Vancomycin resistance in Staphylococcus haemolyticus causing colonization and bloodstream infection

Veach, Lisa A; Pfaller, Michael A.; Barrett, Mary S.; Koontz, Franklin P.; Wenzel, Richard P.

doi:10.1128/jcm.28.9.2064-2068.1990

Cited by 141 publications

(37 citation statements)

References 13 publications

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“…While concern over the possible transfer of the enterococcal resistance mechanism into pathogenic strains of Staphylococcus aureus has been voiced repeatedly, as of now there are no'confirmed reports on clinical isolates of S. aureus isolates with increased vancomycin minimum inhibitory concentration (MIC) values. On the other hand, recovery of coagulase-negative staphylococci with 8-16-fold increased vancomycin MICs has been repeatedly described in the clinical microbiology literature [ 1,2] and S. aureus laboratory mutants with modestly increased vancomycin resistance (MIC values in the range of 4-16 l&/ml) have been described [3-51. The genetic/biochemical basis of resistance in such strains is not well understood, but it seems to differ from the mechanism(s) identi-While studying the effect of a variety of cell wall inhibitors on the expression of methicillin resistance, we isolated a spontaneous S. aureus mutant with modestly increased vancomycin MIC (from 1.5 to 6.0 ng/ml). A few cycles of growth of the mutant in vancomycin-containing medium resulted in further increase in resistance to the glycopeptide (up to an MIC of 100 &ml) and a parallel, steep decrease in the MIC value for methicillin (from 800 ug/ml to 1.5 l&ml).…”

Section: Introductionmentioning

confidence: 99%

A highly vancomycin-resistant laboratory mutant of Staphylococcus aureus

Sieradzki

1996

FEMS Microbiology Letters

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A resistant mutant with vancomycin MIC of 100 micrograms/ml was isolated relatively easily through step pressure in the laboratory from a Staphylococcus aureus strain with initial MIC of 1.5 micrograms/ml for the antibiotic. Upon addition of vancomycin (50 micrograms/ml) to the growth medium mass increase of the culture and peptidoglycan synthesis continued but cell division (daughter cell separation), cell wall turnover and autolysis were inhibited, resulting in the production of multicellular clumps of bacteria. Parallel with the increase of culture density, the concentration of vancomycin measured both by biological activity and by HPLC gradually declined in the culture medium. Cell division and wall turnover of the culture resumed with the production of cells of normal morphology at the time when the concentration of the drug in the medium decreased below 0.5-1.0 micrograms/ml. There was no detectable change in the antibiotic concentration in the culture medium during growth of a vancomycin-resistant (vanA-positive) strain of Enterococcus faecium and an intrinsically vancomycin-resistant strain of Leuconostoc. The vancomycin-resistant staphylococcal mutant gave no signal with the vanA or vanB DNA probes and contained no detectable D-lactate terminating cell wall precursors. The biochemical mechanism and clinical significance of such glycopeptide-resistant mutants remained to be established.

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Section: Introductionmentioning

confidence: 99%

A highly vancomycin-resistant laboratory mutant of Staphylococcus aureus

Sieradzki

1996

FEMS Microbiology Letters

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“…Unfortunately, vancomycin resistance has already been reported in isolates of coagulase-negative staphylococci.12. [69][70][71] In addition, genes encoding for vancomycin resistance were successfully passed from enterococci to S. aureus i n the laboratory, indicating that the emergence of a superbug resistant to all available antimicrobial agents may not be far off the horizon. 72 There is clearly an urgent need for the development of new antimicrobial agents, not only to treat VRE, but also in anticipation of the day when we find ourselves faced with vancomycin-and methicillin-resistant S. aureus.…”

Section: Resultsmentioning

confidence: 99%

Vancomycin‐Resistant Enterococci

Palmer,

Rybak

1996

Pharmacotherapy

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Vancomycin‐resistant enterococci (VRE) are a major problem in numerous institutions in the United States. Most VRE are resistant to all available antimicrobial agents, resulting in serious therapeutic dilemmas. The resistance genes are transmitted on transposons, so the potential for dissemination to other species is significant. Risk factors associated with VRE infection and colonization are vancomycin and cephalosporin use, but numerous patient‐related factors also contribute. Although resistant strains appear to arise from the patient's endogenous flora, VRE may be spread through direct contact with contaminated environmental surfaces and hands of caregivers. Published guidelines for preventing such spread suggest implementing infection‐control practices and vancomycin restrictions. The ideal drug regimen for the treatment of VRE is unknown. Various drug combinations have been studied in the laboratory, but patient treatment data are scarce. There is an urgent need for new antimicrobial agents.

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“…The percentage of nonsusceptible CoNS was 0.55%, and we did not observe any increase over the study period. To our knowledge, resistance to teicoplanin among CoNS has been described only as a result of in vitro studies, as sporadic cases, or in studies selecting specific groups of patients (1,2,6,7,9,11,14,15,19,(26)(27)(28); however, the global incidence of the resistance and its clinical significance have not been reported. Moreover, although the emergence of CoNS with decreased levels of susceptibility to teicoplanin has been reported in several studies, the existence of isolates with high levels of resistance has been anecdotal (1,6,22,28).…”

Section: Discussionmentioning

confidence: 99%

Emergence of teicoplanin-resistant coagulase-negative staphylococci

et al. 1996

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Over a period of 5 years we have recovered 32 clinical isolates of coagulase-negative staphylococci (CoNS) exhibiting either decreased levels of susceptibility or true resistance to teicoplanin (MICs, 16 to 128 g/ml); these isolates make up 0.55% of the total CoNS isolated by us. Twenty-nine of the strains were also methicillin resistant, and all were susceptible to vancomycin. Fourteen of the strains were Staphylococcus epidermidis, fourteen were Staphylococcus haemolyticus, and four were Staphylococcus hominis. In one case, a strain of S. haemolyticus was isolated with a vancomycin-resistant, teicoplanin-resistant Enterococcus faecalis strain. All strains were nosocomially acquired and were isolated from 17 different wards. Teicoplanin resistance occurred as a sporadic phenomenon, and none of the isolates were epidemiologically related. The isolates were from 30 patients, 13 of whom presented with true infections (43%). Five (38%) of the 13 patients with true infections had been previously treated with vancomycin. None of the infected patients were previously treated with teicoplanin. The in vivo development of resistance to teicoplanin among CoNS strains limits the therapy of infections by these microorganisms. There is a need for surveillance of nosocomial isolates of CoNS to determine resistance to glycopeptides.

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Vancomycin resistance in Staphylococcus haemolyticus causing colonization and bloodstream infection

Cited by 141 publications

References 13 publications

A highly vancomycin-resistant laboratory mutant of Staphylococcus aureus

A highly vancomycin-resistant laboratory mutant of Staphylococcus aureus

Vancomycin‐Resistant Enterococci

Emergence of teicoplanin-resistant coagulase-negative staphylococci

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