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S Al-Obeid

Publications and source records attributed to S Al-Obeid.

4 recordsLinked to original sources
PubMed1996

Penicillin tolerance and modification of lipoteichoic acid associated with expression of vancomycin resistance in VanB-type Enterococcus faecium D366.

Induction of vancomycin resistance in Enterococcus faecium D366, which exhibits a VanB-type resistance, as well as its constitutive expression in MT9, a derivative of D366, was associated with penicillin tolerance as shown by decreased lysis and killing of the cells. This phenomenon was linked neither to decreased expression of the different autolysins nor to their decreased lytic activity on the different cell walls. The only change observed was that almost twice the normal amount of D-alanine was attached to the lipoteichoic acid.

Anti-Bacterial Agents↗
PubMed1989

Inducible resistance to vancomycin in Enterococcus faecium D366.

Strain D366, a clinical isolate of Enterococcus faecium, is resistant (minimum inhibitory concentration [MIC] 32 mg/L) to vancomycin. When exponential-phase cultures were exposed to half the MIC of vancomycin, a lag of 3-4 h occurred before growth resumed. Cells preexposed to 1/2 MICs of vancomycin did not show any lag. Pregrowth of D366 with vancomycin caused resistance to all glycopeptides tested. Pregrowth in vancomycin resulted in synthesis of a 3.95-kDa cytoplasmic-membrane-associated protein. This protein was correlated with resistance in mutants with high-level resistance, in the presence of NaCl, which inhibited the activity of vancomycin, and when several glycopeptides with varying activities were tested. Vancomycin-grown cells appeared abnormal and lysed at a much slower rate than did normal cells. We conclude that (1) vancomycin resistance in D366 is inducible; (2) resistance is correlated with the synthesis of 39.5-kDa cytoplasmic membrane protein; and (3) this protein play an additional role in the inhibition of normal lytic functions.

Aged↗
PubMed1989

Inducible, transferable resistance to vancomycin in Enterococcus faecium, D399.

Enterococcus faecium D399 was isolated from the blood and peritoneal abscess of a patient with intraabdominal sepsis. The patient had not been treated with vancomycin, but the strain was found to be resistant with a MIC of 1000 mg/l. Resistance was inducible and transferable (probably by conjugation) to JH2-2, and correlated with induction of synthesis of a 39 kDa protein. This mechanism appears to be identical to that previously described for E. faecalis A256, suggesting that dissemination of this form of glycopeptide resistance has already occurred. The resistance phenotype of D399, however, differed somewhat from that found in other enterococcal strains with inducible resistance.

Drug Resistance, Microbial↗