Late blight is a devastating and worldwide potato and tomato disease caused by Phytophthora infestans (Mont.) de Bary. The aim of the study was to compare P. infestans isolates collected from potato and tomato plants by determining their virulence, aggressiveness, and sporulation intensity on both hosts in reciprocal testing with the goal of elucidating possible host specialization of the pathogen. Isolates were multiplied on leaflets of their primary hosts. In total, 76 potato-derived P. infestans (P) isolates and 100 tomato-derived P. infestans (T) isolates collected from 2005 to 2007 were studied in detached-leaflet assay experiments. Virulence was assessed on Black's potato differentials R1-R11 and cv. Bzura, as well as on the set of six tomato genotypes, namely cv. New Yorker (Ph-1 gene), Solanum pimpinellifolium L 3708 (Ph-3), West Virginia'63 (Ph-2), West Virginia 700 (Ph-1, Ph-2), Ottawa 30 (Ph-1, Ph-2), and BALU-30 (Ph-1, Ph-2, fruit resistance). Aggressiveness scored as disease severity and sporulation intensity assessed on a 0-3 grade scale were evaluated on leaflets of susceptible cultivars of both hosts. All 176 of the tested isolates were pathogenic to both hosts, indicating that extreme host specialization has not occurred. However, we did observe differences between P and T virulence spectra and their race structures supporting the notion of host adaptation of P. infestans. P and T isolates were more frequently virulent to differentials of their own hosts. P isolates had higher sporulation intensity on their own hosts than on tomato hosts, while for T isolates a similar sporulation intensity was observed on both hosts. Significantly stronger severity of the disease development on T testers was evoked by T isolates. All isolates showed stronger aggressiveness on susceptible potato than on susceptible tomato hosts, and the latter finding indicates a relatively greater suitability of potato host tissue for P. infestans pathogenicity. The host adaptation observed in this study was not conditioned by an ability to evoke disease, but rather by quantitative differences in pathogenic fitness. Genetic characterization of P and T populations is needed to place the present findings in a fuller context.