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Causes: P. falciparum (severe form), P. malariae (mild form), P. vivax (benign), P. ovale (least common).
Transmission: anopheles mosquito carries organisms in its salivary glands injects them into humans while it feeds. Also transmitted by blood transfusion, ‘dirty’ syringes.
Pathogenesis: enter blood ≫ sporozites ≫ ½ hr ≫ grow in the liver and spread to red blood cells where they reproduce ≫ red cells lyse due to too much organisms ≫released into blood stream ≫ fevers result (i.e.: only when RBC’s burst, are fevers caused. Therefore fevers are intermittent + cyclical). Different species of Plasmodium burst at different time intervals (i.e.: vivax = 48 hrs, falciparum = irregular 24-36 hrs).
Features: periodic episodes of chills + fevers + profuse sweating at 48-72 intervals. These last for 6 hrs, and are associated with rupture of RBCs. 7-14 days: hepatosplenomegaly. As RBC lyse, patient becomes anaemic, leads to ‘sticky RBCs’. P. falciparum is the most dangerous and it will invade up to 30% of your RBCs (very aggressive). The sticky cells will plug up your venules in your kidneys, lung, brain ≫therefore blocking blood delivery to that organ.
Other complications include: Cerebral malaria (seizures, impaired consciousness ≫ coma), renal failure (toxins cause glomeruli to contract – impaired function), GI malaria (collapse of gut circ.).
Dx: Examination of thin & thick films of blood under oil-immersion magnification (1000X) – see trophozoites + schizonts within RBCs. Fluorescently labelled antibodies may be used to identify responsible species.
Treatment: 2 things must be considered: a) geographical pattern of susceptibility of P. falciparum to antimalarial drugs, b) type of Plasmodium species causing infection.
The class of drugs include: CAUSAL PROPHALACTICS, SCHIZONTOCIDAL, GAMETOCYTOCIDAL, and ANTI-RELAPSE.
Category: Microbiology Notes
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