Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

EXAM 6 > Protazoa > Flashcards

Protazoa Flashcards

1
Q

plasmodium falciparum

A

most deadly malaria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

plasmodium vivax

A

most prevalent malaria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

basic malaria lifecycle

A
  1. mosiquito bites and parasites into skin
  2. parasites migrate to liver
  3. parasites infect hepatocytes and multiply
  4. parasites getinto blood and infect erythrocytes - form ring and different structures when multiplying
  5. burst out of RBC into blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

malaria liver stage

A

sporozoites in skin from mosquitoes migrate to the blood and then to the liver to infect hepatocytes

huge amplification - sporozoite produces thousands of merozoites

no pathology

hypnozoites!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

hyponozoites

A

p. vivax and p. ovale

hepatocyte infection can stop in a few cells and result in hypnozoites (dormant infected hepatocytes) - reactivate months/years later —> relapse (blood stage infection and disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

malaria vaccines

A

against liver stage

partial protection

against CS protein fused w hep b protein to make it immunogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

malaria blood stage

A

merozoites released from infected hepatocytes - infect erythrocytes - start symptomatic phase of disease

  1. infect by merozoites
  2. ring stage
  3. trophozoite forms in RBC
  4. schizont forms in RBC
  5. replicate, rupture, release

replication is synchroized - simultaneous release of newly flormed merozoites and high inflamation (fever) - cyclical (every 48h)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

malaria and genetics

A

evolutionary driving force behind sicklecell, thalassemia, g6pd

duffy ag - if don’t express, not infected w p vivax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

sporozoites

A

what mosquitos inject

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

malaria gametocytes

A

what mosquitos take up

mature to sporocytes in mosquitp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

cerebral malaria

A

headache, stiff neck, drowsiness, seizures, coma and death

p. falciparm

only RBC with this can stick to brain endothelial cells and cause capillary clogging, local inflammation, blood brain barrier damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

placental malaria

A

p. falciparum

RBC infected can stick to placental membrane, impeding oxygen-nutrient transfer and causing intrauterine growth retardation and miscarriage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

knobs

A

how infected rbs adhere to brain/endothelial

PfEMP1 - from parasite - binds to membrane of RBC - aggegate in nobs and mediate adhesio to membranes/cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

PfEMP1

A

var gene famly

many different genes - selective expression of one, swithch around for immune evasion in malaria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

P falciparum PfEMP1

A

bind to endothelial cells in all tissues by binding to CD36 on surface of endothelial cells - no pathology

only if express specific - adhere to brain or placental endothelial cells - pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

P. falciparum diagnosis

A

only see ring and gametocytes!

trophozoites and schizonts do not circulate bc they adhere to endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

P. vivax diagnosis

A

find all stages in blood

ring, trophozozite, schizont, gametocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Primaquine

A

malaria drug

added w p. vivax and p. ovale because they can hae hypnozoites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

chloroquine

A

resistince is widespread for p. falciparum - not used as much anymore,

use for most other types thugh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

recrudescence

A

even after treatment malaria can remain at very low levels in the blood and reactivate years later

21
Q

babesiosis

A

transmitted by ticks

common in NE and MW

many have no symptoms, some have flu like symptosm, immunosuppressed can have life threatening diseases (immune escape)

low/unstable BP, anemia, low platelets

22
Q

babeosis life cycle

A

rodents and ticks back and fort

ticks give to humans - transfer through transfusions

rare congenital transfusion

23
Q

toxoplasmosis

A

1/3 of world pop, very mild in immunocompetent - can be severe for immunodeficinet/fetus (maternal transmission)

24
Q

toxoplasmosis life cycle

A

in birds/rats - have tissue cysts - cats eat and get infected - have fecal oocysts

animals can eat fecal oocysts and we eat animals

OR gardening without gloves, changing cat liver - we ingest fecal oocysts

oocysts tranform into tachyzoites (form of the parasite) shortly after ingestion, infect many cell types and develop into tissue cysts in neural and muscle cells - immune keeps under control, no pathology for uears

25
toxoplasmosis transmission
undercooked meat, food/water contaminated w cat feces, gardening without gloves/cleaning litter boxes, blood transfusion/organ transplant, transplacentally
26
toxoplasmosis clinical features
cysts maintained for many years, burst periodically but immune controls impaired immune system can't control eye lesions can be confused with tumors
27
toxoplasmosis and pregnancy
if an immuno-competent woman was infected before pregnancy, there is no risk for the fetus if woman is infected during pregnancy- can have no symptoms but fetus can have problems congential toxoplasmis - prmature birth, eye problems, high mortality
28
toxoplasmia- active or chronic?
IgM and IgG high IgM - acute! low IgM, high IgG - chronic
29
toxoplasmosis treatment
pyrimethamine plus sulfadiazine - expensive drug!
30
trophozoite
intestinal protozoa - develops in intestine transmitted by cysts - oral fecal very resistant and can contaminate water supply
31
Cryptosporidiasis
small cysts, in drinking water problem for immunocompromised
32
Giardiasis
infection w giardia, most freqent intestinal parasite in US drinking untreated water add'l symptoms: gas, greasy stools that tend to float
33
Giardia lifecycle
inject cysts, trophozoites in small intestine, pass cysts and trophozoites in stool but only cysts survive, contaminate in small intestine - triphozoites replicae by binary fission
34
Amebiasis
trophozoites can degrade the intestine and spread (freq liver and lung), can eat RBCs, enter circulation enter as cysts and exit as cysts
35
intestinal protazoa diagnosis
microscopy of fecal samples immuno diagnisis if needed (i.e. ag capture)
36
intestinal protazoa
cryptosporidiosis giardiassis amebiasis
37
trypanosomatid diseases
leishmaniasis human afrincan trypanosomiasis Chagas protazoans - single flagella, mitoc w large genome
38
leishmaniasis
transmitted by sandflies, high prev in mid east also blood and ddrugs dogs are main res infects and lives in microphages - surface protects from lytic enzymes in lysosome, inhibits oxidative burst visceral (systemic - parasits use neutrophils to travel, infect macrophages and extend through body - can be fatal), cutaneous (scar - crater), mucocutaneous
39
kinetoplast
mitoc w large genome - always assoc w basal body of flagellum
40
diagnosis and treatment of Leishmanaisis
microscopy of tissues, abs, ag detection treatment - depends
41
Human African Trypanosomiasis
Trypanosoma brucei, rhodesiense, gambinse tse tse fly African sleeping sickness trypanosomes live and reproduce free in blood invasion of cns --\> coma and death ag variation! always ag uniform but small numbers are divergent, also packing of VSG - abs can't find contagious ag
42
Treatment and diagnosis of Human African Trypansomiasis
microscopy of blood/ln before CNS vs after CNS drugs - identify early
43
Chagas
Trypanosoma cruzi bite of triatomid bug obligate intracellular replication S America
44
Chagas disease
acute - usually not treated chronic - infected for life persists in smooth muscle - cardiac, GI, can lead to death reactivate w HIV
45
T. cruzi life cycle
46
Transmission of T. cruzi
unknowingly rubbing feces or urine into eyes, mouth blood tranfusion mother to fetus uncooked food
47
Diagnosis of T. Cruzi
blood smear for acute phase (impossible in chronic) abs - can tell of has had chagas but not if currently infected PCR - doesn't detect all chronic cases bc parasite load in blood is low
48
t. cruzi treatment
high toxicity drugs good efficacy in acute phase, partial in chronic phase

EXAM 6 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions