Preterm birth is the leading cause of death among children aged under 5 years of age worldwide. Maternal genitourinary tract infections (GUTIs) are among the few modifiable risk factors for spontaneous preterm labor (sPTL), yet the gap between association and effective intervention remains unresolved. This narrative review consolidates recent evidence on GUTIs and sPTL, integrating pathogens, ascending and hematogenous pathways, and prevention. MEDLINE, Embase, the Cochrane Library, and Scopus were searched (January 2000–January 2026); evidence was synthesized narratively and stratified by preterm‐birth subtype where possible. Pooled estimates showed increased odds of preterm birth with urinary tract infection (odds ratio [OR] 1.92, 95% confidence interval [CI] 1.62–2.27), asymptomatic bacteriuria (ASB; OR 1.62, 95% CI 1.30–2.01), bacterial vaginosis (OR 1.79, 95% CI 1.32–2.43), Ureaplasma colonization (OR 2.76, 95% CI 1.63–4.68), Trichomonas vaginalis (relative risk 1.42, 95% CI 1.15–1.75), and Chlamydia trachomatis (OR 1.57, 95% CI 1.11–2.22). A 2026 Swedish register cohort ( n = 684 595) demonstrates that the hazard for preterm birth after urinary tract infection (UTI) diagnosis is highest in the first 6 days and declines with advancing gestation (adjusted hazard ratios 18.5, 13.5, and 6.7 at 22–27, 28–31, and 32–36 weeks). Gene–environment analyses further indicate that preterm birth subtypes differ in susceptibility to UTI versus vaginal infection. Antibiotic treatment of ASB reduces pyelonephritis (RR 0.24), but its effect on preterm birth in unselected populations is uncertain. Ascending infection drives decidual cytokine release and premature myometrial activation; amniotic‐fluid sludge on transvaginal ultrasound is an accessible marker of subclinical intra‐amniotic infection. Targeted screening, evidence‐based antibiotic selection, and antimicrobial stewardship remain the practical priorities.
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Malik et al. (2026) studied this question.
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