Chen H Y, Livermore D M
Department of Medical Microbiology, London Hospital Medical College, UK.
J Antimicrob Chemother. 1994 May;33(5):949-58. doi: 10.1093/jac/33.5.949.
The activity of biapenem (L-627, LJC-10627), a new carbapenem, was investigated against Pseudomonas aeruginosa strains, mutants and isolates with known resistance mechanisms to other beta-lactams. The behaviour of biapenem closely resembled that of imipenem, although it showed minor differences compared with meropenem, Inducible (i.e. normal) or derepressed chromosomal beta-lactamase expression gave slight protection against biapenem and imipenem, but insufficient to raise the MICs above clinically significant limits. This behaviour correlated with the slight lability of these compounds to the purified enzyme and with their strong capacity to induce beta-lactamase synthesis. Inducible or derepressed enzyme gave no protection against meropenem, possibly reflecting this compound's particular ability to deactivate the enzyme. Biapenem also has some ability to reversibly deactivate the enzyme. None of several plasmid-mediated beta-lactamases (TEM-2, PSE-1, -3 or -4; OXA-3,-6,-10,-11; NPS-1 or LCR-1) introduced into a P. aeruginosa PU21 recipient strain reduced susceptibility to biapenem or other carbapenems. Amongst permeability mutants, those lacking the D2 'carbapenem-specific' porin had reduced susceptibility to biapenem as well as to imipenem and meropenem. Biapenem and imipenem insusceptibility in these D2 porin-deficient mutants required continued expression of the chromosomal beta-lactamase, although this did not apply to meropenem. P. aeruginosa isolates and mutants with broad-spectrum insusceptibility ('intrinsic resistance') to penicillins, cephalosporins and unrelated drugs remained fully susceptible to biapenem and imipenem, whilst showing slightly reduced susceptibility to meropenem. Overall, these findings suggest that biapenem, like the earlier carbapenems, should prove to be a useful antipseudomonal agent, overcoming the mechanisms that commonly confer resistance to other classes of antipseudomonal beta-lactams.
研究了新型碳青霉烯类药物比阿培南(L-627,LJC-10627)对铜绿假单胞菌菌株、突变体以及对其他β-内酰胺类药物具有已知耐药机制的分离株的抗菌活性。比阿培南的表现与亚胺培南非常相似,不过与美罗培南相比存在细微差异。可诱导(即正常)或去阻遏的染色体β-内酰胺酶表达对比阿培南和亚胺培南有轻微的保护作用,但不足以使最低抑菌浓度(MIC)升高至临床显著水平以上。这种现象与这些化合物对纯化酶的轻微不稳定性及其诱导β-内酰胺酶合成的强大能力相关。可诱导或去阻遏的酶对美罗培南没有保护作用,这可能反映了该化合物使酶失活的特殊能力。比阿培南也有一定能力使该酶可逆性失活。导入铜绿假单胞菌PU21受体菌株的几种质粒介导的β-内酰胺酶(TEM-2、PSE-1、-3或-4;OXA-3、-6、-10、-11;NPS-1或LCR-1)均未降低对比阿培南或其他碳青霉烯类药物的敏感性。在通透性突变体中,那些缺乏D2“碳青霉烯类特异性”孔蛋白的突变体对比阿培南以及亚胺培南和美罗培南的敏感性降低。在这些缺乏D2孔蛋白的突变体中,对比阿培南和亚胺培南不敏感需要染色体β-内酰胺酶持续表达,不过美罗培南不存在这种情况。对青霉素、头孢菌素及无关药物具有广谱不敏感性(“固有耐药性”)的铜绿假单胞菌分离株和突变体对比阿培南和亚胺培南仍完全敏感,而对美罗培南的敏感性略有降低。总体而言,这些发现表明,与早期的碳青霉烯类药物一样,比阿培南应被证明是一种有用的抗铜绿假单胞菌药物,可克服通常导致对其他类抗铜绿假单胞菌β-内酰胺类药物耐药的机制。