The role of Gram-positive and drug-resistant bacteria in bacterial infections in cirrhosis

A. Alexopoulou, I. Mani, L. Vasilieva
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Abstract

© Digestive Medicine Research. All rights reserved. Dig Med Res 2021;4:26 | http://dx.doi.org/10.21037/dmr-21-35 Bacterial infections are a frequent complication of cirrhosis, with a 5-fold higher incidence than that reported in the general population (1,2). Infections in cirrhosis are lifethreatening as they increased mortality fourfold; Shortterm mortality is 30% at one month and about 60% at 12 months (2). Despite advances in the understanding of the pathogenetic mechanisms and management, bacterial infections are associated with the development of complications leading to hospitalization of cirrhotic patients in common wards or in intensive care units (ICUs) (2). Types of bacterial infections in cirrhosis are spontaneous bacterial peritonitis (SBP), pneumonia, urinary tract infections, skin or soft tissue infections and spontaneous or secondary bacteremia (1,3). SBP and spontaneous bacteremia are characteristic for patients with decompensated liver cirrhosis and are originated from the intestinal tract (endogenous infections) (3). The pathogenetic process leading to the development of SBP or spontaneous bacteremia is the traverse of viable microorganisms from the intestinal tract through the gut wall to the mesenteric lymph nodes, passing to the systemic circulation (development of spontaneous bacteremia) and entrance to the peritoneal fluid through the l iver (development of SBP). This mechanism was first depicted in 1979 and was named bacterial translocation (4). The components that enhance bacterial translocation in cirrhosis are disturbed bacterial overgrowth, increased gut permeability and impaired gut-associatedlymphatic tissue (5). Gram-negative usually Enterobacteriaceae SBP are the most prevalent bacteria causing SBP (6). Since 1990, a change in epidemiology of type of bacteria associated with infections in cirrhosis was reported. Initially, quinolone-resistant bacteria were observed due to wide use of this family of antibiotics for SBP prophylaxis (7). This phenomenon was followed by a growing rate of infections with Gram-positive bacteria (cocci) (8-10). In a Spanish study of 405 patients with cirrhosis, Grampositive bacteria were isolated in 53% patients overall and in 59% of nosocomial infections (1). Infections by Gram-positive bacteria were associated with hospital environment and interventional techniques such as ligation of esophageal varices, insertion of central catheters and chemoembolization (1,9). The emergence of vancomycinresistant enterococci (VRE) strains was firstly observed in US hospitals and Liver Centers and was attributed to the avoparcin enrichment of the animal food and the transmission to humans through food chain (11). It was reported that VRE distribution varied globally from less than 1% in Finland, France, Iceland and Sweden to 40–50% in Latin America or Ireland and >70% in USA (11). Recently, Piano et al. in a worldwide multicenter study including 1,302 patients with cirrhosis and bacterial or fungal infections found that the global prevalence of Gram-positive bacteria was 38% and differed in geographical areas, being higher in Europe (43%) and lower in Asia (28%) (12). The most important shift in epidemiology is the growing incidence of bacterial infections induced by multi-drug-resistant organisms (MDRO). The MDRO are classified as multidrug-resistant (MDR), extensivelydrug-resistant (XDR) or pandrug-resistant (13). Even though extended-spectrum-b-lactamase-producing Editorial
革兰氏阳性和耐药细菌在肝硬化细菌性感染中的作用
©消化医学研究。保留所有权利。Dig Med Res 2021;4:26|http://dx.doi.org/10.21037/dmr-21-35细菌感染是肝硬化的常见并发症,其发病率是普通人群的5倍(1,2)。肝硬化感染会使死亡率增加四倍,从而危及生命;短期死亡率在一个月时为30%,在12个月时约为60%(2)。尽管对发病机制和管理的理解有所进步,但细菌感染与并发症的发展有关,导致肝硬化患者在普通病房或重症监护室住院(2)。肝硬化的细菌感染类型包括自发性细菌性腹膜炎(SBP)、肺炎、尿路感染、皮肤或软组织感染以及自发性或继发性菌血症(1,3)。SBP和自发性菌血症是失代偿性肝硬化患者的特征,起源于肠道(内源性感染)(3)。导致SBP或自发性菌血症发展的致病过程是有活力的微生物从肠道穿过肠壁到达肠系膜淋巴结,进入系统循环(自发性菌血症的发展),并通过肝脏进入腹膜液(SBP的发展)。这种机制于1979年首次被描述,并被命名为细菌易位(4)。肝硬化中增强细菌移位的成分是细菌过度生长紊乱、肠道通透性增加和肠道相关淋巴组织受损(5)。革兰氏阴性通常是肠杆菌科SBP是引起SBP最常见的细菌(6)。自1990年以来,有报道称肝硬化感染相关细菌类型的流行病学发生了变化。最初,由于广泛使用该类抗生素预防SBP,观察到了喹诺酮类耐药细菌(7)。这种现象之后,革兰氏阳性菌(球菌)的感染率不断上升(8-10)。在西班牙一项针对405名肝硬化患者的研究中,53%的患者和59%的医院感染患者分离出革兰氏阳性菌(1)。革兰氏阳性菌感染与医院环境和介入技术有关,如食管静脉曲张结扎、插入中心导管和化疗栓塞(1,9)。耐万古霉素肠球菌(VRE)菌株的出现首次在美国医院和肝脏中心观察到,并归因于动物食物中的avoparcin富集和通过食物链传播给人类(11)。据报道,VRE在全球的分布各不相同,从芬兰、法国、冰岛和瑞典的不到1%,到拉丁美洲或爱尔兰的40-50%,再到美国的>70%(11)。最近,Piano等人在一项包括1302名肝硬化和细菌或真菌感染患者的全球多中心研究中发现,全球革兰氏阳性菌的患病率为38%,并且在地理区域有所不同,欧洲较高(43%),亚洲较低(28%)(12)。流行病学中最重要的转变是耐多药生物(MDRO)引起的细菌感染的发病率不断上升。MDRO分为多药耐药(MDR)、广泛耐药(XDR)或泛药耐药(13)。即使是扩展谱b-内酰胺酶生产社论
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