Bouza Emilio, Cercenado Emilia
Servicio de Microbiología Clínica and Enfermedades Infecciosas, Hospital General Universitario "Gregorio Marañón," Universidad Complutense de Madrid, Madrid, Spain.
Semin Respir Infect. 2002 Sep;17(3):215-30. doi: 10.1053/srin.2002.34693.
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.
克雷伯菌属和肠杆菌属在环境中广泛存在，也寄生于人体。这两个菌属都是公认的社区和医院病原体，可引起严重感染。它们是呼吸道和非呼吸道感染的常见病因。克雷伯菌属导致1%至5%的社区获得性肺炎病例，在医院获得性肺炎病例中占0%至23%，在酒精性患者中其发生率更高。大多数病例位于右上叶后段，为单侧病变。肺脓肿可在肺炎病程后发生，或继发于克雷伯菌属感染，发病率和死亡率较高。肺炎克雷伯菌是导致脓胸的最常见微生物之一。克雷伯菌属和肠杆菌属分别是医院获得性肺炎的第四和第三大病因，主要发生在机械通气早期的患者中。克雷伯菌属对青霉素天然耐药，由于产生质粒介导的超广谱β-内酰胺酶（ESBLs），可获得对第三代和第四代头孢菌素的耐药性。这些质粒通常携带氨基糖苷类修饰酶。肠杆菌属由于产生组成型AmpCβ-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天然耐药。该酶的去阻遏在临床分离株中越来越常见，可导致对第三代头孢菌素、脲基青霉素和羧基青霉素耐药；第四代头孢菌素对去阻遏菌株仍保持合理活性。大多数克雷伯菌属和肠杆菌属分离株对氟喹诺酮类、甲氧苄啶-磺胺甲恶唑、氨基糖苷类和碳青霉烯类敏感。在某些情况下，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）与氨基糖苷类的联合使用。由于治疗期间出现耐药的风险很高，治疗期间应密切观察所有严重感染。
