Klebsiella and enterobacter: antibiotic resistance and treatment implications.

Klebsiella and enterobacter: antibiotic resistance and treatment implications.
复制标题

DOI:
10.1053/srin.2002.34693
复制
发表时间:
2002-09-01
期刊:
Seminars in respiratory infections
影响因子:
--
通讯作者:
Cercenado, Emilia
Cercenado, Emilia
中科院分区:
其他
文献类型:
--
作者:
Bouza, Emilio;Cercenado, Emilia

文献摘要

被引文献

相似文献

克雷伯氏菌属:和肠杆菌属(Enterobacter spp.)广泛分布于环境中,也由人类携带。这两个属都是公认的社区和医院病原体,并引起重大感染。它们是呼吸道和非呼吸道感染的常见原因。克雷伯菌属占所有社区获得性肺炎病例的1%至5%,占医院获得性肺炎病例的0%至23%,其在酒精中毒患者中的发生率更高。大多数病例为单侧右上叶后段。肺脓肿可发生在肺炎过程后或继发于克雷伯菌属。感染率高,发病率和死亡率高。K.肺炎是导致脓胸的最常见微生物之一。克雷伯菌属和肠杆菌属(Enterobacter spp.)医院获得性肺炎主要发生在机械通气早期,分别居第四位和第三位。克雷伯菌属对青霉素具有内在耐药性,并且由于质粒介导的超广谱β-内酰胺酶(ESBLs)的产生,可以获得对第三代和第四代头孢菌素的耐药性。这些质粒经常携带氨基糖苷类修饰酶。肠杆菌属由于产生组成型AmpC β-内酰胺酶,对氨苄西林、阿莫西林、阿莫西林-克拉维酸、第一代头孢菌素和头孢西丁具有内在耐药性。这种酶的去阻遏在临床分离株中越来越频繁,并赋予对第三代头孢菌素、脲基青霉素和羧基青霉素的耐药性;第四代头孢菌素保留了对抑制菌株的合理活性。克雷伯氏菌属的大多数分离株。和肠杆菌属。对氟喹诺酮类、磺胺甲恶唑、氨基糖苷类和碳青霉烯类敏感。在某些情况下,由这些微生物引起的严重感染的治疗可能受益于β-内酰胺类(或氟喹诺酮类)与氨基糖苷类的组合。由于在治疗期间产生耐药性的风险很高,因此在治疗期间应仔细观察所有严重感染。
KLEBSIELLA: spp. and Enterobacter spp. are widespread throughout the environment and also carried by humans. Both genera are well-recognized community and nosocomial pathogens and cause significant infections. They are a common cause of respiratory and nonrespiratory infections. Klebsiella spp. is responsible for 1% to 5% of all cases of community-acquired pneumonia and between 0% to 23% of those acquired in the hospital, and its frequency is greater in alcoholic patients. The majority of cases are unilateral in the posterior segment of the right upper lobe. Lung abscess can occur after a pneumonic process or secondarily to Klebsiella spp. infections and have high rates of morbidity and mortality. K. pneumoniae is one of the most common microorganisms responsible for empyema. Klebsiella spp. and Enterobacter spp. rank fourth and third, respectively, as causes of hospital-acquired pneumonia mainly in patients during the early period of mechanical ventilation. Klebsiella spp. are intrinsically resistant to penicillins and can acquire resistance to third- and fourth-generation cephalosporins owing to the production of plasmid-mediated extended-spectrum beta-lactamases (ESBLs). These plasmids frequently carry aminoglycoside-modifying enzymes. Enterobacter spp. are intrinsically resistant to ampicillin, amoxicillin, amoxicillin-clavulanate, first-generation cephalosporins, and cefoxitin owing to the production of constitutive AmpC beta-lactamase. The derepression of this enzyme is increasingly frequent among clinical isolates and confers resistance to third-generation cephalosporins, and ureido- and carboxypenicillins; fourth-generation cephalosporins retain reasonable activity against depressed strains. Most isolates of Klebsiella spp. and Enterobacter spp. are susceptible to fluoroquinolones, trimethoprimsulfamethoxazole, aminoglycosides, and carbapenems. In some instances, treatment of severe infections caused by these microorganisms may benefit from the combination of beta-lactams (or fluoroquinolones) with aminoglycosides. Because of the high risk for developing resistance during treatment, all severe infections should be carefully watched during therapy.