Inflammation and infection

The role of inflammation and infection in PTB has been recog­nized for many decades. Infection is frequently associated with PTL in both humans and animal models. In pregnant mammals, systemic administration of a microbial load can induce labour (17).

The amniotic fluid cavity is a sterile environment, therefore posi­tive cultures of amniotic fluid are considered pathological. The re­ported rates of positive culture of amniotic fluid detected in women presenting in PTL with intact membranes is 13%, higher than rates of non-l abouring preterm patients and term labourers. In women with PPROM, this rises to 32%, and again to 75% by the time these women subsequently labour, demonstrating colonization of mi­crobes both before and during the latent period (19). A third mech­anism of infection unrelated to the cervix is haematological spread through the placenta causing microbial invasion of the amniotic cavity (19). This route of infection is supported by the fact that extrauterine infection such as asymptomatic bacteriuria and pyelo­nephritis (20), periodontal infection (21), and malaria (22) are all associated with an increased risk of PTB.

Changes in cervical ripening during labour have been associ­ated with increased production of inflammatory cytokines such as interleukin (IL)-1, IL-6, IL-8, tumour necrosis factor, and prosta­glandins (23). Influx of inflammatory cells into the cervix release matrix metalloproteins, contributing to collagen breakdown, and ultimately a softening or ripening of the cervix.