Thoughts on CCD

from December 2008 BEE CULTURE

The following is distilled from the reams of disparate dispatches from the CCD front. I have tried to condense this mass of information into a coherent whole. None of what follows is original — all has been expressed in one form or another by others.

When CCD first came on the stage in 2006-2007, a number of possible causes entered the stage at, or close to, the same time:

Drought in many areas
Difficulty in controlling varroa mites
Nosema ceranae (believed to be widespread since at least 2006)
Decreased bee pasture + increased corn acreage
Chemical buildup in comb
Neonicotinoid pesticides

A good argument can be made for any one of these as the main, or sole cause of CCD; a better argument for a combination of two or more. If only one of the above had occurred, it would have been much simpler to either designate or eliminate it as the cause of CCD.

Based on field reports, CCD can devastate a given apiary in a short period of time, sweeping from one end to the other, leaving previously populous colonies with only a handful of bees and a queen. Since rapid decline of an organism (consider, as many have, a honey bee colony to be an individual organism) is typical of a pathogen, current thinking is that a pathogen, either N. ceranae or a virus (or a combination of both) is the basic cause of CCD.

If a virus causes CCD, is it a new “super” virus, or one of the known bee viruses – Kashmir, DWV, APV et al. — or perhaps a mutation of a known virus to a more virulent form? We don’t know, but assuming that a virus causes CCD allows us to speculate on remedial measures.

Consider other CCD-like problems in humans and plants:

Main Vector
W.Nile virus

In each of the above instances, the Target can withstand the Vector in the absence of the Pathogen – mosquitoes are a minor concern to us if they don’t harbor a pathogen; without a pathogen, psyllids, sharpshooters and aphids are far less devastating to crops. Honey bees are faced with a formidable double (or triple) whammy: the pathogen and either of two vectors, varroa or the Nosema ceranae fungus (also a pathogen) can take down a colony. In most areas, Apis mellifera has not had enough time to be able to co-exist with these two relatively new vectors.

In the human-plant list (above) control of the pathogen (and thus the disease) is achieved by controlling the vector (except for flu). Beekeepers are aware that varroa control, and now Nosema control, are vital in protecting colonies from CCD. At the January 2008 Sacramento meetings, Brett Adee arrived late for the CCD panel and had time for only a few words (as I remember them): Control varroa and you solve CCD. Sometimes profound wisdom can be expressed in just a few words. Lyle Johnston has a little different take: control N. ceranae and you won’t have CCD. A third opinion comes from David Mendes: I’m guessing that nutrition trumps varroa and Nosema control. The three aforementioned worthies would make most lists of Top Ten US beekeepers and as such their opinions deserve serious consideration, especially since all three are speaking from personal hands-on experience. Let’s look at the three CCD candidates more closely:

Brett Adee has strong backing from the scientific community that controlling varroa can eliminate (or minimize) CCD. A study, published in 2001 by UK scientist Stephen Martin, The Role of Varroa and viral pathogens in the collapse of honeybee colonies: a modelling approach, indicated that a relatively small number of varroa could take down a colony in the presence of certain viruses (J. of Applied Ecology, 38:1082-1093, 2001). Note particularly the use of the word collapse in the title of the article and the year (2001) that it was published, both indications that CCD has been around longer than many of us might think. In 2004, Martin teamed with a mathematician to expand his 2001 article (see The dynamics of virus epidemics in Varroa infested honey bee colonies, J. of Animal Ecology, 73:51-63, 2004). Recent work showing that varroa mites impair the already limited immune system of honey bees, leaving the bees more susceptible to a wide spectrum of health hazards, gives further support to Brett Adee’s thesis. The fact that the increase in CCD problems over the past two years coincides with the decreased effectiveness of mite-control chemicals over the same period also supports the varroa-CCD connection.

Nosema Ceranae
Lyle’s contention that controlling N. ceranae is vital in avoiding colony collapse is supported by the fact that Joe DeRisi found that all CCD colonies contained N. ceranae. Nosema may not transmit viruses directly but, by damaging a bee’s gut, can provide an entry path for viruses. The direct pathogenic effect of N. ceranae may be far more harmful than its possible role in virus transmission. The consensus now is that N. ceranae has been with us for a number of years. Much of the recent work on N. ceranae has been done by Mariano Higes, in Spain, where N. ceranae is also prevalent. N. ceranae has taken over from the less virulent N. apis and the timeline for this takeover mirrors the timeline of increasing CCD problems throughout the world. Nosema apis was classified as a cool-weather problem and beekeepers in warm areas (Florida and Southern California) didn’t treat for Nosema. Beekeepers in warm areas are now treating for N. ceranae and their bees look better as a result. High spore counts of N. ceranae are being found this summer and fall and many beekeepers are convinced that N. control is critical towards getting colonies to make it through the winter. The fact that N. spores can survive in empty equipment for months could explain the finding that when equipment from CCD colonies is placed on good colonies, the good colonies come down with CCD. For more information on N. ceranae see where Randy Oliver has posted a number of his articles.

Dave Mendes’ contention that nutrition may trump varroa and nosema control also has support from both the scientific community and from beekeepers. Frank Eischen has found that colonies that are well supplied with supplemental protein patties are better able to withstand both varroa and nosema. Beekeepers that are on a strong supplemental feeding program feel such a program gives them more robust colonies. In a human population, the elderly are more susceptible to the flu virus; in a honey bee colony, old bees are more susceptible to virus attack. Young bees contain vitellogenin (dubbed by Randy Oliver as the “fountain of youth” substance; see Randy’s site, above, for an informed discussion of young and old bees). A well-fed colony contains more young bees.

A good case can be made that a virus, spread by varroa (and possibly N. ceranae) is the sole cause of CCD. An equally good case can be made that N. ceranae, by itself, is the sole cause of CCD (and possibly an indirect cause, by spreading a virus). Certainly, a combination of N. ceranae, varroa and virus is a possible cause. Undoubtedly, optimum nutrition will give bees a stronger immune system that in turn will provide some protection from both viruses and Nosema. To date there is not enough evidence to indict neonicotinoids.

Attacking CCD
If the above discussion is credible, a 3-pronged attack is necessary to escape CCD: varroa control, nosema control and nutrition. I believe that Brett, Lyle and Dave would agree. I know of no beekeeper that has a good handle on these 3 entities + good tracheal mite control, that has had CCD problems. Because most bee colonies look great in May-June-July a beekeeper can be lulled into thinking he will not have CCD in Nov.-Dec.-Jan. But if those summer colonies carry a virus load + significant varroa or nosema populations or if they carry a high nosema load alone, they could (will?) succumb to CCD later on. Beekeepers that avoid CCD make it a point to treat for varroa in August; they sacrifice a part of their August honey crop in order to keep viruses from spreading. (A pitfall of this approach is that colonies can plug out leaving little room for brood development and less young, resistant bees for the winter). Sacrificing an August honey crop and making sure colonies have ample room for brood add significantly to management costs, but these expenses can be offset by significantly less winter loss. Like Lyle, many beekeepers now feel that controlling N. ceranae is critical to avoiding CCD. Until more information is forthcoming on neonicotinoids it would be prudent to avoid areas where topical or water-run applications of these materials are used.

Is it possible that neonicotinoid pesticides are contributing to CCD? Absolutely! A number of highly respected beekeepers, including Dave Mendes, are convinced of a CCD-neonicotinoid connection but to date, there is no definitive evidence. The circumstantial evidence is impressive: the neonics cause memory loss and impair the immune system, both of which can be linked with CCD. US and Canadian studies with neonic-treated seed have shown no problems with melons or canola but there is scant or no information on topical or water-run applications. Project ApisM is funding a 2009 study on neonic-treated blueberries and cranberries that, hopefully, will shed some much-needed light on the subject. In a perfect world, the EPA should have screened the neonics for bee hazards before they were introduced and the EPA, rather than beekeepers, should be funding current neonic-bee tests.

The Future
Many believe that current chemical controls for both varroa and nosema are not sustainable and that it is a matter of time before such chemicals will be found in honey at concentrations high enough to torpedo the honey market. The ultimate solution is genetically improved stock that is resistant to viruses, varroa and nosema and much work is being done on these lines. Some beekeepers are having good luck with survivor stock from a few selected breeders. Until resistant stock is widely available, CCD problems will continue to plague the bee industry and beekeepers must use the few weapons currently in their arsenal, some only temporary, others of limited effectiveness.