The Learning Curve – Part 2: Killing Mites without Killing Your Bees
“U.S. beekeepers crossed the Rubicon of pesticide application when Varroa mites were introduced in the late 1980s. They literally “tore down the fence,” as one wag put it, quickly transforming themselves from anti-pesticide fundamentalists into willing pesticide applicators.”—Dr. Malcolm Sanford (2008).
Those of us who remember the arrival of varroa, and the devastation that it initially caused, can easily understand why beekeepers (generally reluctantly) were more or less forced into becoming pesticide applicators. The introduction of the miticide fluvalinate, in the forms of Mavrik® and Apistan®, was arguably the best, and simultaneously the worst, thing that could have happened at that time. It was the best since it was an incredibly effective miticide, which appeared to be a virtually nontoxic to bees and humans. One shot a year with the “Silver Bullet” was all that was needed to keep varroa in check. Unfortunately, it was too good to last, but while it did, it set us down the path of focusing on finding new Silver Bullets, rather than developing sustainable mite management methods.
Forward to today. Hobby and sideline beekeepers everywhere are eschewing synthetic miticides, with some considerable degree of success. Commercial beekeepers, for whom mite management is a more difficult problem due to the large numbers of colonies kept in close proximity, are at their wit’s end. They are acutely aware of the fact that the dumping of miticides into their hives is tough on the bees, and that the problem is getting worse each year. I speak with a large number of commercial beekeepers, and have yet to meet one who wouldn’t eagerly give up miticides if there were reliable and cost-effective alternatives.
I’m continually impressed by the ingenuity and intelligence of the large commercial beekeepers. These guys really know their bees, and are keen observers of what makes their bees thrive, and what hurts them. Their field observations are a valuable adjunct to laboratory research with its high-tech analytic tools, microscopy, and statistics.
The commercial guys were thrown to the wolves when varroa developed resistance to all legally registered miticides. At that point, they were forced to experiment with “off label” use of chemicals to attempt to kill the mite. This is not an easy job, since any chemical used for mite control should not be noticeably harmful to the bees, contaminate the honey, or accumulate in the combs. A great number of colonies suffered in the course of experimentation, either from one or more of the aforementioned problems, or due to the treatment simply not being effective at killing enough mites to save the colony.
Luckily, there are recent products on the market, some of which are quite effective. However, let me make one point clear—I have yet to see any miticide, synthetic or “natural,” that does not have some degree of negative effect upon the colony. The issue then is whether the benefit outweighs the cost, and whether there are insidious cumulative sublethal effects within the hive, perhaps in synergy with other miticides, agricultural chemicals, or certain parasites.
Worldwide Colony Collapses and Neonicotinoids
The widespread unusual collapses of colonies worldwide these past few years have encouraged the research community to peer closely into the biological and chemical workings within the hive. Some of their findings were surprises, such as the discovery of Nosema ceranae, which appears to be associated with colony collapse in many areas. Less surprising was clarification of the negative effects of nutritional stress, and the value of supplemental protein feeding.
In Europe, beekeepers reported colony collapses when bees were moved to fields of sunflowers and corn that were treated with neonicotinoid insecticides. This class of insecticides are distributed systemically within the plant, rather than simply being contact pesticides sprayed onto the leaves. This is generally an ideal way to apply a pesticide, since it minimizes the exposure of nontarget organisms to the chemical. Unfortunately, the plant may translocate, or even concentrate, the active ingredient or a degradation product to the pollen, nectar, or sap exudates, which may then be consumed by honey bees. (However, the Bayer label for Admire® insecticide (imidacloprid) states: “Admire® will generally not control insects infesting flowers, blooms or fruit.”)
The author’s bees collecting pollen from corn tassels. One of the neonicotinoids, clothianidin, is used as a seed treatment on corn, and may translocate to some small extent to the pollen.
Many European beekeepers strongly believed that the neonics were responsible for their losses. However, there were several other possible factors that were present concurrently, such as poor nutrition due to drought and the deficient food value of corn and sunflower pollen, the arrival of N. ceranae, high varroa levels due to the failure of miticides, and bee toxicity due to the cumulative levels of beekeeper-applied miticides.
Indeed, long-term, blue-ribbon research reports from Germany, France, and Spain all came to the politically unpopular conclusions the collapses were likely due to the other factors, rather than directly from the neonics. They simply couldn’t find any “smoking gun” directly implicating the insecticides (note that these papers were published prior to the identification of Nosema ceranae). Allow me to quote the authors of the German final paper (Forster 2005) “If the residue concentration of 10–20 ppb, which is also safe in the long term for bees [documented earlier in the paper], is compared with the average residue concentrations in pollen and nectar of less than 5 ppb, it becomes clear that bees cannot be damaged by seed dressing with imidacloprid. This conclusion is confirmed by findings from over 30 semi-field and field tests on bee colonies carried out under various climatic and soil conditions on all significant crops. In none of these on-farm trials could harmful effects on bees be observed. In particular, the symptoms reported by French beekeepers were not observed in any of the studies.”
The French, however, are a bit more circumspect (Doucet-Personeni 2003), and are still testing for behavioral effects (some cynics suggest that researchers may be milking a politically popular cow). These sort of studies on the effects of minuscule amounts of pesticides on bee behavior are devilishly difficult, as evidenced by Aliquane (2009): “The toxic action of thiamethoxam is then related to its rapid conversion to clothianidin, a metabolite compound….However, we failed to ﬁnd any relevant biological effect of thiamethoxam on the honeybee after acute sublethal treatment, and we observed only a limited impairment of sucrose sensitivity and olfactory learning after chronic treatment (present study). No explanations can be put forward for these results, as bioassays in honeybees have shown comparable toxic effects of imidacloprid, thiamethoxam, and clothianidin” [italics mine].
There are those who are currently calling for a total ban on the use of neonics in the U.S. (Schacker 2008). In reality, this would cause substantial hardship for the growers of many crops, who find that a single treatment with a neonics may replace a half dozen treatments with other pesticides, some of which cause serious environmental damage and human health issues. Imidacloprid is also the pesticide of choice for urban pest control, especially in Florida (which uses a third of all the urban pesticides in the U.S.!). It also replaces vast quantities of pesticides formerly used for termite and ant control, including gases that damage the ozone or contribute to global warming. Applicators prefer it in hot weather, since they don’t need to wear respirators. I’m no salesman for pesticides, and don’t use them myself, but my research has forced me to look at the environmental tradeoffs that a ban would cause. I am heartened by the current cooperation between Bayer CropScience and the national beekeeping associations, which may result in the rewriting of labels to help avoid problems to bees.
Now that I’ve raised the hackles of the anti-neonic crowd, let me say that neonics don’t have a spotless bill of health. Researchers are continuing to sort out behavioral and multigenerational effects of exposure. Several commercial beekeepers (for whom I have the greatest respect) report that their colonies go downhill after placing them on crops treated with neonics (although this may not occur until later dearth or cold weather events, which are serious colony stressors on their own right). On the other hand, there are commercial beekeepers whose bees are on neonic-treated canola every year, yet don’t appear to have any problems as a result. So I’m not sure if the association between neonics and sick colonies is coincidental or causal. Of course there could be contributing factors, such as misapplication of the products, bees drinking treated “chemigation” water, or concentration of the product by a specific weed in an orchard.
Neonics may also have long residual lives (some single treatments are claimed to protect plants from sucking insects for years), and may build up in the soil (where they may be too tightly bound to be taken up by plants, but could conceivably get into hives via soil dust clinging to the bees’ bodies). In any case, few studies have been able to find any residues of neonics in sick colonies anywhere in the world. However, researchers have commonly found plenty of other pesticides, fungicides, and beekeeper-applied miticides in hives.
I’m not yet ready to reach any conclusions about the neonics, and indeed will return to them in a bit. As I follow the worldwide honey bee health research, the impression that I get is that the investigators have rounded up a lineup of the usual, and some new, suspects. However, instead of finding any single culprit guilty, all the suspects appear to be associated with what appears to be an epidemic of crimes. Some beekeepers find such lack of a single guilty culprit unsatisfying and too complex for their taste—unfortunately, things are sometimes not simple in real life.
There are some causes of colony loss that we can mitigate, such as by supplemental feeding in response to drought, or better management of mite and nosema levels. We may have fewer options to directly manage virus epidemics. However, there is one aspect that affects overall colony health over which beekeepers may exert some considerable control…
The Elephant in the Living Room
You may be wondering why I digressed into the subject of agricultural pesticides. The plain truth is that a colony of bees does not differentiate between agricultural pesticides, and beekeeper-applied miticides. What actually affects the colony is the cumulative load of all toxins that the colony is exposed to, whether from smokestack pollution, dust drifted over from China, pesticides sprayed by farmers, or miticides applied by beekeepers with the best intentions.
Honey bees are essentially “flying dust mops” whose bodies pick up the dust of any toxin in the environment. Dr. Jerry Bromenshenk, who has decades of experience in documenting pesticide and heavy metal contamination of bees, has documented that bees have a long history of being exposed to multiple toxins.
One result of all the CCD research is that we now know which pesticides are present in sick colonies, as well as in those that are apparently healthy. Although the usual agricultural pesticides and fungicides are often found, all the blue-ribbon research panels have pointed their fingers squarely at the contribution of beekeeper-applied chemicals—notably the miticides fluvalinate and coumaphos. Of secondary, but additional, concern are paradichlorobenzene (commonly used to fumigate combs to control wax moth), the wood preservative copper napthenate, and various chemicals used to control small hive beetle, ants, and other hive pests. The elephant that we have been ignoring is the beekeeper contribution to the cumulative effect of all the toxins in our hives.
None of the beekeeper-applied chemicals generally cause frank toxicity problems on their own right. Nor may properly-applied agricultural pesticides and fungicides. What happens is that the Law of Unintended Consequences kicks in: two or more chemicals may exhibit synergistic effects. A recent study by Laetz (2009) determined the effects of exposing juvenile salmon to pairings of normally “safe” doses of common pesticides. They found that some combinations were far more toxic than from simple additive effects. Their conclusion is worth our attention: “Salmon exposed to mixtures containing some of the most intensively used insecticides in the western United States showed either concentration-additive or synergistic neurotoxicity as well as unpredicted mortality. This implies that single-chemical assessments will systematically underestimate actual risks….”
Drs. Marion Ellis and Reed Johnson are investigating the synergies between pesticides when applied to bees. Such synergies are most likely if the pesticides have similar modes of action, that is, they affect the same metabolic process in the bee.
Guess what! The two most common pesticides found in colonies, fluvalinate and coumaphos, both appear to be detoxified in the bee by the same mechanism–cytochrome P450 (Johnson 2006). Thus, the presence of one effectively makes the other more toxic to bees! In other words, a normally safe dose of fluvalinate might be toxic to bees if coumaphos is already present in the hive.
This is a huge red flag! I’ve often heard beekeepers who didn’t get a good kill with the first miticide, then applying a second or third product. It’s not uncommon to see more than one treatment strip, stick, towel, or colored patty on waxed paper in hives. This practice is essentially an experiment in which the beekeeper keeps adding poisons to see who eventually suffers first—the mites or the bees!
So what other interactions and synergies are taking place between miticides and/or agricultural pesticides? Dr. Johnson told me: “No one knows too much about the interactions between pesticides in honey bees—unfortunately these sorts of things are notoriously difficult to nail down.” However, he and Dr. Ellis are going to take on that challenge this summer.
It is likely that coumaphos will also be found to synergize with carbamate pesticides (such as Sevin®), since they both have a similar mode of action. Since commercial bee combs typically test positive for coumaphos, this may well make the bees in such colonies more susceptible to harm from this common ag chemical.
Another red flag for me are the reports of high fungicide levels found in bee-collected pollen. Dr. Eric Mussen has been following reports from California beekeepers whose colonies show signs of damage after fungicide exposure. Dr. Johnson suggests that “any chemical that interferes with P450s is likely to synergize with fluvalinate—some of the ergosterol biosynthesis inhibiting fungicides are probably the most likely to increase the toxicity of fluvalinate” (see also Schmuck 2003).
Ruben Alarcón (Tucson Bee Lab) reports that “research has shown that feeding larval honeybees pollen contaminated with fungicides can lead to increased mortality. Exposure to pollen containing captan, ziram, or iprodione led to 100 percent mortality of larvae.
“One possible reason – when honey bees collect pollen contaminated with fungicides the levels of the compounds become higher in the stored pollen than in the pollen brought back to the hive by the foragers.
“High levels of fungicides in stored pollen might also inhibit the growth of certain strains of fungus that are necessary to convert pollen into bee bread. The loss of the beneficial fungus could reduce the nutritional value of the pollen to bees.”
So ag fungicides, which are often freely applied to flowering crops, may actually have serious detrimental effects upon bees, especially if the combs have fluvalinate residues.
We caught this prune grower making a halfhearted attempt to wait until dusk to spray a fungicide. Fungicides sprayed directly onto the blossoms to straight into the hive when the bees collect pollen. Marysville, CA photo by Larry Merrit.
A Toxic Stew
I was taken to task after a recent article by some individuals who took offense when I stated the obvious fact that beekeepers had a “visceral distrust” of pesticide manufacturers. All beekeepers should have a visceral distrust of pesticides, and of any associated with their sales or application! My point was that we shouldn’t allow our distrust to cloud our objective analysis of the reality of the situation.
When I perused the Bayer website, it made me queasy to see the vast array of poisons that the company offers to homeowners. However, as a journalist and scientist I force myself to set aside my personal distastes and prejudices, and to report the truth. All pesticides are poisons, and in my personal life I go out of my way to avoid them. However, I realize that if we wish to feed the current human population, pesticides are a necessary evil, since it is unlikely that our farmers could otherwise win the battle against insects, fungi, and competing plants. The best that we can do is to call for the development of more environmentally benign products, and to educate those who use them to apply them to do so carefully and sparingly.
One glimmer of hope is that there appears to be progress on this issue. The Europeans are ahead of us as far as the public demanding a more chemical-free environment. And only yesterday I saw a nesting pair of bald eagles near my home—a bird that appeared destined for extinction due to insecticides only a few decades ago. The fact is that some of the newer pesticides are less environmentally harmful than their predecessors (I hesitate to use the term “environmentally friendly”).
Unfortunately, we all drink from the same cup on this planet, and all our bodies are testing ground for the new combinations of novel chemicals that we spew into the environment. I am concerned about the insidious effects of this toxic stew upon the health and well being of living organisms.
So what happens when you mix a brew of chemical toxins within a bee hive? Research by Maryann Frazier found that East Coast bees in commercial operations test positive for six pesticides on average. Historically, this is not unusual, and indeed, some of today’s pesticides are less overtly toxic to bees. Unfortunately, few beekeepers are immune to pesticide issues—if your apiaries are within flight range of, or downwind from, any farm, orchard, golf course, public park, waterway, West Nile Virus area, suburban or urban area, you can assume that your bees pick up pesticides. Not to mention that the beeswax used for most commercial foundation comes already contaminated with coumaphos and fluvalinate!
For commercial beekeepers who make their living by providing pollination services to the agricultural sector, exposure to pesticides can be a major and recurring problem. A colony can often recover and rebuild after a single pesticide exposure, if given “clean,” nutritious forage and some “time off.” Unfortunately, the next pollination contracts may be calling, and the colony gets moved to yet another monoculture, with perhaps a different spectrum of pesticides, and heavy competition from other colonies.
Let’s digress into plant and insect coevolution. Many insects eat plant leaves. Plants fight back by loading their tissues with natural chemicals to deter insects. That’s why plants of the tobacco family produce nicotine—to discourage insects (and mammals) from eating them. So insects that specialize on eating those plants developed genetic mechanisms for detoxifying the plant-produced insecticides. When we tweak a natural insecticide, such as nicotine, into synthetic pesticides such as the neonicotinoids (meaning “new-nicotine-like”), they may work well to kill insects that don’t naturally feed on the parent plant. However, it isn’t much of a trick for insects like the Colorado potato beetle, which naturally feeds upon plants in the tobacco family, to develop resistance to neonics, which they have already done!
But how about the honey bee? Bees don’t eat leaves, and plants willingly feed them pollen and nectar. So the honey bee did not need to develop or maintain many genes to detoxify natural plant insecticides. As a general result, neither can it detoxify man-made pesticides as well as can the typical leaf eating or sap sucking insect. Since ag pesticides are developed to target plant-eating insects, the poor bees are relatively defenseless!
The Colorado potato beetle. This insect, which evolved to eat plants of the tobacco family, easily developed resistance to neonicotinoids. Honey bees, since they don’t eat toxin-rich plant leaves, do not have as many innate resistance mechanisms to pesticides. Photo USDA.
Beekeepers report that the bees just don’t recover as well as they used to. Some blame single pesticides, but the actual situation may be more complicated. The ongoing evolution between bees, the mites, viruses, and now Nosema ceranae, coupled with a colony’s constant exposure to miticide residues in the combs, means that bees are forced to adapt to an entirely new and changing set of challenges.
Overt pesticide kills are fairly easy to spot—there are piles of dying bees with their tongues sticking out twitching in front of your hives. Unfortunately, sublethal pesticide toxicity is another matter, especially when more than one pesticide is involved. To further complicate matters, there are also often “compounding risk factors” (Repetto 1996). These include the quality of nutrition available to the bees, the age of individual bees, temperature, genetics (some stocks are more pesticide resistant), and parasites (including mites, nosema, bacteria, and viruses). Indeed, it is virtually impossible to make any concrete statement about the toxicity of any particular pesticide to bees for all circumstances!
An apple grower in Chile sprayed the insecticide carbaryl on trees in bloom, for an entirely different purpose—it is used to thin the apple crop. Unfortunately, the nearby colonies belonging to beekeeper Juanse Barros suffered considerable loss of their field force. Photo courtesy Juanse Barros.
This is a problem, since pesticide manufacturers don’t test for pesticide toxicity to sick animals. Therefore, they don’t test for pesticide effects on parasitized, stressed, or miticide-contaminated bee colonies! So a manufacturer’s legitimate determination of safe application rates may not truly apply to the real world situation.
Furthermore, the active ingredient of the pesticide may be only part of the problem. Pesticides are often mixed with “adjuvants” such as solvents, emulsifiers, stickers, and spreaders, which may be separately toxic on their own right. Formulations may also include synergists to accentuate the active ingredient’s pesticidal activity. Finally there are “breakdown products” or “metabolites” that may be even more toxic than the original active ingredient! And some of these may have long residual lives in dust, in plant sap, or especially in beeswax.
I’ve spoken to a number of commercial pollinators who see serious health issues in their hives following agricultural pollination, as opposed to those hives that “stay home” and remain healthy. Although they can’t pinpoint any specific PPP (Plant Protection Product—which includes insecticides, miticides, fungicides, and herbicides), it appears that the bees are exposed to something that has insidious sublethal effects.
Since many colonies are exposed to combinations of pesticides from without, the question then, is how much do beekeepers contribute to the overall problem by the application of miticides, pesticides, and antibiotics within the hive. These clearly are products that the beekeeper has direct control over.
Pesticide toxicity is typically measured by the LD50—the amount required to kill 50% of the test subjects. This type of measurement is fine for fast-acting pesticides that are sprayed onto crops, and that degrade quickly. However, with bees, chemicals may be brought into the hive in pollen and nectar, and stored in the beebread or be absorbed by the beeswax combs, later to have an effect upon developing brood or the next generation of adults.
Such effects may be brood toxicity, longer developmental time, decreased body weight, or shortened lifespan—any of which will affect overall colony population dynamics, and which may prevent a colony from realizing its full potential.
Several recent studies, and practical field observations, have indicated that commonly used hive miticides may affect the queen’s egglaying and the development or mortality of brood. This is true for both the “natural” treatments, as well as the synthetics.
The sublethal effect that really catches my attention is the potential impairment of immune function. This can be a difficult effect to quantify, as explained by Repetto (1996): “In healthy people, some immunosuppression may occur without discernible effects, because the immune system has overlapping and redundant capacity to deal with challenges. Perhaps for this reason, many studies that measured changes in the immune system after chemical exposure detected no health consequences. More to the point, several clinical studies have examined the possibility that organophosphates [coumaphos] and carbamates [aldicarb, furadan, Sevin] bind to and alter esterases, vital membrane-bound proteins that help immune system cells interact with and destroy foreign organisms.” Bees also use esterases as part of their immune systems.
The most serious pathogens of bees are viruses. Dr. Diana Cox-Foster found that treating colonies with various miticides changed the prevalence of different viruses. But what happens when we have colonies that are already infected with viruses (as most are) and nosema, plus miticides and ag chemicals? Dave Wick’s IVDS machine, and Dr. Joe DeRisi’s microarray may give us windows to observe the interactions.
OK, I told you that I would revisit imidacloprid. It is common practice in biological control of insects to increase the effectiveness of a fungal pathogen by the application of a sublethal dose of imidacloprid (Santos 2007). Recent research by Dr. Jeff Pettis found that bees inoculated with Nosema ceranae suffered from greater rates of infection when simultaneously exposed to low doses of imidacloprid. This is a stunning finding, which suggests that we need to look more closely at the effects of the chemical stew in our colonies when potentially virulent pathogens such as N. ceranae and viruses are involved.
So now let me add yet another juicy tidbit: Reardon (2004) found that corn borer caterpillars succumbed more readily to nosema infections when fed the toxin found in genetically modified BT corn! These facts sure make me curious about reports of beekeepers having major N. ceranae problems when corn begins to tassel…
Sublethal Effects upon Queens and Drones
Anyone seriously interested in the effects of miticides upon reproductive bees should read the excellent introduction to Lisa Marie Burley’s Master’s Thesis (2007). She details the history of miticide use in honey bee colonies, and reviews the published literature on miticide effects upon queens and drones.
To make a long story short, formic acid treatment can kill the drones before they reach sexual maturity, fluvalinate wipes out their sperm, and coumaphos residues can simply prevent colonies from being able to produce queens, and negatively affect queen survival. Even if queens survive, miticide residues can reduce the viability of the sperm stored in their spermatheca, which may lead to early queen failure and unsuccessful supersedure.
Deleterious effects of miticides are often most apparent in queens and drones. Queens may not develop, and drone sperm production may be impaired.
I’ve been speaking with Australian researcher Dr. Boris Baer. He is studying how the glandular secretions of queens and drones function to allow honey bee sperm to survive for years in a mated queen (den Boer, et al., 2009). It will be of great interest to see how various miticides affect the proteins responsible for sperm viability.
Most beekeepers have noticed that queens today often do not hold up as well as queens of yore. Sudgen and Furgala (1982) documented that good queens once exhibited over 80% survival for 16 months (two full seasons), had expected acceptance and 30-day survival of 90-100%, and winter survival in Minnesota of 100%. This is a far cry from the high failure rate and depressed longevity of queens in commercial operations today.
Dr. Eric Mussen’s newsletters have reported on problems experienced by queen producers following the introduction of each miticide, and also following exposure to various fungicides applied to crops. The current bad boy is Pristine® fungicide, which contaminates the pollen of the almond trees that bloom just prior to queen production.
Queens and drones in essence function as the “canaries in the coal mine”—we see effects upon their survival and reproductive success prior to noticing more subtle effects in the workers. The commercial queen producers are often the first to sound an alarm after the introduction of a new miticide or pesticide, when they experience problems with queen production or survival.
The irony of this situation should not go unacknowledged. Those very beekeepers who are most in the position to shift the genetics of our bee populations toward mite resistance—the queen breeders and producers—are the very ones who most feel the negative effects of miticide use.
The Current Situation
Our history with miticide use against varroa reminds me of a quote from Karl Marx: “History repeats itself—first as tragedy, second as farce.” Beekeepers watched fluvalinate go from a “miracle cure” to an ineffective hive contaminant in just a few years. Ditto with coumaphos. Once we blew through those formerly effective miticides, anti-varroa alchemy shifted to other synthetics, or to the essential oils and organic acids. Many commercial U.S. beekeepers owe their current survival to amitraz (although it is not legally registered for use). Unfortunately, that chemical started to show serious signs of failure about two years ago, and many do not trust it to provide adequate mite control this year.
That leads us to the new kid on the block, Hivastan®. Despite years of expensive development and testing, it is dang near impossible for any manufacturer to foresee all the potential problems that might occur once the product goes to market. In reality, beekeepers become the guinea pigs for large-scale field testing.
Hivastan was a difficult product to work the bugs out of, with nagging issues of adult bee mortality. I commend the manufacturer on their perseverance, and do not in any way intend to bad mouth the product. Beekeepers who used the product last summer were quite happy with it, and only noted a small amount of adult bee mortality for the first day or two, which, as a trade off for good varroa control, is likely no big deal.
Then, early this spring, several commercial beekeepers applied Hivastan (sometimes at only a third of the label dose) to broodright colonies in cool weather. Shortly thereafter, the colonies suffered from serious worker, and sometimes queen, mortality—much to the beekeepers’ (and the manufacturer’s) dismay. Tens of thousands of doses were hurriedly scraped out of hives.
I’ve looked at the chemical analyses of the dying workers—surprisingly, the amount of active ingredient (fenpyroximate) in the bees was far below the published LD50, so it wasn’t a simple toxicity issue. It appears that the product hadn’t been specifically tested under cold weather conditions. The affected bees appeared to be young workers that were bloated with pollen or pollen supplement (depending upon what the colonies were eating). Perhaps the restriction of foraging due to the cool weather changed the normal distribution of the product among the bees, and interfered with the digestive process. As with several other varroa control products, the application label may need to be revised after more widespread field experience.
Let me repeat—this problem is not a condemnation of the product. Hivastan got good reports from beekeepers who tested it last season. The manufacturer, due to urgent requests from beekeepers for a new product, released it conditional upon beekeepers signing a waiver acknowledging that the product may cause some adult bee mortality. I’d just be a little cautious about giving it to all my colonies if it looks like a possibility of cold weather ahead. (This may sound like common sense, but I hear time and again of beekeepers who try a product for the first time on all their colonies!)
There isn’t a beekeeper I’ve met who isn’t acutely aware of the “too many poisons in the beehive” problem, and who wouldn’t love to go back to chemical-free beekeeping. I’m heartened by the fact that as I listen to beekeepers throughout the country, a number small commercial operators actually have! Or at least gone solely to “natural treatments.” These guys, in my opinion, are the leading edge of the future.
And here’s the part that I like best: these aren’t smug, holier-than-thou, wear-it-on-your-sleeve, “organic” beekeepers—they are regular guys who simply got tired of the synthetic chemical conveyer, took a deep breath, and stepped off. They don’t make a big deal out of it, and generally suffered a painful learning curve. But I meet some in dang near every state. They don’t hold anything against their colleagues, and aren’t trying to prove anything, except to themselves. But they are being successful!
The reality is, that the larger an operation gets, the harder it is to manage mite levels. A cheap, effective synthetic chemical that can be applied by moderately-skilled labor, may appear be the most cost-effective mite control, at least in the short run (although actual cost/benefit studies of IPM management have demonstrated otherwise).
To me, an analogy with the agricultural industry is enlightening. I’ve read the California Farm Bureau newspaper every week for years. What I’ve seen is a slow acceptance of sustainable farming practices–that were once considered to be on the “organic farming” fringe–becoming widely accepted by the mainstream as the economics of farming and markets change. Indeed, there are now huge commercial “organic” farms and dairies. Although these bear little resemblance to the ideal of the small, labor-intensive sustainable family farm, they demonstrate how even large-scale production can forego synthetic chemicals, and their associated problems (not to say that plenty of other problems won’t take their places).
This evolution in farming is analogous to what is occurring in beekeeping (see recent articles in this Journal by Dr. Wyatt Mangum, Kirk Webster, and Mea McNeil). Smaller beekeepers are leading the way, and as they figure out how to keep their bees alive without major chemical (synthetic or natural) inputs, their methods will be slowly adopted by others in a snowball effect. Eventually, we will reach a tip point where overall commercial bee genetics shift to mite-adapted stocks, and the need for miticides will subside. This process is already well underway, and I feel pretty optimistic about the future.
Let me insert a reality check here. I was recently chatting with a major organic farming consultant on the West Coast (who bought a few hives from me after a long absence from beekeeping). I told him that keeping bees alive without chemical treatments wasn’t as simple as just not using treatments. He laughed and said that a similar misconception also exists when folk want to start organic farming—they think that they can simply give up chemicals, without making any other changes. The transition to reduced chemical beekeeping requires changing the genetic stock of your bees, as well as possible changes to your management strategies.
In my own efforts to “walk the walk,” I found that colony losses prior to my critical February almond pollination contracts required me to really stay on top of mite monitoring, and to incorporate the judicious use of an assortment of “natural” treatments and biotechnical methods, since not a large enough proportion of my colonies exhibited enough innate mite resistance to make it without some help. I’m slowly weaning my bees off even the natural miticides, but they are not yet ready to stand fully on their own.
I’ve been able to keep mite varroa in check the past two years, but I was chagrined this spring that my mite levels were higher in almonds than normal. Perhaps the mite will eat me alive this year. Or maybe my hives will be wiped out by imidacloprid. I wouldn’t be the first beekeeper to be blindsided by the unexpected!
I seem to have digressed from varroa control to pesticide toxicity. I’ll return to an evaluation of the available miticides next month.
Aliquane, Y, et al (2009) Subchronic exposure of honeybees to sublethal doses of pesticides: effects on behavior. Environmental Toxicology and Chemistry 28(1): 113–122.
Burley, LM (2007) The Effects of Miticides on the Reproductive Physiology of Honey Bee (Apis mellifera L.) Queens and Drones scholar.lib.vt.edu/theses/available/etd-08162007-092313/unrestricted/lmburley.pdf
den Boer, S.P.A., et al., (2009) Honey bee males and queens use glandular secretions to enhance sperm viability before and after storage. J. Insect Physiol. (in press)
Doucet-Personeni, C (2003) Imidaclopride utilisé en enrobage de semences (Gaucho®) et troubles des abeilles Rapport final. Centre d’Etudes et de Recherche Sur le Médicament de Normandie
Forster, RE Bode, D Brasse (2005) Das “Bienensterben” im Winter 2002/2003 in Deutschland. www.bvl.bund.de
Johnson, RM Z Wen, MA Schuler, and MR Berenbaum(2006) Mediation of Pyrethroid Insecticide Toxicity to Honey Bees (Hymenoptera: Apidae) by Cytochrome P450 Monooxygenases. Journal of Economic Entomology 99(4):1046-1050.
Laetz, C, et al (2009) The Synergistic Toxicity of Pesticide Mixtures: Implications for Risk Assessment and the Conservation of Endangered Pacific Salmon. Environmental Health Perspectives 117(3): 348-353
Reardon, B.J., Hellmich II, R.L., Sumerford, D.V., Lewis, L.C. 2004. Growth, development, and survival of Nosema pyrausta-infected European corn borers (Lepidoptera: Crambidae) reared on meridic diet and Cry1Ab. Journal of Economic Entomology. 97:1198-1201.
Repetto, R and S Baliga (1996) Pesticides and the Immune System: The Public Health Risks. World Resources Institute
Sanford, MT (2008) Insecticides and CCD, Part I. Bee Culture 136 (7): 17-18
Santos AV, BL de Oliveira and RI Samuels (2007) Selection of entomopathogenic fungi for use in combination with sub-lethal doses of imidacloprid: perspectives for the control of the leaf-cutting ant Atta sexdens rubropilosa Forel (Hymenoptera: Formicidae). Mycopathologia 163(4):233-40.
Schacker, M (2008) A Spring without Bees. The Lyons Press
Schmuck, R, T Stadler, H-W Schmidt (2003) Field relevance of a synergistic effect observed in the laboratory between an EBI fungicide and a chloronicotinyl insecticide in the honeybee (Apis mellifera L, Hymenoptera). Pest Manag Sci 59:279–286
Sudgen MA, Furgala B (1982) Evaluation of six commercial honey bee (Apis mellifera L) stocks used in Minnesota. Part 1: Wintering ability and queen longevity. Am Bee J 122: 105-109.