PARASITES
DISEASE CLINICAL FINDINGS IMPORTANT PROPERTIES PATHOGENESIS DIAGNOSIS TX PREVENTION
INTESTINAL PROTOZOA
Entamoeba histolytica
Amebic dysentery Acute: lower abdominal Transmission: ingestion of cysts via •No animal reservoir •identification of the Metronidazole •Avoid fecal
(bloody, mucus discomfort, flatulence, tenesmus, fecal-oral route in contaminated food •Trophozoites invade organism in the stool or (Flagyl®) = a contamination of
diarrhea) and liver constipation & water (also oral-anal) colonic epithelium & tissues via: mixed food & water
abscess Chronic: low-grade symptoms - Lifecycle: secrete enzymes »» local O & P Test: trophozoites in amebicide
occasional diarrhea, weight loss, •Ingestion of cysts (4 nuclei (central necrosis »» “teardrop” diarrheal stool or cysts in effective against •Observe good
fatigue dot w/ dense peripheral chromatin & ulcer »» may non-diarrheal stool; note that both luminal personal hygiene
90% infected = asymptomatic chromatoidal bars=ribosomes), disseminate, esp. to there will not be large and systemic (hand washing)
carriers nonmotile, rigid cell wall, right lobe of liver where numbers of forms of the
Amebic abscess of liver nondividing, 10-20 microns in it causes abscesses polymorphonuclear disease plus a •purify water
(ameboma): RUQ pain, weight diameter) •worldwide (tropical, leukocytes in stool (vs. luminal supplies
loss, fever, tender, enlarged liver •Trophozoites (motile, phagocytic poor sanitation is most shigellosis, salmonellosis, amebicide like (boiling/filtration is
for RBCs & bacteria, disease- common) ulcerative colitis) diloxanide effective, but
causing, amorphous, 1 •1-2% in USA Biopsy furoate chlorination is not)
nucleus=located eccentrically w/
evenly distributed chromatin) excyst Distinguish between:
in small intestine (1 cyst »» 8 Entamoeba dispar
trophozoites) (nonpathogenic,
•Trophozoites invade tissues of colon morphologically identical)
•Trophozoites encyst in colon OR by PCR or monoclonal
cause pathology (liver abscess, brain Antibodies
abscess, flask-shaped ulcer) Entamoeba hartmani: cysts
•Cysts are passed in feces have 4 nuclei, but are 95% wks after mosquito bite (coincide also, transplacentally, blood RBCs (merozoites & thin (for species id) Giemsa- malaria (mefloquine OR
•P. malariae ~4% w/ cycle between RBCs) transfusion, IVDA spleen) stained smears •kills merozoites chloroquine +
•P. ovale is very rare •periodic cycle of CHILLS, then •P. falciparum is more •ring-shaped trophozoites •does not affect Fansidar
FEVERS, then SWEAT (due to Highlights of Lifecycle: severe: children/elderly can be seen within infected hypnozoites •mosquito netting,
erythrocytic phase) develops •Asexual cycle (schizogony »» most @ risk RBCs window screens,
>200 million infected several days after onset (note that schizonts) in humans (intermediate •Hg is degraded to Primaquine to protective clothing,
>1 million die each yr parasites synchronize themselves) hosts) provide aa’s for protein Diffs between P. falciparum prevent relapses insect repellents
•fever spike (37°C to 41°C) •Sexual cycle (sporogony »» biosynthesis »» heme & others: •kills •protection more
w/nausea, vomiting, & abdominal sporozoites) in mosquitoes released »» Heme •gametocytes are crescent- hypnozoites imp. during the night
pain »» drenching sweats as fever polymerase of shaped, whereas others are •drainage of stagnant
breaks •schizogony=nuclear division plasmodium makes spherical Mefloquine or waters
•Splenomegaly (most) without cell division insoluble hemozoin •infects all RBCs »» higher Quinine- •partial immunity
•Hepatomegaly (1/3) •P. vivax & P. ovale (48hr cycle)- (malarial pigment) parasitemia level (Note: P. Fansidar based on humoral
•Hemolytic Anemia (prominent) benign tertian (recurs every 3rd day) vivax infects reticulocytes, (sulfadoxine- antibodies that block
•Renal damage, esp. P. falciparum •P. falciparum (48hr cycle)- •Susceptibility: whereas P. malariae infects pyrimethamine) merozoites from
•GI problems malignant tertian (every 3 days) blacks 80% if •bilateral rales & rhonchi •extracellular organism found in lungs •immunosuppressed transbronchial biopsy atovaquone are
untreated, ~50% if treated •chest X-ray » diffuse interstitial alternative drugs
•normally a commensal pneumonia Lifecycle: Giemsa-stained lung smears:
•first disease diagnosed in •more gradual onset in infants •cysts inhaled into alveoli •look for trophozoites &
>50% of AIDS pts •inflammatory response causes frothy intracystic bodies (opposed
•worldwide (up to 70% of exudate that blocks oxygen exchange comma-like particles) which are
people have been infected) •organism does not invade lung tissue diagnostic
•pneumonia results when host defenses are
reduced •no serologic test exists
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PARASITES
DISEASE CLINICAL FINDINGS IMPORTANT PROPERTIES PATHOGENESIS DIAGNOSIS TX PREVENTION
Trypanosoma cruzi
Chagas’ disease acute phase: Transmission: through bite of reduviid •most common in children Acute: Acute: •protection from bite of
(American •facial edema & a nodule bug (Triatoma & Rhodnius); also, 12) primary uterine eggs in cow’s intestine & burrow
branches into blood vessel, where they are
carried to skeletal muscle
•in muscle develop into cysticerci
(=larvae) which can then be ingested
by human
Echinococcus granulosus (Dog tapeworm)
Unilocular Hydatid •many are asymptomatic •dog = definitive host •E. granulosus usually •ID of cysts via ultrasound, •Surgical •Do not feed
Cyst Disease (caused by •sheep = intermediate host forms ONE large fluid- CT, MRI removal of cyst entrails of
larva) •hydatic cysts develop slowly •humans = dead-end intermediate filled cyst (unilocular) using extreme slaughtered sheep
•Liver cysts may cause hepatic hosts that contains 1000s of •hydatic sand @ surgery is care not to rupture to dogs!
dysfunction/pain when they reach Lifecycle: individual scoleces + diagnostic cyst
•ONLY 3 proglottids a critical size •1000s of worms in dog’s intestines many daughter cysts
(=one of smallest •Lung cysts can erode into a liberate 1000s of eggs in dog feces & •individual scoleces @ •Microscopic exam •hypertonic
tapeworms) bronchus » bloody sputum, but thereby contaminate environment bottom = “hydatid sand” showing brood capsules saline should be
are usually asymptomatic (grass, etc.) •cyst = space-occupying containing many injected into cyst
•Each protoscolex has •Cerebral cysts can cause •eggs ingested by sheep (or humans) lesion protoscoleces to kill organisms
the potential to become headache and focal neurologic •oncosphere embryos emerge in sm. •cyst fluid contains & prevent
an adult worm signs intestine and migrate to liver (and parasite antigens, which •Serologic tests (indirect accidental
•rupture of the cyst can cause fatal sometimes then to lungs, bones, & can sensitize the host » hemagglutination test) are dissemination
anaphylactic shock brain) anaphylaxis if cyst useful, but may be falsely
•hydatic cysts can become •here, embryos develop into large ruptures negative (15% of liver cysts •Albendazole is
secondarily infected w/ bacteria fluid filled hydatid cysts •Distribution: primarily & 50% of lung cysts have being evaluated
•older cysts may calcify •inner germinal layer of hydatid cysts in sheep-raising areas (S. negative serology) for the prevention
generates many protoscoleces within America, Africa, of spread of cysts
“brood capsules” Mediterranean area, following surgery
•liver containing hydatic cysts of Middle East, Central
slaughtered sheep (=entrails) are Asia, Australia, CA, AZ,
eaten by dogs and cycle continues NM, UT, Alaska, Can.
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PARASITES
DISEASE CLINICAL FINDINGS IMPORTANT PROPERTIES PATHOGENESIS DIAGNOSIS TX PREVENTION
TREMATODES (Flukes)
Schistosoma (S. mansoni, S. japonicum, S. haematobium) - Blood Flukes
Schistosomiasis •most are asymptomatic Lifecycle/Transmission: •eggs in liver, spleen, or S. mansoni & S. japonicum: Praziquantel (all •Proper disposal of
•chronic infections may become •Free-swimming, fork-tailed wall of gut are •eggs in stool, blood in stool, 3 species) human waste
•S. mansoni & S. symptomatic cercariae penetrate skin of humans responsible for most rectal biopsy •eradication of
japonicum affect (=definitive hosts) pathology •prognosis is snail host
gastrointestinal system Acute Phase (shortly after •Cercariae differentiate to larvae Liver: S. haematobium: grave in cases of •avoid swimming
(adults live in cercarial penetration): (schistosomula) and enter the blood •eggs secrete antigens » •eggs in urine, blood in long duration & in in endemic areas
mesenteric veins) •itching, dermatitis •Schistosomula are carried via veins intense immune response urine, bladder biopsy malnourished
•fever, chills, diarrhea, lymph- to arterial circulation (Superior » granulomas » impaired children/people
•S. haematobium affects adenopathy, hepatosplenomegaly Mesenteric artery » portal system » circulation » fibrosis, Distinguish by egg often exposed to
urinary tract (adults live 2-3 wks later liver) hepatomegaly, & portal morphology: cercaria
in urinary bladder) •Intense eosinophilia in response •Become adult flukes in liver HTN » splenomegaly •S. mansoni eggs have a
to migrating larvae •S. mansoni & S. japonicum migrate •hepatocytes undamaged prominent lateral spine
•Adults exist as •Resolves spontaneously against portal flow to reside in •function tests = normal •S. japonicum eggs have a
separate sexes, but live mesenteric venules, whereas S. Intestines: very small lateral spine
attached to each other Chronic: haematobium adults reach the •proteolytic enzymes & •S. haematobium eggs have
(female resides in a •S. mansoni/S. japonicum = GI bladder veins through the venous inflammatory response a terminal spine
groove in the male = the hemorrhage, hepatomegaly, plexus between the rectum & bladder Bladder:
“schist”) massive splenomegaly; death by •Female adult lays fertilized eggs •granulomas » fibrosus »
exsanguination of esophageal •Eggs penetrate vascular carcinoma of bladder Distribution:
•200 million infected & varices; chronic salmonella endothelium to enter lumen (gut or S. mansoni: Africa, Middle
200 thousand death/yr infections, cirrhosis, neurological bladder) Immune Response: East, Latin America
(2nd to malaria) problems •Eggs are excreted (Feces or urine) •Ab dependent, CD4+ (+Puerto Rico)
•S. haematobium = hematuria; •Eggs hatch in fresh water and mediated (IL-4, IL-10)
•2-30 yrs. is prime age superimposed bacterial UTIs, become ciliated larvae (miracidia) •IgE-dep macrophages S. haematobium: Africa,
for infection in endemic calcified bladder, carcinoma of •Miracidia penetrate snails •IgE & IgG-dep Middle East
areas bladder (=intermediate hosts) eosinophils
•Cercariae are formed in snails and •IgE-dep platelets/mast S. japonicum: Orient only
“Swimmer’s Itch”: then released to fresh water where cells (Phillipines, Thailand, Laos,
•due to penetration of the skin by they are able to penetrate human skin •only schistosomula are Cambodia, China); water
cercariae of nonhuman susceptible to immune buffalo, pigs as reservoirs
schistosomes (bird-infective attack
schistosomes), which are
incapable of replicating in Schistosomes evade
humans host defenses
•frequent problem of US lakes •surface coated w/host
antigens (C3 receptor,
IgG receptor, maybe
TNF-alpha receptor)
•SDIF (schistosome-
derived inhibitory factor)
strongly inhibits
lymphocyte proliferation
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PARASITES
DISEASE CLINICAL FINDINGS IMPORTANT PROPERTIES PATHOGENESIS DIAGNOSIS TX PREVENTION
INTESTINAL NEMATODES (Roundworms)
Enterobius vermicularis (Pinworm)
Enterobiasis (or •majority = asymptomatic Transmission/Lifecycle (humans •Worldwide •”Scotch tape” technique to Mebendazole OR None
Pinworm infection) •perianal pruritis (most prominent only): •most common helminth recover eggs from perianal Pyrantel
symptom) •ingestion of eggs or inhalation and in USA skin pamoate
•adult female is 1cm in •scratching predisposes to 2° eventual swallowing of eggs •80% in thickening of skin & loss of nodules (for 10-15yrs) females for 6 •Do not give
endemic areas elasticity »» “onchocercal •female produces microfilariae which months diethylcarbamazin
dermatitis” & “hanging groin” are not sheathed •Suramin kills - it would increase
•male=5cm •microfilariae migrate through adult, but is very pathology of
•female=up to 50cm •microfilariae in eyes can lead to subcutaneous tissue » concentrate in toxic - used for disease
blindness (“river blindness”, eyes eye involvement
because blackflies develop in •microfilariae ingested by another •Skin nodules
rivers & people who live along blackfly removed
those rivers are affected) •infective larvae develop from surgically, but
microfilariae in blackfly normally not
•Humans = only definitive host curative
Loa loa (African eye worm)
Loiasis •Calabar swellings = transient Transmission/Lifecycle: Deerfly •no inflammatory •visualization of sheathed Diethylcarba- •Control deerfly
(2-3 days), localized, (mango fly - Chrysops) deposits response to the microfilariae in blood mazine eliminates with insecticides
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PARASITES
DISEASE CLINICAL FINDINGS IMPORTANT PROPERTIES PATHOGENESIS DIAGNOSIS TX PREVENTION
•Only in tropical Central erythematous, subcutaneous infective larvae on human skin while microfilariae or adults, smear microfilariae &
& West Africa (habitat edema biting but a hypersensitivity may kill the adults
of deerfly) •larvae enter bite wound » wander in rxn is responsible for
•Adult worm crawling across the body » develop into adults Calabar swellings Worms in eyes
•adults = 3-7cm conjunctiva of the eye (harmless, •females release microfilariae may be removed
but disconcerting) •microfilariae enter blood (esp. surgically
during the day)
•microfilariae taken up by deerfly
•differentiate into infective larvae in
deerfly
Dracunculus medinensis (Guinea Worm)
Dracunculiasis •inflammation, blistering, & Transmission/Lifecycle: Humans are •adult female produces a •usually see the head of the Time-honored tx •Filtering or
ulceration of the skin (usually infected when tiny crustaceans substance that causes worm in the skin ulcer consists of boiling drinking
•large areas of tropical lower extremities) (copepods) containing infective clinical symptoms gradually water
Africa, India, & •inflamed papule/nodule burns & larvae are swallowed in drinking extracting the
Pakistan itches (=very painful) water worm by winding
•may become secondarily infected •larvae are released in the small it up on a stick
intestine » migrate into body » over a period of
develop into adults (1 meter long!) days
•meter-long female lives in a nodule
at lower extremities of leg & Niridazole or
produces motile larvae (also metronidazole
responsible for skin pathology) makes the worm
•nodule erupts » release of L1 larvae easier to extract
into environment (fresh water)
•copepods eat larvae
•larvae molt to form infective larvae
(L3 stage) in copepod
•humans eat copepods
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