Scholarlink

<p><i>Streptococcus agalactiae</i> (group B <i>Streptococcus</i>, GBS) is an important cause of invasive infections in infants worldwide, despite widespread implementation of intrapartum antibiotic prophylaxis (IAP). This study aimed to clarify the molecular and clinical characteristics of invasive GBS isolates from infants in Guangzhou, China, over the 10-year period 2013-2022. A total of 131 GBS strains were recovered from blood cultures (<i>n</i> = 98) and cerebrospinal fluid cultures (<i>n</i> = 33) of infants aged ≤ 90 days. All isolates were subjected to capsular serotyping, multilocus sequence typing (MLST), virulence gene profiling (including <i>cylE</i>, <i>hylB</i>, Alp family genes, and pilus island genes), and antimicrobial susceptibility testing. Of the 131 GBS isolates, 37 (28.2%) caused early-onset disease (EOD) and 94 (71.8%) caused late-onset disease (LOD). The hypervirulent III/ST17 clone was the predominant lineage (56.5%) and was associated with LOD. Serotype Ia accounted for 15.3% of all isolates and was correlated with respiratory distress in EOD cases. All isolates carried the <i>cylE</i> and <i>hylB</i> toxin genes, with <i>rib</i> being the most prevalent surface protein gene (71.8%). Pilus island <i>PI-2b</i> (67.9%) was the dominant type and was predominantly detected in serotype III/CC17 strains. Resistance rates to clindamycin, erythromycin, and tetracycline exceeded 80%, while all isolates remained susceptible to penicillin and ampicillin. This study confirms that the III/ST17 clone is the predominant lineage associated with GBS LOD and identifies an association between serotype Ia and respiratory distress in GBS EOD. These findings support ongoing molecular surveillance to guide targeted preventive strategies and improve clinical management of invasive infantile GBS disease.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Invasive Streptococcus agalactiae infections in infants in Guangzhou, Southern China (2013–2022): molecular epidemiology and clinical management implications

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月25日

查看全文
  • Xiao-lan Chen,
  • Hua-min Zhong,
  • Yong-qiang Xie,
  • Wen-shan Chen,
  • Li-Jia Wei,
  • Kan-kan Gao,
  • Bing-shao Liang,
  • Su-fei Zhu,
  • Yun-feng Liu,
  • Fei Gao,
  • Yan Long,
  • Lian-fen Huang

摘要

Streptococcus agalactiae (group B Streptococcus, GBS) is an important cause of invasive infections in infants worldwide, despite widespread implementation of intrapartum antibiotic prophylaxis (IAP). This study aimed to clarify the molecular and clinical characteristics of invasive GBS isolates from infants in Guangzhou, China, over the 10-year period 2013-2022. A total of 131 GBS strains were recovered from blood cultures (n = 98) and cerebrospinal fluid cultures (n = 33) of infants aged ≤ 90 days. All isolates were subjected to capsular serotyping, multilocus sequence typing (MLST), virulence gene profiling (including cylE, hylB, Alp family genes, and pilus island genes), and antimicrobial susceptibility testing. Of the 131 GBS isolates, 37 (28.2%) caused early-onset disease (EOD) and 94 (71.8%) caused late-onset disease (LOD). The hypervirulent III/ST17 clone was the predominant lineage (56.5%) and was associated with LOD. Serotype Ia accounted for 15.3% of all isolates and was correlated with respiratory distress in EOD cases. All isolates carried the cylE and hylB toxin genes, with rib being the most prevalent surface protein gene (71.8%). Pilus island PI-2b (67.9%) was the dominant type and was predominantly detected in serotype III/CC17 strains. Resistance rates to clindamycin, erythromycin, and tetracycline exceeded 80%, while all isolates remained susceptible to penicillin and ampicillin. This study confirms that the III/ST17 clone is the predominant lineage associated with GBS LOD and identifies an association between serotype Ia and respiratory distress in GBS EOD. These findings support ongoing molecular surveillance to guide targeted preventive strategies and improve clinical management of invasive infantile GBS disease.