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Research Article Free access | 10.1172/JCI110813
Division of Infectious Diseases, Department of Medicine, Montefiore Hospital and Medical Center, Albert Einstein College of Medicine, Bronx, New York 10467
The Rockefeller University, New York 10021
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Division of Infectious Diseases, Department of Medicine, Montefiore Hospital and Medical Center, Albert Einstein College of Medicine, Bronx, New York 10467
The Rockefeller University, New York 10021
Find articles by Chang, D. in: JCI | PubMed | Google Scholar
Division of Infectious Diseases, Department of Medicine, Montefiore Hospital and Medical Center, Albert Einstein College of Medicine, Bronx, New York 10467
The Rockefeller University, New York 10021
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Division of Infectious Diseases, Department of Medicine, Montefiore Hospital and Medical Center, Albert Einstein College of Medicine, Bronx, New York 10467
The Rockefeller University, New York 10021
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Division of Infectious Diseases, Department of Medicine, Montefiore Hospital and Medical Center, Albert Einstein College of Medicine, Bronx, New York 10467
The Rockefeller University, New York 10021
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Division of Infectious Diseases, Department of Medicine, Montefiore Hospital and Medical Center, Albert Einstein College of Medicine, Bronx, New York 10467
The Rockefeller University, New York 10021
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Published March 1, 1983 - More info
The effect of penicillin treatment of Streptococcus sanguis in vitro, on subsequent bacterial density in the bloodstream and on cardiac valves in the rabbit model of endocarditis was studied. As experimental tools for this study, isogenic pairs of S. sanguis differing in resistance to streptomycin or rifampin were prepared by genetic transformation. Rabbits with traumatized heart valves received an intravenous inoculation of penicillin treated (1 μg/ml) and untreated S. sanguis, each marked by resistance to either streptomycin or rifampin. The number of penicillin-treated and untreated bacteria attached to the valvular surfaces was determined by differential counting on streptomycin or rifampin containing media. Penicillin pretreatment reduced cardiac valve colonization 5 min after inoculation (“adherence ratio” × 108 was 4.11 for the control and 3.66 for the penicillin-treated bacteria, P < 0.001). The results were not due to differences in serum killing or bacterial densities in the bloodstream. There was no difference in valvular bacterial densities 24 h after bacterial inoculation (adherence ratio × 108, 7.26 untreated vs. 6.34 penicillin-pretreated, P > 0.10).
In vitro experiments were performed using platelet-fibrin surfaces to test the possibility that penicillin-induced loss of lipoteichoic acid was responsible for decreased streptococcal adherence. Pretreatment of S. sanguis cultures with inhibitory concentrations of penicillin or with antiserum against lipoteichoic acid and precoating of the platelet-fibrin surfaces with lipoteichoic acid, all caused reduction in bacterial adherence. The findings are interpreted as support for the role of lipoteichoic acid as an adhesin in S. sanguis interactions with particular host tissue surfaces.