Submitted to: Apidologie
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 1, 2004
Publication Date: June 1, 2004
Citation: Chen, Y., Pettis, J.S., Evans, J.D., Feldlaufer, M.F. 2004. Molecular evidence for transmission of kashmir bee virus in honey bee colonies by ectoparasitic mite, varroa destructor. Apidologie. 35(4):441-448.
Interpretive Summary: Varroa is a parasitic mite of the honey bee, an important pollinator of many agricultural crops. Because this parasitic mite feeds on all stages of the honey bee, the mite has the potential to transmit and spread honey bee viruses. By removing mites from honey bee colonies having a virus infection and placing these mites in honey bee colonies without a virus infection, we were able to assess the ability of these mites to transmit disease. This research, therefore, adds additional importance to parasitic mite control and will be of interest to the beekeeping community at large. The results of this research will also benefit scientists that are interested in the interaction of bee diseases and parasites.
While numerous honey bee viruses are known to exist, their epidemiology is poorly understood. Because the obligate parasitic mite Varroa destructor feeds and moves regularly between brood and adult bees, these mites have the potential to act as either biological or mechanical vectors of bee viruses, though direct evidence for their role in virus transmission is scant. We investigated the role of Varroa in the transmission of Kashmir bee virus (KBV) in honey bee colonies. Using KBV-specific primers and RT-PCR, we were able to identify honey bee colonies that were infected with virus and colonies free of virus. To investigate the vectoring capability of Varroa, we collected live mites from the virus-infected colonies and experimentally inserted one, two, three or four of these mites into the sealed cells of individual bee brood from the virus-free colonies. We found a direct relationship between virus frequency and the number of mites to which recipient bees were exposed. The more donor mites into the brood cell, the greater the incidence of virus was detected in recipient bee brood. This was most evident in bees exposed to four mites, which resulted in 100% infection. Recipient brood that was not exposed to mites showed no signs of infection. Our experimental design involving the introduction of varying numbers of mites allowed us to make a second novel discovery. Following the experiment, it was apparent that virus frequency in mites was directly correlated with the number of mites per cell. Thus, not only did mites transmit viruses to their bee hosts, we have shown evidence of horizontal mite-to-mite transmission of viruses, presumably via a honey bee intermediary. This finding has important epidemiological implications, since infected mites emerge with their host bee, and later infest and parasitize additional host larvae. Mites emerging from multiply-infested cells could therefore play a disproportionate role in the spread of viruses within the colony.