Antibacterial activity of ticarcillin in the presence of clavulanate potassium

Sutherland, Robert L.; Beale, A S; Boon, R. J.; Griffin, Karen E.; Slocombe, B.; Stokes, D. H.; White, Anthony R.

doi:10.1016/0002-9343(85)90124-x

Cited by 29 publications

(16 citation statements)

References 20 publications

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“…Clearly, such strains exist among E. coli and Klebsiella spp., although they are usually a small minority of total isolates examined (5,8,17,22,23). Thus, the availability of a fairly large collection of ticarcillin-potassium clavulanate-resistant members of the Enterobacteriaceae presented the first opportunity to examine this aspect in detail.…”

Section: Discussionmentioning

confidence: 99%

“…Potassium clavulanate is a suicide inhibitor of many 3-lactamases and, in combination with ticarcillin, restores the activity of the latter against members of the family Enterobacteriaceae producing enzymes of essentially all Richmond and Sykes classes except class I, the chromosomal cephalosporinases (5,10,22). However, in a recent survey of piperacillin-resistant members of the Enterobacteriaceae, a number of ticarcillin-potassium clavulanate (Timentin)-resistant strains were found among isolates recovered from patients at the University of Texas M. D. Anderson Cancer Center.…”

mentioning

confidence: 99%

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Resistance to ticarcillin-potassium clavulanate among clinical isolates of the family Enterobacteriaceae: role of PSE-1 beta-lactamase and high levels of TEM-1 and SHV-1 and problems with false susceptibility in disk diffusion tests

Sanders

Iaconis

Bodey

et al. 1988

Antimicrob Agents Chemother

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Thirty-four clinical isolates of the family Enterobacteriaceae from the University of Texas M. D. Anderson Cancer Center appeared resistant to ticarcillin-potassium clavulanate in agar dilution and broth macrodilution tests. Among those isolates producing a single non-class I beta-lactamase, resistance was due to production of high levels of TEM-1, SHV-1, or class IV enzymes. In five Escherichia coli isolates, production of low levels of PSE-1 was responsible for resistance which seemed due to rapid hydrolysis of ticarcillin rather than diminished susceptibility of PSE-1 to inhibition by potassium clavulanate. Comparisons of dilution and disk diffusion tests revealed major discrepancies, with 65% false susceptibility in the disk test. Revision of the interpretive criteria used for disk diffusion tests from less than or equal to 11 to less than or equal to 18 mm for resistance is proposed to resolve these discrepancies until clinical data are obtained which can be used to determine which in vitro test is most predictive of therapeutic outcome. These new criteria would diminish false susceptibility without introducing false resistance.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Resistance to ticarcillin-potassium clavulanate among clinical isolates of the family Enterobacteriaceae: role of PSE-1 beta-lactamase and high levels of TEM-1 and SHV-1 and problems with false susceptibility in disk diffusion tests

Sanders

Iaconis

Bodey

et al. 1988

Antimicrob Agents Chemother

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“…Two doses of ceftazidime given 8 h apart were more effective than the three doses of ticarcillin-clavulanic acid, in keeping with the in vitro activities of these compounds against the infecting organism. These results illustrate the ability of clavulanic acid to penetrate the blood-CSF barrier such that concentrations of the inhibitor in CSF potentiate the activity of ticarcillin against the ticarcillin-resistant, ,-lactamase-producing strain of K. pneumoniae.In the presence of clavulanic acid the antibacterial spectrum of ticarcillin is extended to include ticarcillin-resistant, P-lactamase-producing strains of members of the family Enterobacteriaceae, Pseudomonas aeruginosa, Bacteroides spp., Haemophilus influenzae, and staphylococci (6,8,20). For clavulanic acid to inhibit ,B-lactamases produced in vivo and allow ticarcillin to exert its bactericidal effect, both compounds should display similar distribution characteristics.…”

mentioning

confidence: 99%

“…In the presence of clavulanic acid the antibacterial spectrum of ticarcillin is extended to include ticarcillin-resistant, P-lactamase-producing strains of members of the family Enterobacteriaceae, Pseudomonas aeruginosa, Bacteroides spp., Haemophilus influenzae, and staphylococci (6,8,20). For clavulanic acid to inhibit ,B-lactamases produced in vivo and allow ticarcillin to exert its bactericidal effect, both compounds should display similar distribution characteristics.…”

mentioning

confidence: 99%

Simulation of human serum pharmacokinetics of ticarcillin-clavulanic acid and ceftazidime in rabbits, and efficacy against experimental Klebsiella pneumoniae meningitis

Mizen

Woodnutt

Kernutt

et al. 1989

Antimicrob Agents Chemother

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The penetration into cerebrospinal fluid (CSF) and efficacy of ticarcillin-clavulanic acid, ticarcillin alone, and ceftazidime were compared in rabbits with experimentally induced Klebsiella pneumoniae meningitis. The compounds were administered to simulate in rabbit plasma the concentration-versus-time curves observed in humans after 30-min infusions of Timentin (3 g of ticarcillin plus 100 mg of clavulanic acid), ticarcillin (3 g), and ceftazidime (2 g). Single-and multiple-dosing schedules were used. The penetrations of clavulanic acid into CSF (expressed as [area under the concentration-time curve for CSF/area under the curve for plasma] x 100) after the two dosing schedules were 28 and 24.5%, similar to that for ceftazidime (21%; multiple-dosing only) and greater than those for ticarcillin (8.4 and 9.3%). Ticarcillin was ineffective in reducing viable counts in CSF but, in the presence of clavulanic acid, reduced bacterial numbers by approximately 99% at 4 h after a single dose and by 99.99% at 12 h after three doses given at 4-h intervals. Two doses of ceftazidime given 8 h apart were more effective than the three doses of ticarcillin-clavulanic acid, in keeping with the in vitro activities of these compounds against the infecting organism. These results illustrate the ability of clavulanic acid to penetrate the blood-CSF barrier such that concentrations of the inhibitor in CSF potentiate the activity of ticarcillin against the ticarcillin-resistant, ,-lactamase-producing strain of K. pneumoniae.In the presence of clavulanic acid the antibacterial spectrum of ticarcillin is extended to include ticarcillin-resistant, P-lactamase-producing strains of members of the family Enterobacteriaceae, Pseudomonas aeruginosa, Bacteroides spp., Haemophilus influenzae, and staphylococci (6,8,20). For clavulanic acid to inhibit ,B-lactamases produced in vivo and allow ticarcillin to exert its bactericidal effect, both compounds should display similar distribution characteristics. This has been demonstrated both in animals (4, 5, 24) and in humans (1,3,22). In the study reported here, the penetration into cerebrospinal fluid (CSF) and the efficacy of ticarcillin-clavulanic acid were investigated in a rabbit model of meningitis (18) in which the infecting organism was a strain of Klebsiella pneumoniae.To compensate for the more rapid elimination of ticarcillin (elimination half-life, 0.4 to 0.6 h), clavulanic acid (0.3 to 0.6 h), and ceftazidime (0.75 to 0.88 h) from serum in the rabbit (16, 21, 23; unpublished data) than from serum in humans (half-life, 1.1 ± 0.5, 1.0 + 0.06, and 1.8 ± 0.21, respectively) (7, 9), the antibiotics were administered to infected rabbits by using a procedure designed to simulate in rabbit plasma the concentration-versus-time curves observed in human serum after therapeutic doses. The efficacy of ticarcillinclavulanic acid was compared with results for ticarcillin alone and with those for ceftazidime, a broad-spectrum cephalosporin considered useful for the treatment of gramnegative-bacilliary m...

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“…Ticarcillin is a semi-synth etic penicill in with properties identical to carbenicillin, with exception that it is more active against P aeruginosa [15]. Acylampicillins (meslocillin, azlocillin and piperacillin) have limited role in management of neonatal seps is.…”

Section: Newer Penicillismentioning

confidence: 99%

Neonatal Sepsis

SHARMA

1998

Medical Journal Armed Forces India

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Neonatal sepsis continues to be a major cause of morbidity and mortality in India. To aid the diagnosis several direct and indirect methods are available. Sepsis screen has resulted in decrease in indiscriminate use of antibiotics. C-reactive protein can be easily estimated and is a useful indicator for favourable outcome or complication. The bacterial flora causing sepsis has changed over the years. Antimicrobial chemotherapy should be based on the prevalent organisms in the neonatal ICU. Outcome can be improved by judicious use of newer antibiotics and exchange transfusion when indicated. MJAF11998; 54: 44-46

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Antibacterial activity of ticarcillin in the presence of clavulanate potassium

Cited by 29 publications

References 20 publications

Resistance to ticarcillin-potassium clavulanate among clinical isolates of the family Enterobacteriaceae: role of PSE-1 beta-lactamase and high levels of TEM-1 and SHV-1 and problems with false susceptibility in disk diffusion tests

Resistance to ticarcillin-potassium clavulanate among clinical isolates of the family Enterobacteriaceae: role of PSE-1 beta-lactamase and high levels of TEM-1 and SHV-1 and problems with false susceptibility in disk diffusion tests

Simulation of human serum pharmacokinetics of ticarcillin-clavulanic acid and ceftazidime in rabbits, and efficacy against experimental Klebsiella pneumoniae meningitis

Neonatal Sepsis

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