B组链球菌（group B Streptococcus， GBS）是引起全球新生儿感染的主要病原菌，而孕妇消化道和泌尿生殖道GBS定植是新生儿感染的主要危险因素。全球总体孕妇GBS定植率为18%，其中南亚和东亚地区分别为12.5%和11.0%，中国为11.3%。对于孕妇GBS定植，若不加以干预，50%会垂直传播给胎儿或新生儿，是导致新生儿早发型GBS病的重要原因，可造成新生儿败血症和新生儿脑膜炎等。2015年的一项全球性研究提示，GBS感染引起的新生儿侵袭性疾病导致9万例婴儿死亡，350万例早产，5.7万例死产。目前，一些国家采用了产时抗生素预防（intrapartum antibiotic prophylaxis， IAP），以预防在分娩期间GBS由母亲向新生儿的传播。在IAP中，大环内酯类药物红霉素和林可酰胺类药物克林霉素等作为二线抗生素在抗GBS感染中发挥重要作用。然而，红霉素和克林霉素等抗生素的耐药率居高不下，全球耐药率分别约为25%和27%；中国的耐药率更高，分别约为75%和60%。GBS对以上两类抗生素的耐药机制，主要包括目标修饰、外排泵、核糖体保护ABC-F蛋白和药物灭活，其耐药机制呈现日益多样化，且多与可移动元件有关，加速了其耐药基因的播散。临床迫切需要临床及科研工作者共同努力，严格执行抗菌药物科学化管理、积极研发新型抗菌药物等，以阻止该耐药基因的传播。

Group B Streptococcus (GBS) is a major pathogen causing neonatal infection worldwide, and the colonization of GBS in the digestive and urogenital tracts of pregnant women is the main risk factor for neonatal infection. The global overall maternal GBS colonization rate is 18%, with 12.5% in South Asia, 11% in East Asia, and 11.3% in China. Without intervention, 50% of maternal GBS will be vertically transmitted to the fetus or neonate, which is a major cause of early-onset GBS disease in neonates and can lead to neonatal sepsis and neonatal meningitis. A study in 2015 indicated that neonatal invasive diseases caused by GBS infection globally resulted in 90 000 infant deaths, 3.5 million preterm births, and 57 000 stillbirths. Currently, some countries have adopted intrapartum antibiotic prophylaxis (IAP) to prevent the transmission of GBS from mother to neonate during delivery. In IAP, macrolide antibiotics such as erythromycin and lincosamide antibiotics such as clindamycin serve as second-line antibiotics and play an important role in anti-GBS infection. However, the resistance rates to antibiotics such as erythromycin and clindamycin remain high, with global resistance rates of approximately 25% and 27%, respectively. The resistance rates in China are even higher, at about 75% and 60%, respectively. The resistance mechanisms of GBS to the above two classes of antibiotics mainly include target modification, efflux pumps, ribosome protection by ABC-F proteins, and drug inactivation. These resistance mechanisms are increasingly diverse and mostly associated with mobile elements, accelerating the dissemination of resistance genes. There is an urgent need for clinicians and researchers to work together, strictly implement scientific management of antimicrobial drugs, and actively develop new antimicrobial agents, thereby preventing the spread of resistance genes.