41st Annual Meeting of the Society for Invertebrate Pathology
and 9th International Conference on Bacillus thuringiensis

Colony Collapse Disorder (CCD) was first recognized in 2006 in several beekeeping operations and presented symptoms previously not known.  Collapse of the colony occurred rapidly over a short time, with loss of most workers leaving behind the queen, a small number of newly emerged workers, and brood.  Analysis of remaining bees revealed large numbers of known pathogens in individual bees, without any one pathogen being linked to the symptoms.  This presentation will discuss the collaborative efforts to identify pathogens involved in CCD using a metagenomic analysis of bees taken colonies having identified CCD versus historical and healthy colonies. This analysis resulted in the identification of four pathogens that were strongly linked to CCD, the Israeli Acute Paralysis Virus, the Kashmir Bee Virus, Nosema ceranae, and Nosema apis.  Further examination of IAPV reveals that multiple lineages exist, with at least two being present in CCD colonies in the United States and Canada.  Additional studies will be described in which colonies were exposed to IAPV in containment greenhouses and symptoms observed.  Current questions will be discussed concerning the role of pathogens in Colony Collapse Disorder and bee health worldwide.

In North America, populations of the honey bee Apis mellifera have been in decline since the introduction of the varroa mite, Varroa destructor, in the 1980's. Parasitization by varroa mites still is a major factor underlying most colony losses, most likely through immunosuppression and increased disease instance. However, a new phenomenon was identified in late 2006 that is though to be responsible for large colony losses in affected apiaries: colony collapse disorder (CCD). This condition is identified by a set of unique symptoms: no dead bees in the affected hive or apiary, honey bee brood and food stores are left behind, and secondary pests hesitate to invade affected hive equipment. CCD has continued to have major impact on bee colonies in the United States and significantly add to the already high loss of colonies due to varroa parasitization. In an attempt to determine the cause or causes of CCD, several studies were initiated. Common samples were collected from CCD and non-CCD affected apiaries and shared among various institutions in an attempt to isolate a single causes. No one culprit has yet been found which explain all CCD losses. A longitudinal epidemiological study was also initiated in 2007 that followed individual colonies over time, sampling them repeatedly. This study uncovered several factors which impact bee health but not necessarily how CCD is triggered. This presentation will discuss the approaches being taken to investigate causes of colony losses, and how losses in the United States compares to losses in other countries in terms of magnitude, symptoms and response.

Honey bee colonies face disease threats ranging from viruses to bacteria and mites. Recent severe colony losses in North American honey bees reflect, in part, a rare syndrome during which adult bees disappear from colonies, leaving behind healthy queens and brood with no obvious pathologies. Current hypotheses to explain this syndrome, Colony Collapse Disorder, center on nutritional deficiencies in bees, exposure to harmful exogenous chemicals, and the presence of new or resurgent pathogens. These hypotheses have been tested by genetic analyses of honey bee pathogens and gene-expression analyses of honey bee genes involved in immunity and stress responses. Copy numbers of several bee viruses as well as trypanosomatid parasites are positively correlated with CCD, with a substantial geographic component to the predominant pathogens. Several honey bee genes have emerged as expression biomarkers for CCD, although CCD and control bees do not show systematic differences in the expression of genes related to immune function or stress responses. Genomic resources for honey bees and their major pathogens are also being used to improve honey bee breeding and management for disease resistance. Heritability and efficacy of immune genes targeting the bacterial pathogen Paenibacillus larva will be discussed, along with efforts to use molecular tools to follow bee-bacterium interactions.

Phylogenetically, Microsporidia are now considered highly specialised parasitic fungi. They are all intracellular parasites with a characteristic and unique mode of infection. Microsporidia may infect all life forms and undoubtedly, only a small fraction of the actual number of species have been characterised. In Hymenopteran pollinators, microsporidia infections have been described from four host species only: Nosema apis infecting the European honey bee, Apis mellifera; Nosema ceranae infecting the Asian honey bee, Apis cerana; Nosema bombi, infecting Bombus spp. and Antonospora scoticae infecting Andrena scoticae. N. apis and N. ceranae are cross infective between hosts. However, N. apis does not do well in A. cerana, whereas there is a worldwide process of N. ceranae replacing N. apis in A. mellifera. N. bombi has recently become of particular interest for conservationists, since this parasite may be distributed to areas assumed free from this parasite, thereby presumably endangering endemic bumble bee spp. Furthermore, within-genome rRNA variability in N. bombi suggests that to characterize intraspecific genetic variants in the Microsporidia based on RNA sequences is not straight forward. A. scoticae infects the fat body tissue of A. scotica and may occur with an extreme prevalence in its host.