GI- infections Flashcards

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1
Q

Trypanasoma cruzi- spread

A

South America; reduviid (kissing bug) via feces in bite

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2
Q

Trypanasoma cruzi- presentation

A

Chagas disease: megacolon, dilated cardiomyopathy, and megaesophagus

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3
Q

Trypanasoma cruzi- diagnosis

A

Blood smear (acute), serology (chronic), heart biopsy (rare)

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4
Q

Trypanasoma cruzi- treatment

A

Nifurtimox

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5
Q

Giardia lamblia- spread

A

Water contaminated with cysts, fecal-oral route. “camping, hiking.”

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6
Q

Giardia lamblia- presentation

A

Affects small intestine. Bloating, flatulence, foul-smelling steatorrhea (or watery diarrhea)

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7
Q

Giardia lamblia- diagnosis

A

stool O&P (cysts), ELISA stool antigen test (usually required before stool O&P)

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8
Q

Giardia lamblia- treatment

A

Metronidazole. Furazolidone may be used in children.

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9
Q

Entamoeba histolytica- spread

A

Water contaminated with cysts, anal-oral route. “men who have sex with men.”

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10
Q

Entamoeba histolytica- presentation

A

Affects colon. Bloody diarrhea, “flask-shaped” intestinal ulcerations, liver abscess (usually right lobe; pus smells like “anchovy paste”), right upper quadrant pain, hepatomegaly

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11
Q

Entamoeba histolytica- diagnosis

A

Stool O&P (trophozoites with endocytosed RBCs), ELISA stool/serum antigen tests. Serology should only be used in cases of suspected invasion.

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12
Q

Entamoeba histolytica- treatment

A

Metronidazole and luminal agents (paramomycin, iodoquinol)

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13
Q

Cryptosporidium- spread

A

Oocysts (containing 4 motile sporozoites) released in water. Fecal-oral route. “campers, swimmers, etc.” Common in HIV/AIDS.

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14
Q

Cryptosporidium- presentation

A

Targets small intestine. Severe diarrhea in AIDS/immunocompromised patients. Mild watery diarrhea in immunocompetent patients. Sporozoites attach to intestinal wall- usually the small intestine but can also cause colitis.

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15
Q

Cryptosporidium- diagnosis

A

Acid-fast staining in stool, antigen test, demonstration in tissue

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16
Q

Cryptosporidium- treatment

A

Nitazoxanide (immunocompetent only), spiramycin (a macrolide; not FDA-approved)

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17
Q

Staphylococcus aureus- morphology

A

Gram positive cocci in clusters, catylase positive, aerobic

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18
Q

Bacillus cereus- morphology

A

Gram positive rods, spore-forming, aerobe

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19
Q

Fried rice syndrome species

A

Bacillus cereus

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20
Q

Clostridium perfringens- morphology

A

Gram positive rods, spore-forming, anaerobic

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21
Q

Staphylococcus aureus- vomiting mechanism

A

Enterotoxin is a superantigen. Cytokine release stimulates serotonin production, causing emesis.

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22
Q

Staphylococcus aureus- common food and incubation period

A

Mayonnaise, 3-12 hours

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23
Q

Bacillus cereus- vomiting mechanism

A

Cerulide toxin stimulates serotonin receptor directly

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24
Q

Fried rice syndrome- time of onset

A

1-6 hours

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25
Q

Bacillus cereus- toxins

A

Cerulide toxin, hemolysins

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26
Q

Clostridium perfringens- mechanism

A

Enterotoxin (CPE) disrupts tight junctions of enterocytes

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27
Q

Clostridium perfringens- common foods

A

Gravy, potatoes, “BBQ,” etc.

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28
Q

Traveler’s diarrhea- secretory diarrhea species

A

Enterotoxigenic E. coli (ETEC), Vibrio

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29
Q

Reason for dehydration in non-inflammatory gastroenteritis

A

Usually affects small bowel, where most fluid is absorbed

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30
Q

Rotavirus- morphology

A

non-enveloped dsDNA virus

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31
Q

Norovirus- morphology

A

non-enveloped (+) ssRNA

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32
Q

Adenovirus- morphology

A

linear dsDNA

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33
Q

Adenovirus serotypes causing gastroenteritis

A

40, 41

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34
Q

Astrovirus- morphology

A

non-enveloped (+) ssRNA

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35
Q

Typical age for rotavirus

A

About 2 years old

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36
Q

Cruise ship gastroenteritis cause (often)

A

Norovirus, 80%. ETEC is runner-up.

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37
Q

Gastroenteritis associated with raspberries

A

Norovirus

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38
Q

Vibrio cholerae- morphology

A

Curved gram negative rod, oxidase positive, facultative anaerobe

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39
Q

Enterotoxigenic E. coli (ETEC)- morphology

A

Gram negative rod, “coliform”

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40
Q

Enteropathogenic E. coli (EPEC)- morphology

A

Gram negative rod, “coliform”

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41
Q

Vibrio cholerae- virulence

A

Adhesins, cholera toxin, pili, type II secretion

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42
Q

Rice water stools

A

Vibrio cholerae

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43
Q

Shigella- morphology

A

Gram negative rods, “coliform”

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44
Q

Campylobacter jejuni- morphology

A

Curved gram negative rods

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45
Q

Yersinia enterocolitica- morphology

A

Gram negative coccobacilli

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46
Q

Enterotoxigenic E. coli- virulence

A

Heat stable and heat labile toxins cause secretion by cAMP (similar to cholera toxin)

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47
Q

Salmonella enteritidis- morphology

A

Gram negative rods, “coliform”

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48
Q

Salmonella enteritidis- virulence

A

Direct invasion of enterocytes. Type III secretion. Salmonella typhi multiplies in macrophages.

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49
Q

Listeria monocytogenes- morphology

A

Gram positive short bacilli

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50
Q

Listeria monocytogenes- virulence

A

Invasion of epithelial cells. Cell-to-cell spread (rocket). TNFa production.

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51
Q

Shigella- reservoir

A

Humans

52
Q

Shigella- virulence

A

Acid-resistant, low infective dose, host cell invasion (rockets)

53
Q

Post-infectious Guillian-Barre

A

Campylobacter jejuni

54
Q

Infection commonly seen in asplenic/sickle cell disease patients

A

Salmonella

55
Q

Yersinia enterocolitica- animals

A

cattle, pigs, etc.

56
Q

Yersinia pseudotuberculosis- animals

A

rodents, birds

57
Q

Chitterlings, undercooked pork

A

Yersinia

58
Q

Yersinia- common location of effect

A

Terminal ileum, proximal colon

59
Q

Pseudoappendecitis infection

A

Yersinia

60
Q

Yersinia- presentation

A

Abdominal pain, RLQ tenderness, fever, blood in stool

61
Q

Clostridium difficile- morphology

A

Gram positive rods, spore-forming, anaerobic

62
Q

Negative for sorbitol fermenting

A

Enterohemorrhagic E. coli

63
Q

Bacillus anthracis- presentation

A

Black eschar with erythematous ring. Pulmonary anthrax (Woolsorter’s disease- dry cough, hemorrhagic mediastinitis)

64
Q

Bacillus anthracis- morphology

A

Large gram positive rods in chains. Protein capsule (poly D glutamate). Obligate aerobe. Spore-forming.

65
Q

Bacillus anthracis- virulence

A

Two toxins must be present for infection- edema factor (EF) and lethal factor (LF). EF functions as adenylate cyclase (extracellular fluid causes edema, prevents phagocytosis). LF cleaves MAP kinase, ultimately causing necrosis.

66
Q

Bacillus anthracis- treatment

A

Fluoroquinolones. Doxycycline as secondary treatment.

67
Q

Antibiotic that classically leads to C. diff infection

A

Clindamycin

68
Q

Clostridium difficile- virulence

A
Exotoxin A and Exotoxin B.
Exotoxin A (apple) binds brush border and causes watery diarrhea.
Exotoxin B (black licorice) depolymerizes actin (cytoskeleton, causes enterocyte death/necrosis) and pseudomembranous colitis.
69
Q

Clostridium difficile- diagnosis

A

Visualization of pseudomembrane directly or identifying toxin in the school (i.e. PCR)

70
Q

Clostridum difficile- treatment

A

ORAL vancomycin or metronidazole (less severe)

71
Q

How to rule out non-pathogenic Entamoeba dispar in favor of Entamoeba histolytica?

A

Phagocytosed RBC in the trophozoite (hard to tell in smear). Normally, use clinical findings.

72
Q

Entamoeba histolytica cysts transform into trophozoites in what organ?

A

Ileum; primarily affects the colon

73
Q

Entamoeba histolytica- stool O&P findings

A

Fulminant diarrhea will contain trophozoites. More formed stool (slower movement) may have more cysts.

74
Q

Entamboeba histolytica- virulence

A

Chitin wall (temps up to 55’C, stomach acid, chlorine), proteinase (invasion), surface lectins (binding), channel-forming proteins (host cell lysis)

75
Q

Giardia lamblia- other name

A

Giardia duodenalis

76
Q

Giardia lamblia virulence

A

Lectin-based sucker disc

77
Q

Crytosporidium- reservoir

A

Humans and some animals, like cows

78
Q

Cryptosporidium- life cycle

A

Alternating asexual and sexual reproductive cycles. Oocysts exit via feces or may cause autoinfection.

79
Q

Cryptosporidium- virulence

A

Lectin (binding), superficial invasion of cytoplasm (intracellular organisms, so no lysis)

80
Q

Strongyloides stercoralis- reservoir

A

humans

81
Q

Strongyloides stercoralis- location

A

Affects small intestine but may disseminate.

82
Q

Strongyloides stercoralis- lifecycle/spread

A

They live in soil. Larvae penetrate the skin directly and travel to the lungs via circulation. They then climb up the respiratory tree and are swallowed. They mature in the small intestine and lay ova, which are excreted in the feces and hatch. Autoinfection is possible.

83
Q

Strongyloides stercoralis- biology

A

Nematode. 2 forms of larvae: rhabditiform and filariform (infectious).

84
Q

Strongyloides stercoralis- complications

A

Hyperinfection if immunocompromise allows maturation to infectious filariform. Associated gram-negative sepsis or candidemia may also be seen.

85
Q

Strongyloides stercoralis- normal presentation

A

Larvae may cause pneumonitis or eosinophilia. Adult worms cause mild/moderate mucosal inflammation. Rash/pruritis at site of entrance may be seen. Often asymptomatic.

86
Q

Strongyloides stercoralis- hyperinfection

A

Diarrhea, GI hemorrhage, pneumonia, gram-negative meningitis (otherwise uncommon in adults), sepsis

87
Q

Strongyloides stercoralis- treatment

A

Ivermectin, thiabendazole. Treat even after clear.

88
Q

Enterobiasis (pinworm)- reservoir

A

Humans

89
Q

Enterobiasis (pinworm)- presentation

A

Affects colon. Pruritis (itchy butt) may occur.

90
Q

Enterobiasis (pinworm)- spread

A

Ingestion of ova. Classically in children or their parents.

91
Q

Enterobiasis (pinworm)- lifecycle

A

Nematode. After ingestion, ova hatch. Adults live in cecum. Gravid females lay ova on skin. Risk of autoinfection.

92
Q

Enterobiasis (pinworm)- treatment

A

Mebendazole

93
Q

Enterobiasis (pinworm)- diagnsosis

A

Demonstration of ova on perianal skin. Adhesive tape.

94
Q

Taeniasis- reservoir and intermediate hosts

A

Reservoir is humans. Intermediate hosts are pigs and cattle.

95
Q

Taeniasis- spread

A

Ingestion of infected beef/pork

96
Q

Taeniasis- causal organisms

A

Taenia solium (pork tapeworm) and Taenia saginata (beef tapeworm)

97
Q

Taeniasis- lifecycle

A

Cestode. Intermediate host ingests ova. Embryo travels to tissue. Human eats undercooked meat and ingests cystircerci, which are then liberated. Evaginate scolex and attach to small intestine. Ova and gravid proglottids may be passed in feces.

98
Q

Taeniasis- presentation

A

Affects small intestine. May be asymptomatic. May be mild mucosal inflammation.

99
Q

Taeniasis- diagnosis

A

Ova or proglottids in stool.

100
Q

Taeniasis- treatment

A

Praziquantel or niclosamide

101
Q

Cystircercosis- spread

A

Ingestion of Taenia solium ovum by the human, rather than the intermediate host (pig). Burrows into intestine and accesses bloodstream. Autoinfection is possible.

102
Q

Cystircercosis- presentation

A

Cystic lesions in brain, muscle, and skin. Often without inflammation if organism is viable. Inflammation, fibrosis, and calcification if dead.

103
Q

Schistosomiasis- causal organisms

A

Schistosoma mansoni, haematobium, and japonicum

104
Q

Schistosomiasis- spread

A

Trematode. Underdeveloped countries (e.g. Sub-Saharan Africa), inadequate water supplies (dams and irrigation systems increase risk). Ova in water mature into miracidium, which infect snail.. Cercaria from snails (intermediate host) go into contaminated water. Direct skin penetration of human. Travel to venous plexuses and mature in pairs, then lay eggs which are excreted.

105
Q

Schistosomiasis- virulence

A

Mature organisms incorporation of host proteins into their own membranes (antigenic mimicry). Ova are highly immunogenic, causing granulamatous inflammation, fibrosis, and even allergy.

106
Q

Schistosomiasis- presentation

A

Intestinal, liver, bladder, and skin penetration site symptoms

107
Q

Schistosomiasis- treatment

A

Antihistamines, corticosteroids for snail fever. Praziquantel.

108
Q

Traveler’s diarrhea- bloody diarrhea species

A

Shigella, salmonella, EHEC, EIEC, campylobacter

109
Q

Most common nematode infection worldwide

A

Ascariasis

110
Q

Ascariasis- spread

A

Contact with contaminated soil or ingestion of eggs (fecal-oral route)

111
Q

Ascariasis- presentation

A

Abdominal pain, nausea/vomiting, cough/wheezing/dyspnea, jaundice, peripheral eosinophilia. May cause small bowel obstruction.

112
Q

Enteropathogenic E. coli- presentation

A

Noninflammatory diarrhea in infants in developing countries

113
Q

Enteropathogenic E. coli (EPEC)- virulence

A

Adherence to M cells, rearrangement of actin and effacement of brush border villi

114
Q

Shiga-like toxin mechanism

A

N-glycosylation of the 28S rRNA, inhibiting the 60S ribosomal subunit. AKA “verotoxin”

115
Q

Echinococcus granulosus- spread

A

Cestode, usually ingested as eggs from dog feces in rural settings

116
Q

Echinococcus granulosus- presentation

A

Asymptomatic at first. Later, they develop vague abdominal symptoms, weight loss, vomiting, diarrhea, fatigue, hepatomegaly. Hydatid cysts found in liver, but may be found in kidney and spleen as well.

117
Q

Echinococcus granulosus- treatment

A

Surgical intervention (may cause anaphylaxis) or albendazole

118
Q

Schistosoma mansoni and japonicum venous location and presentation

A

mesenteric veins and portal veins, causing portal hypertension leading to cirrhosis and even liver failure

119
Q

Schistosoma haematobium venous location and presentation

A

Veins of bladder, leading to hematuria and bladder cancer

120
Q

Schistosoma mansoni O&P findings

A

Egg with large lateral spine

121
Q

Schistosoma japonicum O&P findings

A

Egg with small spine, round

122
Q

Schistosoma haematobium

A

Egg with large terminal spine

123
Q

Clonorchis sinesis- spread

A

Trematode. Snails are intermediate hosts. Larvae are ingested by humans from undercooked fish. Worms mature and reside in biliary system.

124
Q

Clonorchis sinesis- presentation

A

Biliary tract fibrosis, pigmented gallstones, choleangiocarcinoma

125
Q

Clonorchis sinesis- O&P findings

A

Operculated eggs

126
Q

Clonorchis sinesis- treatment

A

Praziquantel