Parasitology Test 1 Lec 2 Flashcards

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malaria pt. 2



genes where polymorphism that provide resistance to malaria

  • a-globin (a-thalassemias)
  • B-globin (B-thalassemias)
  • B-globin (Hemoglobinopathy S)
  • B-globin (hemoglobinopathy C)
  • B-globin (hemoglobinopathy E)
  • erythrocyte band (ovalocytosis)
  • spectin (spherocytosis/elliptocytosis)
    • genetic, change shape

ppl w/ these are more resistant to malaria

  • erythrocyte glucose-6-phosphate gehydrogenase (G6PD)

if deficient, can have extreme pathology from malaria ( hemolytic anemia )


resistance continued

  • melanesian (band III)
    • alters shape of RBC so cant be in it
  • duffy antigen negativity
    • (vivax)
  • failure of invasion
    • (vivax)
  • failure of invasion
    • (falciparum)
  • glycophorin B deficiency
    • (falciparum)
    • falciparum wont affect nearly as much
  • blood group O
  • poor rosette formation
    • blood form chains in vessels - if bad formation = not as many parasites


temperature chart for 3 types of malaria

card image
  • can tell diff malarias apart based on fever peaks
  • vivax - as virus break out of RBC (2nd peak)
    • every 48 hrs fever peaks
  • malarie - peaks longer
  • falciparum - most pathogenic
    • fever peaks all over the place, harder ti tell
    • can be every day, every other day, etc.


malaria febrile paroxysms

classic 3 stages after infection gets established for 1 week

  1. cold stage - chills (15 mins-1 hr)
  2. hot stage - high fever 106 F (2 - 6 hrs)
    • + headaches, vomiting, delirium, anxiety, restlessness
  3. sweating stage - profuse sweating + fever subsides (2 - 4 hrs)


can diagnose malaria w/

  • fevers
  • spleen enlargement
  • person develop anemia


palpation of spleen

pic of enlarged spleen from malaria


spleen w/ hemozoin

card image

spleen with the pigment from the malaria parasite

  • when the parasites lyse RBC
  • -> release pigment
  • macrophages pick it up
  • go to the spleen + liver
  • spleen / liver turn black
  • -> must process to get rid of it
  • spleen/liver get enlarged
    • can rupture


what does the hemozoin do to the spleen / kidney?

turns it black

becomes enlarged

bc processing these things



  • enlarged spleen
  • due to increase in antibody producing cells + increase in reticulocytes leading to splenomegaly
  • spleen can rupture
  • spleen filters abnormal RBCs
  • deformability of RBCs
  • if get malaria when missing spleen - can quickly be fatal
    • bc spleen so important for immune system / protection


malaria liver w/ hemozoin (pigment)

card image


jaundice due to liver pathology

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  • can get jaundice from malaria bc of liver
  • yellow = person is very sick


mechanisms of jaundice

jaundice - from liver pathology from large increases of Kuppfer cells being produced to pick up garbage from all infected RBCs lysing releasing membranes + malarial pigment (hemozoin)


cerebral malaria morbidities

10% children surviving cerebral malaria left w/ neurologic sequelae

  • ehmiplegia
  • aplasia
  • decerebratev rigidity
  • psychosis
  • tremors
  • epilepsy
  • cortical blindness
  • ataxia
  • behavioral disturbances
  • mental retardation
  • learning difficulties



can kill by getting into brain

  • mimic epilepsy
  • heart attack
  • if young, interfere w/ learning capacity


rheological properties of RBCs deformability of normal RBCs

RBCs must deform considerably during multiple passages through the microvasculature and sinusoids of the spleen

RBC deform when go thru spleen

  • malaria causes infected cell to be rigid, so cant pass thru spleen -> spleen pick them out + destroy them


deformability of falciparum in fatal RBCs

  • falciparum infect RBCs + become rigid (lose deformability) as mature + avoid spleen clearance by sticking in capillaries
  • vivax does NOT do this
    • vivax infected cells dont become rigid
  • falciparum DOES do this
    • makes the knobs (stick to epithelial cells, bind RBC)
    • knobs advantage to parasite -> tried to make vaccines to avoid knob formation, none work


vivax does NOT

make infected RBCs become rigid


mechanism for this loss of deformability of falciparum infected RBCs

card image
  1. knobs on infected RBCs
  2. falciparum RBC membrane protein 3
  3. integral RBC membrane protein - band 3
  4. oxidative stress exerted on RBC membrane by metabolic byproduct from parasite
  5. increased internal viscosity of infected RBC
  6. infected RBC becomes more spherical + has reduced surface area to volume ration (spherocytosis)


deformability of vivax infected RBCs

  • remain deformable
  • but dont sequester (isolate/hide)
  • deformability of infected RBC actually increases as the parasite so matures it avoids the splenic entrapment
  • no problem going thru spleen
  • no knobs - gametocytes or rings -> go thru spleen -> allow gametocyte to be picked up by mosquito + can go into other cells + make rings



card image

adhesion w/ knobs -> inflammation -> loss of endothelial barrier... etc. see slide he said


cerebral malaria prognosis

mortality = deaths

in adult cases - fatality rate = 15-25%

in children fatality rate = 40%

hard to get good stats bc many are from rural areas where dont do autopsies, so probably even more deaths from it


urine from cerebral malaria patient

card image

overload kidneys capability to break down -> lysed stuff gets in urine


child with cerebral malaria body becomes rigid

in final stages


parasties in situ blood vessels of the brain

RBC filled w/ parasites

lot of clogging -> severe malariacan


malaria in pregnancies

malaria can cross placenta -> infect baby

many times both do not make it

parasites overwhelm baby


placenta w/ falciparum

card image

placenta w/ infected RBC filled w/ malarial parasites



card image


effect of aspirin

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no aspirin - vascular occlusion can occur bc falciparum infected erythrocytes (platelets) clump

  • aggregate

aspirin - inhibition of platelet aggregation


pathology - clogging vessels

card image
  • brain
  • placenta
  • microvascular adhesion



5-10% parasitemia

  • high level of parasites
  • 5-10% of RBC infected

usually will kill someone unless treated quickly

  • poor prognosis
  • treat by exchange transfusion



card image

enlarged spleen


mechanisms of anemia

  • RBC lysis by mature asexual parasites
  • suppression of erythropoiesis by cytokines (TNFa)
  • destruction of RBCs by spleen bc of loss of RBC deformability
  • autoantibodies to normal RBCs


worms and malaria

  • most ppl in malaria endemic areas infected w/ 1 or more worms
  • several worms shown to induce immune response that does not fight malarial parasites
  • some vaccines do not take in ppl infected w/ certain worms
  • must get rid of worms bc vaccine wont take well if high levels of worms
  • must deworm first before vaccine


treat worm infections

  • if worm infections treated, then malarial infections can be treated better/immunity develops faster
  • worms stimulate an immune response that leads to more TH2 cells which the HIV organism uses to develop within


schistosomes and malaria

schistosomes also stimulate an immune response different than one that is needed for elimination of malarial parasites


antibody subclasses increasing during an ascaris infection

  • IgG2 isotype
  • IgG4 isotype
  • both increase during an infection with ascaris worm
  • therefore, worms stimulate an immune response not favorable to the hosts ability to eliminate malaria


antibody subclasses important for fighting malarial infections

  • IgG1 isotype
  • IgG3 isotype
  • these Abs bind to receptors on monocytes leading to an ADCC mechanism killing of the malarial parasites


optiMAL dipstick P. falciparum and P. vivax

card image

neg band

vivax = 1 line

falciparum = 2 lines


malaria chemotherapy funded by DOD

chemotherapy program started in 1960 funded by the DOD and ended december 2012

evaluated over 320k compounds for antimalarial activity in mice


3 new drugs approved by the FDA

  • mefloquine - lariam
  • halofantrine - halfan
    • cause cardiac toxicity
  • tafenoquine - krintafel / arakoda
    • kills all stages
    • only drug that does this
    • cannot take if G6PD deficient
  • always take combinations of drugs for malaria (never just 1)


lecture finished (did not finish slides)