Clinical overview
Infection in pregnancy is core FCOG(SA) business because, in South Africa, sexually transmitted infections and their downstream complications sit at the intersection of two of the country's largest maternal and perinatal burdens: a generalised HIV epidemic and a high background prevalence of treatable STIs. The triennial Saving Mothers reports (NCCEMD) consistently place non-pregnancy-related infections — overwhelmingly HIV/AIDS and its complications — among the leading causes of maternal death, while syphilis and untreated STIs drive stillbirth, preterm birth, low birthweight and neonatal sepsis. Many of these losses are avoidable with a cheap, well-rehearsed package: screen early, treat the woman and her partner, retest, and protect the baby at delivery.
The objective focuses you on three threads that recur in every antenatal clinic: syphilis (a screenable, curable cause of devastating but preventable congenital disease), Group B Streptococcus (GBS) (a commensal that becomes the most important cause of early-onset neonatal sepsis), and the broader basket of STIs — chlamydia, gonorrhoea, trichomoniasis, bacterial vaginosis, herpes and the syndromic presentations of vaginal discharge and genital ulcer disease. Throughout, HIV is the silent co-traveller: it amplifies STI transmission and complications, and STIs amplify HIV transmission. The SA approach is syndromic management at primary care, layered on universal antenatal screening for syphilis, HIV and (increasingly) other infections, all anchored in the National Integrated Maternal and Perinatal Care Guideline (NDoH, 2024). Read this chapter alongside HIV in pregnancy, Antenatal booking and Preterm birth and pprom.
Core knowledge
Syphilis
Syphilis is caused by the spirochaete Treponema pallidum. It is transmitted sexually and transplacentally at any gestation and in any stage of maternal disease, with vertical transmission risk highest in early (primary, secondary, early latent) infection where spirochaetaemia is greatest. Untreated maternal syphilis classically causes a spectrum: miscarriage, stillbirth, hydrops, preterm birth, fetal growth restriction, neonatal death, and the stigmata of congenital syphilis (rhinitis/"snuffles", hepatosplenomegaly, rash, periostitis, and late features such as Hutchinson teeth and interstitial keratitis). Stillbirth and perinatal death are the dominant SA burden.
Staging matters because it determines treatment duration:
- Primary — painless chancre at inoculation site.
- Secondary — disseminated: maculopapular rash (including palms/soles), condylomata lata, mucous patches, lymphadenopathy.
- Early latent — asymptomatic, infection acquired within the preceding ~12 months.
- Late latent / latent of unknown duration — asymptomatic, beyond ~12 months or unknown.
- Tertiary — gummatous, cardiovascular, neurosyphilis (uncommon in pregnant women).
Serology underpins diagnosis. Treponemal tests (TPHA/TPPA, treponemal EIA, and rapid point-of-care treponemal tests) confirm exposure but stay positive for life. Non-treponemal tests (RPR, VDRL) are quantitative, correlate with disease activity, and are used to monitor treatment response — a fourfold (two-dilution) drop in titre signals adequate response. SA antenatal services increasingly use on-site rapid syphilis tests (often dual HIV/syphilis devices) so that a positive result is actioned the same day rather than lost to follow-up.
Group B Streptococcus
Streptococcus agalactiae (Lancefield group B) colonises the gastrointestinal and genital tract of a substantial minority of women asymptomatically. It is the leading cause of early-onset neonatal sepsis (EONS) — sepsis, pneumonia or meningitis in the first week of life (most within 24–48 hours), acquired by vertical transmission during labour and delivery. Late-onset disease (after the first week) is less clearly prevented by intrapartum measures.
The protective strategy is intrapartum antibiotic prophylaxis (IAP) to the mother, which suppresses transmission during passage through the colonised tract; antenatal treatment of colonisation does not prevent EONS because recolonisation occurs. Two strategies exist internationally: universal antenatal culture-based screening (a recto-vaginal swab at around 35–37 weeks, as favoured in some high-income settings) versus a risk-factor-based approach. RCOG Green-top Guideline 36 sets out the UK position and the recognised risk factors. South African public-sector practice, constrained by laboratory capacity, has historically leaned on a risk-factor approach rather than universal culture; you must follow the current local protocol and the NDoH Maternity Guideline (NDoH, 2024). Key recognised risk factors include: previous infant with invasive GBS disease, GBS bacteriuria in the current pregnancy, intrapartum pyrexia, prematurity (<37 weeks), and prolonged rupture of membranes.