Intrapartum Antibiotics Led to Increase in Resistant, Late-Onset Group B Streptococcal Disease

Group B streptococcus
Group B streptococcus
Researchers assessed the influence of intrapartum antibiotic prophylaxis on the emergence of antimicrobial resistant Group B streptococcal isolates.

Results of a study published in Clinical Infectious Diseases found that an intrapartum antibiotic prophylaxis (IAP) program was associated with an expansion of Group B Streptococcus (GBS) clonal complex (CC) 17 and an increase in late-onset disease (LOD).

Newborns and infants admitted to the Linkou Chang Gung Memorial Hospital in Taiwan between 1998 and 2020 with invasive GBS due to sepsis were included in this study. Isolates of GBS were collected from patients and women who were pregnant. Isolates were sequenced, serotyped, and evaluated for antimicrobial susceptibility.

A total of 238 GBS genomes were evaluated. The genomes ranged in size from 1.9 to 2.2 megabase pairs (Mb). The isolates comprised 7 serotypes (Ia, Ib, II, III, V, VI, and VII) and 6 unique strains (CC1, CC10, CC17, CC19, and CC24). Of note, 2 strains were unable to be classified into any CC.

There were 112 isolates with resistance to clindamycin and 114 isolates with resistance to erythromycin, of which 96.4% and 93.9% also conferred resistance to lincosamide and macrolide, respectively. Fourteen resistance genes were observed in at least 1 of the GBS genomes, the most common of which was the peptide antimicrobial resistant gene mprF found among all 238 GBS isolates. Other resistant genes found among the GBS isolates included tetM in 169, ermB in 126, Sat-4 in 120, tetO in 116, and tet(45) in 32.

The researchers found that CC17 isolates were dominant (66%) among the 164 patients with LOD, defined as GBS onset between days 7 and 89 of life. Of note, CC17 has been expanding over time, with approximately 30% of LOD diagnoses comprising CC17 before 2009 to more than 65% after 2012.

Among a total of 34,304 single nucleotide polymorphisms (SNPs), 1955 were specific to CC17. These CC17-specific SNPs were associated with penicillin-binding proteins (n=7), recombination regulator RecX (n=6), CPBP family intermembrane metalloprotease (n=5), and pneumococcal histidine triad protein (n=4).

In a genetic resistance analysis, more than 70% of CC17 isolates were resistant to tetracycline, aminoglycoside, lincosamide, clindamycin, macrolides, nucleoside, and streptogramin; 45.5% to phenicol; 31.8% to pleuromutilin; and 27.6% to oxazolidinone.

The findings of this study may reflect local patterns of GBS and may not be generalizable to other geographic locations.

“Although the susceptibility of CC17 to antibiotics is not significantly different from other sequence types at present, GBS with phenotypic resistance to antimicrobials may emerge in the future given the environmental selection pressure and the continued accumulation of SNP mutations,” the researchers noted.


Zhou Y, Wang L-Q, Yan Q, et al. Genomic analysis of group B Streptococcus from neonatal sepsis reveals CC17 clonal expansion and insights into virulence- and resistance-associated traits after intrapartum antibiotic prophylaxis. Clin Infect Dis. 2022;ciac331. doi:10.1093/cid/ciac331