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Malaria acquired during pregnancy is one of the major causes of maternal morbidity that may lead to poor maternal and birth outcomes in tropical areas endemic for this disease.1–5 The clinical manifestations of malaria in pregnancy depend on the levels of transmission in a particular population with different levels of immunity.1,6,7 Although some women may be semi-immune to malaria, pregnancy may render them at risk of complications of malaria because they may lose much of that previous immunity during pregnancy.5,8 Severe anemia predominates as the main feature of severe malaria in areas with high levels of transmission, while hypoglycemia, respiratory failure, and cerebral malaria may predominate in areas with low levels of malaria transmission.1,5 Malaria during pregnancy is associated with maternal anemia and low birth weight.1–5,9–12 In some areas, infection with Plasmodium falciparum may be associated with up to 35% of preventable low birth weight deliveries.7 Furthermore, pregnancy outcomes such as stillbirths, miscarriages, and preterm births are common in pregnant women with malaria, particularly P. falciparum malaria.1,9,10,12
Plasmodium vivax malaria is prevalent in many areas of Asia and South America.13 It is more common than P. falciparum malaria in northeastern Venezuela.14 Despite its high prevalence and a possible association with important complications,12,15–18 research into its effects has lagged disproportionately compared with research on the impact of P. falciparum malaria,19–21 especially its impact during pregnancy where the effects of the other malaria species have not been well characterized.10 Some recent studies have reported that P. vivax malaria is associated with mild maternal anemia and significantly decreased birthweight,5,10,11,22 but miscarriage, stillbirth, or preterm delivery has been infrequently reported in those with P. vivax infections.10,11,22 We report the clinical features and pregnancy outcomes in 12 cases of P. vivax infection in pregnant women complicated in some by either miscarriages or premature deliveries. Furthermore, some of them developed significant degrees of anemia and thrombocytopenia during the malaria episode.
A prospective observational study was conducted at the Hospital Santos Anibal Dominicci in Sucre in northeastern Venezuela from January 1, 2000 to December 30, 2002 to evaluate the clinical features and outcomes of pregnant women infected with P. vivax. The study was reviewed and approved by the ad hoc committee of the Coordination of Environmental Health and Sanitary Surveillance of the General Direction of Environmental Health and Sanitary Control of the Ministry of Health of Venezuela. Most patients with symptomatic P. vivax infection during pregnancy are seen at their local clinics and treated as outpatients following national treatment guidelines (chloroquine, 25 mg/kg given as 10, 10, and 5 mg/kg over a three-day period, followed by 5 mg/kg per week during the rest of the pregnancy). Those patients who require hospital admission on the basis of individual clinical decisions are then referred to the Hospital Santos Anibal Dominicci for further evaluation and treatment. During the study period, 12 pregnant women with P. vivax malaria were seen at this institution. Plasmodium vivax was identified by thick and thin blood smears with external quality (5% of total number of pregnant women admitted during 2002).
Underlying medical conditions and other obstetric co-morbidities were ruled out by detailed clinical evaluation, routine laboratory analysis (complete blood counts with differential counts, liver function tests, blood chemistries, coagulation times, blood cultures, urinalyses, urine cultures, and viral serologies), and obstetric ultrasonography. There were 6 (50%) primigravidae and 6 (50%) multigravidae and the mean age was 27 years. The mean gestational age at presentation to the institution was 29 weeks. Clinical characteristics of patients are shown in Table 1
. The mean hemoglobin level on admission was 8.8 g/dL; all patients developed anemia (< 12.0 g/dL) (one with severe anemia, hemoglobin < 7.0 g/dL). The mean platelet count on admission was 131,333 cells/mm3. Among these patients, 9 (75%) of 12 developed thrombocytopenia (< 150,000 cells/mm3) and among these women, 3 (33%) of 9 had severe thrombocytopenia (< 60,000 cells/mm3). Severe thrombocytopenia and bleeding were treated with platelet transfusions in 3 (25%) of 12 patients. Miscarriage was observed in two patients (no. 1 and 7, Table 1). Preterm delivery occurred in three patients (No. 3, 5, and 11, table 1). Normal birth weight newborns were delivered by the other seven patients (No. 2, 4, 6, 8, 9, 10, and 12, Table 1). The number of registered miscarriages in the hospital due to other medical reasons during the study period was 3 (1 in 2000, 1 in 2001, and 1 in 2002). The number of preterm deliveries during this same period was 16 (7 in 2000, 6 in 2001, and 3 in 2002). After antimalarial treatment with chloroquine (25 mg/kg given as 10, 10, and 5 mg/kg over a three-day period, followed by 5 mg/kg per week during the rest of the pregnancy), intravenous quinine (10 mg/kg in only one case of oral intolerance), and supportive care, all patients were successfully discharged. No maternal deaths or additional complications were seen in these women.
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To our knowledge, this is the first report of pregnant women in Latin America infected with P. vivax whose outcome was either miscarriage or preterm delivery. Although many pathologic aspects of P. vivax infection in pregnancy are still not understood, this parasite may be able to sequester for a long time in the placenta,4,5,24 and this could be the pathogenic mechanism underlying these complications during pregnancy. Any infectious process may lead to adverse maternal and perinatal outcomes, particularly, shortened duration of pregnancy. Therefore, the perinatal outcomes seen in our study may be due to either the parasitic infection or to systemic effects of the infection such as fever and other cytokine-mediated processes.3,5
The mechanisms of resistance or susceptibility to infection and malaria pathogenesis in pregnant women may differ according to Plasmodium species.1,4,5 Since P. vivax has a predilection for reticulocytes compared with P. falciparum, pregnant women who receive iron and folate supplementation, which is important for treating other pregnancy-related hematologic abnormalities, may put pregnant women at greater risk of developing P. vivax malaria.25 Our findings suggest that chemoprophylaxis against P. vivax infection in pregnancy may be justified in populations where P. vivax is endemic.10
We were unable to determine levels of parasitemia in the pregnant women and associate these levels with clinical outcomes. However, despite the limitations of our study, we believe that P. vivax malaria may negatively impact maternal and perinatal outcomes. Most of the studies evaluating the effect of P. vivax have been conducted in low transmission areas of Asia. Moreover, P. vivax is increasingly recognized as a cause of significant morbidity in pregnant women, and there is little information on the clinical, epidemiologic, and molecular aspects of this infection during pregnancy.1,10 Our study highlights the need to further evaluate and define at both molecular and clinical levels the impact of P. vivax infection in pregnancy, particularly in areas, such as Latin America, where P. vivax is the predominant Plasmodium species. To achieve this goal, we are currently conducting a larger cohort study to further characterize the epidemiologic, clinical, and molecular interactions of P. vivax malaria in pregnancy.
Received September 29, 2005. Accepted for publication November 29, 2005.
Acknowledgments: This work was previously presented in part at XIV National Infectious Diseases Meeting, Puerto La Cruz, Venezuela, November 2003 (abstract 57).
Disclosure: None of the authors have any conflicts of interest.
* Address correspondence to Carlos Franco-Paredes, Division of Infectious Diseases, Emory University, 69 Jesse Hill Jr. Drive, Atlanta, GA 30303. E-mail: cfranco{at}sph.emory.edu 
Authors’ addresses: Alfonso J. Rodriguez-Morales, Instituto Experimental José Witremundo Torrealba, Universidad de Los Andes, Trujillo, Venezuela. Elia Sanchez, Miguel Vargas, Carmelina Piccolo, Rosa Colina, and Melissa Arria, Infectious Diseases Service, Hospital Santos Anibal Dominicci, Carúpano, Sucre, Venezuela. Carlos Franco-Paredes, Division of Infectious Diseases, Emory University, 69 Jess Hill Jr. Drive, Atlanta, GA 30303, and Hospital Infantil de Mexico, Federico Gómez, Mexico City, Mexico, Telephone: 404-616-3600, Fax: 404-880-9305, E-mail: cfranco{at}sph.emory.edu.
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