Submitted to: Journal of Apicultural Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: March 30, 2004
Publication Date: March 1, 2005
Citation: Evans, J.D., Armstrong, T.N. 2005. Selective screening for honey bee bacterial symbionts that inhibit a key bacterial pathogen, paenibacillus larvae. Journal of Apicultural Research. 44:168-171. Interpretive Summary: Among the honey bee diseases, American Foulbrood disease (AFB) is especially widespread and damaging. This disease is caused by a single species of bacteria, Paenibacillus larvae. We used inhibition assays and genetic screens to identify several bacterial species found in natural bee populations that strongly inhibit P. larvae. These newly identified bacteria are candidates for novel control strategies against P. larvae and other honey bee disease agents. They also can help explain great variation across bees and colonies in disease rates when exposed to P. larvae. The results can be used to help develop novel strategies that reduce the need for antibiotics and other controls for this disease.
Technical Abstract: Insects harbor diverse bacterial symbionts and it is increasingly evident that many of these symbionts play important facultative roles as mutualists. While honey bees possess a diverse microbial flora, the impacts of most of these species on honey bee health remains unresolved. Here, in vitro inhibition assays were used to identify bacteria isolated from larval honey bees that inhibit the gram-positive bacterium Paenibacillus larvae larvae, the primary pathogen of bees. Among the diverse bacteria cultured from larval bees, strains placed in the genera Stenotrophomonas, Acitenobacter, Brevibacillus and Bacillus showed the most consistent inhibition of this widespread pathogen. These species were present in approximately 10% of the larvae from an age class that is susceptible to P. l. larvae. Accordingly, symbiotic bacteria including those described here are plausible antagonists toward this important pathogen. The results suggest a tradeoff between the maintenance of potentially beneficial bacterial symbionts versus mechanisms at the individual or colony level to reduce infection by pathogens.