ABSTRACT
Pregnant women are at increased risk of malaria, but in Angola, epidemiologic data from this group is almost inexistent. We conducted a cross-sectional study to determine the prevalence and risk factors of Plasmodium falciparum infections in 567 pregnant Angolan women living in Luanda province. One in five women had P. falciparum at delivery, diagnosed by PCR assay. Age, residence and history of malaria during pregnancy were significantly associated with P. falciparum infection, but gravidity and use of anti-malarial drugs were not. Placental infections were significantly more common in women ≤18 years old and in primigravidae, but we could not correlate placental infections with poor pregnancy outcomes. These findings are relevant to malaria control policies in Luanda, Angola.
Subject(s)
Antimalarials/therapeutic use , Malaria, Falciparum/epidemiology , Parasitemia/diagnosis , Plasmodium falciparum/isolation & purification , Pregnancy Complications, Parasitic/epidemiology , Adolescent , Adult , Age Factors , Angola/epidemiology , Cross-Sectional Studies , Educational Status , Female , Fetal Blood/parasitology , Gravidity , Humans , Malaria, Falciparum/diagnosis , Odds Ratio , Parasitemia/parasitology , Parity , Placenta/parasitology , Plasmodium falciparum/genetics , Pregnancy , Pregnancy Complications, Parasitic/diagnosis , Pregnancy Outcome/epidemiology , Prevalence , Risk FactorsABSTRACT
Our understanding about the role of the maternal genetic factors on placental malaria is scarce. The general aim of this work was to examine whether common polymorphisms of genes involved in chondroitin sulphate A (CSA) synthesis influence susceptibility to and manifestation of malaria during pregnancy. To achieve this, 96 women with placental malaria and 180 healthy controls without malaria from the province of Luanda, Angola, were genotyped using six microsatellite loci. No associations were found between polymorphisms of genes involved in CSA synthesis and placental malaria. All these findings suggest that there is no genetic susceptibility or increased risk attributed to polymorphisms of the enzymes involved on the synthesis of CSA.
