REPLY
Urinary Tract Infection with Enterococcus faecalis
Henry S. Fraimow and
James Dean
1 February 1995 | Volume 122 Issue 3 | Page 238
IN RESPONSE:
Dr. Jacoby is correct in noting that we were not the first to report a clinical isolate that required an antimicrobial agent for growth [1]. In addition to being a well-described laboratory phenomenon, streptomycin dependence has also been reported in several clinical isolates [2]. Of note, many of these antibiotic-dependent strains were also isolated from the urinary tract, an environment in which a large inoculum of organisms may be continuously exposed to high antibiotic concentrations for prolonged periods and in which an antibiotic-resistant organism may take the "next" evolutionary step toward the development of antibiotic dependence. As Dr. Jacoby has observed, various antibiotic-dependent strains have been isolated in the laboratory. In addition to their novelty, such strains can also be powerful tools for studying the basic mechanisms of antibiotic action and resistance [3]. It is perhaps not surprising that antibiotics can serve as positive regulators of bacterial growth, given that most of these compounds are natural products of soil organisms and that they may have once functioned as primitive cellular effector molecules [4, 5]. We agree that the prevalence of antibiotic-dependent bacteria is unknown and will remain so until we begin to search for such strains in the appropriate clinical settings.
1. Fraimow HS, Jungkind DL, Lander DW, Delso DR, Dean JL. Urinary tract infection with an Enterococcus faecalis isolate that requires vancomycin for growth. Ann Intern Med. 1994; 121:22-6.
2. Finland M. Emergence of antibiotic resistant bacteria. N Engl J Med. 1955; 253:1019-28.
3. Dabbs ER. New tool for studying interactions of components of ribonucleic acid polymerase: rifampin-dependent mutants. J Bacteriol. 1979; 139:1072-4.
4. Davies J. What are antibiotics? Archaic functions for modern activities. Mol Microbiol. 1990; 4:1227-32.
5. Amabile-Cuevas CF. Origin, evolution and spread of antibiotic resistance genes. Austin, Texas: R.G. Landes; 1993:1-4.
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