In plants, strong structural and biochemical barriers are shown to delay fungus entry by deterring their establishment. Additionally, these alterations induce a cascade of reactions in plant that often lead to resistance against pathogens. Nevertheless, faster kinetics and amplitude of these defence mechanisms define resistance and susceptibility. The infection process of two Ascochyta lentis isolates (FT14069 and FT13082) on three lentil hosts (ILWL 180, ILL 7537 and ILL 6002) using histopathology revealed significant differences in early behaviour of two isolates among three hosts. Both isolates recorded significantly lower germination, shorter germ tubes and delayed appresorium formation on the resistant genotypes (ILWL 180 and ILL 7537) compared to the susceptible genotype (ILL 6002). Further, these were more pronounced on ILWL 180 than on ILL 7537. Both isolates germinated within 6 hours post inoculation (hpi) and a significant increase in germination % was observed in ILL 7537 compared to ILWL 180 at all-time points (6, 12, 20 and 30 hpi). Isolate FT14069 germinated faster on ILL 7537 and reached a maximum of 28.26% compared to 15.49% on ILWL 180. Similarly, significantly shorter germ tube lengths were observed for both isolates on ILWL 180 (ranging from 4 µm to 17.63µm) than on ILL 7537 (ranging from 7.14 µm to 21.09 µm). Although appresorium formation was delayed on both genotypes until 20 hpi and 30 hpi for isolates FT14069 and FT13082, respectively, unlike on ILL 6002, significantly higher appresorium formation was observed on ILL 7537 (4.87 % for isolate FT14069 and 2.58 % for isolate FT13082) than on ILWL 180 (3.82 % for isolate FT14069 and 1.87 % for isolate FT13082) at 30 hpi. Although early and faster recognition of A. lentis might be the reason for observed resistance in ILWL 180, this initial finding requires further validation through histochemical and gene expression studies.