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Inducible resistance to vancomycin in Enterococcus faecium D366.

R Williamson¹, S Al-Obeid, J H Shlaes

¹Laboratoire de Microbiologie Médicale, Université de Paris VI, France.

The Journal of Infectious Diseases

|June 1, 1989

Summary

Vancomycin resistance in Enterococcus faecium is inducible, triggered by exposure to the antibiotic. This resistance correlates with the production of a specific cytoplasmic membrane protein that also affects cell lysis.

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Area of Science:

Microbiology
Molecular Biology
Drug Resistance

Background:

Enterococcus faecium is a common cause of hospital-acquired infections.
Vancomycin is a critical antibiotic for treating infections caused by Gram-positive bacteria.
Emergence of vancomycin resistance in E. faecium poses a significant public health threat.

Purpose of the Study:

To investigate the inducibility and mechanisms of vancomycin resistance in a clinical isolate of Enterococcus faecium (Strain D366).
To identify potential molecular correlates of vancomycin resistance.
To understand the functional implications of induced resistance on bacterial physiology.

Main Methods:

Exposure of exponential-phase cultures of E. faecium D366 to sub-inhibitory concentrations of vancomycin.

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Assessment of growth kinetics and resistance profiles to vancomycin and other glycopeptides.

Analysis of protein synthesis using techniques to identify novel proteins.

Correlation of protein expression with resistance levels and cellular functions.

Main Results:

Vancomycin exposure induced a lag phase in growth, which was abolished by pre-exposure.
Pre-exposure to vancomycin resulted in cross-resistance to other glycopeptides.
A 39.5-kDa cytoplasmic membrane protein was synthesized upon vancomycin exposure.
This protein was associated with high-level resistance and altered lytic functions.

Conclusions:

Vancomycin resistance in E. faecium D366 is an inducible phenomenon.
The induced resistance is mediated by a 39.5-kDa cytoplasmic membrane protein.
This protein plays a role in both vancomycin resistance and the inhibition of normal cell lysis.