Submitted to: Book Chapter
Publication Type: Book / Chapter
Publication Acceptance Date: 8/30/2001
Publication Date: N/A
Citation: N/A Interpretive Summary: The use of wasp parasitoids to control agricultural insect pests is ecologically sound and as part of an IPM program, should reduce the use of chemical pesticides. The mechanism(s) of action used by the parasite to maniplate host hormone levels to create conditions that are favorable for parasite development are not well-understood. Artificial methods that mimic the techniques used by parasitic wasps to inhibit insect growth and development would be a boon to the implementation of new biorational strategies for controlling pest insects. Here we analyze the methods used by Cotesia congregata, a parasitic wasp, to induce developmental arrest in its host, the tobacco hornworm. In addition, we examine the effects of a juvenile hormone mimic commonly used to control pest insects on parasitoid survival, and report that this insect growth regulator causes abnormal wasp metamorphosis and results in high rates of parasitoid mortality. Information should be useful to other scientists investigating the mechanism(s) of action by which parasites induce developmental arrest in their host insects and to IPM specialists who desire to control insect pests with minimum damage to natural enemies. The ultimate goal is to capitalize on the techniques used by parasitic wasps to prevent the host from completing its life cycle to design new, effective biorational strategies for controlling insect pests, while at the same time minimizing damage to natural enemies.
Technical Abstract: Manduca sexta larvae parasitized by the wasp, Cotesia congregata, exhibit many physiological and behavioral changes, especially during their last instar. The parasitoid manipulates host hormone levels causing host development to be halted in the last larval stage. Host hemolymph juvenile hormone titers are elevated, JH esterase is undetectable and prothoracicotropic hormone (PTTH) and other neuropeptides accumulate in the brain, ventral nerve cord and midgut endocrine cells. In addition, host prothoracic glands appear to be refractory to stimulation by PTTH and hemolymph ecdysteroid titers remain relatively low. However, the parasitoids induce a small ecdysteroid peak just prior to and during their last larval molt and concomitant emergence from the host. Results indicate that both secretion by the parasitoids and parasitoid-controlled secretion of ecdysteroid by host prothoracic glands (PTGs) contribute to this peak. Importantly, the parasitoid appears able to uncouple the normal mechanisms by which the brain regulates PTG activity. Thus, PTGs do not respond to PTTH, but neither are these glands subject to the normal inhbitory signals that maintain ecdysteroid synthesis/release at optimum levels for host development. Treatment of last instar day-2 larvae with 200 micograms of methoprene, a juvenile hormone mimic, delays the emergence of the parasitoids and likewise delays the ecdysteroid peak associated with this emergence. Reduced numbers of wasps emerge from these methoprene-treated hosts and the wasps that do emerge exhibit abnormal metamorphosis, typically dying within the pupal cocoon.