We used selection to test for a genetic component to the pattern of emergence of infective juveniles from the host cadaver in the entomopathogenic nematode, Steinernema glaseri (Steiner), and whether other traits would respond to selection on this major and complex life-history character. We selected for early (‘ fast’) and late (‘ slow’) emerging lines by perpetuating nematodes that emerged on the first and after the seventh day of emergence respectively. After 12 cycles of selection, the pattern for the slow line but not the fast line differed significantly from the base population. Cumulative emergence for the slow line was less than the base population from Days 4 to 14 of the 18-day emergence period. The maximum difference occurred on the fourth day when 72·6% of emergence was complete for the base population but only 55·4% for the slow line. Decreases in infective juvenile size over the emergence period were consistent with the change in emergence pattern, but variation in sex ratios was not. No differences in infectivity were found. These results indicate that the emergence pattern has a genetic component, and that genetic variability for this trait occurs in natural populations. Furthermore, the asymmetric response to selection suggests that our field population is under strong selection for a highly skewed early emergence.

Entomopathogenic nematode infective juveniles are likely to encounter both uninfected and infected insects and host quality depends on the stage of the infection. We hypothesized that nematode response to infected hosts will change over the course of an infection. Here, we tested this hypothesis by focusing on the influence of host infection status on long-range attraction to host volatile cues. The attraction response of 3 nematode species (Steinernema carpocapsae, S. glaseri and S. riobrave) with different foraging strategies to infected and uninfected insects (Galleria mellonella and Tenebrio molitor) was tested at 24 h intervals from start of infection to emergence of infective juveniles from depleted host. As expected, based on their foraging strategies, S. carpocapsae was not very responsive to hosts, S. glaseri was highly responsive and S. riobrave was intermediate. Generally, the level of attraction did not change with time after infection and was similar between infected and uninfected hosts. An exception was S. glaseri infected T. molitor, which tended to be less attractive to S. glaseri than uninfected hosts. These results suggest that any influence of host infection status on infection behaviour is occurring at subsequent steps in the host-infection process than host attraction, or involves non-volatile cues.

Many studies of entomopathogenic nematodes (Heterorhabditidae and Steinernematidae) have reported that only a small proportion (typically <40%) of infective stages (dauers), even under apparently ideal conditions, actually infect a host. The ‘phased infectivity hypothesis’ is most frequently invoked to explain this pattern of low infection with entomopathogenic nematodes. It proposes that at a given point in time not all individuals are infectious i.e. infectiousness is delayed in some individuals. We tested experimentally several predictions based on this hypothesis. Specifically, if phased infectivity occurs, we should be able to expose dauers to increasing numbers of potential hosts until dauers no longer infect and still be able to recover viable dauers. These recovered dauers which did not infect should be infectious at some later point in time. However, our results do not support the phased infectivity hypothesis for 3 species of Steinernema: most dauers could be recovered in one sampling round when provided with sufficient suitable hosts. In contrast, Heterorhabditis bacteriophora frequently did not infect all available hosts, and infectious dauers were recovered in subsequent sampling rounds. This result is more consistent with the phased infectivity hypothesis, but further research is needed before we can be more confident in the hypothesis. For all species tested, the number of available hosts influenced population levels of nematode infectivity. This suggests that the infection status of hosts can influence whether a dauer infects. Our results indicate that phased infectivity is not a common phenomenon in entomopathogenic nematode dauers, despite the widespread acceptance of this hypothesis.