It's been quite awhile since there's been anything of substance to say about the condition of the honey bees in this country, or even the rest of the world, relative to Colony Collapse Disorder. Beekeepers and scientists pretty much know what they know ... pesticides are involved, both those from people other than beekeepers, and those applied by beekeepers; viruses are involved, both normal and exotic; diseases are involved, both regular and exotic; nutrition is involved, both enough, and good enough; and of course the root cause ... money, lots of money is involved, both from the research side, and from the beekeeper side.
During the past couple of years, snatches of all this have been revealed in publications by the many beekeeping scientists looking at these various issues, from beekeepers who have made discoveries on their own, and by researchers not even remotely associated with the beekeeping industry, but who have been brought in because they have a technology, a technique, a skill or experience that has helped those involved. Colony Collapse Disorder has brought together, and split apart, a complex and diverse assortment of practical and applied scientists, theoretical and specialized scientists, and everyday beekeepers.
Yet, we still don't have the answer as to why most of the adult bees in a hive leave and do not return, abandoning their home, their queen and their future the brood left behind. Nor do we know why secondary pests don't immediately move in and consume the delicacies there for the taking; nor do we know why, when bees are reintroduced to the equipment that housed Colony Collapsed bees, the second batch does not fare well at all; nor do we know when, or if, any of the promised federal dollars will ever arrive to apply to the issues that still remain.
But we do know lots of differences between colonies that succumbed to CCD and those that did not. "You can't tell what something is until you can tell what it isn't" is the philosophy I suppose, and Colony Collapse Disorder A Descriptive Study, which came out last week, does just that ... it spells out all the differences.
After studying the paper for a bit, it became obvious that there is little we didn't already know in the world of really sick honey bees. But that wasn't the goal of this work ... rather, they wanted to measure the risk factors any given set of colonies had of coming down with CCD when compared to ... well, compared to colonies that probably wouldn't come down with CCD. Briefly, below is what they found. But above, I mentioned one of the factors scientists haven't looked at ... and won't because they don't include the relationship between income potential, CCD, and the bottom line of a family business. It's not in their DNA to include a variable they can't measure, quantify or explain. I will, below.
But first, the conclusions of the paper, from the authors (emphasis mine):
This is the first comprehensive survey of CCD-affected bee populations that suggests CCD involves an interaction between pathogens and other stress factors. Evidence is presented that this condition is contagious or the result of exposure to a common risk factor. Potentially important areas for future hypothesis-driven research, including the possible legacy effect of mite parasitism and the role of honey bee resistance to pesticides, are highlighted in this work.
91 colonies were in the sampling process. 79 were living, the rest not. Sampled colonies were noted for brood infections and brood patterns. Adult bees were taken to be measured for pathogen, protein and pesticide analysis, varroa and tracheal mite presence and nosema spore load. Comb samples containing pollen, wax, and brood and bee bread (bee-processed pollen) samples were taken. They also measured the strength of the colonies right next to those they took samples from, and obviously sampled apiaries that had colonies in the process of collapsing and not collapsing. And then they did the statistics. If you want the particulars, and there are lots of particulars, find a comfortable chair, a strong cup of coffee, or something stronger, and settle in ... there's lots to read. The authors sum up their results....
This descriptive epidemiological study was initiated to better characterize CCD and compare risk-factor exposure between control and afflicted populations in hopes of identifying factors that cause or contribute to Colony Collapse Disorder. Of the more than 200 variables we quantified in this study, 61 were found with enough frequency to permit meaningful comparisons between populations. None of these measures on its own could distinguish CCD from control colonies. Moreover, no single risk factor was found consistently or sufficiently abundantly in CCD colonies to suggest a single causal agent. Nonetheless, our results help to elucidate this poorly understood affliction of the honey bee colonies and provide insight into the planning of hypothesis-driven research.
CCD apiaries contained more dead and weak colonies than did control apiaries and the distribution of dead and weak colonies in CCD apiaries was not random. Dead and weak colonies were more likely to neighbor each other in CCD apiaries as compared to control apiaries suggesting that an infectious agent or the exposure to a common risk factor may be involved in colony collapse.
While no single pathogen or parasite was found with sufficient frequency to conclude a single organism was involved in CCD, pathogens seem likely to play a critical (albeit secondary) role. CCD colonies generally had higher virus loads and were co-infected with a greater number of disease agents than control colonies. Elevated virus and Nosema spp. levels potentially explain the symptoms associated with CCD. One possible way honey bees regulate pathogen and parasite loads within a colony is for infected individuals to emigrate from their hive. This behavior has been proposed to explain the rapid loss of adult populations in colonies collapsing from N. ceranae. Whether infected individuals die away from the hive as the result of an evolved response (suicidal pathogen removal or from a sudden debilitating process by which forager bees cannot return to the hive is irrelevant to understanding how colony collapse can unfold. Premature loss of worker bees does not preclude non-pathogenic causes; recent work has shown that worker bee longevity can be reduced when they are exposed to sub-lethal levels of coumaphos during the larval and pupal stages (Pettis, unpublished). The premature loss of forager bees, the older cohort in a colony, results in younger bees prematurely becoming forager bees. If these replacement bees die at a rate that exceeds the colony's ability to replace them, the result would be rapid depopulation, a reduction in the bee-to-brood ratio, and eventually colony failure.
In addition ....
The intrinsic bias associated with sampling only surviving (and presumably the least-sick) bees did not prevent us from establishing that workers in CCD colonies were more ill than those in control colonies. Co-infection with both Nosema species was 2.6 times greater in CCD colonies when compared to control colonies, and colonies co-infected with 4 or more viruses were 3.7 times more frequent in CCD colonies than in control colonies. While honey bee colonies are commonly infected with one or more pathogens, often without exhibiting overt signs of illness, the greater prevalence and abundance of infectious agents in CCD colonies does suggest that either they were exposed to a greater number of pathogens or their ability to fight infection had been compromised.
This is the first descriptive epizootiological survey of honey bee colonies that provides evidence that the condition known as CCD is consistent with a contagious condition or reflective of common risk factors within apiaries Of the 61 variables quantified (including adult bee physiology, pathogen loads, and pesticide levels), no single factor was found with enough consistency to suggest one causal agent. Bees in CCD colonies had higher pathogen loads and were co-infected with more pathogens than control populations, suggesting either greater pathogen exposure or reduced defenses in CCD bees. Levels of the miticide coumaphos were higher in control populations than CCD-affected populations. Potentially important areas for future hypothesis-driven research, including the possible legacy effect of mite parasitism and role of honey bee resistance to pesticides, are highlighted.
So ... lots of things, it seems, cause a colony to crash and burn with no single factor standing out. The details, however, are wonderfully explained. Read the paper for them all. Stress, however plays a role in all of this too, and stress is definitely enhanced by putting bees in harm's way with commercial pollination. So here's another, even more difficult to measure factor in the role of CCD ... the price of almonds.
The California almond crop, which uses half of the honey bees in the U.S. each spring, is affected by available water, the going price of almonds, the going price of honey bee pollination, and a few other, less important factors. Less water availability this year has made growers contract their holdings, reducing the need for bees and decreasing demand; meanwhile problems like CCD reduce the availability of bees, decreasing supply and increasing demand. Almond prices affect grower inputs and cash flow and increase, or decrease bee demand, depending on the sale of almonds worldwide. And honey, too, drives colony rental prices ... high honey prices because of world shortages reduce the number of bees available to pollinate because they stay home and make honey, reducing supply, driving up prices, reducing demand, increasing supply ... Don't you wish you had paid more attention in Econ 101, back in the day?
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