Congenital Malaria

Risk and Pathogenesis

Congenital malaria is thought to be a rare occurrence, with a historically reported incidence of 0.3% in immune mothers and up to 7.4% of nonimmune mothers (7). More recent studies have shown incidence rates of 7-17% when testing infant blood after delivery (8,9). Studies utilizing cord blood as a marker for neonatal malaria transmission are of limited significance as it has been shown that cord blood parasitemia does not correlate with development of congenital malaria (10,11). It is thought that transmission of malaria from mother to infant occurs at the time of delivery via breakdown of maternofetal placental blood barriers during parturition (12,13).

Because the exact timing of neonatal infection is clinically difficult to determine, congenital malaria in this review refers to all malaria that is felt to be acquired vertically either in utero or peripartum from the mother and not from the bite of an infected mosquito. In general, the fetus in utero appears to be relatively resistant to Plasmodium infection. Factors preventing infection are thought to include the high percentage of fetal hemoglobin and low oxygen tension in fetal circulation and the function of the placenta as a barrier and filter for the parasites (12,14). However, little research has been performed to investigate the clinical and molecular aspects of congenital malaria.

Pregnant women are more susceptible to malaria than nonpregnant individuals. It is thought that the immune suppression associated with pregnancy contributes to malarial disease severity (15). Primigravidas demonstrate fever and heavy parasitemias, particularly during the first trimester, even when previously immune (15,16). A prospective study of 60 primigravid women in Nigeria showed that malaria parasitemia incidence and density of infection was higher in pregnant women compared to the same women before pregnancy and to a control group of similar age (17). Malaria during pregnancy contributes to maternal anemia and low birth weight in neonates (12,18,19). Stillbirth, spontaneous abortion, and severe maternal disease may also occur with maternal infection in areas of low endemicity (15,16).

Clearly, the placenta plays a major role in preventing congenital malaria. It is well documented that the placenta may harbor a high parasite load even in the absence of maternal peripheral parasitemia (7,20,21). It is thought that the placenta may preferentially sequester parasitized erythrocytes via preferential cytoadherence mediated by Plasmodium-encoded surface antigens (22). However, despite this high local parasite load, numerous studies of placentas and infants demonstrated a low rate of transmission to the infant from infected placentas (10,23-25). The mechanism of this protection is not well understood (12).

Clinical Presentation: Mothers and Infants

Most studies of congenital malaria in endemic areas are limited by the lack of medical resources in those areas of the world. However, reports from the US Centers for Disease Control and Prevention in the 1990s documented the clinical presentation and course of 24 infants born in the United States who clearly contracted congenital ma laria from maternal transmission (2,26-34). In these cases, infants generally presented with fever 3-8 weeks after delivery, although some who developed symptoms in the first week of life were not diagnosed until later. Two infants were born prematurely. It is not clear whether maternal malaria precipitated the preterm delivery, although both mothers had positive blood smears at delivery. Most infants also presented with symptoms of poor feeding, irritability, or lethargy. Anemia and thrombocytopenia were reported in several cases, although other infants reportedly had normal laboratory parameters. The diagnosis was made in all infants by thick and thin blood smears. P. vivax malaria was reported for 18 infants (75%), P. falciparum malaria was found in 4 infants (17%), and P. malariae was detected in 2 infants (8%). Most infants were treated with chloroquine. Other treatment regimens included chloroquine with primaquine (4 cases), quinine or intravenous quinidine (2 cases), and mefloquine (1 case). All infants recovered and no deaths were reported. No infant was treated immediately after delivery, even when the mother was found to be parasitemic during delivery. Interestingly, 1 infant diagnosed with congenital malaria had an asymptomatic, unaffected twin who never required antimalarial treatment.

Mothers of these infants with congenital malaria all originally lived in malaria-endemic areas. Most had immigrated to the United States either shortly before or during pregnancy. However, 3 mothers had left the malarious region 2-8 years prior to the pregnancy and had no subsequent malaria exposure. Some mothers reported receiving treatment abroad for malaria during pregnancy, but the type and duration of treatment were not documented. Some mothers took chloroquine for prophylaxis or treatment of malaria during pregnancy. At the time of delivery, most mothers were asymptomatic. Two mothers had symptoms (fever, anemia, thrombocytopenia) at the time of delivery but only received treatment for malaria peri- and postpartum. Neither of those infants received malaria treatment after delivery. At the time of their infants' diagnosis, mothers' smears were reported as negative in 9 cases, positive in 8 cases, and unreported in 7 cases. Additional testing of some mothers revealed positive serologies against the Plasmodium species infecting the infant as well as positive serologies against other species not found in the infant. One mother whose smears were negative underwent blood PCR testing, which was also negative.

Findings from this small case series generally reflect findings noted in other case series reviews and individual case reports of congenital malaria occurring in nonendemic countries (13,35-40). In nonendemic countries, the diagnosis of congenital malaria is rarely made at the time of delivery but is suspected when clinical symptoms arise several weeks after delivery. It is likely that in malaria-endemic countries, infants presenting with congenital malaria in the first few weeks of life cannot be distinguished from those with postnatally acquired malaria. Therefore, it is quite difficult to determine a true incidence of congenital malaria transmission in endemic areas, and as a consequence it most likely is underreported.

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