Pathozone behaviour of soil-borne plant pathogenic fungi is characterized by curves for the change in probability of infection with distance of inoculum from a host. We identify three major components that give rise to the pathozone profile for infection efficiency: the germinability of inoculum, given that it occurs in the pathozone (P1), the growth of the resulting fungal colony outwards to make contact with the host (P2), and the infectivity of mycelium once contact is made (P3). The probability of infection (P) is then given by the product, P1 × P2 × P3. Using Raphanus sativus and two contrasting types of inoculum of Rhizoctonia solani as a model experimental system, we measured each of the three components by quantifying germinability, colony architecture (to determine the chance of contact by one or more hyphae) and the change in susceptibility over time as a measure of infectivity as mycelium arrives from different distances away. The germinability of inoculum is uniform across the pathozone whereas the probability of contact declines with distance, and the net effect of host susceptibility and infectivity increases. The characteristics of these components result in pathozone profiles that vary in shape. Infection efficiency can decline in an exponential or sigmoidal fashion with increasing distance from the host or follow a curve that rises close to the host and then falls asymptotically to zero with increasing distance. Colony architecture was summarized by the distribution of the furthest extent of hyphal growth amongst colonies growing out from single inoculum units (described, because of its asymmetrical pattern, by a gamma distribution) and by the radial density of hyphae on concentric circles at different distances from the centre of the colony (described by a negative binomial distribution with parameters changing with distance).

The mechanistic model for the components of pathozone behaviour is tested by comparing the magnitude and shape of pathozone profiles predicted by the model with independent estimates for P obtained by placing inoculum at fixed distances from the host, and measuring the proportion of successful infections. The shape depends on the relative magnitudes and change with distance of the three components, P1, P2 and P3, which differed between the two types of inoculum. The profiles could be reproduced accurately when the probability of contact was based on the distribution and density of hyphae reaching the host rather than on the furthest extent of hyphal growth amongst colonies. The model is used to analyse the effects of replication and stochastic variability in the components of pathozone behaviour on the comparison of treatments for disease control.