Micro U2 L1 pt 2. Flashcards
(46 cards)
How does transmission of most parasitic infections spread?
mosquitos, ticks, specific flies, other arthropods
What is human to most parasitic infections?
intermediate host. sexual reproduction occurs in vector associated with transmission of agent
Plasmodium
protozoan parasite - malaria
Which area of the world is most affected by malaria and why?
africa - very efficient mosquito (anophele gambiae complex); predominant parasite species is plasmodium falciparum; warm weather = year round
What transmits malaria?
anopheles mosquitos - usually by female mosquitos
What are the four parasite species that cause malaria in humans?
plamodium falciparum, vivax, malariae, ovale
Plasmodium falciparum
most fatal outcomes - sub saharan africa, SE asia, S america
Plasmodium vivax
most common, seen in US - NOT seen in sub saharan africa
Plasmodium malariae
all malarious areas, but spotty
Plasmodium ovale
tropical areas - africa; SE asia, S america
What are the clinical symptoms of malaria due to?
schizont rupture and destruction of erythrocytes
What are the prodromal symptoms of malaria?
fever, chills, headaches, diaphoresis
What are malarial paroxysms?
febrile attacks following the prodromal symptoms - exhibit periodicities (24 hrs for vivax, ovale, falciparum and 72 hr for malariae)
What are natural protections against malaria?
- hg C, S (sickle cell) 2. Duffy antigen - lack this = low incidence 3. thalassemia
What are the stages of the malaria paroxysm?
- cold stage (lysis of RBC) - intense cold feeling, shivering, 15-20 min 2. hot stage - due to circulating and innate immune response - intense heat, dry burning skin, throbbing headache, 2-6 hr 3. sweating stage due to infection of additional erythrocytes and immune system shutting off - profuse sweating, declining temp, exhausted and weak, 2-4 hr
What are the major complications of severe malaria?
cerebral malaria, pulmonary edema, acute renal failure, severe anemia, bleeding
What are the most common metabolic complications of malaria?
acidosis and hypoglycemia
PfEMP-1 antigen
on 100% of RBCs
What causes stable stationary adherence of the parasitized RBCs?
CD36 and chondroitin sulphate A (CSA) - surface of P falciparum trophozoite and schizont infected RBCs is covered with knob-like excrescences made up of the PfEMP-1 antigen
How does p falciparum modify the surface of RBCs so that asexual parasites and gametocytes can adhere to the endothelium and asexual parasites can adhere to the placenta?
knob-like excresences made up of PfEMP-1 antigen
Cerebral malaria
most severe neurological complication of infection with plasmodium falciparum - breakdown of BBB due to cytoadherence of infected RBCs and vascular sequestration of infected erythrocytes
Placental malaria
accumulation of parasitized erythrocytes and monocytes in the placenta, direct adverse birth outcomes
Malaria relapse
reactivation of infection via hypozoites released from the liver (with vivid and ovale only) - second drug should be given with these types to help prevent relapses
Malaria recrudescence
parasitemia falls below detectable levels and later increases to detectible level = re-attack of malaria due to surviving malaria parasites in RBCs. Due to: 1. incomplete or inadequate treatment 2. antigenic variation 3. multiple infections