Location:2010 Annual Report
1a. Objectives (from AD-416)
1) Develop improved understanding of factors weakening hive vigor and foraging efficiency, and provide economically sound integrated pest management (IPM) approaches to lessen the effects of these factors. Improve IPM tactics for control of key pests of honey bees, including Varroa mites, and the small hive beetle. Develop IPM strategies to lessen pesticide/antibiotic use in managed honey bee colonies, biorational compounds, and sustainable agricultural practices/IPM tactics for use in crop production that will lessen bee exposure to pesticides. 1A) Develop IPM tools and methodologies for control of key pests, and miticide resistance management programs to preserve useful chemical options. 1B) Determine the impact of the small hive beetle on colony development and longevity, and develop management systems for controlling the beetle in hives, including use of antifeedants for protection of protein supplements from small hive beetle damage. Develop effective control programs for management of small hive beetle in bee hives, with the goal to prevent contamination of bee products. 1C) Determine impacts of pesticides on foragers, both acute lethal effects and sub-lethal effects on bee behavior due to chronic exposure, and develop methods to mitigate bee losses due to pesticides, including management strategies for minimizing exposure of bees to pesticides in the field. 2) Use molecular approaches to investigate the physiological basis for bee immune responses to fungal pathogens such as chalkbrood, and develop strategies for controlling natural honey bee diseases. Identify molecular bases for honey bee physiological responses to chalkbrood. Identify and assess the role of genes that could potentially be involved in the anti-fungal activity.
1b. Approach (from AD-416)
Objective will be achieved through development of a combination of different IPM tactics (e.g., soft pesticides, acaricide rotation program, traps, lures) for control of pests, parasites, and diseases of the honey bee, and protection of hive products. It will also involve molecular studies to better understand the genetic basis of insect resistance to the fungal pathogen Ascosphaera apis, the causative agent of chalkbrood disease in honey bees. We will conduct a genome–wide screening of the honey bee immune cDNAs and will monitor the expression profile of larval genes by direct comparison of immune vs. pre-immune cDNAs. We will then utilize qRT-PCR approach to monitor expression profiles of the selected genes, identified through the genomic screens of bee's cDNAs, to better understand the correlation between changes in the level of gene transcripts and the progression of the disease.
3. Progress Report
In 2009, a preliminary field trial was conducted in Weslaco, TX, to test experimental (Pfizer) products controlling Varroa destructor, which showed good efficacy with minor impact on honey bee health. Another field trial with 150 colonies was conducted in Shafter, CA. We tested the impact of currently used acaricides for varroa control on almond pollen collection. We investigated the physiological basis for bee immune responses to honey bee fungal pathogens by using molecular approaches in order to develop strategies for controlling natural honey bee diseases. In this study, we analyzed honey bee transcriptional response to Ascosphaera apis, an infection, using in vitro larval bioassay and natural mode of larval infection. Differentially expressed transcripts were identified in infected vs. healthy honey bee larvae. These transcripts were cloned, sequenced, and analyzed. The most promising target molecules were analyzed using quantitative RT-PCR. Data showed a direct correlation between health status of the animals and their nutritional status. These results will be incorporated in a new disease management plan to help bees sustain the impact of an infectious disease. Several laboratory Small Hive Beetle studies were initiated to determine population dynamics (pupation rate and daily oviposition). A computer-based IPM simulation model of small hive beetle population dynamics is now in development.
1. Chalkbrood effect on honey bee immune competence, nutritional status, and general stress responses. Diseases and other stress factors working synergistically weaken honey bee health and may play a major role in the loss of bee populations in recent years. Among a large number of bee diseases, chalkbrood has been on the rise. Scientists at the Honey Bee Research Unit in Weslaco, Texas, identified honey bee genes that were differentially expressed in response to infection of honey bee larvae with the chalkbrood fungus. Data from this study (infected vs. healthy honey bee larva) was analyzed as it relates to honey bee health, nutritional status, and stress in general. A wide variety of molecules were found that can potentially be involved in the activity against fungus, degradation of damaged proteins, immunological resistance, and nutrition. This data supports the theory that there is a trade off between activation of immune stimulation and nutritional status of the honey bee.
2. Comparative virulence of Nosema apis and Nosema ceranae in cage experiment. In recent years, Nosema infection in honey bees has been implicated in significant losses of bee populations. In three independent trials conducted in 2009 and 2010, scientists at the Honey Bee Research Unit developed the laboratory bioassay methodology for infecting honey bees in small cages. This new laboratory methodology allows for development of more precise experimental design, which we cannot achieve in the field. Our methodology ensures that mortality of caged bees is not associated with the stress due to handling of newly emerged bees and/or rearing conditions of bees in cages. Following our new infection protocol we have determined the level of bee mortality for different species of Nosema by using a range of spore concentrations.Metz, B.N., Pankiw, T., Tichy, S.E., Aronstein, K.A., Crewe, R.M. 2010. Variation in and responses to brood pheromone of the honey bee (Apis mellifera L.). Journal of Chemical Ecology. 36(4):432-440.