Martínez-Beltrán J, Calderón C, Sierra M P, Alvarez M, Cantón R
Servicio de Microbiología, Hospital Ramón y Cajal, Madrid.
Enferm Infecc Microbiol Clin. 1997 Sep;15 Suppl 1:20-6.
Resistance to imipenem and meropenem, reported sporadically in Enterobacteriaceae and more frequently in Pseudomonas aeruginosa, can be caused, among other mechanisms, by the combination of changes in permeability and hyperproduction of inducible chromosomal beta-lactamases. In this study, the in vitro activity of imipenem and meropenem was analysed by the agar dilution method against cefotaxime, ceftazidime, and aztreonam resistant clinical strains of Enterobacteriaceae (n = 202) and P. aeruginosa (n = 90). This phenotype is consistent with the hyperproduction of group 1 chromosomal beta-lactamases and was previously determined in stably derepressed mutants in the same species, obtained from strains with inducible beta-lactamase expression by selection with cefotaxime and ceftazidime. Likewise, the activity of imipenem and meropenem against the same number of clinical isolates susceptible to cefotaxime, ceftazidime, and aztreonam was evaluated. In general, imipenem and meropenem showed an excellent activity, which was intrinsically greater for meropenem against Enterobacteriaceae and P. aeruginosa organisms. Nevertheless, imipenem and meropenem activity was slightly affected on cefotaxime, ceftazidime, and aztreonam resistant isolates of E. cloacae (MIC90, 1 and 0.2 microgram/ml, respectively), E. aerogenes (1 and 0.2 microgram/ml), C. freundii (1 and 0.1 microgram/ml), M. morganii (1 and 0.5 microgram/ml), and S. marcescens (4 and 0.5 micrograms/ml). On the other hand, the activity of imipenem and meropenem against ceftazidime and aztreonam resistant isolates of P. aeruginosa was more significantly affected, with MIC90 values of 64 and 16 micrograms/ml, respectively.
对亚胺培南和美罗培南的耐药性在肠杆菌科中偶有报道，而在铜绿假单胞菌中更为常见，除其他机制外，可能是由通透性改变和诱导性染色体β-内酰胺酶过度产生共同导致的。在本研究中，采用琼脂稀释法分析了亚胺培南和美罗培南对头孢噻肟、头孢他啶和氨曲南耐药的肠杆菌科临床菌株（n = 202）和铜绿假单胞菌临床菌株（n = 90）的体外活性。这种表型与1类染色体β-内酰胺酶的过度产生一致，先前在同一物种的稳定去阻遏突变体中得到证实，这些突变体是通过用头孢噻肟和头孢他啶进行筛选，从具有诱导性β-内酰胺酶表达的菌株中获得的。同样，评估了亚胺培南和美罗培南对相同数量的对头孢噻肟、头孢他啶和氨曲南敏感的临床分离株的活性。总体而言，亚胺培南和美罗培南表现出优异的活性，美罗培南对肠杆菌科和铜绿假单胞菌的内在活性更高。然而，亚胺培南和美罗培南的活性在阴沟肠杆菌（MIC90分别为1和0.2微克/毫升）、产气肠杆菌（1和0.2微克/毫升）、弗氏柠檬酸杆菌（1和0.1微克/毫升）、摩根摩根菌（1和0.5微克/毫升）和粘质沙雷氏菌（4和0.5微克/毫升）的对头孢噻肟、头孢他啶和氨曲南耐药的分离株中受到轻微影响。另一方面，亚胺培南和美罗培南对铜绿假单胞菌的对头孢他啶和氨曲南耐药的分离株的活性受到更显著的影响，MIC90值分别为64和16微克/毫升。
