PubMed · 2143668
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1990. Roerig extends antibiotic guarantee.. https://pubmed.ncbi.nlm.nih.gov/2143668/
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OBJECTIVE: To investigate the status of the drug resistance and the ampC gene expression of Enterobacter cloacae. METHODS: Disk diffusion tests were made for detecting the susceptibility of antimicrobial agents against Enterobacter cloacae. AmpC gene was amplified by polymerase chain reaction (PCR) and verified by DNA sequencing. AmpC gene expression was analyzed according to antimicrobial agent sensitive phenotype. RESULTS: The sensitivity rates of 144 strains to imipenam, cefepime and cefoperazone/sulbactam were 98.61%, 65.97% and 63.89%, respectively. The sensitivity rates of 144 strains to other antimicrobial agents were lower. Among the 144 strains 120 were found to be positive by PCR for ampC. The PCR product showed high homology to the GenBank ampC sequence. Stably derepressed strains, hyperinducible strains and unexpressing or lower level expressing strains accounted for 30.0% (36/120), 37.5% (45/120), and 32.5% (39/120), respectively. Fifty-six out of 120 strains (46.67%) also produced extended spectrum beta-lactamases (ESBLs). The hyperinducible strains were highly sensitive to all the antimicrobial agents except amoxicillin/clavulanic acid and cefuroxime, while the stably derepressed strains were only sensitive to imipenam and cefepime. However, sensitivity to cefepime decreased if the strains also produced ESBLs. CONCLUSIONS: The drug resistant status of Enterobacter cloacae is severe. Clearing out the expressive status of ampC gene will be helpful in selection of antimicrobial agents in the treatment of clinical infection.
A high performance frontal analysis(HPFA) method was developed to determine the unbound concentration of drugs in drug-human serum albumin (HSA) mixture under binding equilibrium. The sample was injected directly onto an internal-surface reversed-phase silica column (ISRP). The mobile phase was 67 mmol/L phosphate buffer (pH 7.4, I = 0.17 mol/L). When a large volume of sample solution under drug-HSA binding equilibrium was directly injected, the drug was eluted as a trapezoidal peak with a plateau, and the drug concentration in this region was the same as that of the unbound drug in the sample solution. The eluate of plateau region was collected and a small volume was injected onto a reversed-phase HPLC column. This HPFA-HPLC method was employed in the determination of unbound concentration in both ketoprofen (KP)-HSA and cefoperazone (CP)-HSA mixtures. The unbound concentrations of drugs obtained by using HPFA-HPLC were compared with those determined with ultrafiltration-HPLC. The effects of sample volume and flow rate of mobile phase on the plateau formation were investigated. It was found that the minimum injection volume to achieve a trapezoidal peak varied with drugs. The flow rate showed no effect on the trapezoidal peak formation. The unbound concentrations of KP and CP obtained were about the same by using HPFA-HPLC or ultrafiltration-HPLC and precisions were similar for both methods.
OBJECTIVE: To investigate the characterization of cefoperazone resistance gene (CPZr) on plasmid pFC in E. coli HX88108 and inquire into the mechanism of resistance to CPZ at the molecular level. METHODS: E. coli HX88108 strain which demonstrated high-level resistance to cefoperazone (MIC, > 512 micrograms/ml) was isolated from a severely infected patient in 1988. Five plasmids coexisting in the strain were designated pFC, pFT1; pFT2, pFT3 and pFX, respectively. Four plasmids except pFX conferred CPZ resistance. Cefoperazone resistance gene (CPZr) has been cloned from plasmid pFC. beta-lactamase assays with Nitrocefin were performed. RESULTS: The expression product of CPZr was beta-lactamase. The high level beta-lactamase enzymatic activities against cephaloridine of CPZr transformants which were detected spectrophotometrically at 260 nm wave length demonstrated high level similarities to that of pFC. MICs of 18 antibiotics were determined according to a guideline of NCCLS by broth dilution method. CPZr transformants showed moderate level resistance to ampicillin, cefazolin, cefazolin, cefamandole and CPZ (MIC, 64 micrograms/ml). Meanwhile, susceptibility testing results demonstrated that the level of resistance to CPZ of pFC transformant in this study (MIC, 64 micrograms/ml) was much lower than that in 1988 (MIC, > 512 micrograms/ml) and resistance to nofloxacin and aminoglycosides was not observed. Induction experiment and temperature-sensitive mutation of CPZ resistance were performed. CPZr colonal strains revealed the higher-level of resistance to CPZ (MIC, 512 micrograms/ml) due to antibiotic CPZ induction rather than temperature sensitive mutation. CONCLUSION: This observation suggests that resistance to antibiotics encoded by plasmid might have been lower or lost under no antibiotic stress in a certain period, but higher under heavy stress.