Identification and Discrimination of Volatiles Associated With Chalkbrood Infection in European Honey Bees (Apis Mellifera), Eastern Australia

Abstract

Abstract Chalkbrood disease in honey bees is caused by the fungal pathogen Ascosphaera apis. Transmission occurs when developing larvae are fed brood food containing infectious spores. These spores germinate in the larval gut producing hyphae which penetrate the larval cuticle and can sporulate on the cadaver. Infection with A. apis can trigger changes in larval volatile profiles, producing chemical cues that influence colony behaviour. For example, the production of phenethyl acetate by infected larvae is known to elicit cannibalism and/or removal in highly hygienic honey bees providing a colony level protection from chalkbrood disease however, recent evidence in Australia suggests that hygienic behaviour is failing to confer chalkbrood resistance. To better understand this host-pathogen relationship the present study identified semiochemicals produced by infected larvae and measured the response of bees from hygienic colonies in a field assay. In field trials, bees from hygienic colonies responded to brood cappings topically treated with phenethyl acetate within three hours, significantly faster than cappings treated with phenethyl alcohol or gamma decalactone. Gamma decalactone, was associated with uncapping at 24 hours in hygienic colonies, but this response appears insufficient to influence colony level disease. These findings indicate that A. apis in Australia does produce phenethyl acetate and that hygienic bees are able to discriminate and respond to the compound. However, more research is needed to better understand the host-pathogen relationship in the Australian context in order to pursue genetic improvement of honey bee stocks for disease resistance.