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EXAM 6 > Protazoa > Flashcards

Protazoa Flashcards

1
Q

plasmodium falciparum

A

most deadly malaria

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2
Q

plasmodium vivax

A

most prevalent malaria

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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
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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!

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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)

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6
Q

malaria vaccines

A

against liver stage

partial protection

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

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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)

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8
Q

malaria and genetics

A

evolutionary driving force behind sicklecell, thalassemia, g6pd

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

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9
Q

sporozoites

A

what mosquitos inject

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10
Q

malaria gametocytes

A

what mosquitos take up

mature to sporocytes in mosquitp

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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

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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

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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

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14
Q

PfEMP1

A

var gene famly

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

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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

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16
Q

P. falciparum diagnosis

A

only see ring and gametocytes!

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

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17
Q

P. vivax diagnosis

A

find all stages in blood

ring, trophozozite, schizont, gametocyte

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18
Q

Primaquine

A

malaria drug

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

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19
Q

chloroquine

A

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

use for most other types thugh

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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
Q

toxoplasmosis transmission

A

undercooked meat, food/water contaminated w cat feces, gardening without gloves/cleaning litter boxes, blood transfusion/organ transplant, transplacentally

26
Q

toxoplasmosis clinical features

A

cysts maintained for many years, burst periodically but immune controls

impaired immune system can’t control

eye lesions can be confused with tumors

27
Q

toxoplasmosis and pregnancy

A

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
Q

toxoplasmia- active or chronic?

A

IgM and IgG

high IgM - acute!

low IgM, high IgG - chronic

29
Q

toxoplasmosis treatment

A

pyrimethamine plus sulfadiazine - expensive drug!

30
Q

trophozoite

A

intestinal protozoa - develops in intestine

transmitted by cysts - oral fecal

very resistant and can contaminate water supply

31
Q

Cryptosporidiasis

A

small cysts, in drinking water

problem for immunocompromised

32
Q

Giardiasis

A

infection w giardia, most freqent intestinal parasite in US drinking untreated water

add’l symptoms: gas, greasy stools that tend to float

33
Q

Giardia lifecycle

A

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
Q

Amebiasis

A

trophozoites can degrade the intestine and spread (freq liver and lung), can eat RBCs, enter circulation

enter as cysts and exit as cysts

35
Q

intestinal protazoa diagnosis

A

microscopy of fecal samples

immuno diagnisis if needed (i.e. ag capture)

36
Q

intestinal protazoa

A

cryptosporidiosis

giardiassis

amebiasis

37
Q

trypanosomatid diseases

A

leishmaniasis

human afrincan trypanosomiasis

Chagas

protazoans - single flagella, mitoc w large genome

38
Q

leishmaniasis

A

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
Q

kinetoplast

A

mitoc w large genome - always assoc w basal body of flagellum

40
Q

diagnosis and treatment of Leishmanaisis

A

microscopy of tissues, abs, ag detection

treatment - depends

41
Q

Human African Trypanosomiasis

A

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
Q

Treatment and diagnosis of Human African Trypansomiasis

A

microscopy of blood/ln

before CNS vs after CNS drugs - identify early

43
Q

Chagas

A

Trypanosoma cruzi

bite of triatomid bug

obligate intracellular replication

S America

44
Q

Chagas disease

A

acute - usually not treated

chronic - infected for life

persists in smooth muscle - cardiac, GI, can lead to death

reactivate w HIV

45
Q

T. cruzi life cycle

A
46
Q

Transmission of T. cruzi

A

unknowingly rubbing feces or urine into eyes, mouth

blood tranfusion

mother to fetus

uncooked food

47
Q

Diagnosis of T. Cruzi

A

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
Q

t. cruzi treatment

A

high toxicity drugs

good efficacy in acute phase, partial in chronic phase

EXAM 6 (4 decks)

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