Abstract:

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.

Key words: Group B Streptococcus, Erythromycin, Clindamycin, Resistance mechanisms