Currently, the most convincing evidence for a possible interaction between HIV-1 and malaria comes from studies of pregnant women. HIV-1 infected pregnant women in Malawi showed a higher prevalence and density of P. falciparum parasitemia than their non-HIV-1 infected counterparts (Steketee et al., 1996). This finding has been confirmed in other studies of pregnant African women (Ladner et al., 2002; van Eijk et al., 2003). Pregnant HIV-infected women also are more likely to be anemic (van den Broek et al., 1998; Meda et al., 1999; van Eijk et al., 2001) and to respond less well to intermittent preventive treatment with sulfadoxine-pyrimethamine than HIV uninfected women (Parise et al., 1998). Postnatal mortality in infants also is increased in mothers co-infected with HIV-1 and malaria than infants of mothers with only one infection (Bloland et al., 1995).

An important question still unanswered is whether or not placental malaria increases mother-to-child HIV transmission. In a recent study of 746 HIV-positive mother-infant pairs in Uganda, the increased risk of mother-to-child transmission associated with placental malaria was 2.89 (Brahmbhatt et al., 2003); however another study completed in Kenya found no association between placental malaria and HIV transmission in utero or peripartum (Inion et al., 2003).

Plasmodium vivax

Plasmodium vivax malaria is widely distributed throughout the world—predominantly in Asia, the Western Pacific, and the Americas—and accounts for over half of all malaria infections outside Africa, and roughly 10 percent of infections in Africa (Mendis et al., 2001). It has recently made a comeback in Korea, Peru, Indonesia, and China (Sleigh et al., 1998; Sharma, 1999; Chai, 1999; Roper et al., 2000; Barcus et al., 2002), and currently produces an estimated 75 million acute malarial episodes every year (Sina, 2002).

In humans, the fact that P. vivax invades only young RBCs (reticulocytes) limits its total parasite load and disease severity. In addition, P. vivax can only attach to human RBCs possessing the Duffy blood group cell surface antigen (Miller et al., 1976). Since most residents of West Africa lack genetic expression of the Duffy blood group antigen, the disease is essentially absent from the region.

The hallmark of vivax malaria is its sudden, dramatic paroxysm, trig-

Front Matter (R1-R20)

Executive Summary (1-16)

Part 1: A Response to the Current Crisis1 Malaria Today (17-60)

2 The Cost and Cost-Effectiveness of Antimalarial Drugs (61-78)

3 The Case for a Global Subsidy of Antimalarial Drugs (79-111)

4 An International System for Procuring Anitmalarial Drugs (112-122)

Part 2: Malaria Basics5 A Brief History of Malaria (123-135)

6 The Parasite, the Mosquito, and the Disease (136-167)

7 The Human and Economic Burden of Malaria (168-196)

8 Malaria Control (197-251)

9 Antimalarial Drugs and Drug Resistance (252-298)

Part 3: Advancing Toward Better Malaria Control10 Research and Development for New Antimalarial Drugs (299-311)

11 Maximizing the Effective Use of Antimalarial Drugs (312-328)

Acronyms and Abbreviations (329-333)

Glossary (334-346)

Index (347-364)