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CSP - Exam 4 > Ohl - Parasites - JK > Flashcards

Ohl - Parasites - JK Flashcards

1
Q

what does a parasite need?

A

motility, don’t harm the host, don’t cause inflammation, disease, when does it cause problems? when there is too much, or a build up, cause mechanical failure or blockage

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2
Q

What are the 2 kinds of hosts?

A

Definitive host

Intermediate host

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3
Q

What is a Definitive Host?

A

Definitive host is one in which the parasite reaches sexual maturity

i. e. Malaria, the mosquito is the definitive host
i. e. Schistosoma: the human is the definitive host

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4
Q

What is an Intermediate Host?

A

Intermediate host is one which is required for parasite development but one in which the parasite does not reach sexual maturity – i.e. Malaria, humans are the intermediate host i.e. Schistomsoma: the snail is the intermediate host

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5
Q

In Malaria, humans are the ___ host.

A

intermediate host

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6
Q

In schistomsoma, the snail is the:

A

intermediate host

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7
Q

Parasites are a problem in developing countries because _____ share the living space with humans.

A

chicken, water foul, pigs, etc

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8
Q

Parasites are eukaryotic and can be ____.

A

single-celled or multi-celled

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9
Q

Helminths

A

Life cycles complex. Almost always requires an intermediate host.
Humans can be the only host.
The intermediate host or the definitive host.
An accidental or “dead-end” host occurs when a helminth that usually infects another animal attempts to invade or infect a human but cannot complete the necessary stage of its life cycle. Still can cause a self limited illness/disease. Usually, unless re-exposed, the human infection lasts only as long as the life-span of the adult worm or the intermediate stage, Thus the intensity of infection can increase only with repeated re-exposures.

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10
Q

explain dead end host:

A

An accidental or “dead-end” host occurs when a helminth that usually infects another animal attempts to invade or infect a human but cannot complete the necessary stage of its life cycle. Still can cause a self limited illness/disease. Usually, unless re-exposed the human infection lasts only as long as the life-span of the adult worm or the intermediate stage

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11
Q

immune response to helminths

A

Eosinophilia common. Eosinophisl are integral to the immune response to parasites. Seen only in tissue invasion or migratory portions of the life cycle. Not seen with adult worms in intestinal lumen. Not seen with protozoal infections.

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12
Q

if parasite is not invasive (i.e. hookworm) there will be….

A

no eosinophils in the biopsy

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13
Q

______ will not cause eosinophilia

A

single cell parasites (protazoa)

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14
Q

entamoeba have usually _____ in it’s _____

A

2 nuclei in its trophozoite stages,

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15
Q

trophozoite stage:

A

secretes virulence factors, invades, moves, etc, it is the active stage!

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16
Q

cyst stage

A

sleep stage, cysts prevents damage, etc (trophozoite is more sensitive and prone to injury)

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17
Q

when trying to control parasite you seek to reach it at the:

A

cyst stage

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18
Q

entamoeba:

A

engulf rbcs, transform to trophozoite, moves to colon, invades colon, perforates, causes abscesses

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19
Q

virulance factor of entamoeba:

A

Galactosamine adherence lectin. Proteinases

Lysis of WBC’s

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20
Q

how do you contract giardia?

A

Cysts found in surface waters where mammalian reservoirs frequent (beaver the prototype)Transmission: water&raquo_space; food, person-to-person, zoonosis (dog or cat). Most common enteric parasite in the USA and Canada. Sporadic infection in US seen in outdoor adventurers. Small epidemics seen associated with day-care or swimming pools.congregate water sports!wading pool: shallow, warm, fecal deposition, feces get in the water, large people populations, cholrine won’t kill

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21
Q

difference between giardia and amoeba

A

troph cyst cyst troph, giardia doesn’t penetrate colon, amoeba does

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22
Q

crptosporridium

A

intracellular, gets inside cell (giardia extracellular and attaches, amoeba are invasive) insert into microvilli

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23
Q

cryptosporidium loves to contaminate

A

cows, contaminated foods, apple cider, sprouts, lettuce, cabbage, bigger risk in swimming bc it’s super resistant to water, chlorination doesn’t do much

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24
Q

cryptosporidium can:

A

kill hiv patients, hard to treat, etc

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25
Q

epidemeology of malaria

A

40% of world population at riskTropical and subtropical regions80% of cases occur in Africa300-500 million cases a year1.5 – 2.7 million deaths a year90% in sub-Saharan Africa½ in children less than 5 yrs of ageAlso high risk in pregnant women and non-immune travelers12 billion dollars in lost revenue/year in Africa

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26
Q

4 types of malaria

A

P. falciparumMost dangerousP. vivax & P. ovaleLess dangerousCan relapse because of “hidden” liver stage that can persist despite drug treatmentP. malariaeRareDifferent distributions of species depending on geography

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27
Q

2 main groups of malaria: ___ and ____, which are dangerous and reoccurring

A

falciforum, vivax&ovale

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28
Q

Malaria transmission

A

Anopheline mosquito (female only)Aggressive night time biter (dusk to dawn)Reservoirs of infected and uninfected humansNeeds opportunity for host-vector contactMostly tropical and subtropical, altitudes below 1500mAlso can be transmitted by transfusion, needles, and transplacentally

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29
Q

life cycle of mosquito

A

Anopheles mosquito inoculates sporozoites into humanExoerythrocytic schizogony:Sporozoites infect liver cells Mature into schizonts, then rupture and release merozoites P.ovale and P.vivax have a dormant stage (hypnozoites) in liver and can persist for years, causing relapses when they invade bloodstream

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30
Q

the ______ mosquito inoculates ______ into _____

A

anopheles, sporozoites, humans

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31
Q

Exoerythrocytic schizogony:

A

Sporozoites infect liver cells Mature into schizonts, then rupture and release merozoites P.ovale and P.vivax have a dormant stage (hypnozoites) in liver and can persist for years, causing relapses when they invade bloodstream

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32
Q

Erythrocytic schizogony:

A

Erythrocytic schizogony (asexual reproduction)Merozoites infect red blood cellsRing stage trophozoites mature into schizontsSchizonts rupture and release merozoites

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33
Q

Sexual erythrocytic stage

A

Sexual erythrocytic stage Some form gametocytesIngested by mosquito

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34
Q

sporogonic cycle:

A

Sporogonic cycle (in the mosquito)Micro and macro gametocytes develop into zygotes then ookinetesOokinetes invade midgut wall, become oocystsOocysts rupture and release sporozoites which travel to salivary glands for injection into human host

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35
Q

need to know: when a mosquito bites a human, it injects a:

A

sporazoite (need to know)

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36
Q

_____ infect liver cells, and then the ____ which are released upon rupture

A

hepatic schizonts, merozoites

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37
Q

the _____ can infect the rbc after they:

A

merozoite, have matured from the sporazoite and then are ruptured

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38
Q

when merozite infects RBC, it matures and forms___ or a ___

A

trophozoite or gametozite

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39
Q

disease is introduced from:

A

liver

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40
Q

_____ get involved with sexual reproduction

A

gametocytes and the sporite is formed

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41
Q

one response can be:

A

immune response against sporazoite (immunization)

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42
Q

another place to attack

A

the liver cells, as sporozoite infects liver cell and forms shizonts and mirazoite, you could attack it

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43
Q

you could also attack in

A

the erythrocytic cycle

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44
Q

a backwards approach would be

A

prevent mosquitos from getting the disease, transmission blocking vaccine

45
Q

transmission blocking vaccine

A

prevents the mosquito from getting the disease

46
Q

infected RBC you can find by identifying the:

A

trophozoytes

47
Q

malaria gametocyte look like:

A

bananas

48
Q

malaria causes most damage in:

A

brain kidneys heart

49
Q

risk factors for malaria

A

Risk of severe disease greatest in young children and travellers to areaNo specific protective antibodies or cell-mediated immunity found Partial immunity develops over timeNormal spleen function importantRemoves parasitized RBCs from circulation because they are less deformable

50
Q

important to know about malaria resistance:

A

continuously exposed, you will develop partial immunity, and this will help control or keep you from dying… won’t keep you from getting the infection, still get it. AFricans who have been infected several times may learn to deal with the disease and not die (thus pregnant women and children have most susceptibility) partial immunity is not long lasting!

51
Q

risk of malaria:

A

native africans, who had immunity, then come to us, then go back… immunity has worn off

52
Q

for travelers, they look at fever thinking:

A

fever usually goes up, then drops back down during replication phase, then jumps up again 48 hours later, but travelers can take 2 weeks to synchronize to this schedule and by this time you’re in the icu (synchronization is only in endemic areas)

53
Q

babesio ____, translated by ___

A

microti tick

54
Q

looks like malaria, sounds like malaria, never been outside us

A

babesio

55
Q

________ disease is transmitted via___ which are able to ______, and is found in _____

A

trypanasoma brucei, chase down animals, africa

56
Q

life cycle of Trypanasome brucei:

A

promastagote insect stage, amastigote tissue infections stage. Promastagote enters human blood stream and is distributed to tropic areas

57
Q

important: how does trypanosomiasis avoid immune system:

A

periodically changes is glycoprotein coat, antigenic coat, so antibodies form, moves its genetic cassette around and switches up antibodies

58
Q

trypanosomiasis in us is transmitted via

A

reduvid bug (parasite lives in gut of bug and it’s deficated into slit that it makes while it’s lapping up your blood)

59
Q

trypanasoma cruzia presents with:

A

lymphadenapothy behind ears, then encephalitis, then smooth muscle, organs, etc leading cause of congestive heart failure in brazil

60
Q

toxoplasma:

A

pregnant women who get toxoplasma WILL infect baby and it will cause retardation (transferred through the placenta)

61
Q

hookworm:

A

globally 1x10^9 people infected, risk has to do with the life cycle, people sleep on the ground, bare foot, etc,

62
Q

life cycle of hookworm:

A

infective larvae, infects skin, infects venuole, matures in lungs, swallowed, back into gi, hooks onto the gi tract, lives off rbcs and matures,

63
Q

what part of the lifecycle is hookworm detected by immune system?

A

eosinophilia: when the tissue migratory phase, when hook worm is burrowing through the lung, causes PNU

64
Q

hookworm was erradicated in nc by interferring in the life cycle at:

A

larvae penetrate the skin

65
Q

dog or cat hookworm lack

A

enzymes to enter human venoules

66
Q

schistosomiasis

A

wet areas of africa, lakes, etc, either still water or fresh

67
Q

schisto life cycle starts with:

A

sercaria released by snail, enters human through skin, migrates to one of two blood supplies

68
Q

what 2 blood supplies do schisto migrate to?

A

portal ciculation of gut, hematomium the plexus of the bladder, they then live there and copulate their entire life, the eggs go downstream from gut and get stuck in liver

69
Q

(know) long term effect of schistoma mansoni

A

liver cirrhosis, 20 years later, kills human, in bladder it scars up, bladder infections, possible bladder cancer

70
Q

eggs can break out of bladder, and the eggs will be pooped or peed into environment:

A

egg gets into water source, gets into snail and matures further, snail is intermediate host

71
Q

pond with schistasomiasis in it, you can get rid of it by:

A

killing every snail in the pond, can’t do it

72
Q

bc schistasomiasis is invasive,

A

it causes eosinophilia

73
Q

to avoid immune system, schisto

A

puts host antibody proteins on surface

74
Q

(know this) schistasomiasis can be detected and treated for:

A

cirrhosis of liver or bladder cancer down the road

75
Q

tape worms:

A

t. saginata (cow), t. soleum (pig), diphyllobathrium (fish), can only get B12 from host

76
Q

adult tape worm:

A

asymptomatic, until you pass pieces in your stool

77
Q

adult tape worm can:

A

cause cysticercal phase, human ingests eggs and cysticerci will end up in tissues and brain

78
Q

adult tape worms show ______

A

little or no eosinophilia

79
Q

life cycle of tape worm in intestine:

A

egg hatches in animal, forms larvae, burrows through, goes through tissue, brain, incystacircus has skullix in it, the incysticircus falls apart, skullix comes out, attaches to our gut, etc

80
Q

also could eat tapeworm egg via

A

hands in dirt, get on hand, eat eggs, egg hatches, flariform larvae comes out, burrows through intestine, goes through muscles and to brain

81
Q

cysticircae in the brain:

A

they die, causes inflammation in the brain, this causes a seizure, most common cause seizures in central america, mexico,

82
Q

(know) cysticircae is an example of

A

when the human can be the intermediate host or the difinitive host

83
Q

definitive host:

A

host where sexual maturity occurs

84
Q

intermediate host:

A

maturation in an intermediate life form adult tape worm is where sexual maturity happens, in our gut, that’s us as a definitive, cysticircae is an example of us being an intermediate host

85
Q

anti-malaria drugs:

A

ChloroquineMefloquine (Lariam®)Atovaquone/proguanil (Malarone®)DoxycyclineArtemether/lumefantrine (ACT)Quinine/Quinidine (IV for Rx)Primaquine

86
Q

how does chloroquine work?

A

Inhibits heme polymerase. Trophozoites that are maturing are chewing up hemoglobin in rbc. When it does that, it gets small pieces of heme ring (heme ring is toxic to trophozoite) so trophozoite makes a heme polymerase (bunches it up and cleaves it until its no longer toxic). If you inhibit heme polymerase, the heme builds up in the blood and the trophozoite dies.Resistance occurs through drug effluxActive against ERYTHOCYTIC states (non-liver stages) of

87
Q

what stage of the life cycle does chloroquine work on?

A

Liver stage? no, no heme! the erythrocytic stage (non-liver stage) where heme is being matabolized

88
Q

plasmodium falcipirum is resistant to chloroquine

A

in c. america, n. guinea, hispanola

89
Q

chloroquine:

A

orally, long time, weekly, well tolerated, etc

90
Q

mefloquine

A

works against all chloroquine resistant drugs, half life is 5-7 weeks, have to take 2 weeks to start building up immunity, causes dreams

91
Q

malarone

A

works against the liver stage! other 2 you have to take for weeks, you interrupt early with malarone, prevention or treatment, no dream issues, etc, take daily

92
Q

doxycycline

A

effective against chloroquine but causes rash in sun

93
Q

quinine

A

too much resistance, unless used with doxycycline (synergystic) we always have it, heart monitoring

94
Q

big advance in malaria therapy:

A

artemisin, wormwood plant, works on erythrocytic stage by binding iron, breaking down peroxide bridges and causes free radicals that damage parasite proteins

95
Q

_______ decreases parasitemia the fastest

A

artemisin (starting next year this will be the new staple drug in the us)

96
Q

how does resistance occur?

A

people don’t take medication properly, not long enough or not the right amount

97
Q

What is the current strategy for preventing resistance to artemisin?

A

combination therapy “ACT” artemisin plus lumefantrine

98
Q

primaquine:

A

only active against liver stages, both active hepatic schizade and sleeping hypnozoite, thus used for terminal prophylaxis, not active against retrocytic stages, vivax and ovale

99
Q

what is terminal prophylaxis

A

prophylaxis that is given at the very end of it of the other prophylaxis that we do, and that’s because it’s effective against that liver stage

100
Q

fear of prophylaxis?

A

G6PD deficiency, can cause dangerous anemia

101
Q

for treatment or prevention?

A

use a drug against erythrocytic stage: chloroquine, methoquine, quinine/quinidine, doxycycline, artemis artemisens (easier to remember the drugs that work against liver)

102
Q

(know) what drugs work against the liver stage?

A

atovaquone and proquanal, and primaquine, they interfere with schizade production and the rupture of the schuzade

103
Q

(know) two species that cause relapse in malaria?

A

vivax and ovale, how? hepatic schizade goes to sleep in liver, so instead of maturing and rupturing, it’s a hiddenzoic, sleeps for months or years, wakes up, then transforms back to an active schizade, ruptures and goes out

104
Q

atovaquone and proguanal cannot: (know)

A

work against the hypnozoite

105
Q

you get vivax malaria…

A

treated with chloroquine to get rid of erythrocytic stage, then the last two weeks, primquine to kill off any hypnozoites that may have happened during that infection, same thing with prevention if you’re going to an area where there’s vivax and ovale, at the end of chloroquine treatment, you get primaquin (terminal prophylaxis)

106
Q

what is the only drug that works against hypnozoite? (know)

A

primaquin

107
Q

What drug do we use against the liver phase? (know)

A

atoloquone and proguanal (malorone)

108
Q

prophylaxis in non resistant areas? resistant? (know)

A

chloroquine. meflo, doxy, malarone (dreams, rash, pocket book)

CSP - Exam 4 (22 decks)

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