<i>In-vitro</i> effects of vancomycin, rifampicin, and fusidic acid, alone and in combination, against methicillin-resistant <i>Staphylococcus aureus</i>

Foldes, Mary; Munro, Rosemary; Sorrell, Tania C.; Shanker, S.; Toohey, M.

doi:10.1093/jac/11.1.21

Cited by 60 publications

(39 citation statements)

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“…Although fusidic acid and novobiocin are no longer available in the United States, they may be available elsewhere in the world for use with rifampin, especially for the treatment of complicated staphylococcal infections, in particular MRSA (124). The rifampin-fusidic acid combination appears to demonstrate synergy rather than indifference by several in vitro studies (82,86,254). The rifampin-novobiocin combination demonstrates synergy or indifference by in vitro studies, especially when there are heavy inocula of bacteria (48,135,258).…”

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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Section: Staphylococcimentioning

confidence: 99%

Rifampin Combination Therapy for Nonmycobacterial Infections

2010

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“…Vancomycin-group glycopeptides are important antibiotics that are frequently used as a last line of defense against methicillin-resistant Staphylococcus aureus (1). However, the recent emergence of vancomycin-resistant strains raises the possibility that vancomycin may soon be rendered ineffective over time and that other therapeutic agents must be developed (2).…”

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confidence: 99%

“…The backbone of a third unusual amino acid in these antibiotics, (S)-3,5-dihydroxyphenylglycine, was shown to be derived from acetate, and a polyketide synthase (PKS) 1 reaction was proposed (10). Therefore, it was of considerable interest that the biosynthetic gene cluster of balhimycin does not contain genes for typical bacterial PKS (type I or II) but a gene for a protein related to the plant-specific polyketide synthases of the chalcone synthase family (reviewed in Ref.…”

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confidence: 99%

A Polyketide Synthase in Glycopeptide Biosynthesis

Pfeifer¹,

Nicholson²,

Ries³

et al. 2001

Journal of Biological Chemistry

139

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Balhimycin, a vancomycin-type antibiotic from Amycolatopsis mediterranei, contains the unusual amino acid (S)-3,5-dihydroxyphenylglycine (Dpg), with an acetate-derived carbon backbone. After sequence analysis of the biosynthetic gene cluster, one gene, dpgA, for a predicted polyketide synthase (PKS) was identified, sharing 20 -30% identity with plant chalcone synthases. Inactivation of dpgA resulted in loss of balhimycin production, and restoration was achieved by supplementation with 3,5-dihydroxyphenylacetic acid, which is both a possible product of a PKS reaction and a likely precursor of Dpg. Enzyme assays with the protein expressed in Streptomyces lividans showed that this PKS uses only malonyl-CoA as substrate to synthesize 3,5-dihydroxyphenylacetic acid. The PKS gene is organized in an operon-like structure with three downstream genes that are similar to enoyl-CoA-hydratase genes and a dehydrogenase gene. The heterologous co-expression of all four genes led to accumulation of 3,5-dihydroxyphenylglyoxylic acid. Therefore, we now propose a reaction sequence. The final step in the pathway to Dpg is a transamination. A predicted transaminase gene was inactivated, resulting in abolished antibiotic production and accumulation of 3,5-dihydroxyphenylglyoxylic acid. Interestingly, restoration was only possible by simultaneous supplementation with (S)-3,5-dihydroxyphenylglycine and (S)-4-hydroxyphenylglycine, indicating that the transaminase is essential for the formation of both amino acids.

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“…These strains have become established hospital flora, with infections caused by methicillin-resistant S. aureus becoming increasingly prevalent (13,16). Vancomycin (VM) hydrochloride is generally effective in the treatment of infections involving methicillinresistant S. aureus, although poor clinical responses have been observed, perhaps caused by the tolerance of S. aureus to VM (5,7,15). The combination of trimethoprim (TMP)-sulfamethoxazole (SMX) has been reported to be active in vitro against these resistant strains, although only a limited number of isolates have been examined.…”

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confidence: 99%

In vitro and in vivo efficacy of the combination trimethoprim-sulfamethoxazole against clinical isolates of methicillin-resistant Staphylococcus aureus

Elwell¹,

Wilson²,

Knick³

et al. 1986

Antimicrob Agents Chemother

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The in vitro susceptibilities of 16 independent, geographically distinct clinical isolates of methicillin-resistant Staphylococcus aureus to trimethoprim (TMP) in combination with sulfamethoxazole (SMX) were evaluated. Although methicillin-resistant S. aureus strains appear to be universally resistant to SMX, the combination TMP-SMX was found to be synergistic in vitro (in combination, the MICs of both drugs decreased 6- to 25-fold) as well as in vivo (5- to 6-fold reduction in TMP at 50% effective doses).

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In-vitro effects of vancomycin, rifampicin, and fusidic acid, alone and in combination, against methicillin-resistant Staphylococcus aureus

Cited by 60 publications

References 0 publications

Rifampin Combination Therapy for Nonmycobacterial Infections

Rifampin Combination Therapy for Nonmycobacterial Infections

A Polyketide Synthase in Glycopeptide Biosynthesis

In vitro and in vivo efficacy of the combination trimethoprim-sulfamethoxazole against clinical isolates of methicillin-resistant Staphylococcus aureus

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