Clinical trial of the efficacy and safety of ticarcillin and clavulanic acid

Roselle, Gary A.; Bode, R B; Hamilton, Brett; Bibler, Mark R.; Sullivan, Rebecca; Douce, Richard W.; Staneck, Joseph L.; Bullock, Ward E.

doi:10.1128/aac.27.3.291

Cited by 37 publications

(10 citation statements)

References 19 publications

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“…In principle, if the resistance mechanisms were to be inhibited, the antibacterial activity of various aminoglycosides could be restored. This concept is inspired by the successful introduction into clinical use of the first inhibitor of ␤-lactamases, enzymes that produce resistance to ␤-lactam antibiotics (164,247). The combination of the inhibitor, clavulanic acid, and amoxicillin, a penicillin, has been marketed for two decades.…”

Section: Strategies To Counter Resistancementioning

confidence: 99%

Versatility of Aminoglycosides and Prospects for Their Future

2003

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Aminoglycoside antibiotics have had a major impact on our ability to treat bacterial infections for the past half century. Whereas the interest in these versatile antibiotics continues to be high, their clinical utility has been compromised by widespread instances of resistance. The multitude of mechanisms of resistance is disconcerting but also illuminates how nature can manifest resistance when bacteria are confronted by antibiotics. This article reviews the most recent knowledge about the mechanisms of aminoglycoside action and the mechanisms of resistance to these antibiotics

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Section: Strategies To Counter Resistancementioning

confidence: 99%

Versatility of Aminoglycosides and Prospects for Their Future

2003

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“…The most recent combination (TIC-CA) has activity against many pathogens including Pseudomonas aeruginosa. In vitro studies (7,10,18) and clinical trials with the TIC-CA combination have been promising (6, 19). …”

mentioning

confidence: 99%

Effect of clavulanic acid on the activity of ticarcillin against Pseudomonas aeruginosa

Tausk¹,

Stratton²

1986

Antimicrob Agents Chemother

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We studied the ability of clavulanic acid (CA) to induce beta-lactamase in Pseudomonas aeruginosa isolates and what effect this might have on the susceptibilities to beta-lactam agents. We first used a disk approximation method to test 4 laboratory and 16 clinical P. aeruginosa isolates against antipseudomonal beta-lactam agents for truncation by CA and found this to be very common. All antimicrobial compounds except imipenem demonstrated truncation in the vicinity of CA. We also evaluated the extent to which chromosomal beta-lactamase is induced by CA and found this to occur to some degree in most isolates and to be dependent on the concentration of CA. Finally, we performed time kill curves on these isolates to compare bacterial growth in ticarcillin alone with growth in ticarcillin-CA (the CA at 2 or 4 micrograms/ml). We found that CA at this concentration has neither an antagonistic nor a synergistic antibacterial effect in combination with ticarcillin.

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“…Clavulanic acid has become a useful supplement to penicillins that are susceptible to hydrolysis by plasmid-mediated P-lactamases. This 3-lactamase inactivator works well when it is combined with amoxicillin or ticarcillin to treat infections caused by bacteria that produce many kinds of penicillinases or P-lactamases with broadspectrum hydrolyzing activities (1,17). However, recent reports indicate that occasional antagonism of penicillin activity has been observed when antibiotic combinations with clavulanic acid are added to selected gram-negative rods (19,21).…”

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confidence: 98%

Effect of clavulanic acid on activity of beta-lactam antibiotics in Serratia marcescens isolates producing both a TEM beta-lactamase and a chromosomal cephalosporinase

Bush

Flamm

Ohringer

et al. 1991

Antimicrob Agents Chemother

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An isolate of Serratia marcescens that produced both an inducible chromosomal and a plasmid-mediated TEM-1 _j-lactamase was resistant to ampicillin and amoxicillin and also demonstrated decreased susceptibility to extended-spectrum P-lactam antibiotics (ESBAs). Clavulanic acid did not lower the MICs of the ESBAs, but it decreased the MICs of the penicillins. The TEM-l-producing plasmid was transferred to a more susceptible S. marcescens strain that produced a well-characterized inducible chromosomal 13-lactamase. The MICs of the ESBAs remained at a low level for the transconjugant. Ampicillin and amoxicillin, which were good substrates for the plasmid-mediated enzyme, were not well hydrolyzed by the chromosomal enzymes; the ESBAs were hydrolyzed slowly by all the enzymes. When each of the S. marcescens strains was grown with these 3-lactam antibiotics, at least modest increases in chromosomal 3-lactamase activity were observed. When organisms were grown in the presence of clavulanic acid and an ESBA, no enhanced induction was observed. The increases in the MICs of the ESBAs observed for the initial clinical isolate may have been due to a combination of low inducibility, slow hydrolysis, and differences in permeability between the S. marcescens isolates. When clavulanic acid and a penicillin were added to strains that produced both a plasmid-mediated TEM and a chromosomal P-lactamase, much higher levels of chromosomal j3-lactamase activity were present than were observed in cultures induced by the penicillin alone. This was due to the higher levels of penicillin that were available for induction as a result of inhibition of the TEM enzyme by clavulanate.Resistance to P-lactam antibiotics is caused to a great extent by the presence of P-lactamases, enzymes that are capable of destroying the antibacterial activities of many of these agents. Clavulanic acid has become a useful supplement to penicillins that are susceptible to hydrolysis by plasmid-mediated P-lactamases. This 3-lactamase inactivator works well when it is combined with amoxicillin or ticarcillin to treat infections caused by bacteria that produce many kinds of penicillinases or P-lactamases with broadspectrum hydrolyzing activities (1, 17). However, recent reports indicate that occasional antagonism of penicillin activity has been observed when antibiotic combinations with clavulanic acid are added to selected gram-negative rods (19,21). In certain isolates, the lack of synergy observed has been attributed to the induction of chromosomal cephalosporinases (10, 12, 22), P-lactamases that are not well inhibited by clavulanate. Although most studies have included organisms that produce only a single inducible chromosomal cephalosporinase, some resistant isolates have been identified as strains that produce multiple P-lactamases (8,19 Bio-Rad (Richmond, Calif.).Organisms. S. marcescens SC 15071, which produces cephalosporinase S1 and the plasmid-mediated TEM-1 P-lactamase (plasmid pSVA071), was from a group of clinical isolates selected at the Seattle Ve...

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Clinical trial of the efficacy and safety of ticarcillin and clavulanic acid

Cited by 37 publications

References 19 publications

Versatility of Aminoglycosides and Prospects for Their Future

Versatility of Aminoglycosides and Prospects for Their Future

Effect of clavulanic acid on the activity of ticarcillin against Pseudomonas aeruginosa

Effect of clavulanic acid on activity of beta-lactam antibiotics in Serratia marcescens isolates producing both a TEM beta-lactamase and a chromosomal cephalosporinase

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