symptoms than veterans who suffered combat wounds. The report raises questions about the potential for cerebral malaria to produce subtle, persistent neurologic deficits that may not have been apparent in examinations conducted during routine medical treatment and followup (Shamo 2001).
The committee concludes that there is limited or suggestive evidence of an association between Plasmodium vivax and Plasmodium falciparum infections and demyelinating polyneuropathy and Guillain-Barré syndrome.
The committee concludes that there is limited or suggestive evidence of an association between Plasmodium falciparum infection and neurologic disease, neuropsychiatric disease, or both, months to years after the acute infection.
Chronic untreated P. malariae infection can be manifested with chronic glomerulonephritis even years after the onset of infection (Eiam-Ong 2003; Kibukamusoke 1986). In contrast, the nephrotic syndrome and acute glomerulonephritis are far more common near the onset of infection (days to weeks later), may be associated with any malaria infection, and would be manifested after months or years only very rarely.
The committee concludes that there is sufficient evidence of an association between Plasmodium malariae infection and the manifestation of immune-complex glomerulonephritis years to decades later.
The committee concludes that there is sufficient evidence of a causal relationship between malaria infection and renal disease, especially the nephrotic syndrome that may occur weeks to months after acute infection.
Some P. vivax and P. ovale parasites remain dormant as hypnozoites in the liver for months after primary infection. The latent period is generally 6-11 months (Mandell et al. 2005), although one report found the latent period to be less than 4 months (Oh et al. 2001).
At the end of their dormancy, P. vivax or P. ovale hypnozoites initiate the same process that occurs during acute malaria, generating tissue schizonts that rupture and release merozoites into the bloodstream. When the merozoites invade and lyse red blood cells, the patient experiences a relapse with acute symptoms resembling de novo infection (Mandell et al. 2005). Such relapses have been described as occurring periodically but irregularly almost always within 2 years after primary infection (Eliades et al. 2005; Shute et al. 1977).
Thus, relapse of malaria may occur after either symptomatic or asymptomatic infection by P. vivax and P. ovale, particularly in people who are taking such prophylactic antimalarials as chloroquine that neither prevent Plasmodium spp. from infecting hepatocytes nor eliminate Plasmodium hypnozoites (Guerrant et al. 1999). In contrast, treatment with primaquine mitigates hepatic infection, reducing the risk of relapse after primary infection by P. vivax or P. ovale (Baird 2005; Shanks and Edstein 2005; Taylor and White 2004). The diagnosis of persistent hepatic infection by P. vivax or P. ovale can be made only if relapse occurs and blood smears or other suitable diagnostics are confirmatory.
The phenomenon of persistent latent hepatic infection does not occur with P. falciparum or P. malariae. However, there are other mechanisms whereby both these species can lead to hepatic disease months or years after the acute infection. Delayed recurrence or delay in onset