Editor's Choice

With the introduction of penicillin in the 1940s, the near-eradication of malaria soon after and the extinction of smallpox by vaccination, the scourge of infection appeared nearly beaten. However, celebration was probably premature. Malaria reappeared in a more resistant form as dichlorodiphenyltrichloroethane (DDT) was phased out and failed to keep its initial promise. The rise of human immunodeficiency virus (HIV) infection and, more recently, the severe acute respiratory syndrome (SARS) virus have reminded doctors of the importance of infection. This month, we publish several articles about the central role of infection in areas of obstetrics that continue to defy full scientific elucidation: fetal brain injury, pre-eclampsia and preterm labour. While the association between intrauterine infection and white matter injury in the fetus is clear, it is not known whether infection itself causes the damage or just potentiates other factors, such as hypoxia. Peebles et al. (pages 735–743) investigated the part played by antenatal cerebral ischaemia in the pathogenesis of periventricular leucomalacia and cerebral palsy associated with fetal infection. They chronically instrumented nine fetal sheep and measured changes in fetal heart rate, mean arterial pressure and carotid blood flow after administration of endotoxin as Escherichia coli lipopolysaccharide. Three lambs died within 12 hours, but in the survivors, there was an increase in the fetal heart rate, decrease in mean arterial pressure and an increase in carotid blood flow. Histology revealed periventricular leucomalacia in three of the six brains studied. It appears that hypoperfusion is not the primary factor in brain injury after exposure to bacterial infection. The exquisite sensitivity of the antenatal brain to the products of bacterial infection themselves maybe more important. Von Dadelszen et al. from Vancouver (pages 725–730) are not the first to wonder if early onset pre-eclampsia may be a different condition from late onset disease. The latter might be an evolutionary adaptation, offering survival advantages to the fetus with minimally increased maternal risks, but the same can hardly be said for early onset disease. The development of pre-eclampsia predicts later cardiovascular morbidity and mortality through atherosclerosis, and the initiation of atherosclerosis may be, in part, due to chronic infection. These authors postulated a link between chronic infection with cytomegalovirus (CMV) and noted an increase in seroprevalence to Chl. pneumoniae in pregnancies complicated by pre-eclampsia. They studied stored sera from four groups of women: those with early onset pre-eclampsia, late onset pre-eclampsia, normotensive IUGR and matched controls. Anti-CMV and anti-Chl. pneumoniae antibodies were higher in the early onset pre-eclampsia group. Although the hypothesis remains tentative, pre-eclampsia may yet justify its old appellation of ‘toxaemia of pregnancy’! The case report from Waghorn and Robson (pages 780–781) reminds us that, even in the developed world, we are not immune from the effects of zoonoses. A vet developed pyrexia 10 days before the onset of preterm labour at 34 weeks of gestation. Delivery was effected with forceps because of maternal pyrexia and the neonate remained healthy. However, Pasturella multocida, a mouth and gastrointestinal tract commensal of domestic cats and dogs, was isolated from a high vaginal swab and blood cultures. The authors postulate a blood-bourne infection with a source of entry from the vet's hands. Childbirth is the sort of activity that attracts a multiplicity of visions from interest groups about the values to be placed on such things as mode of delivery, care in labour or place of birth. Readers may wonder why practising obstetricians should worry about economic evaluation of childbirth interventions. We are, after all, encouraged to place the woman at the centre of decision-making and allow her values to predominate, not the economics of healthcare provision. Nevertheless, the article from Tracy and Tracy (pages 717–724) adds important cost information. Taken in combination with the evidence base surrounding successful vaginal birth, it debunks the myth that continuous one-to-one midwifery support in labour is expensive. Indeed, it seems that the cascade of interventions from medicalised childbirth leads to high use of epidural anaesthesia and steep increases in costs. Conversely, one-to-one support achieves lower use of epidural and lower rates of operative delivery. Those of us involved in management as clinical directors can now argue that more midwives are a cheap alternative to costly, high intervention medicalised birth. This article will, at least contribute to the ‘facts’ rather than the ‘unfacts’ that surround the debate on the mode of delivery (see the letter from Danielian and Nikolaou on page 784). The costs and capacity of the NHS may be decisive factors in the decision about mode of delivery, given the evidence comparing vaginal delivery with elective caesarean section, which shows small differences with respect to perinatal and maternal morbidity. How ironic if finally the tide of fashion is turned by economics, instead of clinical considerations, or the priorities of women themselves!

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