Could an infectious trigger explain the differential maternal response to the shared placental pathology of preeclampsia and normotensive intrauterine growth restriction?

Preeclampsia/eclampsia remains an important cause of maternal and perinatal morbidity and mortality. Its origins lie in a mismatch between fetoplacental demands and the ability of the uteroplacental arteries to supply those demands, a situation that also arises in normotensive intrauterine growth restriction (the fetal syndrome of preeclampsia in isolation). Why is there this differential response to the same underlying pathology? This review summarises the evidence surrounding a potential trigger for the differential response, namely infection. This builds on the inflammatory model of preeclampsia for which there is increasing support. The evidence for an infectious trigger is principally indirect, linking the similarities between acute atherosis in preeclampsia and atherosclerosis, the increased likelihood of developing cardiovascular disease later in life following a preeclampsia pregnancy, and the association between chronic infection and atherogenesis. Also reviewed is the human and animal model evidence for an infectious trigger for preeclampsia. Perhaps preeclampsia truly is the 'toxemia' of pregnancy.