Pakistan reported more than 125,000 laboratory-confirmed cases in 2003, 4 million probable cases, and 14 deaths. Of the laboratory-confirmed cases, almost 70% were caused by P. vivax. The primary mosquito vectors of malaria in Pakistan are A. culicifacies and A. stephensi (RBM 2005f).

In Iran, three provinces in the southeastern corner account for most of the 23,000 cases reported in 2003, 21% of which were caused by P. falciparum. Primary mosquito vectors include A. fluviatilis, A. stephensi, and A. culicifacies (RBM 2005d).

Acute Malaria

All four Plasmodium species can cause cyclic fevers, particularly in naïve populations. Known as malarial paroxysms, the cycles are characterized by rapid onset of high fever with chills followed by rapid resolution, often with intense diaphoresis. The cycles are associated with erythrocyte lysis that occurs at the end of the erythrocytic cycle of infection. The classical (but infrequently observed) periodic attacks occur every second day with the "tertian" parasites (P. falciparum, P. vivax, and P. ovale) and every third day with the "quartan" parasite (P. malariae).

Among populations in endemic areas, the development of partial immunity leads to milder illness and even asymptomatic infections. However, the immune response does not block repeated infections or infections with multiple strains or species. In temperate climates, the long latent phase with P. vivax and P. ovale appears to provide the opportunity for the resumption of transmission when the mosquito season returns in the next year (Guerrant et al. 1999).

Malaria is diagnosed with microscopic examination of blood smears stained with Giemsa or Wright’s stain. An experienced technician can diagnose most cases with examination of routine blood smears (thin smears), but examination of thick smears is more sensitive in detecting those with less severe parasitemia. The key to diagnosis is recognizing the potential for malaria in a potentially exposed person who has fever, anemia, and thrombocytopenia. Deaths from malaria in travelers returning to the United States, most notably with P. falciparum, continue to occur, often in association with delays in diagnosis and in effective therapy (Newman et al. 2004). Other diagnostic techniques have been developed, including fluorescence microscopy, immunologic diagnosis of falciparum malaria with antibodies to the protein HRP2, DNA probes specifically for P. falciparum, and PCR methods (Amino et al. 2005; Berry et al. 2005; Wilson et al. 2005).

Treatments for Malaria and Related Long-Term Toxicity

Resistance to chloroquine and multiple-drug resistance are major problems with P. falciparum in most of Africa, Asia, and South America. Drug-resistant P. falciparum has also been found in the Middle East and southwest Asia, including Iraq (Guerrant et al. 1999). Resistance to chloroquine is an emergent problem with P. vivax in some parts of Asia, Oceania, and South America (Kurcer et al. 2006).

Antimalarial drugs have well-documented acute adverse effects on the skin, gastrointestinal tract, central nervous system, and other organ systems, but evidence of long-term adverse health outcomes is sparse (Taylor and White 2004). Moderate to severe neuropsychiatric complications have been reported in association with mefloquine, doxycycline, combined chloroquine and proguanil, and combined atovaquone and proguanil (Schlagenhauf et al. 2003; Taylor and White 2004). Although retinopathy associated with high-dose long-term chloroquine use has been described, it has rarely been associated with modern prophylaxis. Additional



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