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129 Cards in this Set
- Front
- Back
giardia lamblia life cycle (4)
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1. cysts ingested in water/food
2. in GIT, cysts excyst, releasing trophozoites 3. trophozoites colonize duodenum 4. 2 trophozoites encyst and leave in feces |
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cysts have ___ nuclei, trophozoites have ___
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4
2 |
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___ are reservoir for G. lamblia
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beavers
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g. lamblia symptoms
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diarrhea (not bloody)
dehydration |
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diarrhea from g. lamblia is very smelly because
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fat is not digested in small intestine and is fermented by colonic bacteria
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g. lamblia drugs
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metronidazole
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Trichomonas vaginalis has ___ flagella and ___ nuclei
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4
1 |
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T. vaginalis is endemic to ___. It is the only ___ parasite
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worldwide
sexually transmitted |
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T. vaginalis requires an abnormally high ___ to survive
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vaginal pH
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T. vaginalis drugs
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metronidazole
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T/F: 90% of those infected with Entamoeba histolytica are asymptomatic
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true
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T/F: 50% of those infected with E. dispar are asymptomatic
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false: 100%
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E. histolytica grows on ___ culture, whereas E. dispar grows on ___ culture.
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axenic (no bacteria)
xenic |
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E. histolytica eats ___ (2) and lyses ___
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bacteria
RBCs host cells |
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E. histolytica life cycle (5)
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1. trophozoites in intestine encyst
2. cysts released in feces 3. cysts ingested in water/food 4. cysts excyst in intestine 5. trophozoites colonize large intestine |
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trophozoites can leave large intestine and go to ___ (3). This move may be triggered by ___
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brain
liver lungs drop in intestinal Fe |
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if a trophozoite goes to the liver, it can only ___; it can't ___
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release hepatotoxins
encyst |
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E. histolytica have ___ nuclei and lack ___
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4
mitochondria |
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chronic E. histolytica amebiasis causes ___. ___ effects are rare
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mucosal ulceration of GIT
brain |
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E. histolytica uses ___ to adhere to epithlium. This binds ___ and ___ on epithelial cells. It has ___ subunits linked by ___. Adhesion can be inhibited by adding ___.
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Gal-lectin
Gal GalNAc 2 disulfide Gal |
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E. histolytica uses ___ to kill cells
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amebapores
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amebapore activity is ___ dependent
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pH
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although E. dispar expresses amebapores, it causes less damage because ___ (2)
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it makes less of them
it makes a less active version |
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E. histolytica drugs
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metronidazole
iodoquinol |
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metronidazole mechanism
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converted by amebic pyruvate-ferridoxin oxidoreductase to a nitroso free radical
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E. histolytica ___ can be observed in solid feces, but ___ can be observed in diarrhea, because it has intestinal mucus
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cysts
trophozoites |
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Cryptosporidium parvum life cycle (4)
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1. thick-walled oocyst leaves ileal epithelial cell
2. oocyst released in feces 3. oocyst ingested in contaminated water 4. oocyst releases sporozoites (yeasts) to ileum |
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c. parvum may be identified with ___ stain
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Ziehl-Neelsen
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c. parvum has ___ as revervoir
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domestic animals
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c. parvum drugs
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spiramycine
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3 forms of leishmaniasis
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cutaneous
mucocutaneous visceral |
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cutaneous leishmaniasis is aka ___. it is caused by ___ (3)
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oriental sore
l. tropica l. major l. mexicana |
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mucocutaneous leishmaniasis is caused by
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l. braziliensis
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visceral leishmaniasis is aka ___. it is caused by ___ in india and ___ in mediterranean
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kala azar
l. donovani l. infantum |
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the most dangerous kind of leishmaniasis is ___, which is endemic to ___.
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visceral
india |
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Leishmania has 2 stages, ___ and ___. In the former stage, ___ is present, and in the latter, ___ is present. Like ___, it has a ___.
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promastigote
amastigote a flagellum no flagellum trypanosoma kinetoplast |
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leishmania life cycle (7)
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1. promastigotes in blood are eaten by macrophages
2. promastigotes become amastigotes 3. amastigotes proliferate inside macrophage, sometimes lysing it 4. sand fly sucks blood with infected macrophages 5. in fly gut amastigotes are released and switch to promastigotes 6. promstigotes swim from gut to salivary glands 7. sand fly injects promastigotes into human |
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in a sandfly you will see ___ote, and in human you will see ___ote
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promastig
amastig |
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the kinetoplast contains
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supercoiled DNA
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kDNA has genes for (2)
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rRNA
electron transport chain proteins |
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L. major and L. tropicana cause ___ leishmaniasis with a ___ course for ___ weeks followed by ___ in ___months.
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cutaneous
acute 1--3 healing 2--12 |
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reservoirs for L. major and L. tropicana (2)
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rodents
dogs |
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L. mexicana causes ___, located on ___.
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chiclero's ulcer
ear |
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cutaneous leishmaniasis is diagnosed by ___
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scraping from ulcer and examining with LM
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cutaneous leishmaniasis drugs
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antimonials
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mucocutaneous leishmaniasis starts like cutaneous but then spreads via ___. it is endemic to ___
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lymphatics
new world |
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L. braziliensis causes metastatic lesions at ___, and may cause death from ___.
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nasal and buccal mucosae
secondary infection |
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L. braziliensis drugs
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liposomal amphotericin B
antimonials |
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L. braziliensis reservoir (2)
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sloths
anteaters |
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incubation for visceral leishmaniasis is ___
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1--4 months
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L. donovani reservoir is ___
L. infantum reservoir is ___ (3) |
doesn't exist!
dogs jackals foxes |
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visceral leishmaniasis symptoms (4)
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fever
anemia hepatosplenomegaly wasting |
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visceral leismaniasis drugs
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miltefosine
pentamidine isothionate antimonials |
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Leishmania virulence factor categories (4)
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resistance to respiratory burst
lipophosphoglycan gp63 A2 |
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enzymes for respiratory burst resistance (3)
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SOD
catalase trypanothione reductase |
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in the vector, LPG does ___ (2)
in human, LPG does ___ |
inhibits protease release
helps attach to gut inhibit respiratory burst |
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gp63 is present in ___ stage of ___
its function is (2) |
promastigote
L. major mimic fibronectin degrade lysosomal enzymes |
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A2 gene is present in ___ and ___ but only expressed in ___.
its function is ___ |
L. major
L. donovani L. donovani unknown |
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the 2 kinds of trypanosomiasis are
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african sleeping sickness
chagas' disease |
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sleeping sickness is caused by (2)
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T. brucei rhodesiense
T. brucei gambiense |
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Chagas' disease is caused by
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T. cruzi
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T. b. gambiense is localized to ___ and causes a ___ disease.
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rivers
chronic |
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T. b. rhodesiense is localized to ___ and causes a ___ disease. Its hosts are ___ (3)
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savannah
acute humans antilopes deer |
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sleeping sickness vector
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tsetse fly
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trypanosoma in the host is in the ___ stage, and in the vector in the ___ stage
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trypomastigote
epimastigote (and trypomastigote) |
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in fly, trypanosoma switches from ___ stage to ___ stage after ingestion, and then back before injection
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trypomastigote
epimastigote |
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t. brucei is pathogenic because ___
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antigenic shift allows it to evade immune system
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the characteristic lesion of trypanosomiasis is ___, which is
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winterbottom's sign
cervical lymphadenomegaly from T. brucei infiltration |
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somnolence in trypanosomiasis is caused by ___. they also cause ___ (3)
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toxic metabolitates of aromatic AAs
immunosuppression vascular damage temperature change |
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sleeping sickness drugs
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pentamidine
suramin melarsoprol eflornithine |
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suramin is a ___ drug and works by ___. it is used for the ___ phase of disease.
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arsenical
inhibits glycolysis early |
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eflornithine works by ___. it is used for ___ phase of disease.
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inhibiting DNA replication
advanced |
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antigenic variation is provided by ___. there are ___ possible loci to express. ___ of these are expressed at one time.
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variant surface glycoprotein
20 1 |
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___ is used to select the active locus, and ___, which is a modified ___, is used to repress transcription of the inactive ones.
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crossing over
base J uracil |
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Chagas' disease is spread by ___ aka ___
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reduvid bug
assassin bug |
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Chagas' disease life cycle (5)
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1. amastigotes in skin eaten by macrophages and spread via lymp and blood
2. amastigotes ingested by vector 3. amastigotes become epimastigotes 4. epimastigotes become trypomastigotes 5. vector poops trypomastigote on host |
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clinical syndromes of chagas' disease (3)
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asymptomatic
acute chronic |
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in asymptomatic syndrome, no symptoms are present, but ___ is
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anti-T. cruzi IgG
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in acute syndrome, ___ is present, which is a ___. This is called ___ if present on eye. ___ take 10 days to appear in blood
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chagoma
inflammatory nodule romana's sign trypomastigotes |
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___% of people progress from asymptomatic stage to ___. symptoms include enlargement and dysfunction of ___ (5)
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10--30
chronic liver heart spleen esophagus colon |
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T/F: high levels of parasite are present in blood in chronic infection.
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false: low
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T. cruzi triggers autoimmunity via ___ which resembles cardiac myosin and ___ which resembles skeletal muscle
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B13
cruzipain |
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T. cruzi drugs
these help with ___, but not with ___ |
nifurtimox
benzimidazole acute phase chronic phase |
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systemic symptoms in acute chagas' disease take ___ to develop and include ___
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2--3 weeks
fever myalgia CNS symptoms |
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malaria is caused by ___ (4)
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Plasmodium vivax
P. ovale P. malariae P. falciparum |
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The most virulent malaria is caused by ___. The most widespread is caused by ___. The rarest is caused by ___.
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P. falciparum
P. vivax P. ovale |
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The DH of plasmodium is ___. The IH is ___.
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mosquito
human |
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Plasmodium life cycle (12)
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1. oocyst outside mosquito gut ruptures, releasing sporozoites
2. sporozoites travel to salivary gland 3. mosquito injects sporozoites when it bites IH 4. sporozoites home to hepatocytes 5. in liver, sporozoite matures into schizont 6. schizont matures into merozoites 7. merozoites infect RBCs 8. merozoites multiply inside RBCs and lyse them 9. merzoites become gametocytes 10. mosquito sucks RBCs with gametocytes 11. gametocytes fuse in mosquito gut, making zygote 12. zygote matures into oocyst |
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P. ovale and P. vivax have a ___ stage after ___ and before ___.
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hypnozoid
invasion of hepatocyte schizont |
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merozoites inside RBCs can proliferate by becoming ___ which proliferate into ___
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trophozoites
erythrocytic schizonts |
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infection stages (4)
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mild
cold hot sweating |
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cold stage symptoms (3)
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fever
chills shaking |
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hot stage symptoms (4)
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high fever
nausea headache dizziness |
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sweating stages
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sweating
drop in temperature |
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hemolysis occurs at ___ stage
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cold
|
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people feel better after crises because ___
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new RBCs are made with better O2 binding
|
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cerebral malaria is most commonly seen with ___. it is caused by ___ due to ___
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P. falciparum
ischemia emboli of infected and healthy RBCs blocking cerebral capillaries |
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cerebral malaria may be caused by ___. P. falciparum may use this to ___
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P. falciparum erythrocyte membrane proteins (PfEMP)
evade destruction in spleen |
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tertian cycle means fever every ___. quartan cycle means fever every ___.
___ have tertian cycles, and __ has quartan. |
48h
72h P. falciparum P. ovale P. vivax P. malariae |
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___ may cause infections up to 30 years without treatment.
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P. malariae
|
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plasmodium diagnosis is via
|
PCR
serology |
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mosquitos use ___ (2) to directly fight parasitic infection
these degrade ___ and ___ |
proteases
p25, p28 asexual plasmodium gametocytes that haven't formed ookinetes |
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mosquitos use ___ to indirectly fight parasitic infection. ___ inhibits this and enhances plasmodium infection
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gram negative bacteria
antibiotics |
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stages in mosquito gut (4)
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gamete
zygote ookinete oocyst |
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___ is required for invasion of P. vivax
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Duffy Ag
|
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Antibodies against ___ (5) help fight malaria
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sporozoites
infected RBC antigens gametocytes gametes ookinetes |
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___ kills infected RBCs and ___ kills infected hepatocytes
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cytokines
CD8 cells |
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___ (2) can inhibit invasion of liver
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IFNg
cytokines |
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sickle cell trait helps by ___
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lowering intracellular K+
|
|
chloroquine sensitivity is present in ___ (2)
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middle east
mexico |
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___ is recommended prophylactic in sensitive areas. ___ (4) is recommended in resistant areas.
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chloroquine
mefloquine doxycycline malarone primaquine |
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___ can cause CNS symptoms
|
mefloquine
|
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___ is not available in Israel because ___. It works on the ___ stage of ___ (2).
|
primaquine
G6PD function is required hypnozoid p. ovale p. vivax |
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malarone is good but ___. it kills parasites in ___ and ___. it has (fewer/more) side effects than mefloquine. ___ (2) are resistant, though.
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expensive
blood liver fewer p. vivax p. ovale |
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artemisin causes ___ by ___
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denaturation of plasmodium proteins
free radical release |
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___ (2) are antifolate drugs which work on ___
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pyrimethamine
proguanil dihydrofolate reductase |
|
chloroquine works by ___
___ is toxic to plasmodium, but not ___ |
inhibiting Hb aggregation to Hz
Hb Hz |
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DH of Toxoplasma gondii is ___
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cat
|
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T/F T. gondii infection is asymptomatic in most immunocompetent people
|
true
|
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T. gondii can cause ___ in immunosuppressed people and ___ (2) in congenitally infected babies
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CNS disease
blindness mental retardation |
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in cats, T. gondii replicates by ___ (2). In humans, it replicates by ___ in ___.
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schizogony
gametogenesis endodyogeny macrophages |
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T. gondii cysts in cat
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oocyst
pseudocyst |
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humans are infected by ___
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ingesting oocyst or pseudocyst
|
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bradyzoites are present in ___. when they lyse a cell they release ___ into ___.
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pseudocysts
tachyzoites blood |
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tachyzoites stain with
|
giemsa
|
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T. gondii can cause ___ (2) to fetus. Greatest risk for transmission is during ___. ___% have severe damage and ___% abort.
|
abortion
malformation 1st trimester 30 9 |
|
T. gondii diagnosis
|
serology
PCR for immunosuppressed |
|
T. gondii drugs
for mom for fetus (3) for immunosuppressed (2) |
spiramycine
pyramethamine sulfadiazine folinic acid pyramethamine sulfadiazine |
|
E. histolytica drugs (2)
|
metronidazole
iodoquinol |