Epidemiologic models can be useful for evaluating the potential of various management strategies to control the spread of plant pathogens (Jeger and Chan, 1995). In the case of insect-transmitted pathogens, such models suggest that effects on vector fitness that lead to higher rates of population growth on infected plants could significantly affect rates of pathogen spread (Holt et al., 1997; Zhange et al., 2000). One model of the whitefly-transmitted African cassava mosaic virus is based on substantial field data (Holt et al., 1997) which showed that the rate of spread was sensitive both to vector population dynamics (abundance, birth rate, mortality) and to virus transmission rates (inoculation and acquisition). When virus infection of hosts leads to increased vector fecundity, spatial aggregation of vectors is promoted (Zhang et al., 2000). Models predict that vector aggregation should have a dual effect. Within the infected crop, it should reduce the effective contact rate between vector and host and thus lead to lower disease incidence than would be predicted without aggregation. On the other hand, it could cause increased emigration rates of infective vectors to other hosts in the area (Zhang et al., 2000).
Most of the models described here are based on systems in which the vector insect reproduces within the crop. However, when the incidence of disease depends primarily on the immigration of vectors from alternative hosts that act as reservoirs of pathogens and of vectors, other models show that disease incidence is largely insensitive to vector mortality unless the vector population is extremely small, and therefore insecticide treatment is ineffective (Holt et al., 1999). To evaluate the potential of targeting various aspects of the interaction between Xf and its vectors for control, it is essential to understand the population dynamics of vectors inside and outside of the vineyard.
Epidemiologic models have predicted that vector preference behavior will have a significant influence on the rate of pathogen spread, and conventional wisdom postulated that vector preference for infected hosts over healthy ones would promote the spread of disease (e.g., Irwin and Thresh, 1990; Matthews, 1991). However, the results of several recent epidemiologic models suggest that often the reverse is true (McElhany et al., 1995; Real et al., 1992). That is, a preference for healthy plants often leads to greater rates of pathogen spread, because an infective vector is less likely to “waste” a visit to a plant that is already infected. However, the effect of vector preference depends on the frequency of infected plants in the population and on whether the transmission system is persistent, nonpersistent, or semipersistent. Models predict that pathogens with even moderate persistence are likely to have higher rates of spread by vectors that prefer healthy plants at most disease frequencies (McElhany et al., 1995). Given the persistence of Xf in adult sharpshooters, vector preference for healthy grape plants could lead to faster spread of PD.