|ULRICH, KEVIN - University Of Maryland|
|ST. LEGER, RAYMOND - University Of Maryland|
|THORNE, BARBARA - University Of Maryland|
Submitted to: Journal of Economic Entomology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/15/2014
Publication Date: 12/1/2014
Citation: Ulrich, K.R., Feldlaufer, M.F., St. Leger, R.J., Thorne, B.L. 2014. Exposure of bed bugs to metarhizium anisopliae, and the effect of defensive secretions on fungal growth in vitro. Journal of Economic Entomology. 107(6):2190-2195.
Interpretive Summary: Due to insecticide resistance, bed bugs may not be effectively controlled by many chemicals formally used for that purpose. Therefore, new treatment methods and strategies are being sought to control this blood-sucking pest. We investigated the ability of a fungus that attacks insects to kill various stages of bed bugs, and found less than adequate control. We subsequently showed that chemicals produced by the bed bug for defensive purposes were able to kill the fungus before it acted. This information will be used by scientists involved in developing new control methods for bed bugs.
Technical Abstract: Bed bugs Cimex lectularius were treated with conidia of the entomopathogenic fungus Metarhizium anisopliae by topical, spray, and contact exposure. One week post-exposure, inconsistent mortalities were observed, averaging 30% across all treatment groups and replicates. Microscopic examination of topically-treated bed bugs with a M. anisopliae strain that expresses green fluorescent protein (GFP) revealed that while numerous conidia attached to the cuticle, there was no evidence of cuticle penetration. The two major aldehydes produced by bed bugs and considered defensive secretions, (E)-2-hexenal and (E)-2-octenal, were shown to inhibit fungal growth in vitro by contact and fumigation. Exposure by fumigation of M. anisopliae conidia to (E)-2-octenal for as little as 0.5h was sufficient to inhibit all fungal growth. The inhibition of fungal growth by bed bug aldehydes is discussed in the context of other biotic and abiotic barriers to infection.