Anthracnose, caused by Colletotrichum coccodes, is a serious ripe tomato fruit rot disease. Genetic resistance to anthracnose is not available in commercial tomato cultivars, but has been reported in small-fruited Plant Introductions (P.I.), and with lesser intensity in a number of breeding lines. Transfer of high levels of resistance from these breeding lines or P.I.s to elite materials has proven difficult. Inheritance of resistance has been described as complex with at least six loci influencing resistance reactions. Segregating populations originating from a cross between a susceptible tomato breeding line and a large-fruited breeding line (88B147) with resistance derived from Lycopersicon esculentum var. cerasiforme P.I. 272636, were evaluated for anthracnose resistance. Analysis of anthracnose resistance in puncture-inoculated fruit indicated small, but significant, additive genetic effects for resistance. Additional populations were developed from crosses of a susceptible inbred processing tomato cultivar with: 1) the resistant P.I. 272636, 2) an unadapted small-fruited resistant line developed from P.I. 272636, and 3) the large-fruited breeding line 88B147, also with resistance derived from P.I. 272636. Small additive effects identified in large-fruited material, in comparison to the resistant P.I., suggests that resistance loci have been lost during germplasm development. This is consistent with the relatively larger lesions observed in large-fruited lines derived from P.I. 272636. Positive correlations were noted between small fruit size and high levels of anthracnose resistance. Identification of molecular markers linked to resistance genes in the respective populations will be discussed.