Parasitology

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3 kinds of parasites: protozoa
helminths
arthropods
Define arthropods: animals with a segmented body and a chitinous exoskeleton
define the definitive host: (primary host)

host in which the parasite completes the SEXUAL PHASE of its life cycle
Define the intermediate host: (secondary hosst)

other host in which the parasite lives (completes a life-cycle phase, or reproduces asexuxally)
Define vector: organism (usually insect) which transmits a parasite to a host. Also a host.
Reservoir: host (human or otherwise) which serves as a source of parasite transmission to the population of interest.
Where are parasitic diseases more prevalent/increasing in incidence?: Low income countries. Middle/high have successfully eliinated or controlled it
Define parasite: An organism which lives in or on another host and draws its nutriment directly from it
Tropical medicine story: Started out as big deal, companies poured in efforts due to colonialism and war

But by the 1960s tropical medicine became massively underfunded
what is an apicoplast: Organelle derived from chloroplasts that is found in all malaria causers
Definitive malaria host: Vector: female mosquitoes of the genus Anopheles.
When do anophelines bite?: Night, peaking at 1 AM
Human sstages of malaria: 1) pre erythrocytic stages
2) erythrocytic asexual stages
3) erthroctic sexual stages
4) hypnozoite
Clinical course o malaria: 1) Prepatent perioud: asymptomatic, plasmodium multiplis in liver
2) Paroxysm stage: classic sudden onset of shaking chills, then high fever (to 106) when infected RBC burst to release new merozoites. May be periodic (48 to 72 hrs)
Diagnosin gMalaria: 1) Giemsa stainded blood smears
2) thick smear/ thin smear
3) rapid tests
4) travel history
Plasmodium falciparum details: 1) invades red cells of all ages (so it is generally seen in normal sized RBCs) -->high parasitemia
2) sickle shaped gametocyte is unique
3) 48 hour periodicity
4) ONLY rings and banana shaped gametocytes are in circulation
5) most common
6) most dangerous
7) most drug resistant
Plasmodium vivax Plasmodium ovale: 1) invade reticulocytes (young RBC) and live in enlarged red cells (because they are young)
2) produce schuffner's dots
3) produce latent forms (hypnozoites) that remain dormant in liver for months to years and then reinitiate parasetimia (allowing disesse to survive thru wintere to next mosquitoe season)
4) 48 yhhour periodicity
Plasmodium malariae: 1) has no hympnozoites but still may persist in the bloodstream at very low levels
2) 72 hour periodicity
3) tends to invade older RBC cells, so mainly found in norma sized RBC
Why is p. falciparum most lethal yet intermediate stages not seen in periphery?: 1) mature p. falciparum makes proteins in red cell that form knobs on host RBC surface
2) knowbs adhere to caps and are sequestered in the caps (so you don't see it in the periphery)
3) this can block circulation in the brain
4) gametocytes do NOT have knobs so they can be transmitted
What does malaria look lke in areas of high transmission?: Adults immune, disease fonund only in childrine and primigrvidae
Malaria in low transmission areas: Disease seen in all ages and gravidity
Prophylaxis for malaria: 1) chloroquine: some rsistance
2) Lariam (neuro side effects)
3) malarone: expensive
4) doxycycline: cause photosensitivity
5) primaquine: used for p.vivax exposure
what is duffy blood group: Surface antigen required for p. vivax to get into RBC. Duffy negatives are resistant to p. vivax
Things tat can cause resistance to malaria: 1) sickle cel trait
2) thalassemia
3) glucose-6-phosphate dehydrogenase deficiency
4) ovalocytosis
5) duffy blood group negative
Name all of the apicomplexia: 1) plasmodium sp.
2) babesia sp
3) toxoplasma gondii
4) cryptosporidium sp.
5) cyclospora sp.
Origin of the apicomplexa: All contain the apicoplast
Apicoplast has DNA related to algae
Evolved from 2 evolutionary events

1) algae phagocytosed bacteria (chloroplast precursor) and became photosynthetic
2) Plasmo precursor phagoctosed the algae. Algae/organelle loses photosynthetic abiltiy
plasmodium hosts (def/int): DEF: mosquito
INT: human
babesia hosts: DEF: tick
INT: mammals
Toxoplasma gondii hosts: DEF: cat
INT: mammals
Cryptosporidium hosts: DEF: mammals
INT: mammals
Cyclospora hosts: 1) DEF: mammals
2) INT: mammals
P. falciparum life cycle more detailed: 1) sporozoites from mosquito spit invade liver cells
2) sprozoite asexually replicates (exoerythrocytic schizogony)
3) (some become hypnozoites)
4) eventually scizont ruptures and releases merozoites
5) merozoites infect RBCs forming a "ring" form trophozoite
6) trophozoite enlarges, then undergoes multiple nuclear devision and segmentation/budding ito more merozoites
7) merozoites released from ruptured schizont
8) or ring stage trophozoite can differentate into gametocytes.
Cases of malaria in developing word v. us: Developing: 300 million/yr
US: 1000 cases/yr
Babesiosis life cyccle: 1) sporozoites enter human from tick
2) sprorzoites invade RBC to from trophozoite, develops into merozoite
3) reservoir is in MICE, there merozoites can form gametes, which go back into the tick, where sexuar reproduction occurs, and sporogony occurs, making more spores to get into tick spit
4) sporogony does not occur in humans
Describe babesiosis illness: 1) flulike, usually mild
2) severe in SPENECTOMIZZED patients and the elderly
3) may be confused w/ malaria
4) endemic to parts of USA
toxoplasma gondii life cycle: CAT:
1) schoogony
2) sequal reproduction in gut lining
3) eggs passed into stool

Itermediate host (BROAD range):
1) ingested eggs and tissue cytst from other int host transform into tachyzoites after ingestion
2) tachyzoited (trophozoites) (avoids fusion with lysozome). localize in nerual and muscle tissue
3) they then develop into tissue cyst bradyzoites
2 routes of toxoplasmosis infection: 1) ingestion of oocyst from cat feces
2) ingestion of bradyzoite (tissue cyst) from infected undercooked meat
Toxoplasmosis disease: 1) 10-20% get mono-like illness
2) trophozoites in humans can be passed to baby, causing congenital malformations and ocular disease (if 1st trimester) or abortion (2/3 trimesters)
3) If sufficiently immunosuprprses (AIDS), you hever get rid of it. Can reactivate, causing fatal encepalitis and retinal lesaions. Can protect with TMP/SMX prophlaxis
Diagnosis of toxoplamosis: 1) serology (IgM based)
2) culture/innoculation of mice (gold standard)
Treating toxoplasmosis: 1) antifolates
2) atovaquone
T. gondii in a macrophage: 1) endycytosis
2) replication, formation of bradyzoite cyst
3) no fusion with lysozome
4) tachyzoites released by cell rupture
what are tachyzoites?: crescent/oval rapidly dividing trophozoites in toxoplasma gondii
Crytosporidium sp. generally: Long known CATTLE PATHOGEN
Oppoortunistic infection in AIDS patients (see also toxoplasmosis)
Cryptosporidiosis disease: Causes mild diarrhea in immunocompetent, sever diarrhea in immunosupressed
treatment of cryptosporidum: no effective treatmennt
cryptosporidiosis life cycle: 1) oocyst ingested by host
2) oocyst sporulates, sporozoite infects gut cell, releases merozoits that infect more
3) undergoes sex cycle in gut, differetiated into gamets, fertilizig each other
4) oocyst may exit host or may autoinfect host again
cryptosporidium resistance?: Cysts resistant to chlorine
Transmission of cryptosporidium: 1) drinking water
2) pools
3) food

(b/c cysts are chlorine resistnat)
Outbreak sites of crytosporidium: 1) day care centers
2) munnicipal water supplies
3) milwaukee
Molecular epidemioloy: Two genotypes:
1) type 1: humans only
2) type 2: humans and cattle

US: outbreaks mostly type 1, sporadic cases mostly type 2

Developing world: most cases are type 2
Cyclosporiasis details: 1) looks like cryptosporidum but larger
2) lillness loike crytpsporidium (diarrhea)
3) 2-20% prevalence in eveloping country
4) no animal reservoir
5) outbreak in US due to guatemala
Trypansomatids, generally: 1) Include: african and american trpansomes, plus Leishmania
2) reproduce asexually
3) single flaggella
4) kinetoplasts
5) usually vector born
4 life cycle forms of trypanosomatids: 1) amastigaote (intracellular in mammal
2) trpomastigote (in mammal)
3) promastigote (vector)
4) epimastigote (vector)
Kinetoplast details: 1) inside mitochondria
2) <20% of total cell DNA
3) contains minicircles and maxicircles of DNA
4) appeared to code for gibberish
5) but they do actually produce correct mRNA for mito proteins, thanks to RNA editing that inserts U's into specific sites
6) editing directed by guide RNA (gRNA) encoded on minicircles
7) gRNA ancchor region puts it in right spot
8) gRNA guide region direct enzymes that transfer U from 3' tail to spot on the pre-mRNA
African trypansomiasis life cyclye: 1) epimastigotes multiply in fly gut, get to salivary gland
1.5) epimastigote multiplies in salivary gland
1.75) metacyclic trypomastigote form forms in salivary gland (INFECTIVE FORM!!!)
2) enter human blood, multiply in trypomasigote form
3) ingested by fly
Types of african trypanosoma: 1) GAMBIAN: T. gambiense (WEST). Human reservoir, causes chronic disease that takes years to develop.

2) RHODESIAN: T. rhodesiense (EAST). Animal reservoir. Causes acute disease that develops in months
Stages of african trypansomiasis: 1) Primary: causes lyymphadenopathy (Winterbottom's sign)
2) secondary: systemic disease (fever, wasting)
3) Advanced: CNS disease (lethargy, insomnia, seizures, coma)
Antigenic variation in african trypanosoma: 1) VSG: variang surfce glycoprotein forms protective coat around parasite
2) each bug may have 1000+ VSG genes
3) thus no vaccine possible
Trypansosma cruzi life cycle: (American tryponsomiasis--Chagas)

1) epimastigote migrates to bug saliva gland
2) becomes infective metacyclic trpomastigote
3) trypomastigote enters human
4) can become AMASTIGOTE
Amastigote: intracellular form of t. cruzi

1) lives in macrophages or muscle cells
2) FUSES with phagolysosome
3) ehten ESCAPES into cytoplasm
4) then transforms to trypomastigotes in the cytoplasm
Epidemiology of t. cruzi: 1) spread by triatomes/reduviid
2) 10 Mil infected
3) can be in US rodents, racoons
4) triatomes live in mud hut cracks,thatch, forest
Acute Chagas symptoms: 1) romanos sign: swelling of eyelids if bite on face
2) parasitemia, febrile illness (trypomastigotes in the blood)
Chronic chagas: 1) occurs 10-20 years after acute infection
2) chronic cardiomyopathy (20-305)
3) megacolon, megaesophagus (8-10%)

No treatment for chronic disease.
Diagnosis of Chagas: 1) parasites not found in peripheral blood in acute illness--mainly in the tissue
2) xenodiagnosis: get patient bit with sterile bug, get that bug to bite something else and see if it infects acutely
3) immunology: fluorescent A assay, etc.
Pathogenesis in chagas: 1) no parasites found in lesions, suggesting autoimmune mechanism of disease
2) more recent studies using PCTR can find organism DNA in the lesions
Strains of Leishmaniasis: 1) Dermatotrophic strains
liishmania mexicana, braziliensis, major, tropica

2) Viscerotropic strains
L. donovani, infantum, chagasi

BUT EITHER GROUP OF STRAINS CAN CAUSE EITHER TYPE OF DISEASE
Lifecycle of Leishmania: 1) Amastigotes in Humans; REMAIN IN PHAGOLYSOSOME (cf. amastigotes in tryponosoma cruzi, whcih escape phagolysosome) and are released when cell ruptures
2) NO trypomastigote form
3) In SANDFLY as promastigote
Leishmania vector: sandfly
Cutaneous leishmaniasis: causes ugly painless lesions
1-1.5 M cases year
Visceral leishmaniases: Splenomegaly, etc
Can be opportunistic infection in AIDS patients
More on cutansous leishmaniasis: Initially a painless lkin lesion
usually disappears spontaneously
May metastasize to liver, spleen, bone marrow (visceral) or face mucus membrane (mucocutaneous leishmaniais)

HIGH DEATH RATE IF VISCERAL IS UNTREATED
Diagnosis of leishmaniasis: 1) culture
2) leishmanin
3) PCR
4) serology
5) immunohistochemistry
Treatment of leishmaniasis: Antimonials
Pentamidine
Amphotericin B (liposome)
What is the official name of the vector for african trypansomatids?: Glossina
What is an amastigote?: Trypanosomatid stage that

1) lives in Mphage or muscle cell
2) fuses with phagolysosome and then escapes into cytoplasm
3) transforms to trypansomastigotes

(stage in Chagas but not african sl si)
Do leishmania amastigotes stay inside phagolysosome or not?: Remain inside
Is there a trypomastigote form of leishmania?: no
Which parasites can live inside macrophages?: Trypanosoma cruzii
Trypansosoma gondii
Leishmania
Which parasite lives only in the phagosome and causes no fusion with lysosome?: T. gondii
Which parasites can survive lysosme fusion with phagosome?: T. cruzi
Leishmania
Which parasite stays in the phagolysosome?: Leishmania
Which parasite escapes the phagolysosome?: T. cruzi
What are the anaerobic protozoa we studied?: Trichomonas vaginalis
Entamoeba histolytica
Giardia lamblia
describe the generic lifecycle of anaerobic protozoa: 1) Host: trophozoites. Motile, reproductive, and destructive

2) Enivironment: live as CYSTS. Durable daughter cells.
Which anaerobic protozoan has no cyst form?: Trichomonas vaginalis
What is the most common STD in the world?: Trichomonas vaginalis
How do you diagnose trichomonas vaginalis?: Wet smear
Sytmptoms of trichomonaas vaginalis infection: Women: Yellowish vaginal discharge (like YEAST), itching and burning

Men: usually asymptomatic. Maybe urethritis
Describe some possible virulence factors of trichomonas vaginalis: cysteine proteases
adhesins
What drug is usesd to treat all anaerobic protozoans?: Metronidazole (Flagyl)
What is the hydrogenosome?: Organelle in trichomonas vaginalis that uses H+ to reduce H into H2 instead of reducing O2 to H20. Related to mito.
How does Flagyl work?: The drug is reduced by the hydrogenosome pathway, generating free radicals that damage DNA
Where does t. vaginalis live?: vaginal epithelium
What kind of pH does t. vaginalis need to live?: 5-6 (nl is 4-4.5)
How can t. vaginalis develop resistance to flagyl?: If it become more aerotolerant. If it can survive with O2 around, then the O2 competes with flagyl in the reduction process
What are the stages of entamoeba histolytica?: 1) trophozoite: pathogenic stage, single nucleus with central nuclealus. Eats bacteria and dead skin

2) Cyst: infective phase that survives in environment. Contains 1-4 nucleii
Do trophozoites of entamoeba histolytica have hydrogenosome? Mito?: No, no
What are virulence factors for etamoeba trophozoite?: amebapore
cysteine proteases
What kinds of disease can entamoeba histolytica cause?: 1) Lumenal (noninvasive)
2) Hepatic (invasive)
Describe noninvasive entamoeba histolytica disease?: 1) trophozoites invade epithelium of colon and rectum
2) can cause accute or chronic disease
3) may be misdiagnosed as ulcerative colitis

ACUTE: bloody, mucusy diarrhea, fever, cramps

CHRONIC: intermittant. Pass cysts.
Diagnosing entamoeba histolytica: 1) examine stool for cysts. though it may be confused w/ E. dispar

2) Need 3 specimens due to low cyst yield

3) Sigmoidoscope specimens are better

4) can use EIA specific for entamoeba lectin (more accurate)
Diagnosing liver entamoeba histolytica:: 1) serology
2) aspiration of abcess (amoeba live in wall of abscess)
Describe invasive entamoeba histolytica disease: 1) abscesses in liver (fever, pain)
2) can rupture and metastasize
3) hard to diagnose (may be no stoool cysts)
What causes giardiasis?: Giardia lamblia
What is the most common intestinal parasite?: Giardia lamblia
Describe stages of giardia: 1) trophozoite: 4 pairs of flagella, 2 nuclia, ADHESIVE DISC, lectins. Inhabits but does not invade intestine.

2) cyste: 4 nucleii
Does giardia have mito or hydrogensosome?: No, no
How is giardia usually transmitted?: Usually thru water, person to person

Rarely thru food
Describe giardia cysts: 1) HIGHLY INFECTIOUS (need only 10)
2) Cl resistant
3) viable for months in rater
What symptoms of giardia?: Accounts for 2-44% of acute diarrhea episodes, mostly in kids
What is the reservir of giardia: Beaver
What are the forms of giardia disease?: 1) acute: lots of trophs in stool. Diarrhea, nausea, flatulence, weight loss.

2) chronic: intermittent. hard to find csts.
What is the tie of giardia to kid development?: Infection may impair absorption of B12, A, Iron, fat, sugar
What is the connection of breast milk and giardia?: Milk kills giardia trophozoites
What diseases can lice carry?: Rickettsia prowazecki (epidemic typhus)
Borrelia recurrentis (relapsing fever)
Rickettsia quintana (trench fever)
Name of the chigger?: Tunga penetrans
What diseases can fleas carry?: 1) yersinia pestis
2) rickettsia typhi (endemic typhus)
What group do fleas and lice belong to?: Hemiptera
What grou do ticks and mice belong to?: Chelicerata
Soft ticks v. hard ticks: Soft: cant see head
Hard: can see head
How do ticks find spot to bite into?: Hallers organs/Chelicerae sense atp.
What disease can tick directly cause?: Tick paralysis. Female tick bites, symptoms appear in 5-7 days
Diseases ticks are vectors for:: RMSF
Erlichiosis
Lyme
Babesiosis
East Coast Fever
Endemic relapsing fever
Coxiella burnetti
Congo-Crimean Hemorrhagic fever
What are houseflies a vector for?: trachoma
What do you use bacon treatment for?: myasis (fly larvae invading animal tissue)
What kills ticks?: Acaricide
What disease other than paralysis can ticks directly cause?: Anemia in cattle
What causes scabies/mange?: Mite:

Sarcoptes scabei
What kills mites?: DDT
Pyrethrins
How does insectiside resistance develop?: Point mutations in target
Detoxifying enzyme emergence
Pinworm lifecycle: Female lives in large gut

Comes out anus at night to lay sticky eggs, causing itching
How to diagnose pinworm: Scotch tape prep
Roundworm name: Ascaris lumbricoides
Pinworm name: Enterobius vermicularis
Where does ascaris adult live?: Small intestine
Descriibe life cycle/propogation of ascaris: 1) ingestion of eggs
2) eggs hatch in upper intestine
3) hatchlings cross bowel wall and enter bloodstream
4) enters lung by crosing into alveolus
5) coughed up, swallowed
6) develops into mature adult in gut.
7) lays eggs in gut where eggs pass in stool
8) fertilized eggs germinate in soil; require 2 weeks to EMBRYONATE and become infective
Describe symtoms of ascaris while in lung stage?: May produce symptoms of pneumonitis with eosinophilioa
What does ascaris worm burden depend on and why?: Depends on the number of eggs ingested, since worms do NOT multiply within the patient (egg ust leave body to fully reproduce)
Diagnosing ascaris infection: find eggs in the stool
How do ascaris stay in the gut?: just by swimming upstream. no fancy hooks or anything
Name some skin penetrating intestinal nematodes: 1) hookwork (necator americanus, ancylostoma duodenale))

2) Strongyloides stercoralis
WHat are the 2 hookworm species?: Necator americanus
Ancyclostoma duodenale
General method of living of hookworm: Live in small intestine
Have cutting plates/teeth that they use to bit emmucosa and get blood
Change attachment sites often
Major ill host effect is anemia
Hookworm & strongyloies life cycle: 1) invasive larvae penetrate unbroken human skin
2) larvae migrate to bloodstream
3) cross into alveoli
4) coughed up, swallowed
5) mature in the upper GI
6) HOOKWORM females lay eggs in GI lumen, releasing eggs into stool. STRONGYLOIDES lfemales lay eggs in bowel wall.
7) hookworm larvae require maturation in environment before reinfecting.
What is ground itch?: Primary irratation of feet after hookworm larvae penetrate the skin
Diagnosis of hookworm: eggs in stool
Describe STrongyloides life cycle: Like hookworm, EXCEPT females do not lay eggs in lumen of gut, but eggs hatch in the patiens intestine, and motile larvae reemerge and the LARVAE, not the egs, are passed into the soil.

Larvae still must be in environment to become infective
What are filariform larvae?: The infective form of strongyloides larvae produced after gut larvae contact soil
Describe strongyloides auto-reinfection: Larvae can mature/molt on the patient's skin, or even in the intestine. In this way, parasite may perist in host for 50+ years.

May be asymptomatic, or may have larva urrens.

If immunoosuppressed, hyperinfection (life-threatening) may occur. Thus, transplant candidates are screened for strongyloides.
What is larva currens?: Itching of the skin in otherwise asymptomatic cutaneous auto-reinfection of strongyloides
Is there hookworm reinfection?: No. Only eggs reemerge from stool, and these cannot become motile and infective without germinating in the soil
What is larva migrans: Iff egg (ascarid) or larva (hookworm) of dog or cat (not human) infects a human host by accident, the larvae are unable tocomplete their life cyfcle and may migrate or wander in the tissues, causing damage.

There are 2 kinds of larva migrans
Describe cutaneous larva migrans: Dog hookworm enters human skin, producing migrating inflammatory reaction known as CREEPIN ERUPTION.
What is visceral larva migrans: "Humans ingest embrounated dog/cat roundworm eggs. Larvae migrate and end upp in liver. Sometimes can migrate to eye to produce retinal lesions, or to brain, causeing seizures.
Name for tapeworms: Cestodes
Beef tapeworm name: Taenia saginata
Name for pork tapeworms: Taenia solium
General life cycle of cestodes: 1) humans eat undercooked beef/pork infected wihth CYSTEICERI
2) elongates in intesting to form adult tapeworm
3) Scolex attaches to lumen, grows many proglottids
4) gravid proglottids released in stool
5) Cow/big eats egg, which hatch in intestine
6) larvae migrate to muscle tissue, forming cysticeri
Differences between taenia saginata and t. solium: Saginata:
1) intermedite host is cow
2) cannot be passed human to human
3) does not form cysts in humans

Solium
1) intermediate host is pig
2) human to human fecal-oral transmission is possible--Eggs are infective
3) larvae can cause cysticerosis in humans
Symptoms of cestsode infection: Intestinal infection rarely symptomatic--tapeworm simply absorbs nutrients directly from gut contents.
Diagnosis of cestode infection: 1) examine feces for eggs
2) scolex rarely obtained pre-treatment, but if it is you can determine Taenia species (solius has a solar appearance of hooks around its head)
Describe cysticerosis: Complication of Taenia solius infection

1) need not have intestinal adult tapeworm history--can be due to ingeestion of larvae/eggs fecal orally
2) symptoms ay appear long after exposure
3) can cause seizures

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