Is CCD a Murder Mystery?

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Mar 7, 2015 Comments Off Ken Bell



Remember Columbo, the cigar chomping, rain slickered, squinty detective who seemed to bumble his way through the evidence, randomly alighting on this fact or that. A little socially awkward, and even dismissable with just the wave of a hand. A modest, working class guy. Then, at the end of the episode after sharing pleasant, but tense, conversation with yet another smug, sophisticated type, a rain slickered Columbo, disheveled, slightly hunched, back turned, and about to leave pauses, then turns, left finger raised, right hand over his brow, “Just… just, one thing bothering me….”. Well, you can guess the rest.

Looking at the research surrounding CCD for the past few years, many have come to the conclusion that systemic pesticides constitute a “last straw” of stressors which lead to colony collapse. Looking at the available data, particularly the coincidence of pathogens like Nosema, parasites like Varroa mites and the rise of neonicotinoid use, there is a correlation, (but not necessarily causation) in the increase in CCD over the past few years.

The public polarization of this issue is, unfortunately, an artifact of the difficulties of science reporting. The complexities of ecology, genetics, immunology, experimental design and history are difficult to fold into articles, written for a public looking for a “smoking gun” or villain.

CCD in various guises has been around for some time, over 100 years, but only recently has become a global epidemic. What numerous studies show is that there is more than one culprit and that the synergies between what we do to the bees, and, what we do to their environment are the major drivers of CCD. While the proximate cause of colony collapse my be immune suppression the ultimate cause is distributed among many agents.

It’s to be expected that some vested interests will seek to absolve themselves from their contributions and it’s prudent to remain skeptical when reviewing experimental design and always ask, “What does this experiment tell us, and what doesn’t it?”

To this end, the possibilities of synergies between colonies with parasites or Nosema, and clothianidin tainted pollen were excluded from a recent University of Guelph honeybee study:
“A large-scale field study examining the effects of exposure to clothianidin seed-treated canola on honey bee colony health, development, and overwintering success”
10.7717/peerj.652 G Christopher Cutler Cynthia D. Scott-Dupree et al. Accepted: October 14, 2014

Funded by Bayer CropScience, who also helped set up the experimental design.

Page 8.
Colony Preparation and Management
“Colonies also were assessed for the presence of varroa mite, tracheal mite, American foulbrood, European foulbrood, Nosema, and chalkbrood. Before placement in canola fields hives infected with diseases as determined during the initial hive assessments were not used in the study…”

What this experimental setup does, is remove a significant CCD susceptible population from the sample, thus eliminating the measurement of synergies or multiple causes. Rather than moving research ahead, towards real world solutions, experimental designs like these actually stall efforts and promote the “More Study Needed” diversion tactic, so favored by vested interests.
There is, of course, lots of blame to go around and we need to get beyond the “blame-game” and move towards real, solutions.

The findings from a 2013 graduate paper by Angela Carcione, from the University of Delaware, may prove useful when balancing discussions.

by Angela Carcione University of Delaware

“My study examines the genetic structure of non-managed “survivor stock” bee colonies in the Arnot Forest, located in Ithaca, NY, and compares it to bees found in two surrounding apiaries. Nuclear DNA allele frequency comparisons found genetic differentiation (3 distinct clusters) between the feral bees and bees from the two managed apiaries. I found that :
1) the Arnot tree bees are feral as opposed to escaped managed bees filling old nest cavities,
2) these feral bees are persisting in the wild despite treatment for agents such as Varroa and other human manipulations, and;
3) there are barriers to gene flow between feral and managed populations.

I uncovered two mtDNA haplotypes among my samples―Apis mellifera carnica and Apis mellifera ligustica, both subspecies of the western European honey bee.

Based on these findings, I suggest more sustainable management practices of our managed honey bee populations in the hopes that they too well develop a more stable coexistence with the agents causing their decline. Strategies include reducing hive size, discontinuing the selection for low-swarming bees, slowing or discontinuing the use of mite-control treatments, spacing hives further apart, and decreasing transportation induced stress of bees. I believe that by working to ensure bees can foster a balanced relationship with their disease agents, the population decimations across the globe can be reduced.”

The study concludes on Page 33:

“It is our belief that current apiculture  practices are a driving force behind Colony Collapse Disorder, and basic management strategies may help to prevent these losses.
Strategies include:

  • discontinuing the selection for low-swarming bees,
  • slowing or discontinuing the use of mite-control treatments as to allow natural selection to favor the more disease-resistance bees,
  • spacing hives further apart,
  • keeping hives that are smaller in size to encourage healthy levels of swarming (even though honey production might be smaller), 
  • decreasing transportation of colonies which not only puts physiological stress on the bees but also hinders natural selection in closed populations.”


So, healthy, diverse populations that live in uncrowded conditions can deal with environmental stressors and disease better that their domesticated cousins.

Given our taste for cheap honey and unlimited crop yields, I wonder if Lt. Columbo would let anyone leave the room?

Ken Bell