The controversial debate around the placental microbiome

For years now it has been thought that the placenta, the organ that nourishes a developing foetus through the umbilical cord,[1] was home to a small community of bacteria – a placental microbiome. Evidence from a study published in Science Translational Medicine[2] in 2014 found that the placenta is home to a bacterial community similar to the one found in the mouth. Prior to this, some thought the placenta was sterile (as are babies in the womb).

 

Research recent has reignited the debate around the extent of the placental microbiome. The study sought to understand whether pre-eclampsia or pre-term births were associated with the bacteria composite of the human placenta.

 

Interestingly, the study found no evidence to support the existence of a placental microbiome in the majority of placental samples across pregnancies with and without complications. The study concludes that the major source of bacterial DNA in the sample studied is linked to acquisition during labour or contamination from laboratory reagents and equipment[3].

 

The exception to this is the presence of Steptococcus agalactiae  – in general, a non-symptomatic colonizer found in the gastro-intestinal or maternal genitalia[4]. For the minority of placental samples that did show the presence of bacterial DNA, S. agalactiae was present in the placenta of approximately 5% of women before the onset of labour[5].

 While this bacteria may not come from the placenta, a child’s skin microbiome begins to develop from birth, and as such, can be affected by the mode of delivery at birth in the long term. You can read more about this on our blog ‘How birth affects your microbiome‘. 

placental microbiome

 

[1] Science – Placenta Harbors Bacteria, May Impact Fetal Health

[2] Aagaard, K. et al. Science Transl. Med. 6, 237ra65 (2014).

[3] [5] Nature – Human placenta has no microbiome but can contain potential pathogens

[4] US National Library of Medicine National Institutes of Health -Understanding the regulation of Group B Streptococcal virulence factors

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