Nosema Ceranae

Parasites and their hosts live a delicate dance.  If the parasite kills the host, it may lose its habitat and perish as well, so most parasite-host relationships develop such that the parasite is a nuisance, but not life threatening to the host.  The problem we have with our bees at the moment, is that the most troublesome parasites are recently introduced.  Resistance in the host, and reduced virulence in the parasite have not yet had a chance to evolve, and humans keep interfering with medication that slows down the inevitable natural selection process.  Varroa mites are the worst and most persistent new parasite, but troubling as well is Nosema ceranae, a microsporidian  protist. When Nosema spores infect the gut of the bee, the spores “germinate” by releasing a harpoon-like structure that pierces the cell wall and allows the nuclear material of the spore to enter the host cell and mature into the vegetative organism, which eventually grows and produces a multitude of spores.  Eventually the host cell dies and comes apart releasing the spores.

Beekeepers have long had to deal with Nosema apis, a very similar bug that was commonly responsible for bee dysentery, usually a problem during cool weather in early spring.  The tell-tale sign for Nosema apis infection is bee feces spotting inside and on the front of the hive.  Infection is spread by workers cleaning up the mess.  The problem largely disappears on its own once the sick bees can leave the hive with the appearance of warmer weather.

The ceranae strain does not show such obvious signs of infection.  Partly because of this fact, the disease was widely spread before it was even apparent that we had a new problem.  It was identified in the U.S. in about 2007, but had widely spread by that time, so it’s hard to say exactly how long its been here.  Fortunately, for us backyard beekeepers, there is some very good information about Nosema ceranae available from beekeeper and biologist Randy Oliver.  His publications and website offer very readable, insightful and practical information on Nosema ceranae, as well as other topics.  I encourage the serious beekeeper to set aside some time and read through Randy’s entire site.  There were a few interesting points I learned from his last update on Nosema ceranae that can help point the way.  So here is my gleaning from all this.

Spore sampling, even if done with care by taking a reasonable number of active field bees at the entrance, can give paradoxical results.  For instance, in Oliver’s treatment tests, he noted that colony weight gain was positively correlated with spore counts. “Curiously, the stronger colonies had higher infection levels”.  At least part of the explanation for this is that single infected bees can have extremely high spore loads just before the bee succumbs to the infection.  Since spore counts are done by taking the average from a modest number of bees, single highly infected individuals can skew the statistics.  Strong colonies might produce generally healthier bees that can handle a higher level of  Nosema infection before leaving the workforce.  The spore count does not tell us what fraction of the bees are infected, or the age when they became infected, both critical factors in determining the disease progression in the colony.

Several characteristics of Nosema ceranae have been discovered.  The N. apis strain is a cool weather pest because once temperatures rise, the vegetative state of the organism is no longer viable.  N. Ceranae remains viable at warmer temperatures, and hence the infection can remain problematic throughout the year.  The spores or N. ceranae, however, are much more sensitive to cold temperatures than are the N. apis spores.  A few days at “refrigerator” temperatures will kill most N. ceranae spores, whereas N. apis can survive freezing winter without loss of viability.  When various organs in the bee are checked for the presence of Nosema DNA, most of the infection is in the bee’s gut; but with N.ceranae infection, all organs tested had some evidence of infection as well.  What is not clear is the mechanism for infection with N. ceranae.  The fact that infected bees have a more generalized infection suggests that it might be easier for spores to be transferred between bees by normal food sharing and feeding activities.  For whatever reason, the queen does not seem to suffer with N. ceranae, whereas it is more common to lose queens to N. apis.

The progression of the disease is not always fatal, and the results of treatment (or no-treatment) are variable.  In Oliver’s trials, the variation in outcomes for a particular treatment cohort, or control group was as large as any trend for a particular treatment.  The disease is known to disappear on its own, and usually (treatment or not) will somewhat abate during the summer season.  The figure below shows infection rates of Nosema species in bees in northern Germany over five years.  There is a strong annual variation, even without treatment.  All this makes you wonder if treatment is worth very much!

There is evidence that bees inoculated with Nosema do not develop infection to the point of spore formation until the bees are about 20 days old, corresponding roughly to the point when the bees enter the field force. It takes longer for the infection to fully develop in bees infected when they are younger.  The progression of colony collapse starts with the reduction in the field bees, and the inability of the field force to provide for the colony.  Reduced lifespan of the field workers directly affects the ability of the colony to build up in the spring.  The need to maintain a field force, means that house bees will move more quickly to outside work, leaving fewer bees to attend the brood, which will in turn cause a reduction in the size of the brood nest.  The physiological changes when bees move to the field could allow a simmering infection to become manifest, leading to accelerated colony decline.

You can see how the pathogen has evolved to at least give the bees a chance. The delayed onset of  the debilitating phase of the disease, and the fact that the queen remains viable, allows the brood nest to function almost normally. The race against time is with the field force. When bees have limited flight days in the early spring, the disease will likely kill the bee before she wears herself out. In the summer it’s possible that most infected bees will die of natural causes before the disease has a chance to develop fully.  This could be the reason spore loads are seen to decrease naturally during the summer.

Another important study was published in Oct. 2010 on the role of Nosema and viruses as a cause for colony collapse (CCD).  Many viruses were detected in conjunction with collapsing colonies, but one type, the invertebrate iridescent virus (IIV) (Iridoviridae), stood out as highly correlated with colony collapse.  The study demonstrated that Nosema and IIV together were more lethal than either pathogen by itself.  It’s possible that this could be part of the reason for the large variability in the outcome for Nosema infected colonies that Oliver observed.  Some colonies may be infected with IIV, others not, with substantially different outcomes.  The iridoviridae are quite a common pathogen in the insect world, but are not particularly infectious when ingested, much more so when the virus is directly introduced into the insect.  It is certainly possible that the damage caused by even low levels of Nosema spores could allow the IIV particles to more easily establish infection.

In our locality, it seems that Nosema ceranae has arrived to stay.  For the last couple of years beekeepers around here have lost many colonies to Nosema infection, but there are still plenty of healthy bees in our town.  A few more years of losing less resistant bees and over-virulent Nosema strains, and this pest too, will fade from the front page.