GI Parasitology Flashcards
Entamoeba histolytica - geographic distribution
worldwide distribution
Entamoeba histolytica - mode of transmission
*fecal-oral (through contaminated food and water)
*person-to-person spread may occur
Entamoeba dispar
*non-pathogenic
*morphologically indistinguishable from Entamoeba histolytica
*need isoenzyme electrophoresis, specific stool antigen, or PCR tests to differentiate
Entamoeba histolytica - life cycle
- ingested cysts (environmentally resistant) transform to trophozoites upon exposure to stomach acid that colonize and in some individuals subsequently invade mucosa
- invasion of the mucosa causes colitis
- trophozoites can divide and transform to infective cysts in asymptomatic carriers or symptomatic patients
- cysts are passed in the stool and spread to others
Entamoeba histolytica - clinical presentation
*invasive bowel disease (aka intestinal amebiasis)
*DYSENTERY (bloody purulent diarrhea), abdominal tenderness, fever
*complications include: stricture, ameboma, hemorrhage, perforation, etc
*chronic colitis may mimic IBD
*extraintestinal manifestation = hepatic involvement/abscess
*FLASK-SHAPED ULCERS in colon on histology
Entamoeba histolytica - treatment
*invasive disease: METRONIDAZOLE (affects only trophozoites, NOT cysts)
*intestinal cysts: paromomycin, iodoquinol (need to treat with these drugs subsequently to eliminate the cyst-shedding state)
Entamoeba histolytica - diagnosis
*serology, antigen testing, PCR, cysts and/or trophozoites
*3 stool exams for light microscopy for cysts or trophozoites
*stool antigen detection
*aspiration of liver abscess = “ANCHOVY PASTE”
*histology of colon biopsy shows flask-shaped ulcers
what pathogen appears as “anchovy paste”
*Entamoeba histolytica, forming a liver abscess
Giardia lamblia - geographic distribution
*worldwide; found in SURFACE WATERS where mammalian reservoirs frequent (beavers are the prototype)
*sporadic infection in US seen in outdoor adventurers
*small epidemics seen associated with day-care or public swimming pools/recreational water parks
Giardia lamblia - mode of transmission
cysts in water (often surface waters where mammalian reservoirs are frequent)
what is the most common cause of PERSISTENT diarrhea in travelers
Giardia lamblia
Giardia lamblia - clinical presentation
*incubation period: 7-14 days
*manifestation of infection varies widely from asymptomatic to acutely symptomatic diarrheal illness, to chronic diarrhea with malabsorption
*weight loss, nausea, abdominal pain, steatorrhea, flatulence common
*non-inflammatory, steatorrhic (fatty) diarrhea; no blood or mucous in stool; no fever
*waxes and wanes while symptomatic
image of giardia lamblia
trophozoites in the stool
Giardia lamblia - diagnosis
*multiplex PCR panel
*multinucleated trophozoites or cysts in stool
*antigen detection (ELISA)
Giardia lamblia - treatment
METRONIDAZOLE (or quinacrine)
Giardia lamblia - prevention
*water purification, including chlorination
*good sanitation, hand washing
Cryptosporidium parvum - geographic distribution
worldwide
Cryptosporidium parvum - pathogenesis
*intracellular pathogen; microvilli atrophied & blunted
*oocysts move into intestine where excyst to sporozoites; oocytes resistant to disinfection
Cryptosporidium parvum - mode of transmission
oocysts in water
Cryptosporidium parvum - epidemiology
*can cause disease in immunocompetent & immunocompromised hosts
*reservoir = CALVES & cattle
*outbreaks seen in day-care settings, swimming pool associated, and food-borne
*not eliminated by water treatment
Cryptosporidium parvum - clinical presentation
*diarrhea, crampy abdominal pain
*7-10 day incubation period
*varies from intermittent, scant to continuous, watery, voluminous diarrhea
*self-limited in immunocompetent host
*can be devastating in immunocompromised, esp AIDS patients
Cryptosporidium parvum - diagnosis
*multiplex PCR in gastrointestinal panels
*microscopic (modified ACID FAST STAIN)
*ELISA stool antigen detection
Cryptosporidium parvum - treatment
*no treatment for immunocompetent hosts (self-limited)
*Nitazoxanide in children and immunocompromised hosts??
*prevention: filtering city water supplies
Cystoisospora belli
*coccidial
*tropical & subtropical climates; AIDS patients
*occasionally infects travelers
*diarrheal illness
*TREAT with TMP/SXT
*not picked up in PCR stool panels
*fluorescent or acid fast stains of stool
Cyclospora
*coccidial: acid fast organism
*some developed world outbreaks with fresh fruits (raspberries, basil, snow peas, lettuce)
*diarrheal organism
*dx best with PCR or fluorescent or light microscopy of acid fast stained specimen
*TREAT with TMP/SXT
helminths - overview
*roundworms (nematodes), tapeworms (cestodes), and flukes (trematodes)
*complex life cycle, generally with 2+ hosts
*most worms CANNOT reproduce within human host
*little or no eosinophilia from intestinal adult worm
Ascaris lumbricoides - overview
*very common intestinal parasitic infection
*more common in children
*aka ROUNDWORM
Ascaris lumbricoides - geographic distribution
worldwide; more common in tropical regions
Ascaris lumbricoides - mode of transmission
fecal-oral transmission (via contaminated foods or soil-contaminated hands)
Ascaris lumbricoides - life cycle
- ingested eggs hatch in small intestine
- larva pass through intestinal wall into venous system to liver; then through heart to lungs
- in lungs, larvae mature and pass into airways, where they are then coughed up and swallowed
- then, the worms complete development into adult worms in small intestine
*during their passage through tissues (intestinal wall & lungs), they can cause inflammation with eosinophilia
Ascaris lumbricoides - clinical presentation
- larval migratory phase: host reaction in the lung
-pneumonitis: hypersensitivity reaction as parasite migrates through; cough, wheezing, SOB, fever, chills, malaise; EOSINOPHILIA - adult worms:
-most asymptomatic
-vague crampy abdominal pain most common sx if present
*intestinal obstruction possible
*aberrant migration can occur in bile ducts, appendix
Ascaris lumbricoides - diagnosis
*stool examination: ova or adult parasites
*adult worms passed through rectum or “coughed up”
Ascaris lumbricoides - treatment
*ALBENDAZOLE
Enterobius vermicularis - overview
*aka PINWORM
*most widely prevalent nematode of man
*more prevalent in temperate than tropical climates
*pretty common in USA
*predominantly in children
Enterobius vermicularis - pathogenesis
*non-invasive; adults live in cecal area
*local allergic reactions to worm proteins
*susceptibility decreases with age
Enterobius vermicularis - clinical presentation
*perianal itching (ANAL PRURITUS) with subsequent sleep disturbance
*most common in children
Enterobius vermicularis - mode of transmission
fecal-oral
Enterobius vermicularis - diagnosis
“scotch-tape test” or examine the anus
Enterobius vermicularis - treatment
*ALBENDAZOLE
which pathogen presents with anal pruritus in children
Enterobius vermicularis
hookworms (Anyclastoma duodenale & Necator americanus) - geographic distributions
Anyclastoma duodenale = Mediterranean countries, Iran, India, Pakistan, Far East
Necator americanus = North & South America, Central Africa, Indonesia, South Pacific, parts of India
hookworms - risk factors
*skin exposures to fecally contaminated soil in endemic areas (esp people walking barefoot)
hookworms (Anyclastoma duodenale & Necator americanus) - life cycle
- infective larvae penetrate skin that contacts soil
- migrates through systemic venous system to lung
- mature in lung, migrate up trachea & swallowed
- further mature into adults in small intestine; attach to mucosa and cause slow, chronic blood loss & iron deficiency anemia
- eggs passed into stool; EGGS HATCH IN SOIL INTO INFECTIVE LARVAE
*gotta have stool in soil
hookworms (Anyclastoma duodenale & Necator americanus) - clinical presentation
*initial intestinal infection with abdominal pain & eosinophilia
*chronic infestation with high worm burden: symptoms of IRON DEFICIENCY ANEMIA & hypoalbuminemia
*malnutrition
*eosinophilia with lung migration
hookworms (Anyclastoma duodenale & Necator americanus) - diagnosis
*eggs in stool
hookworms (Anyclastoma duodenale & Necator americanus) - treatment
ALBENDAZOLE
cutaneous larva migrana
*aka creeping eruption
*dog or cat hookworm
*pathogenesis: larvae hatch in soil after eggs pass in canine or feline feces; penetrate, migrate in skin producing inflammatory reaction along cutaneous tract pulmonary involvement also occurs
*clinical disease = pruritic, serpiginous lesions develop 1 week post-contact with infected soil
*prevention = shoes
*tx = topical thiabendazole
Strongyloides stercoralis - life cycle
*same life cycle as hookworm but AUTOINFECTION can occur
*eggs can HATCH BEFORE LEAVING INTESTINE and larvae can mature in and around rectum/anus
*larvae then can penetrate perianal skin: cutaneous larvae curans
Strongyloides stercoralis - pathogenesis
*adult worms embedded in small intestinal mucosa lead to local inflammation
*larvae cause tissue inflammation during migration
*penetrating larvae may carry enteric bacteria
Strongyloides stercoralis - clinical presentation
*intestinal phase: diarrhea and malabsorption (esp in heavy infection)
*migratory phase: granulomatous colitis, hepatomegaly, pneumonitis and EOSINOPHILIA, fever, recurrent serpentine urticarial rash, “larva currens”
*hyperinfection syndrome: severe manifestations of above, septicemia, high mortality rate, essentially disseminated strongyloides; often associated with enteric bacteria in blood/csf
Strongyloides stercoralis - diagnosis
eggs/larvae in stool
Strongyloides stercoralis - treatment
IVERMECTIN or thiabendazole
cestodes (tapeworms)
*Taeniasis saginata = beef tapeworm
*Taeniasis solium = pork tapeworm
*Diphyllobothriasis = fish tapeworm
Diphyllobothrium latum
*fish tapeworm (from raw, freshwater fish)
*causes VITAMIN B12 DEFICIENCY in host (pernicious anemia) [tapeworm competes for B12 in intestine]
*transmission = ingestion of larvae in raw freshwater fish
*treatment = albendazole + praziquantal
Taenia solium - life cycle
*pork tapeworm
*human can be definitive or intermediate host
*cysticercosis (cystic CNS lesions and seizures) if ingestion of EGGS IN FOOD (when human is intermediate host)
*intestinal tapeworm if ingestion of LARVAE
*treatment: steroids + ALBENDAZOLE + praziquantal + antiseizure med
