parasite Flashcards
what does a parasite need?
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
What are the 2 kinds of hosts?
Definitive host and intermediate
what is a definitive host?
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
what is intermediate
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
in malaria, humans are:
intermediate host
in schistomsoma, the snail is the:
intermediate host
parasites are a problem in developing countries because _____ share the living space with humans
chicken, water foul, pigs, etc
Parasites are eukaryotic and can be?
Parasites are eukaryotic
one-celled or
muti-cellular
Protozoa are all ____ and include:
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
Helminths
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.
explain dead end 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
immune response to helminths
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
if parasite is not invasive (i.e. hookworm) there will be….
no eosinophils in the biopsy
______ will not cause eosinophilia
single cell parasites (protazoa)
entamoeba have usually _____ in it’s _____
2 nuclei in its trophozoite stages,
trophozoite stage:
secretes viralence factors, invades, moves, etc, it is the active stage!
cyst stage
sleep stage, cysts prevents damage, etc (trophozoite is more sensitive and prone to injury)
when trying to control parasite you seek to reach it at the:
cyst stage
entamoeba:
engulf rbcs, transform to trophozoite, moves to colon, invades colon, perforates, causes abscesses
virulance factor of entamoeba:
Galactosamine adherence lectin
Proteinases
Lysis of WBC’s
how do you contract giardia?
Cysts found in surface waters where mammalian reservoirs frequent (beaver the prototype)
Transmission: water»_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
difference between giardia and amoeba
troph cyst cyst troph, giardia doesn’t penetrate colon, amoeba does
crptosporridium
intracellular, gets inside cell (giardia extracellular and attaches, amoeba are invasive) insert into microvilli
cryptosporidium loves to contaminate
cows, contaminated foods, apple cider, sprouts, lettuce, cabbage, bigger risk in swimming bc it’s super resistant to water, chlorination doesn’t do much
cryptosporidium can:
kill hiv patients, hard to treat, etc
epidemeology of malaria
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
4 types of malaria
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
2 main groups of malaria: ___ and ____, which are dangerous and reoccurring
falciforum, vivax&ovale
Malaria transmission
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
life cycle of mosquito
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
the ______ mosquito inoculates ______ into _____
anopheles, sporozoites, humans
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
Erythrocytic schizogony:
Erythrocytic schizogony (asexual reproduction)
Merozoites infect red blood cells
Ring stage trophozoites mature into schizonts
Schizonts rupture and release merozoites
Sexual erythrocytic stage
Sexual erythrocytic stage
Some form gametocytes
Ingested by mosquito
sporogonic cycle:
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
need to know: when a mosquito bites a human, it injects a:
sporazoite (need to know)
_____ infect liver cells, and then the ____ which are released upon rupture
hepatic schizonts, merozoites
the _____ can infect the rbc after they:
merozoite, have matured from the sporazoite and then are ruptured
when merozite infects RBC, it matures and forms___ or a ___
trophozoite or gametozite
disease is introduced from:
liver
_____ get involved with sexual reproduction
gametocytes and the sporite is formed
one response can be:
immune response against sporazoite (immunization)
another place to attack
the liver cells, as sporozoite infects liver cell and forms shizonts and mirazoite, you could attack it
you could also attack in
the erythrocytic cycle
a backwards approach would be
prevent mosquitos from getting the disease, transmission blocking vaccine
transmission blocking vaccine
prevents the mosquito from getting the disease
infected RBC you can find by identifying the:
trophozoytes
malaria gametocyte look like:
bananas
malaria causes most damage in:
brain kidneys heart
risk factors for malaria
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
important to know about malaria resistance:
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!
risk of malaria:
native africans, who had immunity, then come to us, then go back… immunity has worn off
for travelers, they look at fever thinking:
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)
babesio ____, translated by ___
microti tick
looks like malaria, sounds like malaria, never been outside us
babesio
________ disease is transmitted via___ which are able to ______, and is found in _____
trypanasoma brucei, chase down animals, africa
life cycle of Trypanasome brucei:
promastagote insect stage, amastigote tissue infections stage. Promastagote enters human blood stream and is distributed to tropic areas
important: how does trypanosomiasis avoid immune system:
periodically changes is glycoprotein coat, antigenic coat, so antibodies form, moves its genetic cassette around and switches up antibodies
trypanosomiasis in us is transmitted via
reduvid bug (parasite lives in gut of bug and it’s deficated into slit that it makes while it’s lapping up your blood)
trypanasoma cruzia presents with:
lymphadenapothy behind ears, then encephalitis, then smooth muscle, organs, etc leading cause of congestive heart failure in brazil
toxoplasma:
pregnant women who get toxoplasma WILL infect baby and it will cause retardation (transferred through the placenta)
hookworm:
globally 1x10^9 people infected, risk has to do with the life cycle, people sleep on the ground, bare foot, etc,
life cycle of hookworm:
infective larvae, infects skin, infects venuole, matures in lungs, swallowed, back into gi, hooks onto the gi tract, lives off rbcs and matures,
what part of the lifecycle is hookworm detected by immune system?
eosinophilia: when the tissue migratory phase, when hook worm is burrowing through the lung, causes PNU
hookworm was erradicated in nc by interferring in the life cycle at:
larvae penetrate the skin
dog or cat hookworm lack
enzymes to enter human venoules
schistosomiasis
wet areas of africa, lakes, etc, either still water or fresh
schisto life cycle starts with:
sercaria released by snail, enters human through skin, migrates to one of two blood supplies
what 2 blood supplies do schisto migrate to?
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
(know) long term effect of schistoma mansoni
liver cirrhosis, 20 years later, kills human, in bladder it scars up, bladder infections, possible bladder cancer
eggs can break out of bladder, and the eggs will be pooped or peed into environment:
egg gets into water source, gets into snail and matures further, snail is intermediate host
pond with schistasomiasis in it, you can get rid of it by:
killing every snail in the pond, can’t do it
bc schistasomiasis is invasive,
it causes eosinophilia
to avoid immune system, schisto
puts host antibody proteins on surface
(know this) schistasomiasis can be detected and treated for:
cirrhosis of liver or bladder cancer down the road
tape worms:
t. saginata (cow), t. soleum (pig), diphyllobathrium (fish), can only get B12 from host
adult tape worm:
asymptomatic, until you pass pieces in your stool
adult tape worm can:
cause cysticercal phase, human ingests eggs and cysticerci will end up in tissues and brain
adult tape worms show ______
little or no eosinophilia
life cycle of tape worm in intestine:
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
also could eat tapeworm egg via
hands in dirt, get on hand, eat eggs, egg hatches, flariform larvae comes out, burrows through intestine, goes through muscles and to brain
cysticircae in the brain:
they die, causes inflammation in the brain, this causes a seizure, most common cause seizures in central america, mexico,
(know) cysticircae is an example of
when the human can be the intermediate host or the difinitive host
definitive host:
host where sexual maturity occurs
intermediate host:
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
anti-malaria drugs:
Chloroquine Mefloquine (Lariam®) Atovaquone/proguanil (Malarone®) Doxycycline Artemether/lumefantrine (ACT) Quinine/Quinidine (IV for Rx) Primaquine
how does chloroquine work?
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
what stage of the life cycle does chloroquine work on?
Liver stage? no, no heme! the erythrocytic stage (non-liver stage) where heme is being matabolized
plasmodium falcipirum is resistant to chloroquine
in c. america, n. guinea, hispanola
chloroquine:
orally, long time, weekly, well tolerated, etc
mefloquine
works against all chloroquine resistant drugs, half life is 5-7 weeks, have to take 2 weeks to start building up immunity, causes dreams
malarone
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
doxycycline
effective against chloroquine but causes rash in sun
quinine
too much resistance, unless used with doxycycline (synergystic) we always have it, heart monitoring
big advance in malaria therapy:
artemisin, wormwood plant, works on erythrocytic stage by binding iron, breaking down peroxide bridges and causes free radicals that damage parasite proteins
_______ decreases parasitemia the fastest
artemisin (starting next year this will be the new staple drug in the us)
how does resistance occur?
people don’t take medication properly, not long enough or not the right amount
What is the current strategy for preventing resistance to artemisin?
combination therapy “ACT” artemisin plus lumefantrine
primaquine:
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
what is terminal prophylaxis
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
fear of prophylaxis?
G6PD deficiency, can cause dangerous anemia
for treatment or prevention?
use a drug against erythrocytic stage: chloroquine, methoquine, quinine/quinidine, doxycycline, artemis artemisens (easier to remember the drugs that work against liver)
(know) what drugs work against the liver stage?
atovaquone and proquanal, and primaquine, they interfere with schizade production and the rupture of the schuzade
(know) two species that cause relapse in malaria?
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
atovaquone and proguanal cannot: (know)
work against the hypnozoite
you get vivax malaria…
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)
what is the only drug that works against hypnozoite? (know)
primaquin
What drug do we use against the liver phase? (know)
atoloquone and proguanal (malorone)
prophylaxis in non resistant areas? resistant? (know)
chloroquine. meflo, doxy, malarone (dreams, rash, pocket book)
