Synergy of combinations of vancomycin, gentamicin, and rifampin against methicillin-resistant, coagulase-negative staphylococci

Lowy, Franklin D.; Chang, Dong Suck; Lash, P R

doi:10.1128/aac.23.6.932

Cited by 49 publications

(13 citation statements)

References 6 publications

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“…Our study and others (1,2,5,10,23,29,32,39,43,47,49,51,53) have indicated that vancomycin and rifampin are consistently active against both oxacillin-susceptible and -resistant staphylococci. The clinical efficacy of vancomycin has been established for both heteroresistant S. aureus (8) and S. epidermidis (23,52).…”

Section: Discussionmentioning

confidence: 99%

In vitro susceptibilities of four species of coagulase-negative staphylococci

Fass¹,

Helsel²,

Barnishan³

et al. 1986

Antimicrob Agents Chemother

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The in vitro susceptibilities of 260 strains of coagulase-negative staphylococci to penicillin G, oxacillin, nafcillin, methicillin, cephalothin, and seven non-Il-lactam antimicrobial agents were determined and compared with the susceptibilities of 54 strains of Staphylococcus aureus with known patterns of susceptibility. Penicillin G susceptibility for S. aureus, Staphylococcus epidermidis, Staphylococcus haemolyticus, and Staphylococcus hominis was readily determined by using I-lactamase tests with induced cells and with a standardized microdilution test. MIC criteria for susceptibility used for S. aureus were applicable to the coagulase-negative species. Percentages of organisms susceptible were as follows: S. epidermidis, 7%; S. haemolyticus, 5%; and S. hominis, 47%. Oxacillin susceptibility for these four species was readily determined by using a modification of the microdilution test. MIC criteria for susceptibility used for S. aureus were applicable to S. haemolyticus and S. hominis, but alternate criteria were necessary for S. epidermidis. Percentages of organisms susceptible were as follows: S. epidermidis, 29%; S. haemolyticus, 36%; and S. hominis, 97%. Staphylococcus saprophyticus differed from the other staphylococcal species; all strains were ,-lactamase negative and were penicillin susceptible but had higher penicillin G MICs than did susceptible strains of the other species. There was total cross resistance among the penicillinase-resistant penicillins and cephalothin for the coagulase-negative staphylococci as well as for S. aureus; oxacillin MICs were more reliable than MICs of the other drugs or a standardized disk diffusion test for distinguishing resistant from susceptible strains. Vancomycin, rifampin, and ciprofloxacin were consistently active against all staphylococci. Erythromycin, clindamycin, gentamicin, and trimethoprim-sulfamethoxazole were more active against oxacillinsusceptible staphylococci than against oxacillin-resistant staphylococci.

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Section: Discussionmentioning

confidence: 99%

In vitro susceptibilities of four species of coagulase-negative staphylococci

Fass¹,

Helsel²,

Barnishan³

et al. 1986

Antimicrob Agents Chemother

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“…For example, vancomycin penetration into lung tissue is not sustained, and the same was seen for the meninges and infected bone, whereas rifampin easily penetrates these tissues (61,109,120). The rifampin-vancomycin in vitro interaction appears to range from antagonistic to indifferent, with very few synergistic studies (25,26,112,119,158,218,246,251,258,261). Tuazon et al showed that the rifampin-vancomycin combination had "partial synergism" with only 25% of the MSSA isolates, with the remainder being indifferent, while the nafcillin-rifampin combination had "partial synergism" for 60% of the isolates (246).…”

Section: Staphylococcimentioning

confidence: 99%

Rifampin Combination Therapy for Nonmycobacterial Infections

2010

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SUMMARY The increasing emergence of antimicrobial-resistant organisms, especially methicillin-resistant Staphylococcus aureus (MRSA), has resulted in the increased use of rifampin combination therapy. The data supporting rifampin combination therapy in nonmycobacterial infections are limited by a lack of significantly controlled clinical studies. Therefore, its current use is based upon in vitro or in vivo data or retrospective case series, all with major limitations. A prominent observation from this review is that rifampin combination therapy appears to have improved treatment outcomes in cases in which there is a low organism burden, such as biofilm infections, but is less effective when effective surgery to obtain source control is not performed. The clinical data support rifampin combination therapy for the treatment of prosthetic joint infections due to methicillin-sensitive S. aureus (MSSA) after extensive debridement and for the treatment of prosthetic heart valve infections due to coagulase-negative staphylococci. Importantly, rifampin-vancomycin combination therapy has not shown any benefit over vancomycin monotherapy against MRSA infections either clinically or experimentally. Rifampin combination therapy with daptomycin, fusidic acid, and linezolid needs further exploration for these severe MRSA infections. Lastly, an assessment of the risk-benefits is needed before the addition of rifampin to other antimicrobials is considered to avoid drug interactions or other drug toxicities.

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“…In vitro (22,24, 33) and in vivo (23, 25, 33) studies with Staphylococcus aureus and Staphylococcus epidermidis in our laboratory, however, indicated that a second mechanism by which cell wall-active antibiotics (,-lactams, vancomycin) enhance the bactericidal effect of aminoglycosides (or rifampin) is by preventing regrowth of relatively resistant subpopulations. Twentyfour-hour time kill studies often do not distinguish between the aforementioned mechanisms of drug potentiation, and * Corresponding author.…”

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confidence: 95%

Penicillin-induced effects on streptomycin uptake and early bactericidal activity differ in viridans group and enterococcal streptococci

Miller¹,

El-Sokkary²,

Feinstein³

et al. 1986

Antimicrob Agents Chemother

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In vitro studies with penicillin and [3lHlstreptomycin in four strains of streptococci (S. faecalis, S. sanguis, and S. mitis) were performed by simultaneously measuring the rates of bacterial killing and uptake of streptomycin. In S. faecalis, penicillin stimulated streptomycin uptake, as has been shown by Moellering and Weinberg (R. C. Moellering, Jr., and A. N. Weinberg, J. Clin. Invest. 50:2580-2584). Moreover, the antibiotic combination was associated with an enhanced bactericidal rate which temporally correlated with ,-lactam-induced aminoglycoside uptake. In contrast, in viridans group streptococci (S. sanguis and S. mitis) penicillin had no effect on streptomycin uptake and a minimal effect on bactericidal rate when compared with either drug alone. These data suggested that the stimulation of streptomycin uptake in streptococci by penicillin is strain or species specific and that important differences exist between enterococci and viridans group streptococci regarding the mechanisms of ,-lactam-aminoglycoside potentiation.Antibiotic synergy is perhaps best exemplified by the use of a P-lactam combined with an aminoglycoside in the therapy of enterococcal endocarditis. The enhanced antibacterial activity of the combination has been well established both in clinical trials (26) and in an experimental model of endocarditis (14). In studies on the mechanism of synergy in enterococci, Moellering and colleagues (35, 36) demonstrated that penicillin enhanced intracellular entry of otherwise sublethal concentrations of streptomycin, suggesting that the mechanism of sytergy in Streptococcusfaecalis was similar to that shown earlier in Escherichia coli by Plotz and Davis (36). However, from a mechanistic standpoint it is not clear how penicillin would enhance uptake of aminoglycosides in most gram-positive bacteria since no barrier to aminoglycoside penetration comparable to that of gramnegative bacilli has been described. Time kill studies (35,36) also demonstrated that enhancement of streptomycin entry was associated with an increase in the rate of killing during 24 h as determined by the inability of cells to form colonies on agar after overnight incubation. Twenty-four-hour time kill studies have since become a generally accepted in vitro method for examining bactericidal synergism in both grampositive and gram-negative bacteria.Numerous 24-h in vitro time kill studies have shown apparent synergy (i.e., a >2 logl0 enhanced bactericidal effect) between P-lactams and aminoglycosides in grampositive organisms (5,12,20,21,41,44). In vitro (22,24, 33) and in vivo (23, 25, 33) studies with Staphylococcus aureus and Staphylococcus epidermidis in our laboratory, however, indicated that a second mechanism by which cell wall-active antibiotics (,-lactams, vancomycin) enhance the bactericidal effect of aminoglycosides (or rifampin) is by preventing regrowth of relatively resistant subpopulations. Twentyfour-hour time kill studies often do not distinguish between the aforementioned mechanisms of drug potentiation, and ...

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Synergy of combinations of vancomycin, gentamicin, and rifampin against methicillin-resistant, coagulase-negative staphylococci

Cited by 49 publications

References 6 publications

In vitro susceptibilities of four species of coagulase-negative staphylococci

In vitro susceptibilities of four species of coagulase-negative staphylococci

Rifampin Combination Therapy for Nonmycobacterial Infections

Penicillin-induced effects on streptomycin uptake and early bactericidal activity differ in viridans group and enterococcal streptococci

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