Tuesday, December 16, 2014

Not the Bees!


                  It is an uncomfortable fact to consider that parasites may be the predominant life form on Earth, perhaps even outnumbering free-living species by 4-to-12. It is fortunate then that most parasites exist in a specific niche, only able to parasitize an individual species or a small number of closely related species2. This drives an evolutionary war of sorts, where parasites infect a host population, hosts adapt and send on their genes to offspring, prompting the parasite to respond in turn by improving their parasitizing ability. This gives the host an array of defenses against that specific parasite, but unfortunately that's not always enough. Sometimes the niche occupied by a parasite can be usurped by another, leaving the host to the whims of this new invader. Enter Nosema ceranae, a unicellular parasite that did just that by jumping from the eastern honey bee (Apis nosema) to the western one (Apis mellifera)4.  Ecologically speaking it happened in the blink of an eye, and the consequences have been disastrous.
                  In 2006 and 2007 western honey bee colonies seemed to be disappearing over night, and even those that survived suffered abnormally high levels of attrition following the winter months. This phenomenon was given the label Colony Collapse Disorder (CCD), and has led to a loss of around 34% of the bee population yearly from 2007 to 20103. There is no one cause to CCD, usually being a combination of circumstances7, but a factor common to many cases is the presence of N. ceranae5. The timeline of N. ceranae switching hosts matches events leading up to the large incidence of CCD. Before N. ceranae's jump N. apis was found globally in A. mellifera populations, but post jump it has been  largely displaced becoming limited to northern and western Europe5. Not much is known about how the organism made the jump, but researchers have put the time of the jump somewhere between a decade and two decades ago5, which falls in line with the beginning of the bee die off we are currently experiencing.
                  N. ceranae's effectiveness against A. mellifera is two-fold: First because it jumped from a closely related species it is already effective at co-opting metabolic proteins, and second the infection interferes not only on a physiological level but a behavioral level as well. Bee's collecting pollen can also ingest Nosema spores, and when they return to the colony the spores can spread among the population of bees. This spread was exacerbated by humans, with the accidental transport of infected bees by commercial and hobbyist beekeepers5. Once a bee has ingested some spores the fungi will move to and infect the cells of the midgut, where it proliferates8. The midgut proves to be an ideal environment for the parasite, as it is able to absorb the nutrients it needs to survive right at the source of where the bee breaks down nectar into sugar. Although the mechanism for how it is able to accomplish this is unknown, the parasite further capitalizes on its location by actively suppressing proteins in the bee that utilize or store sugars, and increasing the expression of proteins involved in carbohydrate catabolism8. This creates a dangerous feedback loop for the bee because it will breakdown carbohydrates for sugar to sate its hunger, but being unable to use or store it will continue to breakdown more and more food. Left unchecked this has further consequences impacted not just the infected bee, but also healthy bees within the colony.
                  Normally bees are very social creatures, and returning foragers share the food that they collect with the colony6. Infected bees however, both demonstrate a greater inclination to taking in food stocks from the hive and are much less likely to share collected resources6. While perhaps unsurprising this behavioral change may be the largest contributor to how N. ceranae influences CCD. Because infected bees want to take in more food sources they will spend more time where the food in the hive is, leaving spores to the fungus there(Nosema is orally ingested contributing to infection in the hive). A second issue is that CCD is most prevalent in the winter when bees don't have access to food sources and must rely on what was stored. Infected bees consume more, to compensate for their hunger, and in turn contribute to winter starvation possibly dooming the colony.
                  Certainly this parasitic jump has been awful for global A. mellifera populations, but from the perspective of you are I a fair question remains: so what, who cares? Beyond the obvious association to honey production, the western honey bee has an enormous economic role in agriculture7. They are by and large the largest pollinators in nature3, and up to a third of the food we eat is pollinated by bees9. If A. mellifera were to go extinct the consequence for humans would be dire (think a large spike in unemployment, and starvation). Researchers have been able to narrow down CCD to factors such as N. ceranae, but the mechanisms of how it was able to jump, or how it changes protein expression is still in question. By putting effort into unraveling these mysteries scientists in the future may be able to predict, or even prevent such a future disaster. If that is still unsatisfacotry consider this final point: should the garden variety  A. mellifera go extinct the replacement of choice would be a particular subspecies that has been so far no affected by CCD. It's common name is simply the Killer Bee. And that dear reader is a world I shudder to live in.

1. Bromenshenk, J.J., Henderson, C.B., Wick, C.H., Stanford, M.F., Zulich, A.W., Jabbour, R.E., Deshpande, S.V., McCubbin, P.E., Seccomb, R.A., Welch, P.M., et al. (2010). Iridovirus and microsporidian linked to honey bee colony decline. PLoS ONE 5, e13181.
2. Brooker, R., Widmaier, E., Graham, L., and Stiling, P. (2011). Biology (McGraw-Hill).
3. CCD Steering Committee (2010). Colony Collapse Disorder Progress Report. United States Department of Argriculture 2.
4. Higes, M., Martín, R., and Meana, A. (2006). Nosema ceranae, a new microsporidian parasite in honeybees in Europe. Journal of Invertebrate Pathology 92, 93–95.
5. Klee, J., Besana, A.M., Genersch, E., Gisder, S., Nanetti, A., Tam, D.Q., Chinh, T.X., Puerta, F., Ruz, J.M., Kryger, P., et al. (2007). Widespread dispersal of the microsporidian Nosema ceranae, an emergent pathogen of the western honey bee, Apis mellifera. J. Invertebr. Pathol. 96, 1–10.
6. Naug, D., and Gibbs, A. (2009). Behavioral changes mediated by hunger in honeybees infected with Nosema ceranae. Apidologie 40, 595–599.
7. vanEngelsdorp, D., Evans, J.D., Saegerman, C., Mullin, C., Haubruge, E., Nguyen, B.K., Frazier, M., Frazier, J., Cox-Foster, D., Chen, Y., et al. (2009). Colony Collapse Disorder: A Descriptive Study. PLoS ONE 4, e6481.
8. Vidau, C., Panek, J., Texier, C., Biron, D.G., Belzunces, L.P., Le Gall, M., Broussard, C., Delbac, F., and El Alaoui, H. (2014). Differential proteomic analysis of midguts from Nosema ceranae-infected honeybees reveals manipulation of key host functions. Journal of Invertebrate Pathology 121, 89–96.

9. (2009). The economic value of honeybees. BBC.

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