Colony Collapse Disorder - finally an academic publication

Given the time that has elapsed since the first mention of Colony Collapse Disorder in the popular press, it's nice to finally see some scientific publications trying to address this issue.

Last week, PLoS Biology, the free online scientific journal, published an Unsolved Mystery. Benjamin Oldroyd, a bee entomologist at the University of Sydney, writes about Colony Collapse Disorder:

On February 22, 2007, many Americans woke up to media reports that something was awry with their honey bees. A significant proportion of American beekeepers were complaining of unusually high rates of colony loss as their bees broke from their overwintering clusters. Loss of some colonies (say 10%) in early spring is normal and occurs every year. In 2007, however, losses were particularly heavy and widespread—beekeepers in 22 states (including Hawaii) reported the problem. Some beekeepers lost nearly all of their colonies. And the problem is not just in the United States. Many European beekeepers complain of the same problem. Moreover, beekeepers and researchers do not understand the specific causes of the losses.

He puts it in historical perspective:

Some winter losses are normal, and because the proportion of colonies dying varies enormously from year to year, it is difficult to say when a crisis is occurring and when losses are part of the normal continuum. What is clear is that about one year in ten, apiarists suffer unusually heavy colony losses. This has been going on for a long time. In Ireland, there was a “great mortality of bees” in 950, and again in 992 and 1443 [3]. One of the most famous events was in the spring of 1906, when most beekeepers on the Isle of Wight (United Kingdom) lost all of their colonies [4]. American beekeepers also suffer heavy losses periodically. In 1903, in the Cache valley of Utah, 2000 colonies were lost to a mysterious “disappearing disease” following a “hard winter and cold spring” [5]. More recently, there was an incident in 1995 in which Pennsylvania beekeepers lost 53% of colonies [6].

Often terms such as “disappearing disease” or “spring dwindling” are used to describe the syndrome in which large numbers of colonies die in spring due to a lack of adult bees [7,8,9]. However in 2007, some beekeepers experienced 80–100% losses. This is certainly the extreme end of a continuum, so perhaps there is indeed some new factor in play.

So this has been going on for some time.

He covers several possible causes, but zeroes in on two:

We have seen that a large number of factors can produce CCD-like symptoms. We have also seen that CCD is not new: CCD-like symptoms have been known to beekeepers for more than a hundred years but are sufficiently infrequent that when symptoms are severe, beekeepers become concerned that there is something new afflicting their bees.

Clearly CCD is a multifactorial syndrome. Some researchers have suggested that the bees are suffering immunosuppression. Certainly, expression of immune genes in insects is costly [56–58], and if bees are stressed by other causes, they may be less able to mount an effective immune response to pathogens [see Box 1]. This idea is now eminently testable, because the honey bee genome has been sequenced [59], and this provides researchers with new tools to tackle problems like CCD. A microarray of honey bee immune genes and genes from their pathogens is available [60], and this could be used to determine if the known immune genes are underexpressed in colonies suffering from CCD.

I suggest that another possible cause of CCD might simply be inadequate incubation of the brood. Thus any factor—infections, chronic exposure to insecticides, inadequate nutrition, migration in adult population, and inadequate regulation of brood temperature might cause CCD-like symptoms.

My hypothesis could be easily tested by removing brood from several colonies and incubating some of it at optimal temperature and some at suboptimal temperature. The brood would then be used to constitute new colonies in which some colonies comprise workers raised at low temperature and some comprise workers raised at optimal temperature. I predict that the colonies comprising workers reared at suboptimal temperature will show signs of CCD. Moreover, I would not be surprised if they showed higher levels of stress-related viral infections. These effects could act synergistically—more virus leads to shorter-lived, less efficient workers, that in turn leads to suboptimal temperature regulation, and more short-lived bees.

And he provides tests for his hypothesis. Brilliant!