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Ohl Exam 4 > parasite > Flashcards

parasite 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 and intermediate

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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 intermediate

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:

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

Parasites are eukaryotic
one-celled or
muti-cellular

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9
Q

Protozoa are all ____ and include:

A

Protozoa (unicellular); Blood
Vector borne (mosquito, fly or tick)
Two host life cycle
Ex. Plasmodia sp. (malaria)
Ex. Trypanosoma sp. (Chagas disease and sleeping sickness)
Ex. Babesia (Babesiosis: North America and Europe)Enteric (gut)
Entamoeba sp. (amoebiasis)
Giardia sp. (giardiasis)
Cryptosporidium parvum (cryptosporidiosis)
Generally two form life cycle
Trophozoite –causes disease
Cyst: resists desiccation in the environment
Fecal-oral spread (either direct human to human or through food/water)
Desiccate easily in the environment
Intestinal lumen without invasion
Giardia
Cryptosporidium
Invade intestinal mucosa
Entamoeba

Tissue
Two host cycles
Ex. Toxoplasma
Ex. Leishmania sp. (Leishmaniasis)
Leishmania vector borne
Toxoplasma food borne
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10
Q

Helminths

A

Life cycles complex
Almost always requires an intermediate host
Humans can be
The only host
The intermediate host
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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11
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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12
Q

immune response to helminths

A

Eosinophilia common
Eosinophil is integral to the immune response to parasites
Seen only in tissue invasive or migratory portions of the life cycle
Not seen with adult worms in intestinal lumen
Not seen with protozoal infections

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13
Q

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

A

no eosinophils in the biopsy

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14
Q

______ will not cause eosinophilia

A

single cell parasites (protazoa)

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15
Q

entamoeba have usually _____ in it’s _____

A

2 nuclei in its trophozoite stages,

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16
Q

trophozoite stage:

A

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

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17
Q

cyst stage

A

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

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18
Q

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

A

cyst stage

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19
Q

entamoeba:

A

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

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20
Q

virulance factor of entamoeba:

A

Galactosamine adherence lectin
Proteinases
Lysis of WBC’s

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21
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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22
Q

difference between giardia and amoeba

A

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

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23
Q

crptosporridium

A

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

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24
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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25
Q

cryptosporidium can:

A

kill hiv patients, hard to treat, etc

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26
Q

epidemeology of malaria

A 
40% of world population at risk
Tropical and subtropical regions
80% of cases occur in Africa
300-500 million cases a year
1.5 – 2.7 million deaths a year
90% in sub-Saharan Africa
½ in children less than 5 yrs of age
Also high risk in pregnant women and non-immune travelers
12 billion dollars in lost revenue/year in Africa
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27
Q

4 types of malaria

A 
P. falciparum
Most dangerous
P. vivax & P. ovale
Less dangerous
Can relapse because of “hidden” liver stage that can persist despite drug treatment
P. malariae
Rare
Different distributions of species depending on geography
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28
Q

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

A

falciforum, vivax&ovale

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29
Q

Malaria transmission

A

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

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30
Q

life cycle of mosquito

A

Anopheles mosquito inoculates sporozoites into human
Exoerythrocytic 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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31
Q

the ______ mosquito inoculates ______ into _____

A

anopheles, sporozoites, humans

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32
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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33
Q

Erythrocytic schizogony:

A

Erythrocytic schizogony (asexual reproduction)
Merozoites infect red blood cells
Ring stage trophozoites mature into schizonts
Schizonts rupture and release merozoites

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34
Q

Sexual erythrocytic stage

A

Sexual erythrocytic stage
Some form gametocytes
Ingested by mosquito

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35
Q

sporogonic cycle:

A 
Sporogonic cycle (in the mosquito)
Micro and macro gametocytes develop into zygotes then ookinetes
Ookinetes invade midgut wall, become oocysts
Oocysts rupture and release sporozoites which travel to salivary glands for injection into human host
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36
Q

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

A

sporazoite (need to know)

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37
Q

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

A

hepatic schizonts, merozoites

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38
Q

the _____ can infect the rbc after they:

A

merozoite, have matured from the sporazoite and then are ruptured

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39
Q

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

A

trophozoite or gametozite

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40
Q

disease is introduced from:

A

liver

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41
Q

_____ get involved with sexual reproduction

A

gametocytes and the sporite is formed

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42
Q

one response can be:

A

immune response against sporazoite (immunization)

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43
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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44
Q

you could also attack in

A

the erythrocytic cycle

45
Q

a backwards approach would be

A

prevent mosquitos from getting the disease, transmission blocking vaccine

46
Q

transmission blocking vaccine

A

prevents the mosquito from getting the disease

47
Q

infected RBC you can find by identifying the:

A

trophozoytes

48
Q

malaria gametocyte look like:

A

bananas

49
Q

malaria causes most damage in:

A

brain kidneys heart

50
Q

risk factors for malaria

A

Risk of severe disease greatest in young children and travellers to area
No specific protective antibodies or cell-mediated immunity found
Partial immunity develops over time
Normal spleen function important
Removes parasitized RBCs from circulation because they are less deformable

51
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!

52
Q

risk of malaria:

A

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

53
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)

54
Q

babesio ____, translated by ___

A

microti tick

55
Q

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

A

babesio

56
Q

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

A

trypanasoma brucei, chase down animals, africa

57
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

58
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

59
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)

60
Q

trypanasoma cruzia presents with:

A

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

61
Q

toxoplasma:

A

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

62
Q

hookworm:

A

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

63
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,

64
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

65
Q

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

A

larvae penetrate the skin

66
Q

dog or cat hookworm lack

A

enzymes to enter human venoules

67
Q

schistosomiasis

A

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

68
Q

schisto life cycle starts with:

A

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

69
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

70
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

71
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

72
Q

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

A

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

73
Q

bc schistasomiasis is invasive,

A

it causes eosinophilia

74
Q

to avoid immune system, schisto

A

puts host antibody proteins on surface

75
Q

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

A

cirrhosis of liver or bladder cancer down the road

76
Q

tape worms:

A

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

77
Q

adult tape worm:

A

asymptomatic, until you pass pieces in your stool

78
Q

adult tape worm can:

A

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

79
Q

adult tape worms show ______

A

little or no eosinophilia

80
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

81
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

82
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,

83
Q

(know) cysticircae is an example of

A

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

84
Q

definitive host:

A

host where sexual maturity occurs

85
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

86
Q

anti-malaria drugs:

A 
Chloroquine
Mefloquine (Lariam®)
Atovaquone/proguanil (Malarone®)
Doxycycline
Artemether/lumefantrine (ACT)
Quinine/Quinidine (IV for Rx)
Primaquine
87
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 efflux
Active against ERYTHOCYTIC states (non-liver stages) of

88
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

89
Q

plasmodium falcipirum is resistant to chloroquine

A

in c. america, n. guinea, hispanola

90
Q

chloroquine:

A

orally, long time, weekly, well tolerated, etc

91
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

92
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

93
Q

doxycycline

A

effective against chloroquine but causes rash in sun

94
Q

quinine

A

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

95
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

96
Q

_______ decreases parasitemia the fastest

A

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

97
Q

how does resistance occur?

A

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

98
Q

What is the current strategy for preventing resistance to artemisin?

A

combination therapy “ACT” artemisin plus lumefantrine

99
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

100
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

101
Q

fear of prophylaxis?

A

G6PD deficiency, can cause dangerous anemia

102
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)

103
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

104
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

105
Q

atovaquone and proguanal cannot: (know)

A

work against the hypnozoite

106
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)

107
Q

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

A

primaquin

108
Q

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

A

atoloquone and proguanal (malorone)

109
Q

prophylaxis in non resistant areas? resistant? (know)

A

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

Ohl Exam 4 (5 decks)

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