The role of infection in the aetiology of spontaneous early preterm labour

Lamont, Ronald Francis (1988) The role of infection in the aetiology of spontaneous early preterm labour. University of Southampton, Doctoral Thesis.

Abstract

Preterm labour is an important cause of perinatal mortality and morbidity. The aetiology of preterm labour is multifactorial and infection is thought to be one of these factors. To date, the evidence implicating infection is based largely upon retrospective and circumstantial evidence. Through a clinical and also a laboratory based study, this thesis was conceived to provide better evidence to support the premise that infection is a cause of preterm labour. In a prospective clinical study, a detailed microbiological investigation (including anaerobes, mycoplasmas, ureaplasmas and chlamydiae) was set up to examine the carriage of microorganisms in the genital tract of women in spontaneous early preterm labour compared to a control group. The range and type of microorganisms was different in study and control groups. Benign commensal organisms were found significantly more often in the control group. Conversely, anaerobes, mycoplasmas and ureaplasmas were found significantly more often in the study group. Carriage of pathogenic organisms, such as Chlamydia trachomatis, Neisseria gonorrhoeae and Group G β-haemolytic streptococcus were unique to the study group. Chorioamnionitis was also found to be present significantly more often in the study group. Having provided clinical evidence to support an association between infection and preterm labour, an in-vitro model was set up in an attempt to provide evidence to support a causal relationship. Amnion cells in tissue culture were exposed to the products of a wide range of organisms commonly associated with preterm labour. In response to these bacterial products, amnion cells were induced to produce prostaglandin E_2. This is in keeping with the theory that bacteria, through their ability to produce the enzyme phospholipase A_2, may invade the fetal membranes and cause the release of arachidonic acid from phospholipid pools. This results in an increased synthesis of prostaglandins, which may result in an increase in contractions of the uterine corpus together with a reduction of cervical resistance, leading to progressive labour and delivery. The implications of these findings may affect the management of preterm labour, but more likely may improve the better prediction and prevention of preterm labour. (DX86896)

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