not the way we do it commercially, but this method can be easily practiced by most anyone.
A Simple Method
I’m going show you step by step how to raise about 10 queen cells in a simple queenless cell builder. Here’s a list of everything that you’ll need:
A chosen breeder queen hive.
A strong, healthy donor colony from which to make the cell builder hive.
An empty brood box with a bottom board and cover to use for the cell builder hive.
If there is no nectar flow occurring, a syrup feeder.
If you’re over 40, a lighted magnifying headband [2].
A few Chinese grafting tools [3].
JZ’s BZ’s plastic cell cups [4].
A damp towel
Any sort of nuc boxes or divided hive bodies in which to mate out the queens.
Timing: It’s easiest, and you’ll get the best queens, by raising them during swarming season. Look for when your colonies start building queen cells on the bottom bars, or when they are full of emerged drones.
Day 0—Locate the future queen larvae: Before you start setting up the cell builder, first make sure that you can find larvae of the right age from your chosen breeder queen [5]. Go into her colony and make sure that there’s an older, dark frame containing well-fed freshly-hatched larvae [6]. Mark this frame for later recovery and put it back into the hive. You want to graft from the youngest larvae possible—when they are still the size of an egg, and just starting to curl (as in the photo above).
Choose a donor colony: This is the colony (or colonies) from which you will steal nurse bees to make up your cell builder [7]. It must be healthy, full of brood, and the larvae should be well fed with jelly as an indicator of the nurses being in a good state of nutrition [8]. Locate the queen of your donor colony and temporarily set her and the frame she’s on aside in a nuc box for safekeeping [9].
Set up the cell builder hive: Put down a bottom board with an empty brood box wherever you want to make your queenless cell builder (its entrance should be at least several feet away from the donor colony). Into this box, you are going to put at least 4 frames [10] in the order above (the breeder larvae frame will be added later):
A comb of open larvae: Start with a comb containing some open brood and eggs . This will be the core of the cell builder, around which the nurse bees will cluster. You don’t want a solid frame of young brood competing with the queen cells for feeding—just a patch of young larvae emerging over the next few days to stimulate the nurse bees to produce an abundance of royal jelly. The rest of the frame can be sealed brood, beebread, or whatever.
Cut a channel the width of a hive tool: parallel to the top bar, at least midway up the frame, in either the pollen frame or open brood frame as shown. Scrape out the comb right down to the foundation [11].
Add the nurse bees: Now shake all the bees from all the frames of the donor hive (other than the one that the queen was on) into the cell builder hive [12]. The older bees will quickly fly back to the donor hive [13], leaving your cell builder full of young nurse bees. You have now created a free-flying queenless cell builder colony. At this time you can temporarily add the frame of larvae to be grafted [14].
As you were shaking bees, if there was nectar shaking from the combs, the bees do not need to be fed. If not, then lightly drench all the bees with 1:1 syrup and add a quart of syrup in a top feeder jar. Put a cover on the cell builder and check back in an hour.
One-hour check back for strength: After an hour, your cell builder should look like this—bees covering the frames and hanging from the lid. If there are not this many bees, then shake additional bees (through a sieve box) off of brood combs from other donor colonies. A strong starter like this can rear up to 50 queen cells, even in a snowstorm [15].
Now wait a few to several hours. It takes a few hours for the bees to recognize that they are queenless, and to be ready to start building emergency queen cells. What you are going to now do is to give them chosen larvae from which to rear those cells.
I got the idea for this method from observing my bees building queen cells as in the photo above. It occurred to me that we could duplicate the process with prepared queen cups, thus avoiding the need for the recreational beekeeper to use cell bars to hold the queen cells (commercial guys typically put about 50 grafted cells distributed on 3 cell bars into a special frame).
Down to the nitty gritty—grafting. Yes, I said “grafting.” Don’t have a heart attack–if you are manually adept enough to trim your nose hair, you can use a Chinese grafting tool!
Cell cups: bees love JZ’s BZ’s cell cups, and they eliminate the chance of using contaminated wax. Try ‘em!
A damp towel: To keep the grafted larvae from drying out.
Magnifying head lamp: If you’re over 40, use it! Big tip: graft in a completely dark room (give your eyes a few minutes to adjust). It is a hundred times easier to see what you’re doing. Get a comfortable chair and a table in front of you. Tip up a stand (like a hive cover) to angle the grafting frame perpendicular to your line of sight.
The grafting frame: Now go pull the grafting frame of breeder larvae from the cell builder. At this point, all the old bees should have flown home, so any bees remaining in the cell builder should be gentle as pussycats; so don’t use any smoke–you don’t want to disturb the bees now that they’ve rearranged themselves. Gently brush the bees from the frame (don’t shake it [16]), and wrap it in a damp towel to keep the larvae from drying. Go to the darkroom, set the frame up in front of you, put on your magnifier, turn on the headlamp, and grab your Chinese grafting tool. Take a deep breath and relax.
How to use the Chinese grafting tool: I drew some pictures below. Moisten the blade of the tool; if you’ve used it previously, it will likely be stuck to the plunger. Most graftpersons just lick the tool to keep it clean [17]. Read the instructions below. Practice on a few larger larvae until you get the hang of it. You will see that some of the larvae on the frame have been given extra jelly—these are the ones that you want to graft (since they’ve already been chosen by the bees). The extra jelly makes grafting really easy. With a bit of practice, you’ll be able to transfer a larva in a couple of seconds.
Step 1: Quickly slide the tool straight down the cell wall so that the blade approaches the larva from the outside of its body curve. Do not push down on the plunger at this time.
Step 2. The blade will follow the curve on the rounded bottom of the cell and scoot under the jelly without disturbing the larva.
Step 3. Now pull the tool straight up. The jelly (and larva) will stick like glue to the blade.
Step 4. Hold a plastic cell cup in the fingers of your other hand. Push the tool down into the center of the cup until the blade is slightly bent. Now you push down on the plunger with your index finger to push the jelly (and undisturbed larva) off into the cell cup. With practice, you’ll pull up slightly on the tool at the same time. Easy!
This is what it looks like: Here’s a photo of a larva and jelly on the end of a grafting tool. In this frame, I used the “hunt” method to search for larvae of the right age. If you hold a breeder queen in a small colony to keep her from swarming, she will put eggs into any available empty cell, and the larval ages will be scattered.
Grafting in the field: In this photo I’m showing off to a class, demonstrating how one can graft (if necessary) out in daylight; but it’s much easier in the dark.
This is better! In this photo I’m using a headlamp in a dark room while I graft into a cell bar. Note that sterile technique is not necessary.
Don’t let them dry out! Place the cups face down on a damp towel after you graft each one. This keeps the larvae from drying out.
Push the grafted cells into the top of the channel. Now pull the frame in which you scraped the channel out of the cell builder, and gently push the grafted cells into the comb—they will stick to the warm wax (the cup openings must face downward).Space the cell cups as close as ¾” on center. The channel allows the nurse bees access around the open end of the cup in order to build the queen cell.
Put them back into the cell builder: Now put the frame with the cell cups back into the cell builder; if the cups are on the pollen frame, face them toward the frame of open brood (or vice versa). Replace the lid and put on a syrup feeder if there is no nectar flow. Allow the bees to fly freely out the entrance (use a robbing reducer if indicated).
Allow the bees to build the cells: You really don’t need to open the cell builder for another 11-12 days, but you’ll probably be curious. It’s OK to inspect progress [18]. Again, you shouldn’t need to use any smoke. Here’s what the cells will look like after 24 hours—half full of jelly with a bit of cell wall built. If there is no nectar flow, you should feed the colony with a cup or so of 1:1 syrup each day—you don’t want to overfeed, or the bees will build comb between the queen cells.
Two days later: The cells should be full of jelly, and the queen cells well drawn. The cell in the middle didn’t take. Note that most of the feeding of a queen larva occurs in the first 2-3 days.
Top monitoring: With the clear plastic cell cups you can monitor success by simply looking down from the top. If the cell is full of white jelly, there is a larva being fed.
Now how hard was that? By about Day 4 after grafting, the bees will have completed feeding the larvae, and will cap the cells. Obviously, optimal nutrition is critical for the cell builder for the first days! The queens will typically emerge on Day 11 or 12 after grafting.
Day 9 – 10—make up your mating nucs: I usually make up queenless mating nucs on Day 9 after grafting, usually with 4 frames in a 5-frame nuc box (add another frame of foundation if there is a flow on). For best acceptance, allow the nucs sit for a day or two before inserting a queen cell. I rarely feed my nucs.
Day 10 – 12: Pry out the ripe cells with your hive tool, being careful to only touch the plastic cup! Well-fed ripe queen cells should have plenty of uneaten jelly visible in the plastic cup.
Handle these precious cells gently: Keep the cells at body temperature, and don’t drop or jar them.
Insert the ripe cells into nucs: Spread the two brood frames in the nuc slightly and push the cell gently into the comb, cup end up. Press only on the plastic cup [19]. In cold weather, make sure that the cell is hanging over brood, so that the bees will keep it warm. Pry the frames back together.
Two weeks later—check for mate out: (Up to three weeks if there wasn’t good mating weather). In good flight weather the queens will emerge, mate, and then start laying eggs anywhere from 8-12 days after putting in a ripe queen cell. Look for where the bees have prepared a cleaned brood area— if you’ve got a laying queen, there will be evenly laid eggs in every cell. This is my favorite part of beekeeping—every beautiful new queen is like a daughter to me! Typically, about 4 out of 5 have successfully mated out, so I then take the frames from the dinks and use them to make up the missing frame in the successful nucs.
Now share them! There are pockets of mite-resistant survivor bees naturally evolving in feral populations all over the country. These are an invaluable resource; we need to propagate them! This can be done most effectively away from areas with a large influx of “domesticated” bees, creating an opportunity for the recreational beekeepers of local clubs to work together with each other and with nature to facilitate this natural evolutionary process. I will write more about this subject in the future, but for now, if you have a hive that has indeed survived in good health without mite treatment for more than two seasons, PLEASE raise queens from that bloodline and sell or share them around your local beekeeping community!
More photos and details on the Web: In the interest of space, I kept this article minimally short and sweet. I’ve posted a more expanded, downloadable Powerpoint version, with more details, and the photos at full size to Queens for Pennies .
For sideliners wishing to rear a greater number of queens at a time, see Small Scale Queenrearing.
Footnotes, Tips, and Tricks
1 A colony that has not survived for at least 2 years in good health, without treatment, cannot be considered to be “survivor stock.”
2 Jeweler’s 2.0x headband magnifier Models change regularly—I use an older unlighted one with a backpacker’s headlamp strapped to the headband. You want to be able to focus the light directly into the cell from which you are grafting. I recently tested several models available from Amazon and was quite pleased with the:
Carson Pro Series MagniVisor Deluxe Head-Worn LED Lighted Magnifier with 4 Different Lenses (1.5x, 2x, 2.5x, 3x) (CP-60)
This magnifier costs a bit more, but is comfortable, easily adjustable, has a bright adjustable lamp that runs on AAA batteries, and comes with 4 lenses. The focal length of the 2.0x lens is about 6 inches, meaning that you’ll hold your eyes about 7″ from the grafting frame.
3 There is lots of variation between even those from the same manufacturer, so get more than one; plus you may damage your first in learning to use it. I prefer those with a bamboo plunger, e.g., Mann Lake HD-390). You can use other tools, but I find the Chinese style to be the easiest and quickest once you get the hang of it.
4 E.g., Dadant M00663; Mann Lake QC400
5 A trick is to place a clean, dark drawn comb into the center of your breeder queen colony 4 or 5 days before Day 0. Four days later, it will be full of larvae the right age for grafting.
6 Do not try to graft from a frame that is not darkened from several generations of brood—otherwise the bottoms of the cells will not be rounded enough for the use of a Chinese grafting tool.
7 This can be your breeder colony if you wish. There may actually be an advantage to using nurse bees from the breeder colony, in order to pass on the best gut flora, immune factors, and epigenetic regulators to the queens that you are about to rear.
8 You can feed this colony in advance to prepare it.
9 Believe me, putting her frame aside in a nuc box really helps in keeping track of her! If you have trouble spotting queens, then do this (you can do the previous day):
How to harvest queenless nurse bees without ever spotting the queen: Move the donor colony to the side, and put a bottom board and empty hive body down in its place. From the donor colony, put a couple of frames of brood into the center of the hive body, and then fill it out with drawn comb and honey. Then place another empty box on top to act as a funnel. Shake all the bees off the remaining combs into the “funnel.” When you’re done shaking, gently brush the bees down off the sides of the funnel box, using very gentle smoke wafted above them to guide them. The point of this is to make sure that you’ve gotten the queen into the bottom box.
Once you’ve got all the bees into the bottom box, then put a queen excluder over it, and stack the rest of the combs back over it. The nurse bees will quickly move up through the excluder to cover the brood. In an hour, it will be easy to harvest queenless nurse bees from the upper boxes, and the older bees will return to the lower box to take care of the queen and brood. After harvesting the nurse bees, you can add the combs to other hives.
10 This arrangement is for a basic cell starter. The number of frames is not critical—all that you need is some young brood to stimulate jelly production in the nurses, beebread for them to eat, and empty comb in which they can store incoming nectar.
11 If you’re using wax foundation or foundationless combs, just figure it out! You can place the scraped beebread back on the top bars and the bees will readily consume it.
12 If you have any reason to suspect that there may be a second queen (or virgin) in the donor hive, shake the bees through a “sieve box”—a medium super with a queen excluder screwed to the bottom. It happens!
13 Return the queen to the donor hive. The donor hive will now consist of only a couple of frames of brood and older bees, and will lose any swarm impulse. If you use your breeder hive as the donor, this will keep you from losing your breeder queen to a swarm.
14 This is not necessary, but adding the larvae to be grafted at this time is a trick I use to get a jump on the queen differentiation process. While you leave the bees to recognize their queenlessness, they will start preferentially feeding some young larvae extra jelly in preparation for making them into emergency queens. When you later pull this frame for grafting, you can then use the larvae that the bees have already chosen and started to prepare as royalty.
15 In order to raise only 10 cells, the cell builder could actually be considerably weaker. But no matter, since you can later leave one queen cell in the cell builder to create a kick-ass nuc.
16 Shaking the frame will shift the larvae to the sides of the cells and make grafting more difficult.
17 You’ll wind up eating plenty of royal jelly, so forewarn your spouse, in case it has an aphrodisiacal effect on you.
18 It’s also a good idea to check the brood frame for any volunteer cells, which could theoretically emerge prior to your cells and kill them. Cut out any volunteer cells.
19 Do this bare handed or wearing thin latex gloves. Do not try while wearing clumbsy leather gloves.
Over the past few decades, as a beekeeper/biologist I’ve had the opportunity to watch evolution in action. I’ve observed the catastrophic effects upon colony health due to the introduction of new parasites, periodic pathogen epidemics, and the more subtle effects of changing land use practices and climate change. I’ve also witnessed the evolution of both recreational beekeeping and the bee industry, as we’ve been forced to change our management practices and income streams due to the aforementioned biological and environmental factors, plus changes in markets and the impacts of regulatory decisions.
My point is that things change, each change altering the realized niche of both bees and beekeepers. Neither Nature nor the Market are the least bit sentimental. Those who don’t adapt to change die.
The adaptive process may make headlines, or it may go largely unnoticed. But one thing’s for sure—the more that we understand the changes in the parameters of the bee and beekeeper niches, the better we can successfully engage in the adaptive process.
We Are Two Adaptive Species
Both Apis mellifera, and those Homo sapiens categorized as “beekeepers” have proven to be incredibly adaptive species (ecologists would say that we exhibit a high degree of plasticity). At times, each of our populations face limiting factors that weed out the least fit. And the higher the failure rate of individual colonies or beekeeping operations, the stronger the selective pressure to adapt.
So what sort of failure rate is “normal” for bees under optimal natural conditions (the fundamental niche)? Let’s do the math! Given: an established and stable local population of bees under optimal conditions. In the spring each colony will produce at least one swarm. At that point, the colony population will have temporarily at least doubled. But such a rate of reproductive increase is obviously unsustainable, since by definition a “stable” population ends with the same number of colonies each year. So simple arithmetic tells us that in nature, on average, at least half of all colonies will succumb each season, even under the best of conditions.
Although half the colonies will fail on average, it is not the average colony that fails. The key point is that it is the leastfit that tend to fail, and a greater proportion of the most fit survive. This considerable amount of selective pressure is what drives adaptation and evolution in each natural population of bees.
It’s the same with beekeepers. The failure rate for beginning beekeepers is often even higher than the above. Commercial operations also fail; despite record high prices for honey and pollination services, our recent elevated colony mortality rate is eliminating the profit margin for some operators, who, sadly, will go out of business. But, again, the hard fact is that it is the less fit (or less adaptable) operations that are failing—I speak with plenty of operators who aren’t experiencing egregiously high winter losses, and whose businesses are firmly in the black. It is these operations that are successfully adapting to their realized niche.
Honey Bees Are Designed For Rapid Adaptation
As I study the honey bee reproductive strategy, one principle jumps out:
Everything about the honey bee reproductive process is designed for rapid adaptation to changes in its realized niche, and for the recovery of the bee population from decimation events [1].
Apis mellifera has the highest known rate of genetic recombination of any animal. And those “experimental” recombinations are then filtered for success through the haploid drones, who have only one set of chromosomes, meaning that only the best novel combinations of genes (alleles) have any chance of being passed to the next generation.
The genetic combinations of the fittest drones then predominate in the matings that occur in drone congregation areas, thus ensuring that each virgin queen has the best chance of loading up with the best genetics that the overall bee population in that area has to offer. And she further ensures the maximum diversity of her offspring by mating with multiple drones. Add to this the incredible epigenetic plasticity of the honey bee [2], and we have an organism able to quickly adapt to whatever Nature throws at it!
I observe something similar with beekeepers. Those who are consistently trying new things and adapting to the changing biological and business environments are those who tend to be the most successful in the long run.
The Human-Facilitated Realized Niche Of The Bee
OK, so in nature, half the colonies fail each year. But provided facilitation by human beekeepers, that rate can drop to around 10% for well-managed operations. However, in recent years, U.S. beekeepers have been reporting distressingly high rates of colony failure. Clearly, something in the realized niche of our honey bees has changed in the last decade (one or more limiting factors). In order to attempt to figure out exactly which factors are responsible, let’s first determine what the primary limiting factors were for honey bee populations prior to humans. Perhaps then we can better understand how our actions (and the Earth’s burgeoning human population) are affecting honey bee survival. And maybe then we can take steps to make life easier for our beloved bees (and improve the bottom line of those of us who make our living at keeping ‘em).
The Natural Limiting Factors Of The Honey Bee Population
Limiting Factor: The Weather
The weather would be an obvious limiting factor—colonies are stressed by extreme cold, unfavorable flight weather during the spring or summer, or by lack of forage and water during droughts. Such intermittent weather events may sporadically cull the bee population, but would only affect long-term adaptation if they occurred regularly. So let’s focus upon which factors limited bee populations in favorable years, during which they have the intrinsic ability to increase exponentially.
Limiting Factor: Predation
Honey bees are herbivores. The populations of many herbivores are controlled by predators (Fig. 1). If the population of the prey species becomes dense, predator species ramp up their numbers to take advantage of the food source. The result is typically an oscillating predator/prey population dynamic (this is one of the bases for integrated pest management in agriculture).
Figure 1. Foraging bees face plenty of predators, such as wasps, assassin bugs, birds, spiders, and dragonflies. One of “my” bees (above) became a meal for a robber fly.
Although predators of foraging bees may take a bite out of the population of older bees in the hive, they do not appear to be a primary limiting factor of the overall bee population. An exception to this rule might be the Asian Hornet (Vespa velutina) (now introduced in Europe), which can decimate small colonies of bees by picking off returning foragers [3].
A more serious form of predation is direct invasion of the hive. A healthy colony can generally repel or otherwise deal with small invaders such as ants, wasps, and Small Hive Beetles. More problematic are those large mammalian predators willing to ignore the bees’ defensive stinging, such as bears, skunks, honey badgers, and humans. The bees’ main defense against such predators is to nest in inaccessible fortifications. And that leads us to…
Limiting Factor: Competition For Nest Cavities
Bees are pretty picky about the nest cavities that they choose, strongly preferring elevated tree cavities having small, defendable entrances [4] (Fig. 2). In treeless areas, the lack of suitable nest sites could well have been a limiting factor for the honey bee population. But this is unlikely to have been the primary limiting factor anywhere that patches of ancient forest were within range.
Figure 2. This hollow black oak provides a protected nest cavity impenetrable by our local black bears.
Although a lack of suitable cavities may not the main limiting factor of the bee population, it does bring to mind another fascinating aspect of bee behavior. Please allow me to digress for a bit. Not all beekeepers are aware that intra- and inter-species parasitism is common among bees, wasps, and ants. For example, queens of a number of bumblebee species parasititically invade and take over other bumblebee colonies. And the Cape Bee (Apis mellifera capensis) is famous for its ability to parasitically take over colonies of the Savannah Bee (Apis mellifera scutellata) [5]. This sort of deplorable behavior appears to be ingrained in the bee genome– bees covet the fruits of their neighbors’ hard work.
Part of the Africanized honey bees’ ability to rapidly expand its range in the Americas was likely its ability to invade and usurp the established nests of European bees [6]. Lately, Dr. Wyatt Mangum has been reporting on his observations of similar behavior by ostensibly non-Africanized bees in Virginia [7].
Such takeovers give the usurping swarm a profound advantage. Rather than needing to establish a nest and provision it with stores from scratch, it can simply take over an established colony, essentially hijacking its combs, stores, and entire workforce. Although Mangum, so far as I know, is the first to report such behavior for European honey bees, his observation may answer a question that has been bugging me for years: why do European bees send out what appear to be doomed swarms in late summer?
Bees typically swarm in spring, for the obvious reason that that timing allows the swarm colony to establish and provision a nest in time for winter. But in actuality, there are two peaks of swarming during a season (Fig. 3). I’d long noticed this, and wondered why in the heck a colony would bother to swarm in the late summer—natural selection should have eliminated such suicidal behavior. It just didn’t make sense!
Figure 3. Seasonal timing of swarm emergence dates in New York, showing the main late-spring peak, followed by a lesser peak around the first of September. Why the heck would colonies swarm in late September? After Seeley [[i]].
I assumed that the data was for New York and from the following paper, but I was unable to obtain a copy:
Fell, R. D., et al (1977) The seasonal cycle of swarming in honeybees. J. Apic. Res. 16:170-173.
But Mangum’s observations reminded me that I’ve also seen in past years late-summer swarms landing on hives, and also seen balled queens in hives in late summer. Perhaps I simply never put it all together! Could it be that this is an innate, but previously unrecognized, behavior in European bees?
It is certainly biologically plausible that under certain circumstances European colonies behave like their Africanized brethren (they are, after all, the same species), and send out older queens who have already successfully built up a colony (and perhaps even a second swarm colony), but still have enough vigor left to do an invasive usurpation of a nearby nest. If the colony were already superseding that queen, then it would be an inexpensive gamble to send her out, accompanied by a hit team of experienced workers, to try to take over an unsuspecting colony, its stores, and its workforce shortly before winter.
Pardon my digression—let’s return to our search for the main limiting factor of the natural bee population.
Limiting Factor: Carrying Capacity Of The Habitat
The maximum population density for the realized niche of a population is set by the carrying capacity of that particular environment, typically limited by resources such as food. However, the honey bee is a special case; similar to the bear, the colony can gorge when food is plentiful, and store “fat” (honey and beebread) as reserves for lean times (as during overwintering).
There are indeed areas in which colonies can barely put on enough honey during the main flow in order to make it through the winter. But by definition, such areas would not meet a primary requirement of the fundamental (optimum) niche of the honey bee, so we can disregard such areas from this discussion. What we are interested in is the limiting factor of the bee population in areas that normally produce a good honey flow.
Limiting Factor: The Timing Of The Bloom
Honey bees are defined by their ability to store food reserves—honey and beebread—to see them through lean times. But there are times other than the main honey flow during which the availability of nectar, and especially pollen, are of critical importance to the ability of colonies not only to survive, but also to reproduce. Colonies must build up and produce a swarm early enough in the season that both parent and swarm colony have fighting chances to store enough honey to make it through the following winter [9]. Such buildup requires the initiation of broodrearing in the middle of winter, which is in turn dependent upon having stored a large supply of beebread during the fall pollen flow [10].
What we must keep in mind is that a colony of bees is only effective at putting away a honey surplus if it has grown a large enough population to efficiently forage upon and store the available nectar. Timing is everything. Too large a population at the wrong time of the year would be counterproductive, since those hungry mouths would consume more honey than they were able to store. A locally-adapted population of bees times its buildup to coincide with the main flow, and then quickly shrinks back to survival mode.
Many of us tend to base our idea of typical bee behavior upon that of commercially-selected Italian stock. Such stock, originally adapted to Mediterranean climates, and bred for continuous broodrearing and high honey production, can hardly be expected to be representative of wild type bees adapted to cold-winter areas (I am not dissing Italian-type bees—they are well adapted to build up early for almond pollination).
Bees adapted to colder winters, such as the Carniolans or Russians, are far more responsive to the environment, especially to the availability of pollen. As soon as plants start producing pollen in spring, bees of these races explode into action —working even in cool and wet weather, and madly brood up.
The reason for their frenzy is that they must build up their population early enough to produce a swarm in time for it to have a decent chance at establishing a nest and putting away adequate winter honey stores during the brief main honeyflow (typically May through June; in temperate climates, colonies may only gain weight for a few weeks a year). I’ve previously graphed the bee colony’s amazing ability to quickly build up [11]. An absolute requisite for such a rapid rate of growth is a monster supply of pollen in the early spring.
After the main flow comes the summer dearth. When pollen is unavailable, wild-type bees sit tight in survival mode [12], cooling their heels and conserving their energy. I’ve seen Russian bees cease broodrearing in August in the arid California foothills, appearing as though they were queenless. In the adjacent yards, my Italian stock just keep on rearing brood, and required supplemental feeding of protein in order to keep them in decent shape for going into winter..
So I suspect that the limiting factor for bees in a natural realized niche is not the amount of food available during a brief period of food abundance (the main honey flow), but rather the quality and quantity of forage available during spring and late summer/fall.
Practical application: the realized niche of the honey bee is likely largely defined not by the amount of nectar available during the main honey flow, but rather by the quantity and quality of pollen available prior to and after that period. A successful colony requires a dependable abundance of quality pollen and nectar for early spring buildup; and then adequate late-season pollen to ensure its ability to produce a cluster of protein-rich “winter bees” and to store beebread for midwinter broodrearing.
Nevertheless, prior to man, biologically productive areas typically supported a diversity of native vegetation that produced exactly such an extended season-long buffet of nutrition. Thus, I doubt that during favorable years, a lack of available spring or fall food resources was the limiting factor of the bee population prior to man.
Limiting Factor: Competition For Those Food Resources
Competition for food resources, either against other species or one’s own species, is a common limiting factor of the realized niche. So what sort of competition do bees face?
Anywhere that there are flowering plants, there are pollinators that have coevolved with them. Most are insects (although in some areas, birds, bats, or other mammals may be important). Does competition with other pollinators limit the honey bee population?
Let’s think about it. Since one can place a hive of bees into most any favorable habitat and still make honey despite the presence of established populations of native pollinators, I suspect that competition with other species is not normally the limiting factor of the honey bee population. On the other hand, as any beekeeper quickly recognizes, honey bee colonies certainly compete with one another!
Beekeepers tend to focus upon the amount of nectar available during the main honey flow, and understand that one can overload an area with managed hives. But how about the density of a natural population of bees—does the amount of nectar available during the main flow limit that population?
Again, let’s check easily-verifiable observations. In areas with well-established populations of feral bees (Australia, Hawaii, formerly in the U.S), one can bring in additional managed colonies, yet still produce a substantial honey crop during the main flow—clearly, nectar is produced in excess of what an established natural population of bees can harvest. It follows then that at a “normal” population density of unmanaged colonies, competition for nectar during the main flow was not the limiting factor for colony survival.
On the other hand, competition for pollen during spring or fall could well be a limiting factor. And along with that competition comes…
Limiting Factor: Intercolony Parasitism
Competition between colonies does not occur only for nest sites or at the flower; it can also happen directly at the hive. All’s fair in love, war, and in Nature. If you can save yourself effort by stealing the fruits of another’s labor, so be it. The term for this is kleptoparasitism (kleptoparasite: a bird, insect, or other animal that habitually robs animals of other species of food).
What we call “robbing” is a form of kleptoparasitism, and during early spring or the summer dearth, the robbing pressure between colonies can brutal. There would be a clear competitive advantage to those colonies that successfully robbed honey from others; conversely, there would be an advantage to those colonies best able to defend their hard-won stores.
Robbing behavior may also be more insidious than the overt invasion of a weak colony by a strong colony. Dr. Wyatt Mangum detailed the sneaky “progressive robbing” of one colony by another [13]. Such robbing would constitute an insidious drain upon the victim colony. In areas of high colony population density, I suspect that robbing pressure–at times other than during major honey flows–is a limiting factor in colony density.
And this very robbing behavior brings us to our last suspect factor– that famous Horseman of the Apocolypse, Pestilence.
Limiting Factor: Pathogen Transmission
As most beekeepers soon find out, honey bees are host to a number of parasites and pathogens. To a biologist, a pathogen is a parasite (such as a virus, fungus, or bacterium) that can cause disease. These parasites can cause the bees to suffer from either endemic or epidemic infections. A well-adapted parasite typically does not, under normal circumstances, cause serious disease, but rather smolders in the bee population of each individual colony as an endemic infection; sacbrood virus or Nosema apis follow this model. These well-adapted parasites are typically vertically transmitted, that is, from parent to offspring, or in the case of bees, from mother colony to daughter colony. They can generally be found in a colony, but so long as the colony is not stressed, there are no symptoms of disease.
Other parasites tend to go epidemic, sometimes in recurring cycles; chalkbrood, Chronic Bee Paralysis Virus, American Foulbrood, and European foulbrood fall into this category. Individual colonies are able to “clear” themselves of these parasites; the parasites maintain a presence in the local bee population, but may not be found in every colony. Epidemic parasites are largely dependent upon horizontal transmission from colony to colony, and unlike the well-adapted endemic parasites, actually benefit by the weakening or death of an infected colony. As such, they would be considered to be density dependent infectious diseases. As the density of the host (honey bee colonies) in the environment increases, the opportunities for transmission of the parasite from colony to colony directly increases [14]. The pathogen causing the disease can only persist if the host density exceeds a certain threshold (if bee colonies were scattered beyond flight distance, there would be slim possibility for an infectious pathogen to transmit from one colony to another).
Conversely, not being regularly exposed to a pathogen removes the selective pressure for the bees to maintain genetic (or epigenetic) resistance. Thus, in nature, epidemics of certain pathogens ebb and flow, often decimating a host population one year, at which point the host density is decreased to the extent that the pathogen nearly disappears, struggling to maintain a foothold in the few remaining, and most resistant, hosts. As the host population then recovers over the years, an epidemic may then recur (higher host densities favor virulent mutations of the pathogen). This is a common cyclic pattern in insect species with large populations, and bees are no exception [15].
Practical application: After a plague it may take years for a particular pathogen to again recover its hold in the bee population. And it may take a special combination of environmental circumstances, and perhaps coinfection with other parasites, in order for it to do so.
For most species of wildlife, natural populations tend to reach some sort of dynamic equilibrium, with pestilence being the ultimate limiting factor if all other conditions are optimal. Anderson [16] explains:
It is likely that interplay between the pathogenicity of viral, bacterial, [or] protozoan infections and the nutritional state of the host contributes importantly to the density-dependent regulation of natural populations, with the parasites greatly amplifying the effects of low levels of nutrition.
Such pestilence typically occurs in the form of epidemics, during which the pathogen(s) efficiently spread through a stressed and overcrowded population, the key word being overcrowded. Too many colonies of bees in an area is a recipe for disaster—a ticking time bomb just waiting for the right combination of environmental circumstances and the presence of a virulent pathogen (or combination thereof).
A Special Case: The Viruses
But it’s a bit more complicated when reservoir hosts are involved. That is, when a pathogen is not limited to honey bees as its sole host. And this is the case with the “bee” viruses, most or all of which appear to actually be generic insect viruses that bees pick up when they visit flowers. So it is likely that the density of the bee population is not limited merely by diseases specific to honey bees, but also by the entire pool of viruses that infect pollinating insects [17] (Fig. 4).
Breaking news: As I type these words, a collaboration of researchers associated with the USDA ARS labs is about to release a stunning paper [18], in which they detail how a plant virus is now infecting both honey bees and varroa, and appears to be associated with collapsing colonies. Their findings suggest that varroa may be a key player in the cross-kingdom jump of this virus. The complexity of the bee, mite, plant, and virus web of infection continues to astound us!
Figure 4. These Russian bees near the hive entrance are in the process of cooking a too-bold bald-faced hornet to death [[i]]. Hornets and yellowjackets eat bees, and are thus exposed to bee pathogens. Exposure also goes the other way as the wasps contaminate nectar with virus particles when they visit flowers, or, as in this case, if the dying wasp exudes any body fluids.
[i] Ugajin A, et al. (2012) Detection of neural activity in the brains of Japanese honeybee workers during the formation of a “hot defensive bee ball”. PLoS ONE 7(3): e32902.
Historically (meaning prior to varroa), these viruses were sporadically present in bee colonies, but generally as inapparent (free of noticeable symptoms) infections [20]. It was only under certain circumstances that they went epidemic and caused noticeable morbidity or mortality of colonies:
Taken together, these data indicate that bee virus infections occur persistently in bee populations despite the lack of clinical signs, suggesting that colony disease outbreaks might result from environmental factors that lead to activation of viral replication in bees [21].
In any case, in some years in some localities, such “perfect storms” of environmental factors, virulent mutations of one or more pollinator viruses, and coinfections with other parasites have historically led to serious colony collapse events [22]. This is not a new thing!
Conclusion
My original question was what were the primary limiting factors in the realized niches of the honey bee prior to human influence? I hope that I have adequately covered these factors, since I feel that our understanding of them is critical for us to be better beekeepers, and to make good management decisions.
As always, I prefer to let the reader draw his/her own conclusions, but to me it appears that that the primary limiting factors in colony survival in favorable areas were most likely the density-dependent competition for pollen during spring and fall, coupled with the associated transmission of certain pathogens.
The above factors have long been associated with epidemics in the bee population. It appears to me that our bees today are in the midst of an ongoing and complex multi-pathogen epidemic largely precipitated by the actions of mankind. In the next installment of this article I will explore how this situation came about, examining how changes in world trade, agriculture, the environment, and in beekeeping practices have affected the realized niche of the bee, its parasites and pathogens, and the business models of beekeepers. My hope is that by fully understanding how we inadvertently helped to create the problem, that perhaps we can better take steps to help our poor bees deal with the problem, and for ourselves to stay in business in the process.
Footnotes and Citations
1 “Decimation events” being plagues, droughts, wildfires, extreme weather events, etc.
3 Tan, K, et al (2007) Bee-hawking by the wasp, Vespa velutina, on the honeybees Apis cerana and A. mellifera. Naturwissenschaften 94(6): 469-472. Open access.
4 Seeley TD and RA Morse (1978) Nest site selection by the honey bee, Apis mellifera. Insectes Sociaux 25: 323–337.
5 Martin, S, et al (2002) Usurpation of African Apis mellifera scutellata colonies by parasitic Apis mellifera capensis workers. Apidologie 33: 215-232.
Danka, RG, RL Hellmich, TE Rinderer (1992) Nest usurpation, supersedure and
colony failure contribute to Africanization of commercially managed European honey
bees in Venezuela. Journal of Apicultural Research 31 (3/4): 119-123.
6 Schneider, SS, et al (2004) Seasonal nest usurpation of European colonies by African swarms in Arizona, USA. Insectes Sociaux 51(4):359-364.
7 Mangum, W (2010) The usurpation (takeover) of established colonies by summer swarms in Virginia. ABJ 150(12): 1139-1144.
Mangum, W (2012) Colony takeovers (usurpations) by summer swarms: they chose poorly. ABJ 153(1): 73-75.
Mangum, W (2013) Summer swarms with queen balling. ABJ 153(2): 163-165.
I assumed that the data was for New York and from the following paper, but I was unable to obtain a copy:
Fell, R. D., et al (1977) The seasonal cycle of swarming in honeybees. J. Apic. Res. 16:170-173.
9 Otis, GW and JM Wearing-Wilde (1992) Net reproductive rate of unmanaged honeybee colonies, (Apis mellifera L.). Ins. Soc. 39:157-165.
10 Seeley, TD and PK Visscher (1985) Survival of honeybees in cold climates: the critical timing of colony growth and reproduction. Ecological Entomology10:81-88.
12 This physiological change to diutinus bees occurs when newly-emerged workers sense queen pheromone, but no young brood pheromone, which tells them that the colony is in survival mode. This typically occurs in fall, but can also occur during summer dearth. See https://scientificbeekeeping.com/an-adaptable-workforce/
13 Mangum, W (2012) Robbing: Part 2: Progressive robbing. ABJ 152(8): 761-764.
14 Hudson PJ, et al (2001) The Ecology of Wildlife Diseases. Oxford University Press, Oxford.
16 Anderson, RM and RM May (1979) Population biology of infectious diseases: Part I. Nature 280(2): 361-367.
17 Singh R, et al (2010) RNA viruses in hymenopteran pollinators: evidence of inter-taxa virus transmission via pollen and potential impact on non-Apis hymenopteran species. PLoS ONE 5(12):e14357.
18 Lian JL, Cornman RS, Evans JD, Pettis JS, Zhao Y, Murphy C, Peng WJ, Wu J, Hamilton M, Boncristiani HF, Jr., Zhou L, Hammond J, Chen YP. 2014. Systemic spread and propagation of a plant-pathogenic virus in European honeybees, Apis mellifera. mBio 5(1):e00898-13. doi:10.1128/mBio.00898-13. Open access.
19 Ugajin A, et al. (2012) Detection of neural activity in the brains of Japanese honeybee workers during the formation of a “hot defensive bee ball”. PLoS ONE 7(3): e32902.
20 Hornitzky, M (1987) Prevalence of virus infections of honeybees in eastern Australia. Journal of Apicultural Research 26(3) : 181-185.
Anderson, DL and AJ Gibbs (1988) Inapparent virus infections and their interactions in pupae of the honey bee (Apis mellifera Linnaeus) in Australia. J. Gen. Virol. 69: 1617-1625.
Mouret, C, et al (2013) Prevalence of 12 infectious agents in field colonies of 18 apiaries in western France. Revue Méd. Vét. 164(12): 577-582. http://www.revmedvet.com/2013/RMV164_577_582.pdf
21 Tentcheva, D, et al (2004) Prevalence and seasonal variations of six bee viruses in Apis mellifera L. and Varroa destructor mite populations in France. Appl. Environ. Microbiol 70(12): 7185-7191. http://aem.asm.org/content/70/12/7185.full
First published in: American Bee Journal, February 2014
What’s Happening to the Bees?
Originally published in ABJ Feb 2014
Randy Oliver
ScientificBeekeeping.com
I’m realizing that what I thought was going to be a quick review of CCD has turned into a very long series of detailed articles, and I’m not even near reaching the conclusion. So on this 20th anniversary of my first seeing the parasite that changed beekeeping worldwide, I thought that I’d interrupt the Sick Bees series and attempt to explain, more briefly (hah!), and from an ecological perspective, what’s happening to the bees these days, and how beekeepers are being forced to adapt.
One Wild Ride!
In 1994 I saw my first varroa mite—on a stickyboard that had been placed by the county bee inspector under one of my hives. Little did I know how much that little maroon speck was about to change my life!
Varroa clobbered me (or more precisely my bees). And then did it again; and then again. I finally got pissed off and decided that I should either give up beekeeping altogether, or dust off my scientific training and really learn about bee and mite biology, and how to apply it to practical beekeeping.
What’s interesting is that my very first article (on almond pollination), in the fall of 2006, was published just as Dave Hackenberg’s colonies began to collapse from CCD. The occurrence of CCD put the bee research community into high gear to try to figure out what the heck was happening. And that created a “niche” for a practical beekeeper with a biological background, willing to act as a translator of the scientific findings to an alarmed beekeeping community. I unwittingly stepped into that niche, and it swallowed me up. A mere seven years later, and to my utter surprise, I’ve gone from being an obscure sideline beekeeper to a globetrotting speaker on bee health and management.
I’ve now been fortunate enough to visit both professional and recreational beekeepers in every part of North America and in several other countries. I’ve seen many styles of beekeeping, from the tropics to the Arctic, heard the local problems and concerns, and had the chance to learn from some very smart and successful beekeepers. I’ve attended scores of conferences, read countless scientific papers, and picked the brains of the world’s best apicultural researchers. Then I’ve done my best to share what I’ve learned with others. I’ve met scores of wonderful people and made a lot of new friends, and I’d like to take this opportunity to thank you all for the appreciative and effusive support!
How We’ve Benefitted From CCD
CCD has been a mixed blessing to beekeepers. It brought grown men and women to tears (see the film The Last Beekeeper [1]), and the elevated rate of colony mortality in recent years has made it difficult to keep our operations in the black. But it also pushed our scientific community to learn more about the biology of the honey bee than they had in a great many years. And many of us are much the better beekeepers for it.
Unlike that of other livestock, the true contribution of pollinators to U.S. agricultural production is not reflected by farm gate sales figures, so bees have traditionally not received their fair share of USDA research funding, nor does the beekeeping industry have the lobbying clout of the cattle, poultry, or pork producers. But we’ve benefitted from the public awareness of the plight of pollinators, which has resulted in the shifting of some funding our way [2] (although bees still only get about a tenth the amount of money set aside for research on beef production). In addition, universities, grantors, and other governments have recently supported a great deal of research into honey bee and pollinator health (I only wish that the millions who signed the internet petitions to “save the bees” had instead each donated a single dollar toward bee research).
Misunderstanding And Misinformation
Although CCD refers to a specific set of symptoms [3], the media soon began to use the term for any sort of honey bee mortality (as did many beekeepers). And although the epizootic appears to have largely run its course, speculation ran rampant as to the cause(s) of “CCD,” and continues to do so with every new “documentary” and press release. Although “CCD” remains the poster child of colony losses, a blue-ribbon group of bee researchers cautions:
During the winter of 2008/2009, ∼10% of the 2.3million managed honey bee colonies in the US died with “CCD-like symptoms”, and US beekeepers self-diagnosed CCD as only the 8th most important contributor to colony mortality, behind starvation, queen-related issues, and parasites. The point is, honey bees die from many things. We must be careful to not synonymize CCD with all honey bee losses [4] (emphasis mine).
I’m typing these words as I fly over the beautiful jigsaw-puzzle-like frozen Manitoba landscape on my return from a speaking engagement in Sweden, where the film More than Honey had been recently shown. To my considerable surprise, the Swedish beekeepers (Fig. 1), after viewing the movie, were under the very strong impression that the bee problems in the U.S. were due to our brutal commercial beekeeping practices, and the moving of hives to the deadly almond orchards in California.
Figure 1. Beekeeper Göran Sundström at one of his apiaries in Sweden. Göran typically keeps 12 hives in an apiary, and goes to considerable trouble to comply with some rather arbitrary rules to have his honey certified as “organic.” The red paint is a traditional color for rural buildings in this area.
As it happens, the director of that film had stayed with me during his initial scouting visit to the U.S., and I was responsible for introducing him to my friend John Miller, who was unfortunately (and I’m sure unknowingly) to be cast in the role of the evil bee abuser, so I felt some responsibility to dispel those misconceptions to the concerned audience. And this brings me to my next subject…
Bees are currently enjoying a great deal of attention from a fearful public eager to do something,anything to help them. This could be a really good thing for the bees, for beekeepers, and for the environment as a whole if such public concern and activism could be guided into meaningful actions. I can’t really blame the public for being confused, since the entertaining and sensational docu-dramas about the impending extinction of the honey bee resonate more emotionally than do the dry and qualified explanations by scientists as to the “multifactorial” causes of colony mortality.
As a result of all the misinformation and hysteria out there, an unsure and distrustful public puts pressure their representatives to pass this or that new regulation to “save the bees.” This scares me. I feel that we should heed the sage advice of Thomas Jefferson:
People are inherently capable of making proper judgments when they are properly informed.
And therein lies the problem: due to the complexity of what’s happening with bees these days from the biological, environmental, agricultural, and economic standpoints, it’s danged hard to be “properly informed.” My gosh, just look at me trying to do that “informing”—I first thought that the “Sick Bee” series was only going to be two or three articles long! So what to do?
Challenging One’s Beliefs
One should be careful about embracing the popular stories about why “the bees are dying.” Some of the myths resonate so emotionally that they win uncritical acceptance by the mainstream, despite the fact that they cannot be reconciled with obvious facts (e.g., that bees can indeed thrive surrounded by GMO corn and soy, or on neonic-treated canola). As the popular scientific author Stephen Jay Gould pointed out:
The most erroneous stories are those we think we know best – and therefore never scrutinize or question.
Anyone who knows me (or has had the misfortune of trying to promote an unsubstantiated argument in my presence) can tell you that I’m a challenging and provocative person by nature. I’ve found that the best way to get to the truth is to learn how to argue your opponent’s side of a debate as well as you can argue your own. Therefore, I am more than willing to play Devil’s Advocate any time that I see one side of a legitimate argument being ineffectually presented. And I’m ruthlessly skeptical of any claims that do not jibe with what I see with my own eyes.
As you can imagine, this has earned me my share of vitriol from those who “know the truth” (read [5] for an enlightening discussion). Luckily, my mailbox runs about a hundred to one with thank you letters from beekeepers who appreciate my evaluation of the issues. I take this responsibility seriously; in order to remain objective and unbiased, I go out of my way to constantly question every one of my opinions (I avoid making “conclusions”). I eschew holding any “beliefs,” but rather adhere to the following principles:
That I should respect Nature and all forms of life (my ethical environmentalist side),
That I should thoroughly investigate all research and explanations of any subject, and avoid cherry picking data that suits my ideological convictions (my curious open mindedness and willingness to do my homework).
That I should base my opinions upon information and experimental results which stand up to scrutiny and questioning (my scientific side),
That I should then truth-check those opinions against on-the-ground evidence and observations (my practical side).
Unfortunately, many crusaders allow their commendable environmental consciousness (and innate fear of technology) to override the last three principles, which is understandable, since doing the homework is really hard, and our understanding of the biology involved is as yet incomplete. But I have some suggestions as to where to start…
A Homework Assignment
Allow me to first assign you some required reading. Put down this article and read Berndt Heinrich’s fascinating book Bumblebee Economics [6]. Heinrich studied the minute details of exactly how bees make a living in their ecological niche, focusing upon the economics of energy utilization. His revelationary insights changed my understanding of bee life completely. Then for something entirely different read Ron Miksha’s Bad Beekeeping [7] for a perspective on the economic trials and tribulations faced by professional beekeepers (his comments on p. 243 are especially relevant). I’ll wait ‘til you’re done…
OK, I hope those books were as thought-provoking to you as they were to me! Now let’s take a look at the health of bees and beekeeping from ecological and economic perspectives.
It’s All About Economics
Again and again, I find that everything boils down to economics and finding the right niche. This applies to both honey bees and to the business of beekeeping—either thrives in its ideal niche, and either must either adapt or die if the parameters of the niche change. And boy howdy, how we have changed the parameters of both of our niches in recent years!
Practical application: In this real world, each species, and each business, strives to exploit a niche to which it is particularly well adapted. A change in any of the parameters that define a particular niche may affect the profitability and survival of that species or business. If that species or business is efficient and profitable in its particular niche, then it thrives; if not, if must either adapt or go extinct.
For the remainder of this article, I will view the situation of both bees and beekeepers through the lenses of ecology and economics, and the changes that have occurred in the parameters that define our niches.
Let’s Define Some Terms
Pollinators are in decline over much of the world, and have been for some time [8]. We beekeepers are mainly concerned with our favorite pollinator, the European honey bee, Apis mellifera, native to Europe and Africa, but now introduced worldwide. Unless I specify otherwise, henceforth I will be referring to this species.
It occurs to me that if pollinators have long been in decline worldwide, then that would imply that something has changed in their ecological niches (and that it started before the introductions of cell phones, neonics, or GMO’s). It also occurred to me that the niches occupied by beekeepers have changed substantially (mine sure has; indeed several times). I’ll try not to burden you with too many new terms:
Habitat—where the bee species lives (or could live). The bees in the U.S. are mongrel hybrids of various European or African races [9], each originally adapted to specific microhabitats in their home countries.
Ecological niche—a description of the bees’ “occupation” in its specific microhabitat, including all environmental parameters and interactions with other species.
Fundamental niche— the potential full range of environmental conditions and resources that the honey bee as a species could possibly occupy and use, without the limitations of predation, competition, or other factors.
Realized niche—the less-than-optimal niche that each subspecies of bee actually occupies; constrained by weather, resources, parasites, etc. In its home range, various subspecies of honey bee adapted to narrow realized niches occurring in the warm Mediterranean, the cold Alps, the British heathland, the Egyptian desert, the African savannah, etc. In each of those niches, the bees adapted to the seasonality of local nectar flows, the local plant toxins, temperature, predators, and parasite pressure. Conditions may not have been optimal, but each subspecies was economically successful at “making a living” within those parameters.
So let’s list the most important parameters of the fundamental niche of the European honey bee:
It is a colonial species, existing as a superorganism with generally a single reproductive queen, supported by multiple patrilines of sterile workers, each exhibiting slightly differing genetics, behaviors, and resistance to parasites, toxins, and diseases (this within-hive diversity is extremely important, but often ignored by beekeepers).
It is a generalist species, able to gather food resources from a wide variety of plants. As such, it is adapted to metabolizing a wide range of toxic plant alleleochemicals (and by extension, synthetic pesticides).
It is primarily a pollinator; its diet normally consists solely of nectar and pollen, although those raw foodstuffs are processed into other products (honey, beebread, and jelly) for the actual consumption by the majority of the members of the superorganism.
The bee cannot forage unless the ambient temperature is above roughly 55°F (12°C). This limiting factor constrains its range to those areas that have adequate bloom available when the temperature exceeds that value; any colony with hungry brood when daytime temperatures do not exceed 55°F will soon become stressed due to an inadequate supply of protein (this is a huge management tip).
Unlike other insects, the European honey bee stores vast quantities of processed food for later consumption when resources are scarce.
This allows the colony to do something that no other species of temperate insect can do—maintain an elevated body temperature, and rear brood, throughout the winter.
In order to maintain that colonial body temperature, the European honey bee requires a protective insulated cavity within which to nest (Fig. 2).
Somehow, the European honey bee evolved with remarkably few parasites—the only significant ones being Nosema apis, the bacteria causing the two foulbrood diseases, the fly Braula, rare infection by two opportunistic fungi in pollen (chalkbrood or stonebrood), and what were normally “economically unimportant” infections by any of several insect viruses.
Figure 2. These bees are at the top of the winter cluster at the interface between empty cells and sealed honey. Despite the air temperature being below freezing, the temperature of the bees beneath the surface was 67°F (19°C). This remarkable technique of using stored sugars from the previous summer as an energy source during winter allows the honey bee to overwinter as a populous colony, ready to exploit early spring pollen and nectar sources.
In summary, the honey bee requires a dry cavity, in which it maintains a tropical environment throughout the year, allowing it to exploit food sources any time that the temperature is above 55°F, it is adapted to metabolize a wide variety of plant toxins, it only requires a brief honeyflow to provide it with food stores for the remainder of the year, and it evolved under low parasite pressure.
Practical application: this last point is of huge import when we attempt to understand the biological changes that have occurred in European honey bee populations worldwide in the last decades. To wit, virus infections have become serious “emerging diseases” [10].
Add The Beekeeper
OK, now let’s add one more term:
Facilitation—Optimal conditions in the fundamental niche occur infrequently, if ever. The job of the beekeeper is to optimize the conditions for his bees as best he can, such as by supplemental feeding, medicating for parasites, protecting from predators, providing a larger nest cavity, or providing water or winter insulation. Such “facilitation” may allow bees to survive outside of their fundamental niche.
Practical application: I recently enjoyed a lunchtime conversation with a couple of professional beekeepers who moved their hives from almonds, to the tallow bloom in Texas, to the Dakotas for summer, and then to a mild area in California for wintering (their problem is having too many bees each spring). What they are doing is facilitating the optimal fundamental niche for their bees for the entire year (there are many other ways of doing so).
Practical application flip side: If a beekeeper is keeping colonies alive outside of their fundamental niche, such as in densely-packed apiaries, in areas of crop monoculture or high exposure to toxic chemicals, in flowerless forest or dry grassland, or by the chemical suppression of parasites, should that beekeeper falter in his constant facilitation, his bees may not be able to continue to survive without such help.
Limiting Factors
The realized niche of the honey bee is constrained by limiting factors, which may change from season to season. Common limiting factors for populations of honey bees are:
Climate—bees have very wide “tolerance limits” for cold, heat, rain, and length of seasons. But at the edges of their tolerance limits, colonies will be stressed, and may not be able to deal with other limiting factors.
Competition for food—in some areas there is such an abundance of nectar during the main flow that there is little competition (an important point when speaking with native pollinator advocates). The main competition for food resources occurs at other times of the year; assume that there is serious competition happening if robbing behavior is evident.
Suitability of available food—not all plants produce honey-bee-friendly nectar or pollen, especially outside of the honey bees’ native range. This is clearly evident in America and Australia, where some pollen sources are notably nutritionally inadequate for honey bees (think corn, blueberry, watermelon, pumpkin, some eucalypts). And in some areas or under dearth conditions, bees will unwittingly collect naturally toxic pollen or nectar. And of course, some human-applied pesticides make the available food unsuitable.
Competition for nest sites—without hollow trees or other natural cavities, honey bees cannot survive the winter in temperate climates (Fig. 3).
Figure 3. One of my colonies swarmed late this spring and built open-air combs in a nearby hawthorn tree. We noticed it when the leaves fell in early December, following a week of subfreezing temperatures and a foot of snow. You can’t see it, but there is still a cluster of live bees (which I hope to rescue when I’m done writing this article). The population had obviously grown large enough to build and completely cover all the combs, and could easily have survived the winter had it only found an appropriate cavity in which to build its nest.
Predation—Such as birds, bears, wasps, and ants. The main predator of bees, of course, are humans, who often rob too much honey from the hive, resulting in winter starvation.
Parasitism—Again, natural populations of European honey bees appear to historically have been minimally affected by parasites under normal conditions. We will return to how this has changed.
Transmission of parasites—This is very density dependent—the more colonies within flight range, and the more competition for resources, the greater the transmission of parasites. The swapping of combs by beekeepers also changes this dynamic.
Toxins—Natural plant allelochemicals, soil metals, industrial pollution, agrochemicals, and recently, a huge influx of beekeeper-applied miticides.
Bees have a wide range of tolerance for some limiting factors, and more narrow ranges for others. Usually, several factors interact (sometimes synergistically) to limit bee populations.
Practical application: there is often a single limiting factor that is the determinant for colony survival. A concept used in ecology is “Liebig’s law of the Minimum” (Fig. 4). A beekeeper can work hard all season long to do everything he can for his bees, but should he overlook any single critical limiting factor, Liebig’s Law may come into play, and he may lose his colonies.
Figure 4. An illustration of Liebig’s Law of the Minimum as it applies to the practice of beekeeping. Despite everything else that you do to fill the barrel, the most unfavorable limiting factor(s) (or some combination thereof) at any critical period of time will limit the bees’ (and your) success. Adapted from [[i]].
Practical application: Each race of honey bee in Europe specialized by adapting to certain combinations of limiting factors, and thus gained a fitness advantage in its particular habitat. Since the arrival of varroa, which wiped out much of the feral population, the overall genetics of the U.S. bee population have likely shifted toward those propagated by commercial queen producers [12].
These “all-purpose” bee stocks are typically bred for color, temperament, and honey production, and maintained with a high degree of facilitation by the queen producer (feeding, treatments). There is no reason to expect those stocks to be well adapted for survival without constant facilitation. This is why I strongly support regional queen breeding for locally-adapted stock.
What Are The Limiting Factors For Honey Bees Today?
It would have been so simple had CCD actually been caused by cell phones! We could have banned the danged things, and wouldn’t have to listen to people walking around loudly and obliviously talking to themselves. But alas, it appears to be more complex than that.
So as a biologist, it occurs to me to go back before CCD, in fact, to go back even further in time, and ask the question, “Which factor(s) limited honey bee populations in Europe prior to modern management by humans”? And then we can work forward in time to see what’s changed since then. To be continued…
Footnotes and Citations
1Directed by Jeremy Simmons (2009), and recommended for those who didn’t experience the horror of CCD personally. Unfortunately, I can’t suggest anywhere to purchase a copy of this well-done and heart wrenching film.
2 Pollinator Research.–The Committee is aware that pollinators are responsible for the production of one-third of the Nation’s food supply, but the number of managed honeybee colonies in the United States has dropped in half since 1940. Because of the importance of pollinators in the production of the Nation’s food supply and their impact on the stability of our agricultural economy, the Committee encourages [the Agricultural Research Service] to continue to dedicate resources to protecting the health of both honeybees and other native bees, including continued research into colony collapse disorder. http://www.gpo.gov/fdsys/pkg/CRPT-112srpt73/html/CRPT-112srpt73.htm
3Symptoms of CCD:
1) In collapsed colonies
a) The complete absence of adult bees in colonies, with no or little build up of dead bees in the colonies or in front of those colonies.
b) The presence of capped brood in colonies.
c) The presence of food stores, both honey and bee bread
i) which is not immediately robbed by other bees
ii) when attacked by hive pests such as wax moth and small hive beetle, the attack is noticeably delayed.
2) In cases where the colony appear to be actively collapsing
a) An insufficient workforce to maintain the brood that is present
b) The workforce seems to be made up of young adult bees
c) The queen is present
d) The cluster is reluctant to consume provided feed, such as sugar syrup and protein supplement
From vanEngelsdorp, D, et al (2006, revised Jan 5, 2007) Investigations into the causes of sudden and alarming colony losses experienced by beekeepers in the fall of 2006. Preliminary Report: First Revision.
6 Heinrich, B (2004) Bumblebee Economics. Harvard University Press. I highly recommend all of Heinrich’s books—he’s a brilliant scientist and an engaging writer whose passion it is to understand the details of how organisms survive in their niches.
7 Miksha, R (2004) Bad Beekeeping. Trafford. For a more data-based analysis, see:
Laate, EA (2013) Economics of Beekeeping in Alberta 2011. http://www1.agric.gov.ab.ca/$Department/deptdocs.nsf/all/agdex14472/$FILE/821-62.pdf
Kotthoff, U, et al (2013), Greater past disparity and diversity hints at ancient migrations of European honey bee lineages into Africa and Asia. Journal of Biogeography 40: 1832–1838. http://onlinelibrary.wiley.com/doi/10.1111/jbi.12151/pdf
12 Delaney, DA, et al (2009) Genetic characterization of commercial honey bee (Hymenoptera: Apidae) populations in the United States by using mitochondrial and microsatellite markers. Ann. Entomol. Soc. Am. 102(4): 666-673.
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Thank you!
Randy
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