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1. Predation on vectors of pathogens can indirectly influence infection spread. In addition to the consumptive aspect of predation, non-consumptive, predator-induced changes in various vector traits can lead to trait-mediated indirect effects on pathogen spread, potentially operating in various directions and magnitudes. 2. A widespread non-consumptive effect of predation is the alteration of individual prey development rates. Yet, the implications of this phenomenon for the spread of vector-borne plant pathogens have not been studied. It is hypothesized that the epidemiological effects of predator-induced changes in vector development rate depend on the pattern in which the transmission biology of the vector changes along its ontogeny. 3. A general epidemiological model was developed that considers the role of predation in the infection dynamics of a plant pathogen, while incorporating vector stage structure to allow for variation in its development rate. 4. By contrasting scenarios that represent typical plant disease systems, this study confirms that the magnitude of the effect of altered development rate on infection prevalence depends on the disparity between juvenile and adult vectors in their pathogen transmission potential. 5. The model also reveals that the effect of predator-induced change in development rate can impact pathogen spread counterintuitively. Specifically, slowing down vector development can result in increased pathogen prevalence due to apparent competition between infected and uninfected vector populations. 6. More detailed, stage-specific studies of non-consumptive predator effects on vectors are likely to advance our understanding of plant disease ecology, and the development of more effective biological control practices in agriculture.