Cryptosporidium causes cryptosporidiosis, an infectious diarrheal disease, which can become chronic and life-threatening in immunocompromised individuals. Cryptosporidium parvum and C. hominis are the primary causes of human cryptosporidiosis. Of these species, C. hominis only infects humans while C. parvum additionally infects ruminants, in particular neonatal calves. Therefore, understanding the transmission dynamics of C. parvum, particularly the specific contribution of zoonotic and anthroponotic transmission, is critical to the control of this pathogen. Cryptosporidium parvum genotypes have been identified which appear to be restricted to a single host, which suggests that this may be a heterogeneous species, with varying infection and transmission dynamics. The first objective to this thesis was to determine the population structure of pathogenic C. parvum in the upper Midwest United States. A total of 216 isolates from cases of human cryptosporidiosis in Minnesota and Wisconsin and 64 isolates from diarrheic calves in Minnesota, Wisconsin, and North Dakota were genotyped at 8 polymorphic loci. A total of 213 isolates, 167 from humans and 46 from calves, had complete multilocus types (MLT). There were 93 different Ml Ts and sixty of those Ml Ts were only represented by one isolate. Population analysis revealed a highly recombining, panmictic population that does not have any genetic, geographic, or host sub-structuring. The second objective to this thesis was to determine the variability in the in vitro infectivity of different C. parvum strains, IOWA II and Moredun. A quantitative RT-PCR approach was used to quantify expression of target genes during infection of HCT-8 cells. Fluorescence microscopy was used to quantify life cycle stages during infection. Our data showed that the IOWA II reached its sexual stages earlier and had a greater number of trophozoites/meronts at 24 h p.i. than Moredun. The host used for propagation of C. parvum also affected subsequent infectivity of HCT-8 cells.