FUO - Malaria Flashcards
Plasmodium Falciparum/ P Vivax Char
Sporozoite protozoan (ring structure) - 4 major species
Plasmodium Falciparum/ P Vivax Res
Humans (asexual); mosquitos (sexual)
Plasmodium Falciparum/ P Vivax RF
Travel to endemic areas; autochthonous cases seen
Plasmodium Falciparum/ P Vivax Diag
Blood smear looking for ring structure; rapid tests
Plasmodium Falciparum/ P Vivax Trans
Mosquito bites and blood transfusions
P. Vivax Information
80% of cases - infects only young immature erythrocytes; forms hypnozoites. Requires Duffy Ag. Endemic in Asia; 48 hour cycle.
P. Falciparum Information
15% of cases - infects all erythrocytes, does not form hypnozoites, more severe. Endemic in Africa (irreg cycles)
Malaria Clinical
IR and rupture of RBCs underlie cause of diesease. Signs and symptoms: cyclic paroxysms of fever due to release of toxic substances, chills and rigors, hemolytic anemia, hypoglycemia.
Prodrome is non specific flu like symptoms of HA, muscle pains, nausea and vomit.
P. Falciparum Clinical
Dmg to brain, kidney, and liver due to pigments and debris. Orthostatic hypotension (cap plug due to slugging of infected cells)
Cerebral Malaria
P. Falc induces changes in mental status leading to coma and convulsions. Highly fatal. Risk in children and endemic areas
P falc and kidney
Svr infection in adults leading to dehydration, increased viscosity, hypovolemia, clogged tubules
Sporozoites
Injection from mosquitos into blood, goes to liver via Circumsporozoite protein (CSP). Once it reaches liver it forms merozoites (prolif)
Merozoites
Formed in hepatic cell. It ruptures haptocytes and moves into circulation. P vivax merozoites bind RBC Buffy Ag. P falc merozoites use PfEMP-1 Ag on parasite to bind large range of RBCs.
Trophozoites
Merozoites diff into ring shaped troph within RBC and replicate via Hg as nutrient, produce merozoites to release
Gametocytes
Some merozoites form this sexual stage to be picked up by naive mosquitos