The cues that H. bicruris moths use for oviposition discrimination against diseased plants in S. latifolia are unclear. It is not known whether moths are able to detect and respond to the presence of fungal spores in the flower. Floral scent is known to trigger landing on the flowers, the number of landings being proportional to the intensity of the scent (Brantjes, 1976c). Recently, several of the floral scent compounds responsible for this response have been identified (Dötterl et al., 2005). It would be interesting to see whether there are any infection-induced olfactory cues to which moths can respond with respect to oviposition behaviour. Part of the lower oviposition on diseased plants may not be caused by active discrimination, but may be a consequence of a general density dependence in the oviposition response. For both healthy and diseased plants, we observed a ‘saturation effect’ that has previously been observed in both natural and experimental patches (Elzinga et al., 2005): oviposition decreased with increasing density of conspecifics or decreasing distance to the nearest conspecific. Because of the observed higher incidence of diseased plants in denser patches, part of the lower oviposition on diseased plants might be explained by this general response of moths to host density. This is certainly not the case for responses to variation in floral display. Based on the observed increase in oviposition rate with an increasing number of open flowers on healthy female plants, we would expect higher oviposition rates on diseased plants, which produced larger numbers of open flowers. However, on diseased plants the opposite pattern was found: oviposition per flower decreased with increasing number of open flowers. One possible interpretation of this pattern is that moths are attracted to plants with larger floral displays, but whereas they visit and select a large number of the flowers on such plants for oviposition when they are healthy, they visit or accept only a limited number of flowers for oviposition when they are diseased, resulting in a lower fraction of oviposited flowers on diseased plants as the number of flowers on these plants increase.
At flower level, we found that oviposition rates increased with flower size. As experimental inoculation studies have generally shown that M. violaceum infection results in reduced flower size in S. latifolia and other Caryophylaceous species (Biere & Honders, 1996a; Shykoff & Kaltz, 1998), this trait could be involved in reduced oviposition rates on diseased flowers. However, in our field study we found no evidence for reduced size of diseased flowers. We speculate that this is because visitation and spore deposition rates are higher on plants with larger flowers (cf. Shykoff et al., 1997), hence plants that became diseased had larger flowers to start with, infection reducing their flower size to the average size of flowers on uninfected plants. The most striking difference that we observed between healthy and infected flowers was the reduced size of the aborted ovary on infected plants. In H. bicruris, nectar feeding and oviposition behaviour are strongly related. The former obligately precedes the latter, and experimentally satiating moths results in loss of selectivity with respect to oviposition site. ‘Measuring’ the perimeter of the ovary during nectar feeding to discriminate against diseased flowers during subsequent oviposition therefore appears to be a feasible scenario. On both healthy and on diseased plants, oviposition strongly increased with ovary size. This result should be interpreted with some caution. In principle, larger ovary size could be a result, rather than a cause, of higher oviposition rates; ovaries on which oviposition is recorded are also pollinated and may have grown more quickly than ovaries of unvisited, unfertilized flowers during the hours between pollination and our recording of ovary size and oviposition. However, we argue that this could explain only part of the association. First, increases in oviposition rate with ovary size were observed for both healthy and diseased flowers; as the latter cannot be fertilized, increased growth of fertilized ovaries can be excluded in that case. Second, the period between pollination and recording is probably < 12 h, during which fertilization could result in a c. 7% increase in ovary size (Oostenik, 1976), much smaller than the average size difference between ovaries with and without eggs. If we then interpret the positive association between oviposition rate and ovary size as an oviposition preference for larger ovaries, we could hypothesize that the lower oviposition rates on diseased flowers are caused partly by their smaller ovaries. Surprisingly, a similar hypothesis proposed for the role of the ovary in the almost perfect oviposition discrimination of H. bicruris against healthy staminate (male) compared with healthy pistillate (female) flowers could not be supported by the data (Brantjes, 1976c). Like flowers on diseased plants, flowers on male plants are deceit flowers from the viewpoint of nursery pollination, providing neither shelter nor food, but they do produce nectar, usually in lower quantity but with higher sugar concentration per flower (Shykoff & Bucheli, 1995; Biere & Honders, 1996a; Shykoff, 1997; Shykoff & Kaltz, 1998). They are visited for nectar, but under normal conditions H. bicruris does not oviposit on staminate flowers. However, on the basis of manipulation studies with experimental addition/removal of flower parts, the presence of neither calyx, stigmas, ovary or amount of nectar appeared to be decisive in oviposition discrimination between pistillate and staminate flowers (Brantjes, 1976c). This means either that the H. bicruris response to detached organs differs from that in a natural flower setting, or that the presence and size of ovaries are not an important cue in oviposition decisions.