TRANSMISSION OF ASCOVIRUS FROM HELIOTHIS VIRESCENS (LEPIDOPTERA: NOCTUIDAE) BY THREE PARASITOIDS AND EFFECTS OF VIRUS ON SURVIVAL OF PARASITOID CARDIOCHILES NIGRICEPS (HYMENOPTERA: BRACONIDAE).

Authors: Tillman, Patricia - Glynn; Hamm, John; STYER, E - UNIVERSITY OF GEORGIA; MULLINIX, JR., B - UNIVERSITY OF GEORGIA

Submitted to: Environmental Entomology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/17/2004
Publication Date: 7/1/2004
Citation: Tillman, P.G., Styer, E.L., Hamm, J.J. 2004. Transmission of Ascovirus from Heliothis virescens (Lepidoptera: Noctuidae) by three parasitoids and effects of virus on survival of parasitoid, Cardiochiles nigriceps (Hymenoptera: Braconidae). Environmental Entomology. 33(3):633-643.

Interpretive Summary: Since tobacco budworms (TBW) have developed resistance to pyrethroids, this insect pest can be a serious problem in cotton. Cardiochiles nigriceps (CN) is a parasitic wasp that can contribute substantially to the biological control of TBWs in trap crops in cotton. Tests were designed to determine if CN could transmit a virus to TBW worms, and, if so, what was the effect the TBW virus had on the survival of the immature stages of CN. We determined that a TBW virus was vectored by CN to healthy TBW worms in the field, and laboratory females of CN can transmit the virus by inserting the virus-infected ovipositor into a TBW worm. CN immatures could survive host virus infections that were less than 48h old and those that were initiated toward the end of the 2nd stage of development of CN. The ability of these CN immatures to survive virus infections in their host worms in combination with the inability of these immatures to transmit the virus when they became adults could function as a survival mechanism for CN during extensive field outbreaks of TBW virus in TBW trap crops.

Technical Abstract: We demonstrated that a TBW ascovirus was vectored by the parasitoid Cardiochiles nigriceps (CN) Viereck to healthy TBW larval hosts in the field, and laboratory females of the braconids CN and Microplitis croceipes (MC) Cresson and the ichneumonid Campoletis sonorensis (CS) Cameron can transmit the ascovirus in the laboratory by inserting the ascovirus-infected ovipositor into a TBW larva. The ability of these parasitoids to transmit virus is associated solely with the mechanical ability of the ovipositor to penetrate into the host's body cavity, becoming contaminated with virus through contact with virus-containing tissues or hemolymph or injecting contaminating viruses into a host along with the egg and calyx fluid. CN females were generally able to transmit ascovirus throughout their lifetimes although ascovirus transmission decreased as females aged. CN/CS and MC differed in their ability to transmit ascovirus, but not in the level or extent of infection that developed in host larvae or in the propensity of their ovipositors to become contaminated with ascoviruses. Lower frequency of transmission by MC compared to CN and CS is probably related to the relative shortness of the MC ovipositor compared to the CN and CS ovipositors. Throughout the 12-96 h period following inoculation of source larvae, ascovirus transmission by CN increased linearly at the rate of 1.15% per hour, the equivalent of about 28% per day. Mortality of CN eggs did not begin until around 60 h post-infection and increased thereafter in a curvilinear manner. The relationship between mortality of CN 1st instars and time after inoculation of ascovirus in a source host was biphasic: 1st instar mortality increased from 12 hr to 60 h in a curvilinear manner and then decreased sharply from 60 to 96 h, again in a curvilinear manner. The decrease in 1st instar mortality that began with the 60 hr post inoculation reflects a decrease in the number of eggs that were capable of hatching rather than a diminished rate of mortality among the 1st instar larvae that result from hatching. CN immature parasitoids were able to survive an ascovirus infection only once the immatures developed into second instars. The ability of CN progeny to survive host ascovirus infections that are less than 48h old and those that are initiated toward the end of CN 2nd instar development in combination with the inability of these progeny to transmit ascovirus, could function as survival mechanisms for CN during extensive field outbreaks of TBW ascovirus.