I thank Dr Terry for his informative article [BCMJ 2021;63:383-387 [10]]. Of the many causes of preterm birth, finding an infectious agent gives hope that treatment might prevent recurrence. However, most bacteria identified during autopsies are commonly found in the lower female genital tract. Their culture from fetal surfaces, lung, and stomach may represent colonization during transit through the maternal vagina rather than pathogenicity. The most common bacteria cultured was Group B Streptococcus, a commensal found in the lower genital tract of 20% of women. The second was E. coli, which is ubiquitous. Although occasionally pathogenic, sometimes aggressively so, we cannot eradicate either from a woman’s gut and vaginal flora for the duration of a future pregnancy. How helpful are these culture results? Do they explain the index preterm birth? Can they help prevent a future one?

Why do commensal organisms sometimes become pathogenic? The relationship between bacteria, fetal membranes, and the intra-amniotic cavity is dynamic and poorly understood, as is the maternal immune response to those organisms.[1] Amniocentesis during preterm labor frequently detects inflammatory cytokines without a positive culture, meaning invasion of the amniotic cavity is not required to cause inflammation and preterm birth. Of all the commensal organisms suspected to play an etiological role in infectious/inflammatory preterm birth and bacterial vaginosis, Ureaplasma and Mycoplasma species are perhaps the most amenable to treatment.[2] Identifying them during a preterm loss may help direct care: screening and treatment for bacterial vaginosis early in a future pregnancy and eradication of Ureaplasma and/or Mycoplasma in a woman and her partner before or early in a future pregnancy.

Treatment of atypical bacteria to decrease preterm birth has not been adequately studied.[3] Treatment of bacterial vaginosis with clindamycin appears to have better preventive effect than metronidazole, perhaps because clindamycin also covers Ureaplasma and Mycoplasma, whereas metronidazole does not.[2,4] We have not typically performed fetal cultures for Ureaplasma and Mycoplasma, and they require Universal Transport Medium for identification. Can Dr Terry comment on whether Ureaplasma and Mycoplasma cultures were done in any of the included autopsies? Might he suggest a suitable fetal site if a clinician were to test for them?
—Andrew Kotaska, MD, FRCSC
Obstetrician and Gynecologist, Stanton Territorial Hospital
Assistant Professor, Department of Obstetrics and Gynecology, University of Manitoba
Adjunct Professor, School of Population and Public Health, University of BC
Adjunct Professor, Department of Obstetrics and Gynecology, University of Toronto
Yellowknife, NT

This letter was submitted in response to “The value of ancillary testing in amniotic fluid infection/inflammation-related early pregnancy loss and perinatal death in British Columbia.” [10]

Read the author’s response in “Re: The value of ancillary testing in amniotic fluid infection/inflammation-related early pregnancy loss and perinatal death in British Columbia. Author replies.” [11]

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This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License [12].

References

1.    Combs CA, Gravett M, Garite TJ, et al. Amniotic fluid infection, inflammation, and colonization in preterm labor with intact membranes. Am J Obstet Gynecol 2014;210:125.e1-125.e15.

2.    Morency A-M, Bujold E. The effect of second-trimester antibiotic therapy on the rate of preterm birth. J Obstet Gynaecol Can 2007;29:35-44.

3.    Kotaska A, Paulette L. Genital mycoplasma and preterm birth: A difficult puzzle to solve. BJOG 2022. doi: 10.1111/1471-0528.17069.

4.    Donders G, Van Calsteren K, Bellen G, et al. Predictive value for preterm birth of abnormal vaginal flora, bacterial vaginosis, and aerobic vaginitis during the first trimester of pregnancy. BJOG 2009;116:1315-1324.