Neu H C
Curr Clin Top Infect Dis. 1987;8:37-61.
Alteration of PBPs has proved an effective way for gram-positive bacteria to become resistant to beta-lactams. The gram-positive species have not been able to use decreased permeability or synthesis of novel beta-lactamases to overcome the advances by medicinal chemists. Nonetheless, altered PBPs have proved to be a formidable form of resistance for staphylococci, enterococci, and even some S. pneumoniae. Although isolated examples of resistance of gram-negative species to beta-lactams have been seen for E. coli, Serratia, or P. aeruginosa, in general this form of resistance has not been used by the gram-negative species except by N. gonorrhoeae. Conversely gram-negative bacteria have used beta-lactamases as an effective weapon to overcome the advances in medical chemistry that have provided beta-lactamase inhibitors and structurally stable cephalosporins, monobactams, and carbapenems. Derepression or induction of beta-lactamases has provided species such as E. cloacae and P. aeruginosa the ability to resist destruction by new cephalosporins. The original concept of beta-lactamase as a trap or sponge has been shown to be inaccurate, and we realize that the high concentration of beta-lactamase in the periplasmic space combined with a decreased or slow entry of the beta-lactam allows an efficient acylation of the so-called stable cephalosporins with hydrolysis of these compounds. Although the PBPs and beta-lactamases are clear problems, there is the potential for future modification of beta-lactam structures to increase affinity to PBPs and decrease beta-lactamase affinity. Bacterial populations do have the ability to create transferable resistance even to extended spectrum beta-lactams. It will be necessary to carefully monitor the development of resistance to new beta-lactams. However, advances in the chemistry of beta-lactams should offer solutions to these real but potentially controllable problems.
青霉素结合蛋白(PBPs)的改变已被证明是革兰氏阳性菌对β-内酰胺类药物产生耐药性的有效途径。革兰氏阳性菌无法通过降低通透性或合成新型β-内酰胺酶来克服药物化学家取得的进展。尽管如此,改变后的PBPs已被证明是葡萄球菌、肠球菌甚至一些肺炎链球菌的一种强大耐药形式。虽然大肠杆菌、沙雷氏菌或铜绿假单胞菌等革兰氏阴性菌对β-内酰胺类药物的耐药性有个别例子,但一般来说,除淋病奈瑟菌外,革兰氏阴性菌并未采用这种耐药形式。相反,革兰氏阴性菌利用β-内酰胺酶作为有效武器,来克服医学化学领域提供β-内酰胺酶抑制剂以及结构稳定的头孢菌素、单环β-内酰胺类和碳青霉烯类药物所取得的进展。β-内酰胺酶的去阻遏或诱导使阴沟肠杆菌和铜绿假单胞菌等菌种有能力抵抗新型头孢菌素的破坏。β-内酰胺酶作为陷阱或海绵的原始概念已被证明是不准确的,我们认识到周质空间中高浓度的β-内酰胺酶与β-内酰胺进入减少或缓慢相结合,使得所谓的稳定头孢菌素能够高效酰化并水解这些化合物。虽然PBPs和β-内酰胺酶是明显的问题,但未来有可能对β-内酰胺结构进行修饰,以增加对PBPs的亲和力并降低对β-内酰胺酶的亲和力。细菌群体确实有能力产生甚至对超广谱β-内酰胺类药物的可转移耐药性。有必要仔细监测对新型β-内酰胺类药物耐药性的发展。然而,β-内酰胺类药物化学的进展应该能够为这些实际但潜在可控的问题提供解决方案。