The purpose of the studies contained in this dissertation was to better understand the clinical and pathologic abnormalities caused by infections with Leptospira kirschneri serovar Grippotyphosa and Leptospira interrogans serovars Pomona and Bratislava. Dogs were inoculated with all serovars and additional studies were done with serovar Pomona in guinea pigs. The guinea pig model was used to study binding of leptospires to platelets in vitro.;In the first study, "Clinical and pathologic comparison of acute canine leptospirosis caused by two strains of Leptospira kirschneri serovar Grippotyphosa", it was demonstrated that infection with serovar Grippotyphosa causes severe renal and hepatic failure. Biochemistry profiles were consistent with severe renal and hepatic insufficiency, and infected dogs had lesions in kidney, liver, and pancreas. In the second study, "Experimental canine leptospirosis caused by Leptospira interrogans serovars Pomona and Bratislava", the disease model established in the first study was used to investigate two additional serovars of Leptospira. The serovar Bratislava isolate was obtained from a canine source, but did not cause disease in dogs or hamsters in an experimental setting. The swine derived isolate of serovar Pomona caused lethargy, fever, and diarrhea in infected dogs and was associated with inflammation and hemorrhage in dogs necropsied at days 10, 14, and 20 post-inoculation (PI). As compared to serovar Grippotyphosa; however, there were no biochemical abnormalities suggestive of renal failure. The third manuscript, " Leptospira interrogans serovar Pomona infection in guinea pigs and in vitro evidence of leptospire binding of platelets", demonstrates hemorrhage in a guinea pig model of serovar Pomona infection and provides in vitro evidence of platelet leptospire binding. Microtiter assays show that leptospires bind to platelet monolayers, but do not bind to wells without platelets or wells containing platelet poor plasma or fibrinogen. When activated platelets and leptospires are incubated and fluorescent stained, large aggregates form. Incubation of leptospires with non-activated platelets does not result in the formation of aggregates. Binding was not inhibited with anti-integrin alphaIIbbeta3 antibody. The canine studies reported in this dissertation are important foundation work for further study of the pathogenesis of canine leptospirosis and the development of treatment and prevention strategies.