Umbilical cord-blood infections with Plasmodium falciparum malaria are acquired antenatally in Kenya.

BACKGROUND: It is unknown whether the presence of Plasmodium falciparum malaria parasites in umbilical cord blood denotes infection acquired antenatally or contamination with infected maternal blood at delivery.
METHODS: Parasites were quantified by real-time quantitative polymerase chain reaction (RTQ-PCR) and were genotyped in paired maternal- and cord-blood samples obtained from 632 pregnant Kenyan women and their newborns. Placental alkaline phosphatase (PLAP) and polyclonal immunoglobulin E levels were also quantified in paired maternal- and cord-blood samples, as markers of admixture of maternal blood with cord blood.
RESULTS: Sixty-six cord-blood samples (10.4%) contained falciparum malaria, as detected by RTQ-PCR. For 25 of the infected cord-blood samples, either absence of infection was noted in paired maternal-blood samples at delivery (n=16) or amplicon levels in cord-blood samples were 10-fold higher than those in maternal-blood samples (n=9). Of the paired maternal- and cord-blood samples that were both infected, 57% showed discordant malaria parasite strains. There was no correlation between maternal parasitemia and levels of PLAP and immunoglobulin E in cord blood. PLAP levels, however, were significantly higher in cord-blood samples obtained from newborns of primigravid or secundigravid women with placental malaria, compared with cord-blood samples obtained from newborns of women without placental malaria or multigravid women. These findings indicate that parity and placental malaria are risk factors for maternofetal transfusion.
CONCLUSIONS: Malaria parasites identified in cord blood are acquired antenatally by transplacental transmission of infected erythrocytes. Primigravid and secundigravid women with placental malaria are at increased risk for congenital infection.