Failure of teicoplanin therapy in two neutropenic patients with staphylococcal septicemia who recovered after administration of vancomycin

Brunet, F.; Vedel, G.; Dreyfus, Françoise; Vaxelaire, J. F.; Giraud, T; Schremmer, Bruno; Monsallier, J F

doi:10.1007/bf01963643

Cited by 54 publications

(30 citation statements)

References 14 publications

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“…Similarly to observations described for some laboratory or clinical isolates of moderately glycopeptide-resistant mutants of various coagulase-negative staphylococci and S. aureus (6,(22)(23)(24)(25)34), the highly vancomycin-resistant mutant of S. aureus, VM, also showed changes in several protein bands when analyzed by SDS-PAGE. Some of these proteins showed increased amounts in the mutant (e.g., two proteins with the highest molecular masses of 130 and 110 kDa and the proteins in the molecular mass range of 31.5, 29, 21, 18, and 17.5 kDa), while some others appeared to have decreased representation FIG.…”

Section: Discussionsupporting

confidence: 71%

“…While current concern is directed primarily to interspecific transfer of enterococcal resistance genes, attention has also been paid to other, alternative vancomycin resistance mechanisms that may emerge among S. aureus and coagulase-negative strains of nosocomial staphylococci as a consequence of the extensive use of vancomycin in the hospital environment worldwide (for a review, see reference 42). Moderately increased vancomycin (and teicoplanin) MICs have indeed been noted among some clinical isolates of coagulase-negative staphylococci (3,6,20,31,32,40), and glycopeptide-resistant variants or mutants of staphylococci have also been isolated in several laboratories by the usual step-pressure procedures (5,7,8,16,18,40).…”

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confidence: 99%

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Inhibition of cell wall turnover and autolysis by vancomycin in a highly vancomycin-resistant mutant of Staphylococcus aureus

1997

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A highly vancomycin-resistant mutant (MIC ‫؍‬ 100 g/ml) of Staphylococcus aureus, mutant VM, which was isolated in the laboratory by a step-pressure procedure, continued to grow and synthesize peptidoglycan in the presence of vancomycin (50 g/ml) in the medium, but the antibiotic completely inhibited cell wall turnover and autolysis, resulting in the accumulation of cell wall material at the cell surface and inhibition of daughter cell separation. Cultures of mutant VM removed vancomycin from the growth medium through binding the antibiotic to the cell walls, from which the antibiotic could be quantitatively recovered in biologically active form. Vancomycin blocked the in vitro hydrolysis of cell walls by autolytic enzyme extracts, lysostaphin and mutanolysin. Analysis of UDP-linked peptidoglycan precursors showed no evidence for the presence of Dlactate-terminating muropeptides. While there was no significant difference in the composition of muropeptide units of mutant and parental cell walls, the peptidoglycan of VM had a significantly lower degree of crosslinkage. These observations and the results of vancomycin-binding studies suggest alterations in the structural organization of the mutant cell walls such that access of the vancomycin molecules to the sites of wall biosynthesis is blocked.Multidrug-resistant strains of methicillin-resistant Staphylococcus aureus (MRSA) in which the therapeutic choice is often reduced to a small number of antibiotics, primarily vancomycin, have spread worldwide during the late 1980s and mid1990s. The appearance of vancomycin resistance among clinical isolates of enterococci has raised concern about transfer of the resistance genes to highly virulent strains of MRSA with obvious dire implications for chemotherapy. While current concern is directed primarily to interspecific transfer of enterococcal resistance genes, attention has also been paid to other, alternative vancomycin resistance mechanisms that may emerge among S. aureus and coagulase-negative strains of nosocomial staphylococci as a consequence of the extensive use of vancomycin in the hospital environment worldwide (for a review, see reference 42). Moderately increased vancomycin (and teicoplanin) MICs have indeed been noted among some clinical isolates of coagulase-negative staphylococci (3,6,20,31,32,40), and glycopeptide-resistant variants or mutants of staphylococci have also been isolated in several laboratories by the usual step-pressure procedures (5,7,8,16,18,40).While studying the effect of cell wall synthesis inhibitors on the expression of methicillin resistance in S. aureus, we observed rare staphylococcal cells that were able to form colonies on agar containing 6 and even 12 g of vancomycin per ml. Serial passages of such colonies in vancomycin-containing media (step-pressure procedure) resulted in the emergence of stable variants (mutants) with even higher levels of vancomycin resistance. One mutant for which the vancomycin MIC was 100 g/ml had the unique capacity to quantitatively remove vancomycin f...

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Section: Discussionsupporting

confidence: 71%

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confidence: 99%

Inhibition of cell wall turnover and autolysis by vancomycin in a highly vancomycin-resistant mutant of Staphylococcus aureus

1997

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“…However, the cutoff value of teicoplanin of 12 mg/liter was not sensitive enough for the detection of hVISA in China. It has been reported that a strain of MRSA might become heterogeneously resistant to teicoplanin before it becomes heterogeneously resistant to vancomycin (2,18), a phenomenon that requires further investigation. The points summarized above refer to surveillance studies aimed at measuring or estimating the prevalence rates of hVISA among large numbers of isolates.…”

Section: Discussionmentioning

confidence: 99%

Prevalence and Characterization of Heterogeneous Vancomycin-Intermediate Staphylococcus aureus Isolates from 14 Cities in China

Sun

Chen

Liu

et al. 2009

Antimicrob Agents Chemother

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The prevalence of heterogeneous vancomycin-intermediate Staphylococcus aureus (hVISA) among 1,012 vancomycin-susceptible methicillin (meticillin)-resistant S. aureus isolates collected from 14 cities in China from 2005 to 2007 was 13 to 16%, as determined by a combination of (i) measurement by the modified population analysis profile-area under the curve method (PAP-AUC) and (ii) estimation from the measured sensitivity and specificity of a screening method. Two hundred isolates from blood were chosen as a subset for measurement of the sensitivities and the specificities of several previously described screening methods by using the results of PAP-AUC as the reference. During this testing, one isolate was found to be a vancomycinintermediate S. aureus (VISA) strain so was not used in the evaluation of the screening tests. Of the other 199 isolates, 26 (13.1%) were hVISA, as assessed by PAP-AUC. A screening cascade of culturing the isolates on brain heart infusion agar containing teicoplanin (5 mg/liter) and then subjecting the positive isolates to a macro-Etest method was applied to the 812 non-blood isolates, yielding 149 positive results. From these results and by adjusting for sensitivity (0.423) and specificity (0.861), the prevalence was estimated to be 15.7%. The precision of that estimate was assessed by reapplying the screening cascade to 120 randomly selected isolates from the 812 non-blood isolates and simultaneously determining their heterogeneous vancomycin-intermediate susceptibility status by PAP-AUC. Because PAP-AUC is impractical for use with large numbers of isolates, the screening-based estimation method is useful as a first approximation of the prevalence of hVISA. Of the 27 VISA or hVISA isolates from blood, 22.2% and 74.1% were staphylococcal chromosome cassette mec types II and III, respectively, while 77.8% and 22.2% were agr type 1 and agr type 2, respectively; the MIC ranges were 0.5 to 4 mg/liter for vancomycin and 0.25 to 1 mg/liter for daptomycin.

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“…Both the terms glycopeptide-intermediate S. aureus (GISA) and vancomycin-intermediate S. aureus (VISA) have been used in the literature and in essence are interchangeable. However, it is clear that reduced teicoplanin susceptibility can be present in S. aureus without a clearly demonstrated reduction in vancomycin susceptibility (34,113), whereas generally, VISA strains have demonstrated reduced teicoplanin susceptibility (183). Because the majority of in vitro susceptibility testing uses vancomycin, and much of the literature uses the term vancomycin-intermediate S. aureus (VISA) and heterogeneous VISA (hVISA), this review will use this terminology.…”

Section: Introductionmentioning

confidence: 99%

Reduced Vancomycin Susceptibility inStaphylococcus aureus, Including Vancomycin-Intermediate and Heterogeneous Vancomycin-Intermediate Strains: Resistance Mechanisms, Laboratory Detection, and Clinical Implications

et al. 2010

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SUMMARY The emergence of vancomycin-intermediate Staphylococcus aureus (VISA) and heterogeneous vancomycin-intermediate Staphylococcus aureus (hVISA) over the past decade has provided a challenge to diagnostic microbiologists to detect these strains, clinicians treating patients with infections due to these strains, and researchers attempting to understand the resistance mechanisms. Recent data show that these strains have been detected globally and in many cases are associated with glycopeptide treatment failure; however, more rigorous clinical studies are required to clearly define the contribution of hVISA to glycopeptide treatment outcomes. It is now becoming clear that sequential point mutations in key global regulatory genes contribute to the hVISA and VISA phenotypes, which are associated predominately with cell wall thickening and restricted vancomycin access to its site of activity in the division septum; however, the phenotypic features of these strains can vary because the mutations leading to resistance can vary. Interestingly, changes in the staphylococcal surface and expression of agr are likely to impact host-pathogen interactions in hVISA and VISA infections. Given the subtleties of vancomycin susceptibility testing against S. aureus, it is imperative that diagnostic laboratories use well-standardized methods and have a framework for detecting reduced vancomycin susceptibility in S. aureus.

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Failure of teicoplanin therapy in two neutropenic patients with staphylococcal septicemia who recovered after administration of vancomycin

Cited by 54 publications

References 14 publications

Inhibition of cell wall turnover and autolysis by vancomycin in a highly vancomycin-resistant mutant of Staphylococcus aureus

Inhibition of cell wall turnover and autolysis by vancomycin in a highly vancomycin-resistant mutant of Staphylococcus aureus

Prevalence and Characterization of Heterogeneous Vancomycin-Intermediate Staphylococcus aureus Isolates from 14 Cities in China

Reduced Vancomycin Susceptibility inStaphylococcus aureus, Including Vancomycin-Intermediate and Heterogeneous Vancomycin-Intermediate Strains: Resistance Mechanisms, Laboratory Detection, and Clinical Implications

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