Preterm Birth: Associations With Genital and Possibly Oral Microflora

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Abstract
Opportunistic pathogenic microbes are indigenous to the female lower genital tract and etiologic in many types of pelvic infections and, apparently, a portion of preterm birth (PTB) cases. Bacterial vaginosis (BV) is a clinical syndrome based on an altered genital microflora in which Gardnerella vaginalis; anaerobic species primarily among Prevotella, Porphyromonas, Bacteroides, Peptostreptococcus, and Mobiluncus; Mycoplasma hominis; and Ureaplasma urealyticum become predominant in vaginal secretions. This BV complex of microbes, compared to a normal vaginal microflora dominated by facultative lactobacilli, is associated with significantly increased risks for preterm labor, preterm premature rupture of membranes, PTB, and other perinatal infectious complications. Pathogenetic mechanisms include an ascending route of infection and/or inflammatory process due to microbial products and maternal and/or fetal response(s) with production of prostaglandins and cytokines. In the presence of periodontal disease, oral opportunistic pathogens and/or their inflammatory products also may have a role in prematurity via a hematogenous route. Fusobacterium nucleatum, a common oral species, is the most frequently isolated species from amniotic fluid cultures among women with preterm labor and intact membranes. Also, the species and subspecies of fusobacteria identified from amniotic fluid most closely match those reported from healthy and diseased subgingival sites, namely F. nucleatum subspecies vincentii and F. nucleatum subspecies nucleatum, compared to strains identified from the lower genital tract. Although these fusobacteria also could be acquired through cunnilingus from a partner, new data associating maternal periodontal disease with preterm low birth weight taken with the isolation of F. nucleatum, Capnocytophaga, and other oral species from amniotic fluid support further study of a possible additional route, oral‐hematogenous, to PTB. Ann Periodontol 1998;3:222–232.

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