An epidemic increase in severity and incidence of asochyta blight, caused by Ascochyta rabiei (Pass) Labrousse (teleomorph: Didymella rabiei (Kovachevski) v. Arx. Syn. Mycosphaerella rabiei Kovachevski), has occurred on chickpea (Cicer arietinum L.) crops in Saskatchewan over the past 5 growing seasons. In order to explore the nature of the outbreak, studies assessing population differences in pathogenicity and genetic variability were employed. Isolates of A. rabiei collected in 1998, 2001 and 2002 were inoculated onto 7 differential chickpea genotypes for pathogenicity testing. Significant isolate by differential interaction occurred, but accounted for a low proportion of the total variability suggesting no genotype specific relationship exists between A. rabiei and C. arietinum. Furthermore, it was found that when averaged over all differentials, the isolates from 2001 and 2002 caused significantly greater disease than isolates from 1998, suggesting that the disease epidemic is in part due to a shift in the population to overall greater aggressiveness. The largest increase in disease severity was observed on the cultivar ‘Sanford’, which was widely grown in commercial chickpea fields before 1999. To evaluate the genetic diversity of different A. rabiei populations, 30 isolates from 1998 and 30 isolates from 2002 were compared with random amplified polymorphic DNA fingerprinting. Several clusters of isolates collected from either 1998 or 2002 were approximately 60% genetic similar suggesting divergence of these populations of A. rabiei. However, analysis of molecular variance showed that over 90% of the variation occurred within populations. Pairwise differences and gene diversity over loci showed that genetic diversity of the 2 populations had the same amount of genetic variability. Analysis of mating type distributions revealed that the populations from 1998, 2001 and 2002 did not significantly depart from a 1:1 ratio suggesting random mating of each population. Further supporting the hypothesis of a randomly mating population, linkage disequilibrium for both 1998 and 2002 populations was very low
