In vitro antibacterial activity of the new macrolide azithromycin was tested against 116 strains of Brucella melitensis, isolated from 115 patients in a major tertiary care referral center. Eighty-seven percent of the strains were inhibited by 1.0 mg/l and all the 116 strains by 2.0 mg/l of azithromycin. Comparison was made with tetracycline, gentamicin, trimethoprim-sulfamethoxazole, rifampicin and ciprofloxacin. All the isolates were susceptible to gentamicin, tetracycline, trimethoprim-sulfamethoxazole, rifampicin. One hundred and fifteen of the 115 strains were also susceptible to ciprofloxacin.
The antibacterial activity of the recently developed β-lactamase inhibitor tazobactam with and without piperacillin was studied in recent clinical isolates from patients at a tertiary care center. Although tazobactam by itself had little or no antibacterial activity, the combination with piperacillin was highly effective against piperacillin-resistant Staphylococcus aureus and Enterococci. It was also significantly more inhibitory than piperacillin towards almost all members of Enterobacteriaceae and Pseudomonas aeruginosa tested. The activity was compared with another commercially available combination of penicillin (amoxicillin and β-lactamase inhibitor, clavulanic acid), and other drugs commonly used in clinical practice.
would like to emphasize that piperacillin, a ureidopenicillin, has greater in-vitro activity against Enterococci and other gram-positive bacteria than amino-or carboxy-penicillins. In our paper, we stated that tazobactam has a wide spectrum of affinity that includes classes I, II, IV and V ß-lactamases. The abstract of the paper clearly states that the combination of tazobactam with piperacillin was effective against piperacillin-resistant organisms, including S. aureus and Enterococci. We concur with Dr. Butt that irrespective of the in-vitro activity, the combination could and should only be used against ß-lactamase producers, because tazobactam is nothing but a penicillanic acid sulfone derivative which acts as a ß-lactamase inhibitor and binds to bacterial PBP 1 and PBP 2. We presented the in-vitro activity data which is consistent with other investigators' findings. [1][2][3] We are certain that Dr. Butt knows that many organisms appear susceptible to certain antimicrobials in-vitro without any clinical efficacy. The best examples are the many MRSA which appear susceptible to first-generation cephalosporins, however, microbiologists as well as clinicians know that these drugs are contra-indicative. We feel that Dr. Butt mistook our in-vitro data to mean that we were recommending the use of combination in clinical practice for MRSA, etc. At no point in the article did we say anything about the clinical efficacy of piperacillin/tazobactam against such organisms. Our discussion was centered around the potentiation of piperacillin by the ability of tazobactam to inhibit both plasmid as well as chromosomally mediated ß-lactamases (see paragraphs 1 and 2 of 'Discussion').
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