Flashcards in parisitology review Deck (196):
what are parasites?
eukaryotic pathogens that lack a cell wall (unlike fungi)
what are single cell parasites?
what are multi-cellular parasites?
helminths and arthropods
parasites are separated into what 2 groups?
GI and blood/tissue depending on the usual site of the pathology
what is a definitive host?
the site of sexual reproduction of a parasite
what is an intermediate host?
the site of non-sexual dvpmt of a parasite (ie it matures, but doesn't reproduce)
what is a dead end host?
a host that doesn't transmit the parasite-- that said, the host can become sick and die from the parasite
can vectors be hosts?
the human is a definitive host for which 3 parasites?
2. GI Helminths
3. Taenia Solium
Humans are intermediate hosts for which parasites?
Humans are a dead end host for which parasites
which parasite can use the human as a definitive host or a dead end host depending on the route of ifxn?
what is a vector?
an arthropod that transmits an ifxn-- it can double as a host (ie it is a definitive host for malaria)
anopheles mosquito is the vector for which parasite?
plasmodium species are transmitted by what vector?
triatomine bug is teh vector for which parasite?
trypanosoma cruzi is transmitted by which vector?
Tsetse fly is the vector for which parasite?
Trypanosoma brucei is transmitted by which vector?
the sandfly transmits which parasite?
Leishmania species are transmitted by which vector?
Simulium blackflies transmit which parasite?
onchocerca volvulus are transmitted by which vector?
what is a reservoir?
a non-human site where a pathogen survives
reservoir control is critical for...
4 mechanisms of damage by parasites
1) mechanism impairment
2) kills cells (invasion or cytolysis)
3. competition for nutrients
4) inflammation ---> tissue damage
which 3 parasites damage their hosts via mechanical damage? where is this damage?
1. Echinococcus granulosus - liver
2. Ascaris lumbricoides - intestine
3. Plasmodium falciparum- capillaries, PCV
where does echniococcus granulosus cause mechanical damage, and how does it do it?
in the liver via the formation of hepatic cysts
where does ascaris lumbricoides cause mechanical damage and how does it do it?
intestine, via obstruction
where does plasmodium falciparum cause mechanical damage and how does it do it?
in the capillaries and PCV, via obstruction (by binding RBCs to the endothelium) which causes hypoxia (esp in the brain)
which 3 parasites kill host cells? and where do they do this?
1. Entamoeba histolytica- liver
2. trypanosoma cruzi - heart
3. Leishmania species - macrophages (spleen/liver)
Where does Entamoeba histolytica kill host cells, and what is the resultant damage?
liver ---> necrosis that's like anchovy paste
Where does Trypanosoma cruzi kill host cells, and what is the resultant damage?
heart ---> myocarditis, enlargement
Where do Leishmania species kill host cells, and what is the resultant damage?
macrophages (liver/spleen) ---> splenomegaly and hepatic failure
what are two parasites that compete for nutrients, and where are they located?
1. Hookworms in the GI tract
2. Diphyllobothrium latum in the GI tract
where do Hookworms compete for nutrients and what damage does it cause the host?
in the GI tract-- the worm sucks out blood leading to blood loss ---> anemia
where do Diphyllobothrium latum (tapeworms) compete for nutrients and what damage does it cause the host?
In the GI tract. They adsorb vitamin B12 through their skin ----> anemia
2 parasites that cause damage by inflammation, and where the inflammation is located
1. Onchocerca volulus - in the eye
2. Trypasnosoma cruzi - nerves
Where does Onchocerca volvulus cause inflammation, and what damage results?
in the eye ---> blindness
where does Trypanosoma cruzi cause inflammation and what damage results?
in the nerves ---> megasophagus, megacolon, heart (arrhythmia)
how are protozoa classified?
3 groups of motility by which protozoa are classified
1) flagella -- can swim
3) often non-motile
3 groups of protozoa and their motility
1. flagellates- flagella
2. amebas- pseudopods
3. apicomplexans (coccida) - often non-motile
other features (2):
other features (2): asexual, trophozoite and cyst
other features (1):
other features (1): asexual
other features (3):
motility: often non-motile
other features (3): asexual and sexual. apical complex organelle, intracellular replication
which Apicomplexan protozoan parasites are GI parasites?
which Apicomplexan protozoan parasites are Blood/Tissue parasites? (2)
1. Plasmodium species
2. Toxoplasma gondii
which flagellate protozoan parasites are GI parasites? (1)
which flagellate protozoan parasites are blood/tissue parasites? (2)
1. Trypanosoma species
2. Leishmania species
Which ameba protozoan parasites are GI parasites? (1)
1. Entamoeba histolytica (but it also spreads from there)
Which ameba protozoan parasites are blood/tissue parasites?
none-- although entamoeba histolytica does spread from the GI to other areas
Giardia Lamblia spreads to the host from? via? in what form?
animals and people via fecal oral transmission in cyst form
Giardia Lamblia is what type of protozoa?
pathogenesis of the flagellate Giardia Lamblia? (4)
1. cyst consumed via fecal oral route from people or animals
2. replication in GI tract
3. Giardia adheres to the mucosa of the small intestine
symptoms of giardia?
2. symptmatic: diarrhea, flatus (gas), cramping
entamoeba histolytica is what type of protazoa?
how is entamoeba histolytica spread?
fecal-oral consumption of cysts- spread from person to person
pathogenesis of entamoeba histolytica
1. fecal-oral transmission of cysts
2. replication in the GI tract
3. adheres to colonic mucosa
4. It kills cells with contact
5. it invades and spreads locally
6. causes colonic ulceration and hepatic abscesses (anchovy paste)
Plasmodium species and toxoplasma gondii are what type of protozoa and where do they attack?
they're apicomplexans and they attack blood/tissue
how do you acquire Toxoplasma Gondii? (3)
1. Primary route: ingestion of oocysts from rare meat
2. ingestion of oocysts from cat feces
3. vertical transmission (newly infected mother)
How does Adult (aka post natal) toxoplasmosis gondii spread in the the body?
through the blood
adult toxoplasmosis gondii spreads in the blood, encysts and...
is generally controlled by the immune response
manifestations of Primary infection with toxoplasmosis gondii
asymptomatic or mononucleosis like
what things have mononucleosis like symptoms?
CMV- non-heterophile mono
Acute HIV ifxn
when immunocompromised people with T cell defects (like HIV pts) get toxoplasmosis gondii, what happens?
reactivation/proliferation of toxoplasmosis ---> severe ifxn with encephalitis
What is congenital toxoplasmosis?
when toxoplasmosis gondii spreads in the blood of the mother, crosses the placenta and infects the fetus
why are pregnant women instructed to avoid raw meats and cats?
to avoid Toxoplasmosis gondii
3 different outcomes of congenital toxoplasmosis gondii
1. stillbirth/spontaneous abortion
2. illness at birth with jaundice and hepatosplenamegaly
3. unapparent ifxn at birth
babies with congenital toxoplasmosis who are ill at birth have...
jaundice and hepatosplenomegaly ---> chorioretinitis and CNS abnormalities (calcifications, hydrocephalus and microcephaly)
babies with congenital toxoplasmosis that is unapparent at birth will still get (3)
2, hearing loss
3. developmental delay
plasmodium species are transmitted by which vector?
3 modes of transmission of plasmodium species?
1. anopheles mosquito
2. vertical transmission
why do they ask you about travel when you're giving blood
to screen you for malaria
pathogenesis of plasmodium species
1. transmitted via anopheles mosquito, vertical transmission or blood tranfusion
2. travels in the blood to the liver
3. either becomes latent hynozoites (dormant protozoa) (P. vivax or P ovale) or go into RBCs
4. Once in the RBCs they replicate and dvp gametocytes
5. the gametocytes are picked up by mosquitoes where they sexually reproduce
6. the mosquito bites a new host...
3 different malaria species. Which is the most severe?
plasmodium falciparum -- most severe!!
manifestations of all 3 malaria species (vivax, ovale and falciparum)
1. constitutional symp: fever, headache nausea
2. fever can become cyclical (every 2-3 days)
3. anemia and splenomegaly is variable
severe manifestations of malaria caused by plasmodium falciparum
cerebral malaria: encephalopathy and coma
severe anemia, hypoglycemia, acidosis (bc of damage to kidneys/lysis of RBCs) and renal impairment (bc of damage to kidneys/lysis of RBCs)
2 reasons why Plasmodium falciparum is more virulent than plasmodium vivax/ovale?
1. P falciparum infects RBC of any age (unlike others that only infect really young or really old RBCs) ---> high parasitemia and more severe anemia
2. P falciparum-infected RBCs stick to vascular endothelial cells ---> poor perfusion and hypoxia
what is Pfemp?
the protein that causes Plasmodium falciparum-infected RBCs to bind to endothelium, block blood flow and cause hypoxia
what do early plasmodium Trophozoites look like?
Purple rings inside of RBCs with 1 or 2 darker stained purple dots on them
What to P falciparum gametocytes look like?
bananas or sausages in an RBC with a large, dark granular stain near its middle
trypanosoma and Leishmania species are what type of protozoa and they affect what part of the body?
they're flagellates that infect the blood/tissue
African Trypanosomiasis (trypanosoma brucei) is transmitted by what?
the Tstetse fly
pathogenesis of African Trypanosomiasis (trypanosoma brucei)
1. Tsetse fly bites human
2. replication of trypanosoma brucei in the blood
3. spread to lymph nodes
4. spread to CNS
african trypanosomiasis is aka
Trypanosoma brucei (African Trypanosomiasis ) replication in the skin causes
trypanosoma brucei (African Trypanosomiasis) spread/replication in the blood/lymph causes
fever, sweats, headache, winterbottom's sign
what is winterbottom's sign iand which parasite species is it associated with?
it's swelling of the lymphnodes along the back of the neck on the posterior cervical chain that are evidence that trypanosomes have travelled to the lymph nodes and caused inflammation. it's associated with Trypanosoma brucei (african trypanosomiasis)
Trypanosoma brucei (African Trypanosomiasis) spread/replication in the CNS is associated with?
meningoencephalitis, confusion, somnolence, coma
3 areas of the body often affected by Trypanosoma brucei (African Trypanosomiasis)
1. skin- ulcers
2 subspecies of trypanosoma brucei
1. Trypanosoma brucei gamiense - western africa
2. trypanosoma brucei rhodensiense - eastern
Trypanosoma brucei gambiense
region of africa:
time to death if untreated:
Trypanosoma brucei gambiense
region of africa: western
reservoir: none-- only humans
time to death if untreated: years
why can you live for years with trypanosoma brucei gambiense, but only months with trypanosoma brucei rhodesiense?
gambiense only has human hosts, so it has to be less virulent so that it can continue to live. Rhodesiense has many, many hosts, so it can be more virulent and skip around
trypanosoma brucei rhodesiense
region of africa:
time to death if untreated:
trypanosoma brucei rhodesiense
region of africa: eastern
reservoir: many mammals
time to death if untreated: < 9 months
african sleeping sickness is associated with which species of parasite?
Trypanosoma brucei (African trypanosomiasis)
what do trypanosomes look like in the blood?
longer, really swirly purple things outside of RBCs
American Trypanosomiasis is aka
Trypanosoma cruzi is transmitted from a mammalian reservoir to a human via the
tritomine insect which bites at night and poos the parasite onto your arm. you then spread it into yourself through the eye, or by scratching the bite
pathogenesis of trypanosoma cruzi (American trypanosomiasis)
1. Tritomine insect bites a human and poos out the parasite
2. humans either put the poo in their eyes, or scratch it into the wound
3. replication at the site of entry ---> skin or eye problems
4. spread to the lymph nodes
5. replication in RBCs
6. spread and damage to peripheral nerves and heart
trypanosoma cruzi (american trypanosomiasis) causes manifestations in what 3 places?
1. skin/eye (place of entry)
trypanosoma cruzi (american trypanosomiasis) causes what manifestations at the skin/eye
chagoma ---> resolves
trypanosoma cruzi (american trypanosomiasis) causes what manifestations in the blood
fever, malaise --> hepatosplenamegaly
trypanosoma cruzi (american trypanosomiasis) causes what manifestations in the GI/heart
GI: megaesophagus, megacolon
heart: arrythmia, cardiomyopathy
what is Chaga's disease and what parasite is it associated with?
it includes Romana's Sign (unilateral eye swelling from rubbing parasite latent feces into the eye) and megacolon due to nerve damage/abdominal obstruction and inability to pass stool (this had the picture of the intestine opened up filled with worms)
it's caused by Trypanosoma cruzi (American Trypanosomiasis)
how are Leishmania species transmitted from their mammalian reservoir?
via the sandfly
where do Leishmania speceis replicate?
in Reticuloendothelial Cells (cells of macrophagic origin that are in solid organs)
Pathogenesis of Leishmania species
1. transmitted from mammalian reservoir to humans via the sandfly
2. replicates in reticuloendothelial cells
3. undergoes Disseminated replication (leading to visceral Leishmania) or replicates at the site of entry leading to Cutaneous Leishmania.
4. cutaneous leishmania can either resolve or spread to skin and mucosa (mucocutaneous Leishmania)
3 different manifestations of leishmania
1. Disseminated replication ---> visceral leishmaniasis
2. replication at site of entry ---> cutaneous leishmaniasis (ulcers that will resolve on their own over time due to TH1 response)
3. spread from the site of entry to surrounding skin and mucosa ---> mucocutaneous leishmaniasis crusty and bulbous scarring/inflammation all over due to a TH2 resp)
visceral Leishmaniasis leads to what manifestations?
fever, weight loss (but big tummy/wasting of arms), anemia, thrombocytopenia, neutropenia
the anemia, thrombocytopenia and neutropenia found in visceral leishmaniasis indicates...
that replication is occuring in the bone marrow ---> hemoatopoiesis is affected
how is the protozoa toxoplasma gondii transmitted?
ingestion of raw meat
which 3 important protazoan species are transmitted by vectors?
1. Plasmodium species
2. Trypanosoma species
3. Leishmania species
Which 3 important protozoa are transmitted via the fecal-oral route (including non-human feces)
1. Toxoplasma gondii
2. Giardia lamblia
3. Entamoeba histolytica
how are helminths (worms) classified?
by shape in cross section
what are the 2 major classes of worms?
1. Roundworms (aka nematodes)
what is another name for a roundworm?
what are two types of flatworms?
1. Tapeworms (aka cestodes) which are segmented
2. flukes (aka trematodes) which are leaf shaped and non-segmented
tapeworms are aka
flukes are aka
4 GI Roundworms that we studied?
1. Trichuris trichura
2. Ascaris lumbricoides
4. Strongyloides stercoralis
3 Gi tapeworms
2. Taenia saginata
3. Taenia solium
4 Blood/Tissue Roundworms
1. Loa Loa
2. Lymphatic filaria
3. Onchocerca volvulus
4. Dracunculus medinensis
2 GI Tapeworms
1. Taenia solium
2. Echinococcus granulosus
1 Tissue/Blood Fluke
which parasite is aka the whipworm and why?
Trichuris Trichiura because it has a thick part (which stays in the lumen of the GI tract) and a skinny part (which goes into the mucosa)
how is Trichuris trichuiura (whipworm) transmitted?
eggs mature in the soil and then they're eaten ----> transmitted via fecal oral route, but the eggs have to be in the envt between cycles to mature
pathogenesis of Trichuris trichiura (whipworm) (5)
1. Person sheds eggs in stool
2. eggs mature in the soil and then are eaten (fecal oral transmission)
3. the eggs hatch in the stomach
4. Trichuris trichiura matures and mates in the intestine
5. this causes blood loss and inflammation
How does a light infection of Trichuris Trichiura (whipworm) manifest?
How does a heavy ifxn of Trichuris trichuira manifest? (3)
dysentary (bloody diarrhea), anemia and malnutrition
how do you diagnose someone with Trichuris trichuira
by seeing the eggs in the stool
What is a light manifestation of Ascaris lumbricoides?
asymptomatic, rarely clock biliary or pancreatic ducts
what are the sx of a heavy ifxn of Ascaris lumbricoides?
pneumonitis and GI obstruction
Ascaris lumbicoides is transmitted via:
pathogenesis of Ascaris lumbricoides (9)
1. Person poos out eggs which mature in the soil
2. person eats the eggs
3. eggs hatch in the duodenum
4. larvae enter circulation
5. Lodge in the lung
7. migrate up/get coughed up in into the trachea and swallowed
8. Mature and mate in the intestine
9. poop out the eggs...
what type of host are humans for Ascaris lumbricoides?
two types of hookworms?
1. A duodenale
2. N. americanus
How do hookworms spread?
1. eggs are shed in species, the eggs hatch, mature and the larvae penetrate the skin
pathogenesis of hookworms
1. Larvae penetrate the skin and enter circulation
2. the larvae lodge in the lung and they mature there
3.migrate up, are swallowed
4. mature, mate in the intestine
5. attach and suck blood
6. shed eggs in species which hatch, mature and the larvae penetrate the skin
what are the manifestations of a skin ifxn with hookworms?
1. Hypersensitivity to larva ("ground itch")
what are the manifestations of a heavy hookworm ifxn?
2. blood loss ----> anemia
the image of the raised line of the worm on the foot that is really red/crusty is what?
"ground itch"-- the linear pattern of larvae moving under the skin and the host response to the larva
what's unique about strongyloides stercoralis?
it can autoinfect the host-- uncommonly, larvae mature in the GI ---> autoinfection and superinfection
how is a host infected with strongyloides stercoralis?
immature larvae in feces ---> mature larvae penetrate skin. There are also free livin adults in the envt that produce eggs ---> larvae penetrate skin
pathogenesis of strongyloides stercoralis? (7)
1. immature larvae are passed in stool
2. mature larvae penetrate the skin
3. larvae enter the circulation
4. the larvae lodge in the lung and mature
5. they migrate up and are swallowed
6. they mature and mate in the intestine
7. They produce immature larvae which are passed in the stool
what is "superinfection" referring to in terms of strongyloides stercoralis?
when production of tons of parasites that drag in gram negative bacteria ---> sepsis
what increases the risk of autinfection/superinfection by strongyloides stercoralis
corticosteroids-- they act as sex hormones for worm and drive them twd differentiation
manifestations of strongyloides (3)
1. Ground itch (worm passing around on the foot- like hookworms)
2. GI Ifxn w/o hyperinfection is rarely symptomatic
3. Hyperifxn: fever, abdo pain, diarrhea, dyspnea, wheezing, hemptysis, cough
why does styongyloides stercoralis often leave to wheezing, hemoptysis and cough
because the larvae lodge themselves in the lung where they mature
3 parasites that lead to auto ifxn
1. stongyloides stercoralis (roundworm)
2. pin worms
3. Taenia solium (tapeworm)
how are all filiarial Ifxns are acquired?
vector bites ---> larvae penetrate the skin
pathogenesis of filarial ifxns (5):
1. vector bites ---> larvae penetrates skin
2. larvae mature to long-lived adults
3. adults produce microfilaria
4. microfilaria enter vector during bite
5. vector bites host, larvae penetrates skin...
are manifestations of filarial diseases caused by adults or microfilia?
they can be caused by both
three types of filarial parasites
1. Loa loa (the African eye worm)
2. Lymphatic Filariasis
3.Onchocerca volvulus (River blindness)
the vector for the African Eye Worm: Loa loa (filarial parasite)
pathogenesis of the African Eye Worm (Loa loa-- filarial parasite)
1. Tabanid bites, larvae penetrate skin
2. larvae mature in subqutaneous tissue
3. adults migrate in subQ tissue (inc eye)
4. Microfilaria released into blood stream
5. little host response or damage
adults who are infected with Loa loa (The African Eye worm) get manifestations where? (2)
1. Eye: local edema-- can see the filaria crossing
2. Skin: local edema ---> "calabar swellings" (fugitive, swollen lumps of subcutaneous tissue caused by a parasitic filarial worm, that move with the worms)
calabar swellings and a worm moving across the eye are associated with what parasite?
Loa loa (African Eye Worm)
lymphatic filariasis are spread via
mosquitoes (many species) ---> larvae injected
pathogenesis of lymphatic filariasis
1. mosquito bites ---> larvae injected
2. larvae enter circ
3. larvae lodge in lymph and mature
4. adults release microfilia
5. microfilia in lymph and blood
Early manifestations of lymphatic filariasis
manifestations of Chronic lymphatic filariasis
worms + scarring ---> obstruction of lymph ---> fluid accumulation/elephantiasis
elephantiasis is associated with which parasite?
pathogenesis of River blindness (Onchocerca volvulus)
1. Simulium blackfly bites, larvae is injected
2. Larvae mature in the skin
3. Adults in skin
4. release microfilariae
5. microfilaria in lymph, blood, tissue (eye- conjunctiva)
how is River Blindness (Onchocerca volvulus) transmitted?
manifestations of River blindness (Onchocerca volvulus)
1. Skin and connective tissue: atrophy, depigmentation
2. Eye: blindness due to ifxn of the conjunctiva
Species that causes the disease:
Site and damage (2)
Species that causes the disease: Loa loa (filarial parasite)
Site and damage (2):
1. skin (adult) ---> calabar swelling
2. Eye (adult) ---> pain
species that causes disease (2):
Site and damage (1)
species that causes disease: 1) W. bancrofti and 2)B. malayi
Site and damage (1): Lymphatics (adult) ---> obstruction, lymphedema and elephatiasis
species that causes disease:
Site and damage (2)
species that causes disease: onchocerca volvulus
Site and damage: 1) eye (microfilaria) ---> blindness, 2) skin (microfilaria) ---> pigmentation changes and loss of elasticity
Intestinal tapeworms are all acquired from...
eating larvae in rare meat
pathogenesis of intestinal tapeworms
1. Larvae are ingested in rare meat
2. eggs are passed in stool
3. eggs or larvae are ingested by animals
4. larvae are ingested in rare meat
Tapeworm Taenia solium comes from
tapeworm taenia saginata comes from
tapeworm Diphyllobothrium latum comes from
Sx from Gi ifxn with tapeworm
rarely symptomatic. Diphyllobothrium latum ---> B12 deficiency, anemia
Two forms of Taenia solium- and how you get each
1. GI tapeworm that you get from ingesting pig larvae
2. Cysticerosis-- tissue ifxn caused by eating the eggs shed in human stool rather
T. solium larvae travel to muscles and brain. they die ---> immune response ---> seizures and hydrocephaly
what is neurocysticercosis
cysts of T. Solium in the brain from ingesting eggs from human stool, rather than larvae from rare meat
normal lifecycle for Echinococcus granulosus and how humans fit in
1. carnivore (like a dog) ingests animal with cyst (immature worm) in it ---> GI parasite
2. Carnivore poos out eggs in stool.
3. sheep eats stool with egg in it ---> tissue parasite
4. Sheep gets eaten by dog...
Humans take over the sheep part and get the tissue parasite
Hyatid disease pathogenesis
humans ingest E. granulosus eggs.
2. embryonic worms penetrate intestinal wall and enter circulation
3. they migrate to tissue, usually liver and lung
4. slowly form large cysts full of protoscolices -- asymp. except when they impinge on adjacent structure (bile duct)
5. cysts can rupture ---> anaphalyxes
1. Cercarae mature
2. reach hepatic portal vessels, mature
3. paired adults migrate to veins of mesentary or bladder (no host response)
4. release eggs
how is schisto transmitted?
cercariae penetrate the skin ----> eggs shed in urine/stool ---> infect snails ---> cercariae penetrate skin
3 species of schisto
which 2 types of schisto infect the GI mesenteric veins and shed eggs in the stool?
Schistosoma mansoni and japonicum
which type of schisto infects th bladder veins and sheds eggs in the urine?
manifestations of schisto
1. "swimmer's itch"- dermatitis caused by cercariae as they swim through
2. febrile illness when flukes reach venules
3. eggs ---> granulomas (symp vary with tissue) (liver/spleen: enlarged, portal HTN, ascites, Intestine: colitis, cramps, pain, bleeding, Bladder: hematuria)
how do schisto eggs ---> granulomas in the liver manifest?
liver = enlarged, portal HTN, ascites
how do schisto eggs ---> granulomas in the intestine manifest?
colitis, cramps, pain, bleeding
how do schisto eggs ---> granulomas in the bladder manifest?
What 3 helminths do we get from ingesting meat?
Diphyllobothrium latum (fish)
Taenia saginata (beef)
Taenia solium (pig)
what helminthe do we get via vectors?
which helminths do we get from fecal-oral transmission? (4)
1. Taenia solium (cysticercosis)
2. Trichuris (human feces)
3. Ascaris (human feces)
4. Echinococcus (dog feces)
which helminths can we get from skin penetration? (3)
fever with incubation period of under 14 days is most likely to be one of which 4 things?
1. plasmodium falciparum
2. typhoid fever
4. Campy, Sal, Shig
fever with incubation period of 14 days-6wks is most likely to be
acute HIV or EBV