October 9th, 2010 by Michael Ricciardi
“It” began decimating honeybee colonies across the United States in 2006 and, by the summer of 2009, nearly 40% of US honey bee colonies had collapsed. For awhile it seemed that the disease had tapered off and died out along with the bees, but in the summer of 2010, Colony Collapse Disease returned to once more devastate honey bee colonies throughout the US.
Hundreds of thousands of formerly foraging honey bees (genus Apis) were found far from their hives, apparently “lost”, and mostly dead. The mysterious, bee-killing scourge was soon dubbed “Colony Collapse Disease” (CCD) and scientist from many walks of life began offering theories as to its cause (including GM crops). By 2009, early research had implicated a virus as a likely cause of the disease, while other research had implicated a fungus. But neither seemed to be the sole cause.
Now, as a result of a unique collaboration between military and civilian scientists, the cause — or rather causes — of CCD have been revealed.
In a paper published on the PLoS ONE website on Wednesday, Oct. 6 (Bromenshenk et al), the mysterious cause of Colony Collapse Disease was revealed: a one-two, pathogenic punch from a virus and two species of fungus. But just which throws the primary hit, and which adds the opportunistic “knock out” punch, remains unclear.
Through a genetic analysis tool called mass spectrometry-based proteomics (MSP), an RNA bee virus known as invertebrate iridescent virus (IIV, or iridovirus) and two microsporidia fungus types (Nosema apis and N. ceranae) were identified. The virus and the two, tiny fungal species were found in both healthy and collapsed colonies.
However, the researchers found that IIV “strongly discriminated” amongst strong, failing, and fully collapsed colonies. Bees in failing colonies sampled from US apiaries (between 2006-2007) had both IIV present and the microsporidia fungi. The analysis also included samples from a 2008 “observation hive” and from a recurrence in Florida in 2009
The co-occurrence of the two pathogens was not observed in colonies with no history of CCD. These comparison colonies came from either Australian hives or from a non-migratory bee-keeping operation in Montana.
The fact that these latter colonies were non-migratory and free of CCD, is perhaps the strongest indicator of how CCD was able to spread, as much of the commercial bee industry in the US is highly mobile, with hive owners often traveling many hundreds of miles to augment local bee populations and furnish crops with extra pollinators.In laboratory trials working with a strain of IIV type 6, the scientists were able to confirm that “co-infection with these two pathogens was more lethal to bees than either pathogen alone.”
CCD has also impacted colonies in Europe and Asia. This work supports previous research that had implicated IIV interacting with both Nosema and mites. More research is needed to characterize the life cycle activity of the iridovirus and the microsporidia (and how they work in concert to become so lethal to bees). Once this is accomplished, new management policies will need to be developed to prevent further losses of honeybees.
Read the PLoS ONE paper, Iridovirus and Microsporidia Linked to Honey Bee Colony Decline, and, for more information about the unique collaboration between civilian entomologists and military scientists that led to this discovery, check out the NY Times report by Kirk Johnson here.
Top Photo: Aphaia, on wikipedia; cc – by – sa 3.0
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