Interactions between an entomopathogenic microsporidium and the endoparasitoid Glyptapanteles liparidis within their host, the gypsy moth larva.

Interactions in the host-parasitoid-pathogen system, Lymantria dispar L. (Lep., Lymantriidae)-Glyptapanteles liparidis (Bouché) (Hym., Braconidae)-Vairimorpha sp. (Protista, Microspora), were investigated. Host selection experiments revealed that G. liparidis females did not discriminate between infected and uninfected host larvae for oviposition. Transmission of the microsporidium from infected to uninfected hosts by stinging female wasps could not be ascertained. Females that developed in infected L. dispar larvae did not transmit the pathogen via oviposition. Vairimorpha infection of the host negatively affected the performance of the braconid, when inoculation took place either before or after parasitization. Microsporidiosis of the host caused delayed development, reduced pupation and adult eclosion, reduction in size and weight, and reduction of adult longevity of G. liparidis. Parasitoids themselves were not systemically infected by Vairimorpha sp., but braconid larvae did ingest microsporidian spores at the end of their endoparasitic development and accumulated the undigested and ungerminated spores in the blind midgut. Negative effects of host infection on parasitoid larvae were detectable from the beginning of parasitoid larval development. Lethal time was reduced when L. dispar larvae were infected and parasitized, often at the expense of the parasitoid when G. liparidis were unable to complete endoparasitic development before the host died. Intensity of infection, measured as number of spores produced per milligram fresh weight of L. dispar larva, was slightly higher in parasitized and infected hosts than in unparasitized and infected hosts.