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At least 577 records · Page 32Linked to original sources
PubMed1984

Comparative efficacies of piperacillin, azlocillin, ticarcillin, aztreonam, and tobramycin against experimental Pseudomonas aeruginosa pneumonia.

The therapeutic efficacies of the newer beta-lactam antibiotics piperacillin, azlocillin and aztreonam were compared with the efficacies of ticarcillin and tobramycin in a guinea pig model of experimental Pseudomonas aeruginosa pneumonia. For animals challenged with 2 X 10(8) CFU, tobramycin treatment resulted in survival rates and intrapulmonary killing of pseudomonads which were significantly greater than those found with any of the beta-lactam agents. There were no significant differences noted among the individual beta-lactam agents. When animals were challenged with 200-fold-fewer organisms (10(6) CFU), there was no significant difference between the efficacy of tobramycin and those of the various beta-lactams. These data suggest that tobramycin is particularly valuable in treating more severe P. aeruginosa pneumonia, whereas a number of different beta-lactam agents are of equivalent value in less severe lung infections.

Animals↗
PubMed1984

In vitro activities of aztreonam, piperacillin, and ticarcillin combined with amikacin against amikacin-resistant Pseudomonas aeruginosa and P. cepacia isolates from children with cystic fibrosis.

Amikacin, combined with aztreonam, piperacillin, or ticarcillin, synergistically inhibited amikacin-resistant sputum isolates of Pseudomonas aeruginosa and P. cepacia from children with cystic fibrosis. Ticarcillin-amikacin was the least active combination. Aminoglycoside resistance should not preclude the use of beta-lactam-aminoglycoside combinations in the treatment of pulmonary infections in cystic fibrosis.

Amikacin↗
PubMed1984

Resistance of Pseudomonas aeruginosa mutants with altered control of chromosomal beta-lactamase to piperacillin, ceftazidime, and cefsulodin.

Examination of beta-lactam susceptibility of mutants altered in the control of chromosomal beta-lactamase of Pseudomonas aeruginosa supports the view that a constitutive level of beta-lactamase is not an adequate explanation for resistance to cefsulodin and ceftazidime but could be for resistance to piperacillin which has an efficiency of hydrolysis ca. 10 times higher than does cefsulodin or ceftazidime.

Anti-Bacterial Agents↗
PubMed1985

Enhanced liposome-mediated activity of piperacillin against staphylococci.

This study showed that encapsulation of the beta-lactam antibiotic piperacillin (PIP) by liposomes prepared with phosphatidylcholine and cholesterol (1:1) protected the drug from hydrolysis by staphylococcal beta-lactamase. This was demonstrated by growth inhibition of Staphylococcus aureus in the presence of the liposomal preparation containing PIP at a 50% MIC. Growth inhibition was also seen when exogenous beta-lactamase was added. Furthermore, adsorption of PIP onto the surface of liposomes containing buffer conferred a significant degree of protection against enzymatic hydrolysis of the drug, thus enhancing its antistaphylococcal activity.

Cholesterol↗
PubMed1985

Pharmacokinetics of ceftazidime, alone or in combination with piperacillin or tobramycin, in the sera of cancer patients.

We administered 2 g of ceftazidime intravenously every 8 h to cancer patients for the empiric therapy of febrile episodes. Ceftazidime was administered as monotherapy for patients with granulocyte counts in excess of 1,000/microliter. Febrile, neutropenic patients were randomized to also receive either piperacillin or tobramycin. The pharmacokinetic profile of ceftazidime during a steady-state dosing interval was ascertained in 21 patients. No differences were seen between groups for any of the pharmacokinetic parameters examined. As expected, the observed half-life was longer, the serum clearance was smaller, and the volumes of distribution were larger than in previously reported studies of volunteers. Serum concentrations remained above the MIC for inhibition of 90% of strains of the most common bacteremic pathogens seen in our cancer center for the entire 8-h dosing interval.

Adolescent↗
PubMed1991

Double-blind comparison of teicoplanin versus vancomycin in febrile neutropenic patients receiving concomitant tobramycin and piperacillin: effect on cyclosporin A-associated nephrotoxicity.

A prospective, randomized, and double-blind study comparing teicoplanin with vancomycin in the initial management of febrile neutropenic patients was conducted. Teicoplanin was administered at 6 mg per kg of body weight every 24 h (q24h) intravenously (i.v.) after initial loading at 6 mg/kg q12h for three doses. Vancomycin was administered at 15 mg/kg q12h i.v. Patients also received piperacillin (3 g q4h i.v.) and tobramycin (1.5 to 2.0 mg/kg q8h i.v.). Of 53 patients enrolled, 50 were judged to be evaluable. Among these, 25 received teicoplanin and 25 received vancomycin. At enrollment, both groups were comparable in age, sex, renal function, underlying hematologic condition, and concurrent therapy. Both groups had similar sites of infection and microbial pathogens. Empirical antimicrobial therapy resulted in the cure of or improvement in 23 (92%) teicoplanin patients and 21 (84%) vancomycin patients (P = 0.67). Failures occurred with two vancomycin patients but no teicoplanin patients. Clinical response was indeterminate for two patients in each group. Adverse reactions occurred significantly more often in the vancomycin group than in the teicoplanin group (P = 0.01), and these reactions required the termination of the study regimens of 6 vancomycin versus 0 teicoplanin patients (P = 0.02). Nephrotoxicity was observed more frequently in the vancomycin group (10 versus 2 patients; P = 0.02). Subgroup analysis revealed a significant deterioration of renal function when vancomycin and cyclosporin A, but not teicoplanin and cyclosporin A, were used concurrently (P = 0.02). Among patients who received vancomycin and amphotericin B or teicoplanin and amphotericin B concurrently, deterioration in renal function was equivalent in both groups. Teicoplanin in the dosage employed was tolerated better than vancomycin in the empirical treatment of fever and neutropenia in our patient population.

Adult↗
PubMed1992

Pseudomonas aeruginosa biofilm as a diffusion barrier to piperacillin.

Pseudomonas aeruginosa 579 biofilms formed on dialysis membranes retarded piperacillin diffusion. Treatment of biofilms with 5.0 mM CaCl2.2H2O prevented diffusion. Biofilms permitted equilibration of [14C]glucose. Thin-layer chromatography of fluids distal to untreated (viable and nonviable) and viable Ca(2+)-treated P. aeruginosa 579 biofilms and fluids distal to a viable P. aeruginosa mutant noninducible for the expression of beta-lactamase did not detect piperacillinoic acid.

Chromatography, Thin Layer↗
PubMed1996

Clinical pharmacokinetics of piperacillin-tazobactam combination in patients with major burns and signs of infection.

The pathophysiology associated with major burns is complex and subject to a state of flux. The combination of beta-lactamase inhibitors with powerful penicillins is an interesting and an attractive potential solution to the emergence of bacterial resistance. The kinetics in serum and urine and the clinical safety of a fixed combination of 4 g of piperacillin (PPR) and 0.5 g of tazobactam (TZB) were studied in 10 patients (22 to 50 years old and weighing 45 to 105 kg) with major burns who were infected with Pseudomonas aeruginosa and various entero-bacteria. All of them received additional antimicrobial drugs. Treatment involved one dose every 6 h. The mean body surface area affected by third-degree burns was 30.0% +/- 4.0%. The study took place in accordance with current ethical guidelines. Two series of blood samples were drawn after the first (day 1) and ninth (day 3 at steady state) doses; urine was collected during the same periods. Levels of PPR and TZB in serum and urine were measured by high-pressure liquid chromatography. A noncompartmental method was used for kinetic and graphic analysis of concentration-time pairs. The safety of the treatment was excellent. There was no systemic accumulation of the beta-lactam combination. Residual concentrations measured on days 1 and 3 [mean (standard error of the mean)] were above the MIC for the organism responsible for infection; i.e., C(min)day1 = 26.3 (8.5) and C(min)day3 = 21.0 (9.1) for PPR and C(min)day1 = 1.9 (0.6) and C(min)day3 = 1.4 (0.3) for TZB. There was no statistically significant difference between pharmacokinetic parameters determined for day 1 and day 3. Evidence was found in burn patients, in contrast to healthy subjects, of a marked increase in apparent volumes of distribution, in such a way that the apparent elimination half-lives of the combination were notably prolonged, i.e., 1.8 (0.3) versus 1.5 (0.3) h for PPR in patients and healthy subjects, respectively, and 1.7 (0.3) versus 1.4 (0.3) h for TZB. These findings indicate the possibility of nonrenal translesional diffusion of PPR-TZB in burn patients. The polarity of the association would further support this hypothesis. It has been shown here that the recommended dosage regimen for administration of PPR-TZB must be high in major-burn patients, i.e., 4 g/0.5 g every 6 h. The data obtained provide valuable information, which is suitable for immediate application in everyday clinical practice.

Adult↗
PubMed1997

Open randomized study of cefepime versus piperacillin-gentamicin for treatment of febrile neutropenic cancer patients.

An open-label randomized trial comparing the efficacy and safety of cefepime versus piperacillin plus gentamicin (P+G) given intravenously for the treatment of febrile episodes in neutropenic patients with underlying malignancy was conducted at two oncology centers. Over a 30-month period 111 patients were enrolled and 99 patients were found to be suitable for evaluation. At the 72-h time of evaluation, cefepime monotherapy and P+G combination therapy produced comparable clinical response rates (78% for both). P+G and cefepime produced comparable response rates in microbiologically documented (78 versus 71%), clinically documented (100 versus 100%), and possible (75 versus 79%) infections. The P+G and cefepime treatments achieved comparable microbiological eradication of gram-negative (100 versus 71%) (P = 0.09) and gram-positive (44 versus 70%) (P = 0.37) organisms. There were no statistically significant differences in the rates of superinfection between the groups; however, more superinfections of fungal origin were noted in the P+G group. Cefepime was demonstrated to be an effective and safe treatment for febrile episodes in neutropenic patients with malignancies, and its lack of nephrotoxicity compared to P+G was noteworthy. Cefepime appears to be a candidate for monotherapy in febrile neutropenic cancer patients.

Adult↗
PubMed2000

High-level expression of chromosomally encoded SHV-1 beta-lactamase and an outer membrane protein change confer resistance to ceftazidime and piperacillin-tazobactam in a clinical isolate of Klebsiella pneumoniae.

We describe Klebsiella pneumoniae 15571, a clinical isolate resistant to ceftazidime MIC = 32 microg/ml) and piperacillin-tazobactam (MICs = 1,024 and 128 microg/ml). K. pneumoniae 15571 expresses a single beta-lactamase with a pI of 7.6. However, when cloned in a high-copy-number vector in Escherichia coli, this bla(SHV-1) gene did not confer resistance to ceftazidime, a spectrum consistent with the nucleotide sequence, which was nearly identical to those of previously described bla(SHV-1) genes. Outer membrane protein (OMP) analysis of K. pneumoniae 15571 revealed a decrease in the quantity of a minor 45-kDa OMP in comparison to that in K. pneumoniae 44NR, a low-level ampicillin-resistant strain that also expresses a chromosomally determined bla(SHV-1). Crude beta-lactamase enzyme extracts from K. pneumoniae 15571 produced roughly 200-fold more beta-lactamase activity than K. pneumoniae 44NR. Northern hybridization analysis revealed that this difference was explainable by quantifiable differences in transcription of the bla(SHV-1) gene in the two strains. Primer extension analysis of bla(SHV-1) mRNA from K. pneumoniae 15571 and 44NR indicated that the transcriptional start sites were identical in the two strains. DNA sequencing of the promoter regions upstream of the of bla(SHV-1) open reading frames in the two K. pneumoniae strains revealed an A-->C change in the second position of the -10 region in K. pneumoniae 44NR compared to that in 15571. Site-directed mutagenesis of the cloned K. pneumoniae 15571 bla(SHV-1), in which the A in the second position of the 15571 -10 region was changed to a C, resulted in a substantial lowering of the MIC of ampicillin. When the levels of beta-lactamase enzyme expression in E. coli were compared, the bla(SHV-1) downstream of the altered -10 region produced 17-fold less beta-lactamase enzyme. These results indicate that elevated levels of ceftazidime resistance can result from a combination of increased enzyme production and minor OMP changes and that levels of chromosomally encoded SHV-1 beta-lactamase production can vary substantially with a single-base-pair change in promoter sequence.

Bacterial Outer Membrane Proteins↗
PubMed2004

Synergistic activities of moxifloxacin combined with piperacillin-tazobactam or cefepime against Klebsiella pneumoniae, Enterobacter cloacae, and Acinetobacter baumannii clinical isolates.

The bactericidal activity of moxifloxacin alone and in combination with cefepime or piperacillin-tazobactam against clinical isolates of Klebsiella pneumoniae, Enterobacter cloacae, and Acinetobacter baumannii was evaluated by using time-kill methods and antimicrobial concentrations of one-half and one times the MIC. Synergy was observed in 58 to 88% of the strains and resulted in bactericidal activity against 60 to 100% of the strains. Combinations including moxifloxacin demonstrated enhanced bactericidal activity compared with that of either agent tested alone.

Acinetobacter Infections↗
PubMed2004

In vitro activities of piperacillin against beta-lactamase-negative ampicillin-resistant Haemophilus influenzae.

The in vitro activities of piperacillin (PIP) against beta-lactamase-negative ampicillin (AMP)-resistant (BLNAR) Haemophilus influenzae were compared with those of cefotaxime (CTX) and ceftriaxone (CRO), and the potency of PIP as therapy for meningitis caused by BLNAR is also discussed. PIP showed good activity (MIC at which 90% of strains are inhibited, 0.25 micro g/ml) against 69 BLNAR strains, and its activity was comparable to that of CRO and superior to that of CTX. No significant correlation was observed between the MICs of PIP and CTX or CRO or AMP, whereas a high correlation was observed between the MICs of CTX and CRO. In the killing study, PIP showed potent bactericidal activity compared with those of CTX and CRO. By microscopic examination, PIP caused the formation of a spindle and short filamentous cells with bulges and induced cell lysis in BLNAR strains, while treatment with CTX and CRO resulted in the formation of large, spherical cells without any obvious lysis. The affinity of Bocillin FL, a fluorescent penicillin used for determination of the 50% inhibitory concentration (IC(50)s) for penicillin-binding proteins (PBPs), to PBPs 3a and 3b of BLNAR strains was drastically decreased compared with that to an AMP-susceptible strain (ATCC 33391). In the case of the BLNAR strains, the IC(50)s for PBPs 1a, 1b, and 2 were similar to those for the PBPs of ATCC 33391. Since the affinity of binding to PBPs 3a and 3b of the BLNAR strains decreased drastically, the second targets among the PBPs were PBP 2 for PIP, PBP1 (1a and 1b) for CTX and CRO. In conclusion, PIP showed excellent activities against BLNAR strains in a manner different from those of cephem antibiotics, suggesting that it could be a candidate therapeutic agent for the treatment of meningitis caused by BLNAR strains.

Ampicillin Resistance↗
PubMed1994

Penicillin-binding protein 2b of Streptococcus pneumoniae in piperacillin-resistant laboratory mutants.

In Streptococcus pneumoniae, alterations in penicillin-binding protein 2b (PBP 2b) that reduce the affinity for penicillin binding are observed during development of beta-lactam resistance. The development of resistance was now studied in three independently obtained piperacillin-resistant laboratory mutants isolated after several selection steps on increasing concentrations of the antibiotic. The mutants differed from the clinical isolates in major aspects: first-level resistance could not be correlated with alterations in the known PBP genes, and the first PBP altered was PBP 2b. The point mutations occurring in the PBP 2b genes were characterized. Each mutant contained one single point mutation in the PBP 2b gene. In one mutant, this resulted in a mutation of Gly-617 to Ala within one of the homology boxes common to all PBPs, and in the other two cases, the same Gly-to-Asp substitution at the end of the penicillin-binding domain had occurred. The sites affected were homologous to those determined previously in the S. pneumoniae PBP 2x of mutants resistant to cefotaxime, indicating that, in both PBPs, similar sites are important for interaction with the respective beta-lactams.

Amino Acid Sequence↗
PubMed1981

Quality control limits for ampicillin, carbenicillin, mezlocillin, and piperacillin disk diffusion susceptibility tests: a collaborative study.

A multilaboratory in vitro study was carried out to determine disk diffusion susceptibility testing quality control limits for two new semisynthetic penicillins, mezlocillin and piperacillin. Existing limits for carbenicillin and ampicillin were reevaluated. Multiple tests (which followed standards set by the National Committee for Clinical Laboratory Standards ASM-2 revised) were performed in nine laboratories by different technologists using disks and Mueller-Hinton agar from different manufacturers. Clinically significant differences between disks produced by different manufacturers were not noted. Inhibitory zone diameter measurements from all laboratories were analyzed, and upper and lower control limits were established by using the overall median +/-0.5 the median range of the individual laboratory measurements as determining parameters. Close agreement of the data in this study with the results of national proficiency testing and quality control programs for ampicillin and carbenicillin supports the validity of our approach to making initial recommendations for quality control guidelines for new antimicrobial agents.

Ampicillin↗
PubMed1980

Piperacillin in the treatment of urinary tract infections.

The ureidopenicillin piperacillin was given to 20 patients with urinary tract infections. The infecting microbes all had a minimum inhibitory concentration below 0.6 microgram/ml. One strain of Staphylococcus aureus produced beta-lactamase. All patients were freed of their microbes at the end of 7 days therapy. 1--2 weeks after the end of therapy, 1 relapsed and 3 had superinfections. Among the 16 who were without bacteria or leucocyturia after 1--2 weeks, 2 exhibited a superinfection 4--6 weeks after the end of therapy.

Adult↗
PubMed1984

In vitro combination effects of cefotetan with four aminoglycosides, piperacillin and mezlocillin on gram-positive and gram-negative nosocomial bacteria.

The in vitro efficacy of cefotetan in combination with gentamicin, tobramycin, amikacin, netilmicin against Staphylococcus aureus, Staphylococcus epidermidis and Enterobacter cloacae and with piperacillin and mezlocillin against Escherichia coli, Klebsiella pneumoniae, Serratia marcescens and Enterobacter cloacae was compared by use of the checkerboard agar dilution technique. On average, 60% of the gram-negative and 46% of the gram-positive strains were inhibited by additive, but only 22% of the gram-negative and 2% of the gram-positive bacteria were inhibited by synergistic cefotetan-aminoglycoside combinations. Netilmicin combinations were least active. On gram-negative bacteria, 63% of the cefotetan-penicillin combinations were additive and 11% synergistic. No antagonism occurred with any of the combinations.

Aminoglycosides↗
PubMed1985

Increased minimum inhibitory concentrations with anaerobiasis for tobramycin, gentamicin, and amikacin, compared to latamoxef, piperacillin, chloramphenicol, and clindamycin.

Minimum inhibitory concentrations (MICs) were determined under both routine aerobic and anaerobic conditions for a total of 93 organisms representing nine genera. MICs for the aminoglycosides amikacin, gentamicin, and tobramycin were significantly increased under anaerobic conditions. Tobramycin was most sensitive to the loss of antimicrobial activity with anaerobiasis. MICs for staphylococci were increased by a higher factor than were MICs for gram-negative rods, but even within the latter group increases in MICs for Proteus species were greater than for Salmonella, Klebsiella and Escherichia coli. No change of anaerobic versus aerobic activity was seen for latamoxef, piperacillin, chloramphenicol, or clindamycin.

Amikacin↗
PubMed1985

Pharmacokinetic studies of azlocillin and piperacillin during late pregnancy.

In this paper pharmacokinetic data of acylureidopenicillins (azlocillin and piperacillin) in pregnant women in the last trimenon are compared with those from nonpregnant controls. Four g of each drug was administered as slow bolus injection intravenously. The concentrations in serum and urine of both drugs were determined by polarographic and microbiological methods, for comparison. We used for evaluation of pharmacokinetic data a computer program based on the equations of a two-compartment open pharmacokinetic model. Our investigations show that there are not any different pharmacokinetic values of both antibiotics between pregnant women and healthy nonpregnant volunteers. We can state that both antibiotics are well determined by both analyzing methods which give us identical pharmacokinetic results.

Adult↗