parasitology midterm 2

entamoeba lifecycle

mature cysts ingested, excystation to troph form, troph multiplies into more trophs or into cysts, cyst and troph excreted in feces

entamoeba transmission

ingestion of cysts in contaminated food or water, cysts survive days-week, 1 cyst makes 4 trophs

entamoeba trophozoite

found in diarrheal stool: single nucleus with central karyosome and peripheral chromatin, ground glass cytoplasm

E. histo: erythrophagocytosis

entamoeba cyst

found in formed stool: four nuclei and chromatid body, nucleic acids look like dense rod, size of monocyte

entamoeba laboratory detection

R/O with 3x stool exam, fecal EIA adjunct to microscopy, PCR, EIA for extraintestinal disease

entamoeba treatment and prevention

water treatment: iodination or boiling, chlorination doesn’t work

asymptomatic: eradicate cysts

symptomatic: eradicate trophs with metronidazole then with asymptomatic treatment

E. histolytica doesn’t respond to tetracycline

entaemoeba hartmanni

small E. histo: chromatid bodies with compact karyosome

Entamoeba coli

Large, cyst form >4 nuclei, troph form has large karyosome and vacuolated/dirty cytoplasm

entamoeba polecki

many small pointed/angular chromatid bodies

Entamoeba nana

cyst form has 4 nuclei and lacks peripheral chromatin
troph form has blot like karyosome with granular or vacuolated cytoplasm

Iodamoeba beutschlii

cyst has one large glycogen vacuole, troph is slluggish with large central karyosome

Dientamoeba fragilis

flagellate with no cyst stage, symptomatic and asymptomatic infections possible

balantidium coli

ciliated protozoa that transitions between cyst and troph form

balantidium life cycle

ingestion of contaminated food or water/fecal oral, pigs are reservoir

balantidium disease

dysentery, can be invasive and form colonic ulcers, responds to tetracycline

balantidium coli morphology

large(220-400um), ciliated with kidney bean nucleus, cysts often not seen

Giardia life cycle

1: ingestion of contaminated food or water

2: 1 cyst makes 2 trophs that replicate via longitudinal binary fission

giardia infectivity

cysts are infectious shortly after passage and can survive months in cold water, person-person is possible, if trophs are ingested then no disease/asymptomatic

humans are crucial reservoir and can be asymptomatic carriers

giardia disease

causes non invasive inflammation of jejunum
acute: watery/fatty stools
chronic: fat malabsorption syndrome, loss of vit A,D,E,K can leads to stunted growth or rickets

giardia diagnosis

weird face thing, falling leaf motility
O and P, EIA/RDT kits, PCR

do not use concentrates

giardia treatment and prevention

metronidazole, water treatment with iodination, have good hygiene

trichomonas vaginalis

flagellated protozoan specific to humans, spread through sexual contact

trichomonas vaginalis life cycle

no cyst stage, relies on sexual transmission, resides in female lower genital tract and male urethra/prostate, replicates by binary fission, troph form cannot survive in environment, spreads through sexual contact

trichomonas vaginalis symptoms

Females: more symptomatic, can lead to PID, persists
Males: more asymptomatic, rarely urethritis, epididymitis, prostatitis
neonates: congenital, rare involvement of lung

trichomonas vaginalis morphology

flagella, undulating membrane, twitching motility under wet mount

trichomonas vaginalis diagnosis

wet mount not recommended due to poor sensitivity, must be done <20min
gold standard: anerobic culture, but slow/labor intensive
preferred method is PCR

trichomonas vaginalis treatment and prevention

do whole STD/I panel, safe practices, treat under medical supervision and include all partners of infected person, can treat with metronidazole

taenia saginata/solium lifecycle

Humans: ingestion of raw or undercooked infected meat/muscle tissue with cysticerci, scolex attaches to intestine, adult worm releases eggs/gravid proglottids in feces

intermediate host: cattle and pigs infected by ingesting contaminated vegetation, oncospheres hatch and penetrate intestinal wall, oncospheres circulate and develop into cysticerci in muscle tissue

cysticercosis

T. solium eggs ingested by human hosts, oncospheres hatch and penetrate intestinal wall and circulate to muscle tissue, cysticerci can develop in any organ(brain, eyes, subcutaeneous tissue)

taenia vector

T. saginata: cow
T. solium: pig

taenia disease

eggs can calcify in tissue and rupture later

T. solium: propensity to make cysticerci in brain
T. saginata: no cysticerci in humans
cysticercosis: larvae form cysts in humans

taenia morphology

4 suckers
T. solium: rostellar hooks, proglottid is thinner and more branched
T. saginata: no rostellum, proglottid thicker and less branched

taenia diagnosis

take extreme care in processing specimen, ingestion can cause cystercerosis
O and P: eggs are indistinguishable, usually don’t see proglottid, hooks indicate cestode, differentiate species by striations in eggs

taenia prevention and treatment

post mortem inspection of swine carcass by USDA, stop coprophagia, cook food
treat humans with praziquantel

Echinococcus granulosus/multilocularis definitive hosts

Dogs/canidae, multi(foxes, dogs, cats)

Echinococcus granulosus/multilocularis Intermediate host

Granulosus: sheep, goats, swine, wild herbivores

multilocularis: rodents

Humans are dead end host

diphyllobrothriid(fish tapeworms) lifecycle

unembryonated eggs passed in feces of definitive host, eggs embyronated in water, intermediate host facilitates larvae maturation, infected crustacean ingested by second intermediate host, predator fish eats smaller fish, definitive host ingests plerocercoids in infected fish

fish tapeworm hosts

definitive host: fish eating mammal
intermediate host 1 is crustacean
intermediate host 2 is freshwater fish

fish tapeworm disease

tapeworm absorbs huge quantities of vitb12 which leads to anemia

fish tapeworm morphology

really long(>30ft), width>length of proglottid compared to taenia, “mind the knob”

fish tapeworm prevention

proper cooking/freezing of fish

eneterobius vermincularis(pinworm) lifecycle

embryonated eggs ingested, adult worm lays eggs in gut, mature female worm migrates out of anus and lays eggs at night

eneterobius vermincularis(pinworm) morphology

nematodes: males are curlier and females are longer with tapered ends

enterobius diagnosis

sample collected with clear tape or paddle

enterobius prevention

wash linens, treat family, trim fingernails

enterobius disease

eggs are immediately infectious and easily cause autoinfection/reinfection, causes peri-anal itching

trichuris trichiura(whipworm) lifecycle

embryonated eggs ingested, larvae hatch in small intestine, adults reside in cecum and lay eggs that pass in feces, eggs 15-20 days in soil before development

whipworm(trichuris) disease in normal host

cecum colonized, mostly asymptomatic, coinfections common, can cause malabsorption or inflammation

whipworm(trichuris) disease in compromised kids

severe chronic diarrhea, tenesmus, abd pain, rectal prolapse, allergic manifestations(eosinophilia)

whipworm(trichurius) egg morphology

unembryonated: thick wall with hyaline polar plugs
lookalike: capillaria has striated shell and less prominent polar plugs

ascaris lumbricoides lifecycle

mature eggs release larvae, larvae penetrate GI mucosa, extra GI migration to liver then lungs, cross epiglottis and re enter GI tract, egg laying adults months after exposure

ascaris lumbicoides transmission

common in soil eaters(pica) and kids, love openings, eggs take 18 days to be infectious

ascaris disease

asymptomatic, may crawl out if high fever
worm may migrate to lungs for high O2 and cause pneumonia
may ascend to liver causing jaundice, inflammation
can cause pancreatic block or acute GI blockage

ascaris treatment

deworming with mebendazole/albendazole: binds to beta tubulin and prevents microtubule polymerization, adult worm dies

treatment for 1-3 days

ascaris egg morphology

unfertilized egg: mammalated
fertilized egg: mammalated with curled worm inside
decrotication: loss of outer layer

hookworms

new world: necator americanus
old world: anclyostoma duodenale

hookworm lifecycle

flariform larva penetrates skin, moves from subcutaenous venules to lymphatics and into circulation, enter lungs and cross epiglottis, reaches GI tract, adults 5-9 weeks post exposure

hookworm transmission

resides in small intestines and penetrates bare feet
questing: flariform larvae on blades of grass

hookworm disease

acquired iron deficiency anemia, severity directly correlated to number of parasites, can impair physical/intellectual developement

hookworm morphology

rhabitiform larvae not normally found in stool, must RO strongyloides

old world: sharp teeth
new world: cutting plates

hookworm treatment and prevention

avoid going barefoot, sanitary sewers, educational/deworming campaigns

treat with albendazole

strongyloides lifecycle

flariform larvae penetrate skin and enter circulatory system, transported to lungs and penetrate alveolar spaces, carried to throat and swallowed into small intestine where they become adults, female worm parthogenesis in intestine and can autoinfect, rhabitiform larvae in intestine excreted in stool

stronglyoides signal searching

humans are principle reservoir

non specific signals: CO2, NaCl
specific signals: urocanic acid 5x on foot vs other body parts

strongyloides hyperinfection disease

risk for immunosuppression or HTLV(not HIV): occurs when accelerated autoinfection tremendously increases worm burden
massive tissue invasion leads to malnutrition, hypoproteinemia, polymicrobial infections, septicemia, high mortality

strongyloides disease in normal host

asymptomatic autoinfection up to 40yrs
acute migratory phase induces respiratory symptoms, eosinophilic pulmonary infiltrates(loffler’s)

chronic: digestive issues with minimal inflammation or abd pain

strongyloides morphology

short and sexy, short buccal canal with prominent genital primordium

strongyloides diagnosis

3 O and P for rhabditiform larvae: seldom see eggs

stool concentration important, stool culture for larvae tracks/gliding

strongyloides treatment and prevention

careful with steroid reaction, don’t go barefoot, proper hygiene/sanitation
ivermectin, nasal thiabendazole for hyperinfection

trichinella spiralis(and others) lifecycle

two lifecycles: domestic and sylvatic, humans are dead end hosts
ingestion of uncooked meat, larvae released in small intestine and mature into adults, reside in small intestine >1mo, larvae deposited in mucosa, encysted larvae in striated muscle tissue

trichinella spiralis diagnosis

mainly clinical diagnosis: muscle biopsy, serology, peripheral blood eosinophilia up to 90%
can see curled organism in muscle tissue

trichinella spiralis treatment and prevention

prevent cyst formation(in small intestine >1mo): heat 76.6C for 4min or freeze-29C for 10days, do not microwave, do not freeze T.nativa

USDA prohibits feeding raw meat scraps to hogs

anisakis(sushi parasite) lifecycle

marine mammals excrete unembryonated eggs, eggs embryonated in water, larvae hatch from eggs(free-swimming), larvae ingested by crustacean and mature into L3 larvae, infected crustacean eaten by fish and squid, infected fish or squid ingested by marine/human mammals

anisakis diagnosis

gastroscopic examination