An unlikely hybrid team of researchers - military security experts, interested in using bees to detect explosives, working with university of Montana entomologists - have uncovered clues to the mysterious colony collapse disorder that has wiped out 40% of U.S. honeybee colonies. When the university researchers' hives were hit by colony collapse, they were able to gather molecular clues from the dead bees. A disease caused by a combination of a fungus and a virus appears to have killed the bees.
Dead bees were found to have a combination of viral and fungal proteins at much higher than normal levels.
The research team propose that the both the virus and the fungus killing European honey bees may havejumped from a bee species found in India.
The suspected source of Nosema ceranae in Apis mellifera is the Asian bee Apis cerana [49]. This bee species is also known to be infected by Thai sacbrood virus and by Kashmir bee virus. Kashmir virus was first detected as a contaminant in a sample of iridescent virus from India, as well as IIV-24 [50]. The same virus was linked to bee losses in Canada in the early 1990s [51]. This suggests that perhaps not only the microsporidium N. ceranae, but other pathogens as well may have jumped from Apis cerana to Apis mellifera, as predicted by Bailey and Ball in 1978 [26].
It also implies that if Kashmir bee virus has been in North America for more than twenty years, so might IIV and Nosema ceranae. That would fit the time line of the first observations of this complex of pathogens, and of severe bee losses in India in the 1970s. It also leads us to ask whether the first widespread losses of bees in the USA, described as Disappearing Disease in the 1970s [52], may have been early outbreaks of CCD.
The researchers haven't yet determined how the combination of virus and fungus is killing bees but it appears to affect a bee's gut.
Interestingly, the presence or absence of IIV in a given honey bee colony may explain why in the USA N. ceranae sometimes seems to contribute to severe colony losses (IIV present), and sometimes not (IIV absent), as reported both by researchers and beekeepers [1], [3], [4], [9]. The mechanism by which these two pathogens interact to potentially increase bee mortality is unknown. It may be that damage to gut epithelial and other host cells by the N. ceranae polar tube allows more robust entry of the virus. Alternatively, replication of N. ceranae in honey bee cells may cause a decrease in the bees' ability to ward off viral infections that normally could be controlled. These types of studies await isolation of the definitive virus.
To test the hypothesis that the combination of fungus and virus was more deadly than either factor alone, the researchers ran controlled experiments. Some bees were intentionally infected with only the fungus or the virus. Other bees were left uninfected as controls. And one set of bees was infected with the combination of virus and fungus.
The combination of virus and fungus caused about 75% of the bees in the colony to die in14 days. Survival rates were much higher for control bees and significantly higher for bees affected by only one pathogen.
Our own work, described here, provides multiple lines of correlative evidence from MSP analysis that associate IIVs and Nosema with CCD in the USA. We conclude with results of laboratory inoculations of caged bees with IIV and Nosema that demonstrate the potential for increased lethality of mixed infections of these two pathogens. Our study strongly suggests a correlation between an iridescent virus, Nosema, and CCD. Our inoculation experiments confirmed greater lethality of an IIV/Nosema co-infection compared to infections involving each pathogen alone. Future research using the specific strains of IIV isolated from infected bees will surely confirm whether a synergistic or additive interaction between these two pathogens results in the signs and symptoms of CCD.
Also, see the New York Times for the story about the unusual research team.