Lecture 6 Flashcards

1
Q

why does plasmodium does not wanna get into the spleen

A

because ut has a lot of macrophages that will kill the infected rbcs

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2
Q

what is the role of pfemp1 or pfp proteins

A

they are on the surface of infected rbcs and they help sticking to endothelial cells that line the blood vessels

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3
Q

what does pfps bind to on platelets and what does it cause

A

cr1 and causes cerebral malaria, metabolic acidosis and high mortality

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4
Q

what do pfps bind to on the cerebral microvascular endothelium

A

icam-1
causes cerebral malaria, metabolic acidosis and high mortality

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5
Q

what do pfps bind to on the placental microvascular endothelium and what does it cause

A

csa
causes low birth weight, prematurity and death of fetus

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6
Q

what do pfps bind to on the endothelium and what does it cause

A

cd36 and causes mild malaria

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7
Q

pfemp1 mediated rbc binding causes what

A

rosetting aka the cells stick to eachother and bind to uninfected cells and endothelial cytoadherence
-vascular obstruction causes hypoxia

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8
Q

hypoxia is caused by what and causes what

A

-caused by lack of oxygen resulting in anaerobic glycolysis and lactic acid buildup
-this can cause anemia, cerebral malaria and metabolic acidosis

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9
Q

why are antibodies unable to neutralize pfemp1 surface proteins

A

-over 60 var genes encode for multiple pfemp1 surface proteins
-only 1-2 are expressed at the same time and when antibodies are made against them, the parasite switches to other genes

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10
Q

true or false: var genes encoding pfemp1 are specific to p falcipum

A

true

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11
Q

where are the var genes encoding for pfemp1

A

close to the telomers

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12
Q

true or false: everyone has the same susceptibility to malaria

A

-false depends on your age and if you are living in a region where malaria is endemic
-kids below 5 are the most affected because their body can’t make as much antibodies against pfps
-as you grow older you can also get partial immunity aka they still get disease but your body uses the previously made antibodies
-older peeps get asymptomatic infections due to the build up of antobodies made

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13
Q

what is premunition

A

naturally

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14
Q

what does rifin does

A

-ninds to leucocyte immunoglobulin like receptor B1
-supresses nk cells because it inhibits adcc
-also binds to the same receptor on b cells which reduces the production of antibodies

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15
Q

what does stevor do

A

causes rosetting between infected and non infected rbs

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16
Q

how was trypanosoma brucei discovered

A

colonizers were trying to bring animals to africa and they kept dying
-brucei looked under the microscope

17
Q

trypanosomes come from what name

A

trypano: screw like
soma: body

18
Q

what are the main 2 stages of a trypanosoma brucei infection

A

-swelling of the cervical lymph node: present in blood
-lethargy, confusion and fatal: present in cns

19
Q

what is the vector of trypanosome brucei

A

tsetse fly

20
Q

what is the difference between trypomastigote and epimastigote

A

trypomastigote is from when the tsetse fly gets the blood meal, someone is infected, blood is taken back
-epimastigote is when the trypomastigote leaves the midgut and transforms

21
Q

brucei rhodesiense infects what and where is it

A

cattle and humans and is in esat africa
5%

22
Q

brucei gambiense infects what and where it is

A

only humans, west africa and is 95%

23
Q

treatment of stage 1 brucei

A

pentamidine

24
Q

stage 2 tratment brucie

A

melarsoprol

25
Q

stage 1-2 treatment brucei

A

fexinadazole which just got approved

26
Q
A