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GI Exam > GI Parasitology > Flashcards

GI Parasitology Flashcards

1
Q

Entamoeba histolytica - geographic distribution

A

worldwide distribution

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2
Q

Entamoeba histolytica - mode of transmission

A

*fecal-oral (through contaminated food and water)
*person-to-person spread may occur

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3
Q

Entamoeba dispar

A

*non-pathogenic
*morphologically indistinguishable from Entamoeba histolytica
*need isoenzyme electrophoresis, specific stool antigen, or PCR tests to differentiate

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4
Q

Entamoeba histolytica - life cycle

A
  1. ingested cysts (environmentally resistant) transform to trophozoites upon exposure to stomach acid that colonize and in some individuals subsequently invade mucosa
  2. invasion of the mucosa causes colitis
  3. trophozoites can divide and transform to infective cysts in asymptomatic carriers or symptomatic patients
  4. cysts are passed in the stool and spread to others
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5
Q

Entamoeba histolytica - clinical presentation

A

*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

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6
Q

Entamoeba histolytica - treatment

A

*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)

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7
Q

Entamoeba histolytica - diagnosis

A

*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

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8
Q

what pathogen appears as “anchovy paste”

A

*Entamoeba histolytica, forming a liver abscess

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9
Q

Giardia lamblia - geographic distribution

A

*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

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10
Q

Giardia lamblia - mode of transmission

A

cysts in water (often surface waters where mammalian reservoirs are frequent)

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11
Q

what is the most common cause of PERSISTENT diarrhea in travelers

A

Giardia lamblia

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12
Q

Giardia lamblia - clinical presentation

A

*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

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13
Q

image of giardia lamblia

A

trophozoites in the stool

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14
Q

Giardia lamblia - diagnosis

A

*multiplex PCR panel
*multinucleated trophozoites or cysts in stool
*antigen detection (ELISA)

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15
Q

Giardia lamblia - treatment

A

METRONIDAZOLE (or quinacrine)

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16
Q

Giardia lamblia - prevention

A

*water purification, including chlorination
*good sanitation, hand washing

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17
Q

Cryptosporidium parvum - geographic distribution

A

worldwide

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18
Q

Cryptosporidium parvum - pathogenesis

A

*intracellular pathogen; microvilli atrophied & blunted
*oocysts move into intestine where excyst to sporozoites; oocytes resistant to disinfection

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19
Q

Cryptosporidium parvum - mode of transmission

A

oocysts in water

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20
Q

Cryptosporidium parvum - epidemiology

A

*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

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21
Q

Cryptosporidium parvum - clinical presentation

A

*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

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22
Q

Cryptosporidium parvum - diagnosis

A

*multiplex PCR in gastrointestinal panels
*microscopic (modified ACID FAST STAIN)
*ELISA stool antigen detection

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23
Q

Cryptosporidium parvum - treatment

A

*no treatment for immunocompetent hosts (self-limited)
*Nitazoxanide in children and immunocompromised hosts??
*prevention: filtering city water supplies

24
Q

Cystoisospora belli

A

*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

25
Q

Cyclospora

A

*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

26
Q

helminths - overview

A

*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

27
Q

Ascaris lumbricoides - overview

A

*very common intestinal parasitic infection
*more common in children
*aka ROUNDWORM

28
Q

Ascaris lumbricoides - geographic distribution

A

worldwide; more common in tropical regions

29
Q

Ascaris lumbricoides - mode of transmission

A

fecal-oral transmission (via contaminated foods or soil-contaminated hands)

30
Q

Ascaris lumbricoides - life cycle

A
  1. ingested eggs hatch in small intestine
  2. larva pass through intestinal wall into venous system to liver; then through heart to lungs
  3. in lungs, larvae mature and pass into airways, where they are then coughed up and swallowed
  4. 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

31
Q

Ascaris lumbricoides - clinical presentation

A
  1. larval migratory phase: host reaction in the lung
    -pneumonitis: hypersensitivity reaction as parasite migrates through; cough, wheezing, SOB, fever, chills, malaise; EOSINOPHILIA
  2. adult worms:
    -most asymptomatic
    -vague crampy abdominal pain most common sx if present
    *intestinal obstruction possible
    *aberrant migration can occur in bile ducts, appendix
32
Q

Ascaris lumbricoides - diagnosis

A

*stool examination: ova or adult parasites
*adult worms passed through rectum or “coughed up”

33
Q

Ascaris lumbricoides - treatment

A

*ALBENDAZOLE

34
Q

Enterobius vermicularis - overview

A

*aka PINWORM
*most widely prevalent nematode of man
*more prevalent in temperate than tropical climates
*pretty common in USA
*predominantly in children

35
Q

Enterobius vermicularis - pathogenesis

A

*non-invasive; adults live in cecal area
*local allergic reactions to worm proteins
*susceptibility decreases with age

36
Q

Enterobius vermicularis - clinical presentation

A

*perianal itching (ANAL PRURITUS) with subsequent sleep disturbance
*most common in children

37
Q

Enterobius vermicularis - mode of transmission

A

fecal-oral

38
Q

Enterobius vermicularis - diagnosis

A

“scotch-tape test” or examine the anus

39
Q

Enterobius vermicularis - treatment

A

*ALBENDAZOLE

40
Q

which pathogen presents with anal pruritus in children

A

Enterobius vermicularis

41
Q

hookworms (Anyclastoma duodenale & Necator americanus) - geographic distributions

A

Anyclastoma duodenale = Mediterranean countries, Iran, India, Pakistan, Far East

Necator americanus = North & South America, Central Africa, Indonesia, South Pacific, parts of India

42
Q

hookworms - risk factors

A

*skin exposures to fecally contaminated soil in endemic areas (esp people walking barefoot)

43
Q

hookworms (Anyclastoma duodenale & Necator americanus) - life cycle

A
  1. infective larvae penetrate skin that contacts soil
  2. migrates through systemic venous system to lung
  3. mature in lung, migrate up trachea & swallowed
  4. further mature into adults in small intestine; attach to mucosa and cause slow, chronic blood loss & iron deficiency anemia
  5. eggs passed into stool; EGGS HATCH IN SOIL INTO INFECTIVE LARVAE

*gotta have stool in soil

44
Q

hookworms (Anyclastoma duodenale & Necator americanus) - clinical presentation

A

*initial intestinal infection with abdominal pain & eosinophilia
*chronic infestation with high worm burden: symptoms of IRON DEFICIENCY ANEMIA & hypoalbuminemia
*malnutrition
*eosinophilia with lung migration

45
Q

hookworms (Anyclastoma duodenale & Necator americanus) - diagnosis

A

*eggs in stool

46
Q

hookworms (Anyclastoma duodenale & Necator americanus) - treatment

A

ALBENDAZOLE

47
Q

cutaneous larva migrana

A

*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

48
Q

Strongyloides stercoralis - life cycle

A

*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

49
Q

Strongyloides stercoralis - pathogenesis

A

*adult worms embedded in small intestinal mucosa lead to local inflammation
*larvae cause tissue inflammation during migration
*penetrating larvae may carry enteric bacteria

50
Q

Strongyloides stercoralis - clinical presentation

A

*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

51
Q

Strongyloides stercoralis - diagnosis

A

eggs/larvae in stool

52
Q

Strongyloides stercoralis - treatment

A

IVERMECTIN or thiabendazole

53
Q

cestodes (tapeworms)

A

*Taeniasis saginata = beef tapeworm
*Taeniasis solium = pork tapeworm
*Diphyllobothriasis = fish tapeworm

54
Q

Diphyllobothrium latum

A

*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

55
Q

Taenia solium - life cycle

A

*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

GI Exam (54 decks)

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