# Evolving antimicrobial resistance patterns in group B streptococci: A five-year study in a high-risk pregnancy referral center in northeastern Brazil

**Authors:** Jorhanna Isabelle Araújo de Brito Gomes, Suellen Bernardo de Queiroz, Carlos Gabriel Andrade Barbosa, Larissa Rodrigues Santos Silva, Patrícia Urquiza Lundgren, Eduardo Sergio Soares Sousa, Eloiza Helena Campana, Vinicius Pietta Perez

PMC · DOI: 10.1590/0037-8682-0259-2025 · Revista da Sociedade Brasileira de Medicina Tropical · 2026-03-06

## TL;DR

This study tracks changing antibiotic resistance in group B streptococci among pregnant women in Brazil over five years.

## Contribution

The study provides a five-year analysis of GBS colonization and resistance patterns in a high-risk pregnancy center in Brazil.

## Key findings

- GBS colonization rate was 12% among pregnant women tested.
- Resistance to tetracycline was highest at 82.3%, with tet(M) being the most common resistance gene.
- Erythromycin resistance increased over time, potentially affecting clindamycin efficacy.

## Abstract

Streptococcus agalactiae (commonly referred to as group B
streptococci [GBS]) is a leading cause of neonatal infection. Surveillance
of colonization in pregnant women and the use of intrapartum antibiotic
prophylaxis (IAP) are the primary strategies for preventing early-onset GBS
disease. The increasing rate of antibiotic resistance among GBS isolates is
a concern for the effectiveness of IAP. Our study aimed to evaluate the
prevalence of GBS colonization and characterize antimicrobial resistance
patterns over a five-year period in a high-risk pregnancy referral center in
Northeastern Brazil.

This study was conducted from 2020 to 2024 and included pregnant women at
35-37-week gestation. GBS isolates from anal-vaginal swabs were identified
and tested for susceptibility to penicillin or ampicillin, clindamycin,
erythromycin, levofloxacin, and tetracycline. Isolates stored from 2021 to
2024 were further analyzed for the resistance genes mef(A),
erm(A/TR), erm(B), tet(M), and tet(O).

Of 1469 anal-vaginal samples, the overall GBS colonization rate was 12%. All
isolates were susceptible to either penicillin or ampicillin. The respective
resistance rates for erythromycin, clindamycin, levofloxacin, and
tetracycline were 23.6%, 9.3%, 5.4%, and 82.3%. The main determinant among
macrolide-resistant isolates was mef(A), and
tet(M) was the most frequent tetracycline resistance
gene. Furthermore, we found that erythromycin resistance increased
consistently over the five years, signaling a potential impact on
clindamycin efficacy due to erm genes.

Beta-lactams (penicillin and ampicillin) remained effective for IAP in
northeastern Brazil during the study period. However, high and increasing
resistance to other antibiotic classes reinforces the need for maternal GBS
surveillance and ongoing antimicrobial resistance monitoring.

## Linked entities

- **Genes:** mef(A) (macrolide efflux MFS transporter Mef(A)) [NCBI Gene 45217682], erm(B) (23S rRNA (adenine(2058)-N(6))-methyltransferase Erm(B)) [NCBI Gene 8154416], tet(M) (tetracycline resistance ribosomal protection protein Tet(M)) [NCBI Gene 8154447], tet(O) (tetracycline resistance ribosomal protection protein Tet(O)) [NCBI Gene 8154417]
- **Chemicals:** penicillin (PubChem CID 2349), ampicillin (PubChem CID 6249), clindamycin (PubChem CID 446598), erythromycin (PubChem CID 12560), levofloxacin (PubChem CID 149096), tetracycline (PubChem CID 54675776)
- **Species:** Streptococcus agalactiae (taxon 1311)

## Full-text entities

- **Diseases:** GBS (MESH:D020275), neonatal infection (MESH:D007239)
- **Chemicals:** erythromycin (MESH:D004917), levofloxacin (MESH:D064704), clindamycin (MESH:D002981), macrolide (MESH:D018942), penicillin (MESH:D010406), tetracycline (MESH:D013752), Beta-lactams (MESH:D047090), ampicillin (MESH:D000667)
- **Species:** Homo sapiens (human, species) [taxon 9606], Streptococcus agalactiae (species) [taxon 1311]

## Full text

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## Figures

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## References

18 references — full list in the complete paper: https://tomesphere.com/paper/PMC12971026/full.md

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Source: https://tomesphere.com/paper/PMC12971026