Failure of aminoglycoside antibiotics to kill anaerobic, low-pH, and resistant cultures

Author:

Schlessinger D1

Affiliation:

1. Department of Microbiology and Immunology, Washington University School of Medicine, St. Louis, Missouri 63110.

Abstract

The critical inhibition of ribosome function by aminoglycosides has long been established. But the binding of drug to ribosomes is reversible: why then are aminoglycosides bactericidal? Several groups have shown that irreversible action (lethality) results from irreversible uptake into susceptible cells; conversely, resistance in cases such as anaerobiosis is associated with the failure of uptake. Oddly, the pattern of results excludes all traditional transport mechanisms; most unusual is the apparent dependence of uptake on the interaction of drug with ribosomes. A traditional view that ribosomes may function during uptake as a "sink" for aminoglycosides cannot explain all the data. Instead, the alternative is considered that cycling ribosomes at the cell membrane help to induce "one-way endocytic pores." Although no detailed mechanism is formulated, the results do suggest a way that the permeation of antibiotics might be systematically controllable to render them more cidal.

Publisher

American Society for Microbiology

Subject

Infectious Diseases,Microbiology (medical),Public Health, Environmental and Occupational Health,General Immunology and Microbiology,Epidemiology

Reference36 articles.

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3. Bryan L. E. 1982. Bacterial resistance and susceptibility to chemotherapeutic agents p. 135-160. Cambridge University Press Cambridge.

4. Bryan L. E. 1984. Mechanisms of action of aminoglycoside antibiotics p. 17-36. In R. K. Root and M. A. Sande (ed.) New dimensions in antimicrobial therapy. Churchill Livingstone New York.

5. Mechanism of aminoglycoside antibiotic resistance in anaerobic bacteria: Clostridium perfringens and Bacteroides fragilis;Bryan L. E.;Antimicrob. Agents Chemother.,1979

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