RESUMEN
Background: Bacterial resistance is closely associated with the use of antimicrobial agents. Prolonged therapy with antibiotics can lead to the development of resistance in a microorganism that initially is sensitive to antibiotics, but later it can adapt gradually and develop resistance to antibiotics. Aims: We reviewed whether clavulanic acid plus cephalosporin combinations help to solve the resistance problem. Methods: We evaluated and reviewed this topic via “Antibiotic Resistance”, “Cephalosporin and β-Lactamase Inhibitor Combinations” and our suggestions. Results: Acquired resistance arises from: (1) mutations in cell genes (chromosomal mutation) leading to cross-resistance, (2) gene transfer from one microorganism to other by plasmids (conjugation or transformation), transposons (conjugation), integrons and bacteriophages (transduction). β-Lactamases hydrolyze nearly all β-lactams that have ester and amide bond, e.g., penicillins, cephalosporins, monobactams, andcarbapenems. Serine β-lactamases – cephalosporinases, e.g. AmpC enzyme – are found in Enterobacter spp. and P. aeruginosa and penicillases in S. aureus. Amoxicillin-clavulanate resistance (MIC >16 microg/ml) in Escherichia coli is reported previously. Therefore, development of new drugs or combination is necessary for the antimicrobial resistance. To manage the Cephalosporin resistance, Cephalosporin and β-Lactamase Inhibitor Combinations, such as Ceftolozane/tazobactam or Ceftazidime/avibactam have been used. Conclusion: As resistance to cephalosporins have been increasing, cephalosporin + clavulonate combination will be another choice for managing the antibiotic resistance to the cephalosporins. Our suggestion is based on the success of the clavulonate combination of amoxicillin to manage the antibiotic resistance.
RESUMEN
Background & objectives: Extended-Spectrum Beta-Lactamases (ESBLs) is an important resistance mechanism in Enterobacteriaceae infections. Lack of standard guidelines from Clinical Laboratory Standards Institute (CLSI) for Amp C beta-lactamase detection poses a problem. This study was undertaken to detect ESBLs by phenotypic tests and Amp C beta-lactamase by inhibitor based method. Material and Methods: 200 consecutive non-repetitive isolates of E.coli, Klebsiella and Proteus from clinical samples were screened for ESBLs as per CLSI guidelines and confirmed by PCDT, DDST and E-tests (AB Biodisk, Biomerieux). Amp C beta lactamases were screened by cefoxitin resistance and confirmed by inhibitor (Cloxacillin) based method. Simultaneous occurrence of Amp C and ESBLs was detected by combined disk test (Neo-Sensitabs and Diatabs). Descriptive and Kappa statistics were used. Results: Out of 200 isolates studied, 131 were initially screened as ESBL producers and later 114 (57%) were confirmed by phenotypic methods. E-Test was found most sensitive phenotypic test as compared to PCDT and DDST. 13 strains resistant to cefoxitin (30μg) were found to be pure Amp C producers. Combined disk test detected 36 to be ESBL and Amp C co-producers. Surprisingly, six isolates found sensitive to cefoxitin disk were confirmed as Amp C producers by cloxacillin disk inhibition test. Conclusion: 57% ESBLs and 27.5% Amp C producers were isolated from nosocomial pathogens showing significant resistance to 3rd generation cephalosporins. Phenotypic confirmation by E-test, PCDT & DDST were useful for ESBL identification and for detection of Amp C, cloxacillin was found to be an effective inhibitor.