Genomic identification and characterization of Streptococcus oralis group that causes intraamniotic infection
1
Issued Date
2025-01-01
Resource Type
ISSN
09349723
eISSN
14354373
Scopus ID
2-s2.0-105017454483
Journal Title
European Journal of Clinical Microbiology and Infectious Diseases
Rights Holder(s)
SCOPUS
Bibliographic Citation
European Journal of Clinical Microbiology and Infectious Diseases (2025)
Suggested Citation
Pongchaikul P., Warintaksa P., Wongsurawat T., Jenjaroenpun P., Kruasuwan W., Mongkolsuk P., Vivithanaporn P., Thaipisuttikul I., Singhsnaeh A., Khamphakul J., Hadradchai S., Bhuwapathanapun M., Chaemsaithong P. Genomic identification and characterization of Streptococcus oralis group that causes intraamniotic infection. European Journal of Clinical Microbiology and Infectious Diseases (2025). doi:10.1007/s10096-025-05283-6 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/112458
Title
Genomic identification and characterization of Streptococcus oralis group that causes intraamniotic infection
Corresponding Author(s)
Other Contributor(s)
Abstract
Background: Intraamniotic infection is a cause of spontaneous preterm labor. Streptococcus mitis is a common pathogen identified in intraamniotic infection, with the possible route of hematogenous dissemination from the oral cavity or migration from the vaginal canal. However, there are a few reports on Streptococcus oralis, a member of the S. mitis group, as a cause of pathogen in intraamniotic infection. We reported herein whole genome sequencing and comparative genomic analysis of S. oralis strain RAOG5826 that causes intraamniotic infection. Results: Streptococcus mitis was initially identified from amniotic fluid, vaginal swab, and fetal blood of a patient presenting with preterm prelabor rupture of membranes with intraamniotic infection by the use of conventional microbiological methods (biochemical phenotype, MALDI-ToF, 16 S rRNA). Subsequently, this strain was later identified as S. oralis RAOG5826 by whole-genome hybrid sequencing. Genes involved in macrolide and tetracycline resistance, namely ermB and tet(M), and mutations in penicillin-binding protein were present in the genome. Moreover, potential virulence genes were predicted and compared with other Streptococcal species. Conclusion: We reported a comprehensive genomic analysis of S. oralis, which causes intraamniotic infection. S. mitis was initially identified by conventional microbiological identification. However, whole-genome hybrid sequencing demonstrates S. oralis with complete profiles of antimicrobial resistance genes and potential virulence factors. This study highlights the limitations of traditional techniques and underscores the importance of genomic sequencing for accurate diagnosis and tailored antimicrobial treatment. The study also suggests that S. oralis may be an underestimated pathogen in intraamniotic infection.