{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T00:23:56Z","timestamp":1777767836342,"version":"3.51.4"},"reference-count":0,"publisher":"S. Karger AG","license":[{"start":{"date-parts":[[2009,9,11]],"date-time":"2009-09-11T00:00:00Z","timestamp":1252627200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/karger.com\/pages\/terms-and-conditions"},{"start":{"date-parts":[[2009,9,11]],"date-time":"2009-09-11T00:00:00Z","timestamp":1252627200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/karger.com\/pages\/terms-and-conditions"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Chemotherapy"],"abstract":"<jats:p>Nineteen representative isolates of gentamicin- and methicillin-resistant Staphylococcus aureus (MRSA) were found to comprise three phenotypes; these differed with regard to hydrolysis of nitrocefin and production of staphylococcal enterotoxin A or\/and toxic shock syndrome toxin-1. All MRSA isolates produced a capsule and were susceptible to coumermycin, nitrofurantoin, novobiocin, trimethoprim, trimethoprim-sulfamethoxazole, teicoplanin and vancomycin. All MRSA isolates were resistant to co-amoxiclav, ciprofloxacin, clarithromycin, gentamicin, methicillin, norfloxacin, ofloxacin, oxacillin and polymyxin B. The isolates of the three putative phenotypes differed in susceptibility to ampicillin and sulbactam, ce-famandole, chloramphenicol, clindamycin, josamycin and piperacillin\/tazobactam. Isolates of phenotype I varied in susceptibility to amikacin, fusidic acid, imipenem, meropenem and netilmicin. Isolates of phenotype II were inhibited, but not killed by doxycycline. Some isolates of phenotype II were resistant to mupirocin. Some recent isolates of phenotype I and the two isolates of phenotype III were resistant to rifampin. Pulsed-field gel electrophoresis of SmaI-restricted genomic DNA of the MRSA isolates revealed phenotype I to consist of three subpopulations, designated la, lb and Ic. The isolates comprising phenotypes II and III proved identical, respectively. Time-kill experiments with fresh defibrinated human blood\/broth, using either 1 or 2 \u00b5g\/ml of teicoplanin and vancomycin, respectively, combined with 1 \u00b5g\/ml of fusidic acid, 1 \u00b5g\/ml of netilmicin, 1 \u00b5g\/ml of rifampin, 8 \u00b5g\/ml of nitrofurantoin, 8\/8 \u00b5g\/ml of ampicillin and sulbactam, 8\/4 \u00b5g\/ml of co-amoxiclav, 16\/2 \u00b5g\/ml of piperacillin\/tazobactam and 1\/19 \u00b5g\/ml of co-trimoxazole, respectively, yielded the following results. Human blood (65% v\/v) from 4 donors failed to destroy bacterial inocula(1-2 \u00d7 104 CFU\/ml, time 0). With few exceptions, the antimicrobial drugs were more active in Mueller-Hinton broth (MHB) than in the presence of blood. Overall, on a weight-for-weight basis, vancomycin was more active than teicoplanin in the presence of human blood, but not invariably so. Indifferent effects were obtained with teicoplanin\/vancomycin combined with co-trimoxazole, fusidic acid, netilmicin and rifampin, respectively, against isolates comprising phenotypes II and III. Nitrofurantoin was bactericidal in MHB, but not in the presence of blood. Nitrofurantoin plus teicoplanin yielded an additive effect against 4 of 6 tested MRSA isolates in the presence of blood. Piperacillin\/tazobac-tam plus teicoplanin resulted in an additive effect against 5 of 6 MRSA isolates examined in the presence of human blood; however, replacement of teicoplanin by vancomycin resulted in an additive effect against only 1 of the same 6 MRSA isolates tested although vancomycin alone killed 4 of the 6 isolates. Ampicillin plus sulbactam or co-amoxiclav combined with teicoplanin yielded an additive effect against 2 MRSA isolates of phenotype II which failed to hydrolyze nitrocefin.<\/jats:p>","DOI":"10.1159\/000239419","type":"journal-article","created":{"date-parts":[[2009,9,11]],"date-time":"2009-09-11T09:12:33Z","timestamp":1252660353000},"page":"21-36","source":"Crossref","is-referenced-by-count":4,"title":["Gentamicin- and Methicillin-Resistant Staphylococcus aureus: Phenotypic and Genotypic Characterization of Three Putative Nosocomial Outbreak Strains"],"prefix":"10.1159","author":[{"given":"Walter H.","family":"Traub","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Birgit","family":"Leonhard","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dierk","family":"Bauer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"127","published-online":{"date-parts":[[2009,9,11]]},"container-title":["Chemotherapy"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/239419","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/karger.com\/article-pdf\/doi\/10.1159\/000239419","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T15:45:48Z","timestamp":1777477548000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000239419"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2009,9,11]]},"references-count":0,"URL":"https:\/\/doi.org\/10.1159\/000239419","archive":["Portico"],"relation":{},"ISSN":["0009-3157","1421-9794"],"issn-type":[{"value":"0009-3157","type":"print"},{"value":"1421-9794","type":"electronic"}],"subject":[],"published":{"date-parts":[[2009,9,11]]}}}