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Title: Retention of the cucurbit yellow vine disease bacterium, Serratia marcescens, through transstadial molt of the vector, Anasa tristis (Hemiptera: Coreidae)

Author
item WAYADANDE, ASTRI - OSU, STILLWATER, OK
item Bruton, Benny
item FLETCHER, JACQUELINE - OSU, STILLWATER, OK
item Pair, Sammy
item MITCHELL, FORREST - TAES, STEPHENVILLE, TX

Submitted to: Annals of the Entomological Society of America
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/1/2006
Publication Date: 11/1/2005
Citation: Wayadande, A.C., Bruton, B.D., Fletcher, J., Pair, S.D., Mitchell, F.L. 2005. Retention of the cucurbit yellow vine disease bacterium, Serratia marcescens, through transstadial molt of the vector, Anasa tristis (Hemiptera: Coreidae). Annals of the Entomological Society of America. 98(6):770-774.

Interpretive Summary: Cucurbit Yellow Vine Disease is caused by the bacterium Serratia marcescens and is transmitted by the squash bug (Anasa tristis), a serious pest of cucurbits. Knowledge of how an insect vector acquires and maintains a plant pathogen in it's body is critical to developing integrated control measures for the disease. When we conducted an experiment using S. marcescens and squash bug nymphs, transmission by nymphs was documented (but rare) with two insects known to be 3rd or 4th instar nymphs at the time of inoculation. Of the 82 insects that fed on bacteria-infiltrated cubes as 5th instars, only nine transmitted the bacterium to plants. Four of these nine insects inoculated plants and also molted to the adult stage during the first week, and so it is unknown if these four insects were nymphs or adults at the time of inoculation. Eight of the nine transmitters inoculated plants after molting to the adult stage, and in some cases, several weeks after molting. This evidence, strongly suggests that the bacterium is retained within body fluids and not in glands associated with feeding. Confirmation that S. marcescens is propagative within its squash bug vector is consistent with the adult stage of A. tristis functioning as the overwintering site of the bacterium. However, several questions remain unanswered. How does A. tristis survive S. marcescens infection? What is the long-term survival rate of insects that acquire the pathogen by feeding? Does the bacterium become less lethal to its squash bug host when acquired by feeding? And finally, does A. tristis deposit bacteria directly into the sieve tubes or is some other mechanism of phloem invasion possible? The behavior of vascular-inhabiting plant-pathogenic bacteria within their plant hosts remains poorly understood and is likely to be fundamentally different from that of vascular-inhabiting plant viruses. The answers to these questions await further study and may help us to understand how S. marcescens and other bacterial pathogens adapt to new ecological niches.

Technical Abstract: Retention or loss of transmissibility after molting was tested for adult and nymphal stages of the squash bug, Anasa tristis DeGeer, a natural vector of the plant pathogen, Serratia marcescens Bizio, the causal agent of cucurbit yellow vine disease. Squash bug adults and nymphs fed from bacteria-infiltrated squash cubes were caged on squash test plants and transferred weekly to new plants for eight consecutive weeks. Twelve percent of the bugs that acquired as adults transmitted the bacterium to at least one of the test plants; 75% of these transmitters inoculating more than one plant. All transmitters inoculated plants after three weeks post acquisition. Ten percent of squash bugs that fed on S. marcescens as 5th instar nymphs inoculated plants after molting to the adult stage; 77% of these transmitters inoculated more than one plant. Two insects that fed on S. marcescens as 3rd instar nymphs inoculated squash plants. When examined by scanning electron microscopy, the foregut cibaria of transmitting insects were free of bacteria-like structures. The ability of A. tristis to transmit S. marcescens after molting to the adult stage suggests that the hemocoel acts as the site of retention of transmissible bacteria.