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Sepsis Caused by Contaminated Intravenous Fluids: Epidemiologic, Clinical, and Laboratory Investigation of an Outbreak in One Hospital

STEPHEN K. FELTS, M.D.; WILLIAM SCHAFFNER, M.D., F.A.C.P.; M. ANN MELLY, Ph. D.; and M. GLENN KOENIG, M.D., F.A.C.P.
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Presented in part 21 April 1972 at the Fifty-Third Annual Session of the American College of Physicians, Atlantic City, N.J.

Supported by research grant AI-03082 from the U.S. Public Health Service, Washington, D.C., and training grant AI-00323 from the National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Md. Dr. Felts was supported as a Postdoctoral Trainee and Dr. Koenig was supported as a Research Career Development awardee by the National Institute of Allergy and Infectious Diseases.

▸Requests for reprints should be addressed to William Schaffner, M.D., Vanderbilt University Hospital, Nashville, Ternn. 37232.


Nashville, Tennessee


Ann Intern Med. 1972;77(6):881-890. doi:10.7326/0003-4819-77-6-881
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Thirty-one cases of nosocomial sepsis that occurred from July 1970 through May 1971 in a 500-bed hospital were related to bacterial contamination of intravenous fluid bottles produced by one manufacturer. The responsible microorganisms were Erwinia, Enterobacter cloacae, and Pseudomonas stutzeri. These uncommon bloodstream pathogens caused a persistent Gram-negative sepsis that was refractory to antimicrobial therapy. Discontinuation of intravenous therapy and replacement of the intravenous administration system were the only effective treatments. The organisms multiplied to concentrations of from 105 to 106 bacteria per millilitre in intravenous fluids, although the concentrations were never high enough to cause visible turbidity. Laboratory studies of these epidemic strains showed no significant differences from a control Escherichia coli in serum sensitivity, ease of phagocytosis, endotoxin production, or mouse virulence.

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