Synergy of Penicillin and Gentamicin against Enterococci

Moellering, Robert C.; Wennersten, Christine; Weinberg, Arnold N.

doi:10.1093/infdis/124.supplement_1.s207

Cited by 136 publications

(73 citation statements)

References 3 publications

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“…HH22 was inhibited by 4 ,ug/ml of penicillin using 103 colony-forming units (CFU)/ml but grew readily in 1,024 jAg/ml using 107 CFU/ml. Growth at a high inoculum was not observed with 30 other S. faecalis examined in this laboratory nor with numerous others in the literature (12)(13)(14); the MIC of penicillin for a representative strain, HH54 (also highly resistant to gentamicin), is also shown in Table I. The production of penicillinase, suggested by this inoculum effect (15)(16), was confirmed by demonstrating that HH22 inactivates penicillin (Fig.…”

Section: Methodssupporting

confidence: 55%

“…RESULTS S. faecalis strain HH22 was previously shown to be resistant to streptomycin, kanamycin, tobramycin, and gentamicin (MIC > 2,000 jig/ml), to erythromycin (MIC > 100 lg/ml), and to tetracycline (MIC > 30 ,ug/ml) (12). While investigating the in vitro effects of the combination of aminoglycosides and penicillin, it was observed that with a high inoculum, this organism was not inhibited by the concentration of penicillin (10 U/ml) usually used in enterococcal synergy experiments (12)(13)(14). The results of susceptibility testing using different inocula of organisms are shown in Table I.…”

Section: Methodsmentioning

confidence: 99%

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Transferable beta-lactamase. A new mechanism for in vitro penicillin resistance in Streptococcus faecalis.

Murray¹,

1983

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A B S T R A C T Although enterococci are relatively resistant to penicillin, the mechanism of resistance is largely unknown and enzymatic inactivation does not play a role. In this study, an isolate of Streptococcus faecalis was found to have beta lactamase activity resulting in complete inactivation of penicillin. With a high inoculum, this strain was resistant to >1,000 ,ug/ ml of penicillin. Penicillin resistance and beta lactamase activity were transferred by conjugation at a high frequency to an enterococcal laboratory recipient strain together with two plasmids of molecular size 34 X 106 and 56 X 106, thus demonstrating the emergence of plasmid-mediated penicillin resistance in the genus Streptococcus.

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Section: Methodssupporting

confidence: 55%

Section: Methodsmentioning

confidence: 99%

Transferable beta-lactamase. A new mechanism for in vitro penicillin resistance in Streptococcus faecalis.

Murray¹,

1983

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“…The mechanism of the latter in vitro phenomenon is not known. However, it has been well documented that cell wall-active agents (such as oxacillin) can promote the facilitated uptake of cationic antimicrobial agents (such as aminoglycosides) in antibiotic-resistant bacteria (e.g., enterococci [16]). Thus, it is conceivable that in the presence of oxacillin the intracellular uptake of the cationic peptide tPMP-1 into tPMP-1 r ISP479R cells may also be facilitated.…”

mentioning

confidence: 99%

Thrombin-Induced Platelet Microbicidal Protein Susceptibility Phenotype Influences the Outcome of Oxacillin Prophylaxis and Therapy of Experimental Staphylococcus aureus Endocarditis

Dhawan

Bayer

Yeaman

2000

Antimicrob Agents Chemother

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We previously showed that in vitro susceptibility profiles of Staphylococcus aureus to thrombin-induced platelet microbicidal protein 1 (tPMP-1) impacted the outcome of vancomycin treatment in experimental infective endocarditis. In this same model, treatment with oxacillin (a more rapid staphylocidal agent than vancomycin) enhanced the clearance of both tPMP-1-susceptible and -resistant cells from vegetations. The extent of clearance was greater for tPMP-1-susceptible cells.

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“…Intrinsically resistant to all clinically available cephalosporins, enterococci are also 100-fold more resistant to penicillin than the streptococci with which they are usually compared. Moreover, the characteristic tolerance of these organisms to the activity of all cell wall-active agents necessitates the use of such agents in combination with aminoglycosides to achieve adequate bactericidal activity (15). As a result, the treatment of severe infections due to even relatively susceptible enterococci can pose significant therapeutic difficulties, especially in patients who are allergic to penicillins or who have compromised renal functions.…”

mentioning

confidence: 99%

Chromosomally mediated beta-lactamase production and gentamicin resistance in Enterococcus faecalis

Rice

Eliopoulos

Wennersten

et al. 1991

Antimicrob Agents Chemother

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We have analyzed four distinct strains of multiply resistant, beta-lactamase-producing enterococci isolated during an outbreak of colonization with these strains on an infant-toddler surgical ward at The Children's Hospital in Boston, Mass. All four strains were resistant to erythromycin, penicillin, and tetracycline and to high levels of gentamicin and streptomycin. One strain was also resistant to chloramphenicol. Plasmid profiles revealed four different plasmid patterns, with the number of identified plasmids ranging from zero to three. The gene coding for beta-lactamase production could be transferred at low frequency (less than 10(-8)) to an enterococcal recipient from one strain in conjunction with all of the other resistance determinants. Probes derived from the staphylococcal beta-lactamase gene and gentamicin resistance gene failed to hybridize with any of the detectable plasmids, but both genes were present on restriction fragments of genomic DNA in all strains. Our results indicate that the beta-lactamase genes and gentamicin resistance genes in these strains are integrated into the bacterial chromosome. The cotransmissibility of the resistance determinants raises the possibility of their incorporation into a multiresistance transposable genetic element.

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Synergy of Penicillin and Gentamicin against Enterococci

Cited by 136 publications

References 3 publications

Transferable beta-lactamase. A new mechanism for in vitro penicillin resistance in Streptococcus faecalis.

Transferable beta-lactamase. A new mechanism for in vitro penicillin resistance in Streptococcus faecalis.

Thrombin-Induced Platelet Microbicidal Protein Susceptibility Phenotype Influences the Outcome of Oxacillin Prophylaxis and Therapy of Experimental Staphylococcus aureus Endocarditis

Chromosomally mediated beta-lactamase production and gentamicin resistance in Enterococcus faecalis

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