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Research Article Free access | 10.1172/JCI105507
Department of Medicine, University of Washington School of Medicine, and King County Hospital, Seattle, Wash.
†Epidemic Intelligence Service Officer. Communicable Disease Center, U. S. Public Health Service, assigned to the University of Washington.
‡Address requests for reprints to Dr. Marvin Turck, King County Hospital, Seattle, Wash. 98104.
*Submitted for publication April 25, 1966; accepted September 15, 1966.
This work was supported in part by training grant AI-146-06 and grant AI-06311-02 from the National Institutes of Health, U. S. Public Health Service. Presented in part at the Fifth Interscience Conference on Antimicrobial Agents and Chemotherapy, October 17, 1965.
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Department of Medicine, University of Washington School of Medicine, and King County Hospital, Seattle, Wash.
†Epidemic Intelligence Service Officer. Communicable Disease Center, U. S. Public Health Service, assigned to the University of Washington.
‡Address requests for reprints to Dr. Marvin Turck, King County Hospital, Seattle, Wash. 98104.
*Submitted for publication April 25, 1966; accepted September 15, 1966.
This work was supported in part by training grant AI-146-06 and grant AI-06311-02 from the National Institutes of Health, U. S. Public Health Service. Presented in part at the Fifth Interscience Conference on Antimicrobial Agents and Chemotherapy, October 17, 1965.
Find articles by Turck, M. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Washington School of Medicine, and King County Hospital, Seattle, Wash.
†Epidemic Intelligence Service Officer. Communicable Disease Center, U. S. Public Health Service, assigned to the University of Washington.
‡Address requests for reprints to Dr. Marvin Turck, King County Hospital, Seattle, Wash. 98104.
*Submitted for publication April 25, 1966; accepted September 15, 1966.
This work was supported in part by training grant AI-146-06 and grant AI-06311-02 from the National Institutes of Health, U. S. Public Health Service. Presented in part at the Fifth Interscience Conference on Antimicrobial Agents and Chemotherapy, October 17, 1965.
Find articles by Petersdorf, R. in: JCI | PubMed | Google Scholar
Published January 1, 1967 - More info
Stool carrier rates of Escherichia coli serogroups 4, 6, and 75 were determined on admission and discharge for 190 patients. Persons who were in the hospital 3 weeks or longer had an intestinal carrier rate of 46% compared to a rate of 28% in individuals who had no recent hospital contact. Treatment with broad spectrum antibiotics increased the susceptibility for acquisition of certain specific serologic groups. This was apparently not related to replacement of sensitive E. coli by drug-resistant forms. Studies were made to determine the environmental source for colonization of hospitalized patients and the risk of urinary infection in stool carriers of these strains. A survey of inanimate objects of medical and urological wards demonstrated infrequent isolation of 04, 06, and 075, indicating that extraintestinal foci were an unlikely source for hospital-acquired E. coli. Hemagglutination titers with determination of group-specific O antibody failed to demonstrate any deficiency in hospitalized patients who became colonized with certain coliforms. Similarly, no significant deficit in group-specific serum antibody was found in patients who were community carriers of E. coli 04, 06, or 075. Despite a high rate of acquisition of E. coli serogroups 4, 6, and 75 in the stools of hospitalized patients, only those patients undergoing urinary tract manipulation developed bacteriuria.