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Genital mycoplasmas (which contains well-known and representative species such as Ureaplasma urealyticum, Mycoplasma hominis and Mycoplasma genitalium) are a group of small microorganisms usually found in sexually active women and men. They lack a cell wall and have the propensity to adhere to mucosal surfaces, and sometimes even the ability to enter the cells (as is the case with Mycoplasma genitalium).
One of the characteristics of this group of microorganisms is that they can be found as commensal flora in the female genital tract. Nonetheless, more and more published research shows that genital mycoplasmas are not merely innocuous bystanders in disease development, but often underestimated instigators of adverse pregnancy-related outcomes.
Inflammatory reactions that arise in the genital tissues of the pregnant women are a common pathway that results in labor and delivery – not only in instances of prematurely initiated labor, but also in spontaneous, term labors as well. Still, physicians should watch for certain microbial stimuli that may precipitate inflammatory responses in the gravid uterus, as these could launch the cascade of events that results in an unanticipated delivery.
Such inflammation-inducing events may have exogenous (specific sexually-transmitted pathogens) or endogenous (modified ecology of the customarily present bacterial flora) sources. The “escape” of such normal flora to anatomical sites close to the fetus, as well as the specific genetic profile of pregnant women, may allow altered responses to such microbial challenges. Consequently, inflammation of the cervix, fetal membranes, amniotic fluid, cord or the placenta may ensue.
The role of genital mycoplasmas in this type of inflammation during pregnancy was confirmed by detecting specific anti-mycoplasma antibodies in women developing intra-amniotic infection or presenting with postpartum fevers. Highly characteristic molecular motifs (also known as pathogen-associated molecular patterns or PAMPs) are present in genital mycoplasmas, which could explain how they manage to elicit the inflammatory response that leads to labor.
Furthermore, cervical tissue and trophoblast tissue respond to common constituents of mycoplasma – most notably the lipopeptide segment of the cell membrane. This may result in cytokine release, which is a part of a complex network of reactions that includes both pro-inflammatory and anti-inflammatory factors.
The preponderance of scientific reports implicates Ureaplasma urealyticum and Mycoplasma hominis in prematurity-associated conditions, with Ureaplasma being the most common genital mycoplasma isolated from amniotic fluid and infected placentas. One recent study found a strong link between acute chorioamnionitis and microbial invasion with Ureaplasma urealyticum.
In one study that included 225 women with premature rupture of fetal membranes, 68% of them were colonized by Ureaplasma urealyticum (compared to 17% of controls) and 28% of them were colonized by Mycoplasma hominis (compared to 15% of controls). Likewise, in another cohort of women, Ureaplasma urealyticum was present in 96% of those with premature membrane rupture, compared to only 32% of those without such incident.
Mycoplasma hominis has been isolated from blood in approximately 13% of women with postpartum and postabortion fever, and was found to be an independent risk factor for preterm delivery after 24 weeks of gestation. However, Ureaplasma urealyticum seems to be more frequently encountered and to be the more virulent among genital mycoplasmas with respect to their effect on pregnancy).
The role of Mycoplasma genitalium in adverse pregnancy outcomes is still ill-defined. Several studies have pointed to a conclusion that this species is independently associated with preterm birth, albeit no other syndromes have been correlated to the presence of this mycoplasma.
Despite the possibility that women colonized with genital mycoplasmas may vertically transmit them to their progeny, their mere presence in neonatal surface cultures does not automatically represent the evidence of pathogenicity. Nevertheless, the colonization rates appear to be higher in preterm infants than in full-term infants.