Abstract
Plasmodium falciparum infection during pregnancy leads to adverse outcomes including low birthweight; however, contemporary estimates of the potential burden of malaria in pregnancy in Africa (in the absence of interventions) are poor. We aimed to estimate the need to protect pregnant women from malaria across Africa. Using a mathematical model applied to estimates of the geographical distribution of P falciparum across Africa in 2010, we estimated the number of pregnant women who would have been exposed to infection that year in the absence of pregnancy-specific intervention. We then used estimates of the parity-dependent acquisition of immunity to placental infection and associated risk of low birthweight to estimate the number of women who would have been affected. We estimate that, without pregnancy-specific protection, 12·4 million pregnant women (44·9% of all 27·6 million livebirths in malaria endemic areas in Africa in 2010) would have been exposed to infection, with 11·4 million having placental infection (41·2% of all livebirths). This infection leads to an estimated 900,000 (95% credible interval [CrI] 530,000-1,240,000) low birthweight deliveries per year. Around the end of the first trimester, when the placenta becomes susceptible to infection, is a key period during which we estimate that 65·2% (95% CrI 60·9-70·0) of placental infections first occur. Our calculations are the only contemporary estimates of the geographical distribution of placental infection and associated low birthweight. The risk of placental infection across Africa in unprotected women is high. Prevention of malaria before conception or very early in pregnancy is predicted to greatly reduce incidence of low birthweight, especially in primigravidae. The underlying lifetime risk of low birthweight changes slowly with decreasing transmission, drawing attention to the need to maintain protection as transmission falls. Malaria in Pregnancy Consortium and the Bill & Melinda Gates Foundation.
Highlights
Plasmodium falciparum malaria infection during pregnancy leads to infected erythrocytes sequestering within the placenta.[1]
Incorporation of low birthweight (LBW) into model To estimate the incremental risk of LBW posed by the different placental infection categories, we extended the model to obtain a relation between parity-specific and histology-specific placental infection categories and the risk of LBW in the absence of competing LBW hazards, Angola Benin Botswana Burkina Faso Burundi Cameroon CAR Chad CÔte d’Ivoire Djibouti DRC Equatorial Guinea Eritrea Ethiopia Gabon The Gambia Ghana Guinea Guinea-Bissau Kenya Liberia Madagascar Malawi Mali Mauritania Mozambique Namibia Niger Nigeria Republic of Congo Rwanda Senegal Sierra Leone Somalia South Africa Sudan Swaziland Tanzania Togo Uganda Zambia Zimbabwe
Primigravidae were at the highest risk of placental infection, with an estimated 2∙7 million (48∙2%) of 5∙6 million first pregnancies infected, risk of infection during pregnancy was high in multigravidae, with 8∙7 million (39∙5%) of 22·0 million pregnancies infected
Summary
Plasmodium falciparum malaria infection during pregnancy leads to infected erythrocytes sequestering within the placenta.[1]. A 2010 analysis[4] used estimates of the global distribution of P falciparum transmission[5] to calculate that 31∙3 million pregnancies and 22∙8 million livebirths occur in areas of stable transmission in Africa This analysis provided a useful indication of the potential scope of the population at risk, it did not include estimates of the actual risk of malaria infection in pregnancy and the various heterogeneities in the likelihood and consequences of infection in pregnant women across Africa. Nor did this calculation of risk indicate the fact that, especially in areas of high transmission, women with high parity have much lower risk of the adverse consequence of malaria infection than do those with low parity, because of immunity acquired from infection during previous pregnancies. These estimates relied on infection measured by parasites in the placenta at delivery; they do not adequately take into account the effect of infections early in pregnancy, which are a strong risk factor for LBW.[9,10] These early infections are best captured with placental histology,[11] which enables identification of both active
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