Possible causes of CCD

Here are some theories as reported from wikipedia.org

While the exact mechanisms of CCD are unknown, pathogens, pesticides or mite associations are suspected as causative agents. Whether any single factor is responsible, or a combination of factors (acting independently in different areas affected by CCD, or acting in tandem), is still unknown; it is likewise still uncertain whether this is a genuinely new phenomenon, as opposed to a known phenomenon that previously only had a minor impact.

  • At present, the primary source of information, and presumed “lead” group investigating the phenomenon, is the Colony Collapse Disorder Working Group, based primarily at Penn State University. Their preliminary report pointed out some patterns, but drew no strong conclusions.
  • One such pattern was that all producers in a preliminary survey noted a period of “extraordinary stress” affecting the colonies in question prior to the die-off, most commonly involving poor nutrition and/or drought; accordingly, there is at least some possibility that this phenomenon is correlated to nutritional stress, and may not manifest in healthy, well-nourished colonies.
  • Some researchers have commented that the pathway of propagation functions in the manner of a contagious disease; however, there is some sentiment that the disorder may involve an immunosuppressive mechanism, not unlike the analog of HIV in humans, potentially linked to the aforementioned “stress” leading to a weakened immune system. Specifically, according to researchers at Penn State: “The magnitude of detected infectious agents in the adult bees suggests some type of immunosuppression.” These researchers have further suggested a connection between Varroa destructor mite infestation and CCD, suggesting that a combination of these bee mites, deformed wing virus (which the mites transmit) and bacteria work together to suppress immunity and may be one cause of CCD.  This research group is reported to be focusing on a search for possible viral, bacterial, or fungal pathogens which may be involved.
  • Some researchers have attributed the syndrome to the practice of feeding high fructose corn syrup (HFCS) to supplement winter stores. The variability of HFCS may be relevant to the apparent inconsistencies of results. However, if this were the sole factor involved, this should also lead to the exclusive appearance of CCD in wintering colonies being fed HFCS, but many reports of CCD occur in other contexts, with beekeepers who do not use HFCS.
  • Some have suggested that the syndrome may be an inability by beekeepers to correctly identify known diseases such as European foulbrood or Nosema. The testing and diagnosis of samples from affected colonies (already performed) makes this highly unlikely, as the symptoms are fairly well-known and differ from what is classified as CCD.
  • One of the more common general hypotheses, pesticides (or, more technically, insecticides), is particularly difficult to evaluate for several reasons. First, the variety of pesticides in use makes it difficult to test for all possible pesticides simultaneously. Second, many commercial beekeeping operations are mobile, transporting hives over large geographic distances over the course of a season, potentially exposing the colonies to different pesticides at each location. Third, the bees themselves place pollen and honey into long-term storage, effectively, meaning that there may be a delay of anywhere from days to months before contaminated provisions are fed to the colony, negating any attempts to associate the appearance of symptoms with the actual time at which exposure to pesticides occurred. Pesticides used on bee forage are far more likely to enter the colony via the pollen stores rather than via nectar (because pollen is carried externally on the bees, while nectar is carried internally, and may kill the bee if too toxic), though not all potentially lethal chemicals, either natural or man-made, affect the adult bees - many primarily affect the brood, but brood die-off does not appear to be happening in CCD. Most signficantly, brood are not fed honey, and adult bees consume very little pollen; accordingly, the pattern in CCD suggests that if contaminants or toxins from the environment are responsible, it is most likely to be via the honey, as it is the adults that are dying (or leaving), not the brood. To date, most of the evaluation of possible roles of pesticides in CCD have relied on the use of surveys submitted by beekeepers, but it seems likely that direct testing of samples from affected colonies will be needed, especially given the possible role of systemic insecticides (which are applied to the soil and taken up into the plant’s tissues, including pollen and nectar), which may be applied to a crop when the beekeeper is not present. No detailed studies of toxicity or pesticide residue in remaining honey or pollen in failed colonies are yet published, however.
  • Most beekeepers affected by CCD report that they use antibiotics and miticides in their colonies, though the lack of uniformity as to which particular chemicals are used[3] makes it seem unlikely that any single such chemical is involved. However, it is possible that not all such chemicals in use have been tested for possible effects on honey bees, and could therefore potentially be contributing to the CCD phenomenon.
  • Certain plants’ nectars (and even some pollens) such as rhododendrons, azaleas, Passiflora, almond[citation needed], aconites, hellebore, skunk cabbage, golden rain tree, Jessamine, Aloe littoralis, oleander and Chamaecrista fasciculata (Partridge-pea) are a few of the species known to be mildly toxic to poisonous to bees (and humans). These plants nectar’s are known to include toxic or poisonous substances including alkaloids, anthraquinones, grayanotoxin and andromedotoxin. Catalpa speciosa (makes bees mildly to very enebriated), honey from Kalmia latifolia, the “mountain laurel” of the northern United States, and allied species such as sheep laurel, Kalmia angustifolia, can produce sickness or even death. The nectar of the “wharangi bush”, Melicope ternata, in New Zealand also produces toxic honey, and this has been fatal. Datura plants, belladonna flowers, henbane (Hyoscamus niger), and Serjania lethalis (a liana used in making fish killing mixtures) from Brazil also produce toxins at dangerous to deadly levels in honey. The changing climate, range and other environmental factors are enabling more of some of these plants’ nectars to potentially affect bees and other nectar gatherers.
  • When a colony is dying, and there are other healthy colonies nearby (as is typical in a bee yard), those healthy colonies may enter the dying colony and rob its provisions for their own use. If the dying colony’s provisions were contaminated (by natural or man-made toxins), the resulting pattern (of healthy colonies becoming sick when in proximity to a dying colony) would suggest that of a contagious disease. However, it is often reported in CCD cases that provisions of dying colonies are not being robbed, suggesting that at least this particular factor is not involved in CCD. Furthermore, even if pollen were contaminated in a dead or dying colony, honey bees do not rob pollen stores, only honey.
  • Potential effects of gathering pollen and nectar from genetically modified (GM) crops that produce Bacillus thuringiensis (Bt) toxin have not been investigated in great detail, but the primary crops involved (corn, and tobacco) are not preferred plants for honey bees (if they visit the plants, they typically do so when there is no other food available; they will gather only pollen from corn, and rarely visit tobacco blossoms). Cotton is highly subject to bee visitation for nectar, but there is little evidence of toxicity of GM cotton, other than that from insecticides used during bloom. Furthermore, the effect of Bt on insects is as a larvicide, whereas the CCD phenomenon involves the disappearance of the adult bees. It is therefore highly unlikely the syndrome is related in any way to GM crops. This focus on Bt is only a known toxin. The somewhat to very random approach of creating GM varieties does not include investigating all the ways in which the variety is affected, so other effects, like poisonous pollen or nectar may not be desired in the creation or even been noted by researchers.

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