GI- infections Flashcards
1
Q
Trypanasoma cruzi- spread
A
South America; reduviid (kissing bug) via feces in bite
2
Q
Trypanasoma cruzi- presentation
A
Chagas disease: megacolon, dilated cardiomyopathy, and megaesophagus
3
Q
Trypanasoma cruzi- diagnosis
A
Blood smear (acute), serology (chronic), heart biopsy (rare)
4
Q
Trypanasoma cruzi- treatment
A
Nifurtimox
5
Q
Giardia lamblia- spread
A
Water contaminated with cysts, fecal-oral route. “camping, hiking.”
6
Q
Giardia lamblia- presentation
A
Affects small intestine. Bloating, flatulence, foul-smelling steatorrhea (or watery diarrhea)
7
Q
Giardia lamblia- diagnosis
A
stool O&P (cysts), ELISA stool antigen test (usually required before stool O&P)
8
Q
Giardia lamblia- treatment
A
Metronidazole. Furazolidone may be used in children.
9
Q
Entamoeba histolytica- spread
A
Water contaminated with cysts, anal-oral route. “men who have sex with men.”
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
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.
12
Q
Entamoeba histolytica- treatment
A
Metronidazole and luminal agents (paramomycin, iodoquinol)
13
Q
Cryptosporidium- spread
A
Oocysts (containing 4 motile sporozoites) released in water. Fecal-oral route. “campers, swimmers, etc.” Common in HIV/AIDS.
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.
15
Q
Cryptosporidium- diagnosis
A
Acid-fast staining in stool, antigen test, demonstration in tissue
16
Q
Cryptosporidium- treatment
A
Nitazoxanide (immunocompetent only), spiramycin (a macrolide; not FDA-approved)
17
Q
Staphylococcus aureus- morphology
A
Gram positive cocci in clusters, catylase positive, aerobic
18
Q
Bacillus cereus- morphology
A
Gram positive rods, spore-forming, aerobe
19
Q
Fried rice syndrome species
A
Bacillus cereus
20
Q
Clostridium perfringens- morphology
A
Gram positive rods, spore-forming, anaerobic
21
Q
Staphylococcus aureus- vomiting mechanism
A
Enterotoxin is a superantigen. Cytokine release stimulates serotonin production, causing emesis.
22
Q
Staphylococcus aureus- common food and incubation period
A
Mayonnaise, 3-12 hours
23
Q
Bacillus cereus- vomiting mechanism
A
Cerulide toxin stimulates serotonin receptor directly
24
Q
Fried rice syndrome- time of onset
A
1-6 hours
25
Bacillus cereus- toxins
Cerulide toxin, hemolysins
26
Clostridium perfringens- mechanism
Enterotoxin (CPE) disrupts tight junctions of enterocytes
27
Clostridium perfringens- common foods
Gravy, potatoes, "BBQ," etc.
28
Traveler's diarrhea- secretory diarrhea species
Enterotoxigenic E. coli (ETEC), Vibrio
29
Reason for dehydration in non-inflammatory gastroenteritis
Usually affects small bowel, where most fluid is absorbed
30
Rotavirus- morphology
non-enveloped dsDNA virus
31
Norovirus- morphology
non-enveloped (+) ssRNA
32
Adenovirus- morphology
linear dsDNA
33
Adenovirus serotypes causing gastroenteritis
40, 41
34
Astrovirus- morphology
non-enveloped (+) ssRNA
35
Typical age for rotavirus
About 2 years old
36
Cruise ship gastroenteritis cause (often)
Norovirus, 80%. ETEC is runner-up.
37
Gastroenteritis associated with raspberries
Norovirus
38
Vibrio cholerae- morphology
Curved gram negative rod, oxidase positive, facultative anaerobe
39
Enterotoxigenic E. coli (ETEC)- morphology
Gram negative rod, "coliform"
40
Enteropathogenic E. coli (EPEC)- morphology
Gram negative rod, "coliform"
41
Vibrio cholerae- virulence
Adhesins, cholera toxin, pili, type II secretion
42
Rice water stools
Vibrio cholerae
43
Shigella- morphology
Gram negative rods, "coliform"
44
Campylobacter jejuni- morphology
Curved gram negative rods
45
Yersinia enterocolitica- morphology
Gram negative coccobacilli
46
Enterotoxigenic E. coli- virulence
Heat stable and heat labile toxins cause secretion by cAMP (similar to cholera toxin)
47
Salmonella enteritidis- morphology
Gram negative rods, "coliform"
48
Salmonella enteritidis- virulence
Direct invasion of enterocytes. Type III secretion. Salmonella typhi multiplies in macrophages.
49
Listeria monocytogenes- morphology
Gram positive short bacilli
50
Listeria monocytogenes- virulence
Invasion of epithelial cells. Cell-to-cell spread (rocket). TNFa production.
51
Shigella- reservoir
Humans
52
Shigella- virulence
Acid-resistant, low infective dose, host cell invasion (rockets)
53
Post-infectious Guillian-Barre
Campylobacter jejuni
54
Infection commonly seen in asplenic/sickle cell disease patients
Salmonella
55
Yersinia enterocolitica- animals
cattle, pigs, etc.
56
Yersinia pseudotuberculosis- animals
rodents, birds
57
Chitterlings, undercooked pork
Yersinia
58
Yersinia- common location of effect
Terminal ileum, proximal colon
59
Pseudoappendecitis infection
Yersinia
60
Yersinia- presentation
Abdominal pain, RLQ tenderness, fever, blood in stool
61
Clostridium difficile- morphology
Gram positive rods, spore-forming, anaerobic
62
Negative for sorbitol fermenting
Enterohemorrhagic E. coli
63
Bacillus anthracis- presentation
Black eschar with erythematous ring. Pulmonary anthrax (Woolsorter's disease- dry cough, hemorrhagic mediastinitis)
64
Bacillus anthracis- morphology
Large gram positive rods in chains. Protein capsule (poly D glutamate). Obligate aerobe. Spore-forming.
65
Bacillus anthracis- virulence
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
Bacillus anthracis- treatment
Fluoroquinolones. Doxycycline as secondary treatment.
67
Antibiotic that classically leads to C. diff infection
Clindamycin
68
Clostridium difficile- virulence
```
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
Clostridium difficile- diagnosis
Visualization of pseudomembrane directly or identifying toxin in the school (i.e. PCR)
70
Clostridum difficile- treatment
ORAL vancomycin or metronidazole (less severe)
71
How to rule out non-pathogenic Entamoeba dispar in favor of Entamoeba histolytica?
Phagocytosed RBC in the trophozoite (hard to tell in smear). Normally, use clinical findings.
72
Entamoeba histolytica cysts transform into trophozoites in what organ?
Ileum; primarily affects the colon
73
Entamoeba histolytica- stool O&P findings
Fulminant diarrhea will contain trophozoites. More formed stool (slower movement) may have more cysts.
74
Entamboeba histolytica- virulence
Chitin wall (temps up to 55'C, stomach acid, chlorine), proteinase (invasion), surface lectins (binding), channel-forming proteins (host cell lysis)
75
Giardia lamblia- other name
Giardia duodenalis
76
Giardia lamblia virulence
Lectin-based sucker disc
77
Crytosporidium- reservoir
Humans and some animals, like cows
78
Cryptosporidium- life cycle
Alternating asexual and sexual reproductive cycles. Oocysts exit via feces or may cause autoinfection.
79
Cryptosporidium- virulence
Lectin (binding), superficial invasion of cytoplasm (intracellular organisms, so no lysis)
80
Strongyloides stercoralis- reservoir
humans
81
Strongyloides stercoralis- location
Affects small intestine but may disseminate.
82
Strongyloides stercoralis- lifecycle/spread
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
Strongyloides stercoralis- biology
Nematode. 2 forms of larvae: rhabditiform and filariform (infectious).
84
Strongyloides stercoralis- complications
Hyperinfection if immunocompromise allows maturation to infectious filariform. Associated gram-negative sepsis or candidemia may also be seen.
85
Strongyloides stercoralis- normal presentation
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
Strongyloides stercoralis- hyperinfection
Diarrhea, GI hemorrhage, pneumonia, gram-negative meningitis (otherwise uncommon in adults), sepsis
87
Strongyloides stercoralis- treatment
Ivermectin, thiabendazole. Treat even after clear.
88
Enterobiasis (pinworm)- reservoir
Humans
89
Enterobiasis (pinworm)- presentation
Affects colon. Pruritis (itchy butt) may occur.
90
Enterobiasis (pinworm)- spread
Ingestion of ova. Classically in children or their parents.
91
Enterobiasis (pinworm)- lifecycle
Nematode. After ingestion, ova hatch. Adults live in cecum. Gravid females lay ova on skin. Risk of autoinfection.
92
Enterobiasis (pinworm)- treatment
Mebendazole
93
Enterobiasis (pinworm)- diagnsosis
Demonstration of ova on perianal skin. Adhesive tape.
94
Taeniasis- reservoir and intermediate hosts
Reservoir is humans. Intermediate hosts are pigs and cattle.
95
Taeniasis- spread
Ingestion of infected beef/pork
96
Taeniasis- causal organisms
Taenia solium (pork tapeworm) and Taenia saginata (beef tapeworm)
97
Taeniasis- lifecycle
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
Taeniasis- presentation
Affects small intestine. May be asymptomatic. May be mild mucosal inflammation.
99
Taeniasis- diagnosis
Ova or proglottids in stool.
100
Taeniasis- treatment
Praziquantel or niclosamide
101
Cystircercosis- spread
Ingestion of Taenia solium ovum by the human, rather than the intermediate host (pig). Burrows into intestine and accesses bloodstream. Autoinfection is possible.
102
Cystircercosis- presentation
Cystic lesions in brain, muscle, and skin. Often without inflammation if organism is viable. Inflammation, fibrosis, and calcification if dead.
103
Schistosomiasis- causal organisms
Schistosoma mansoni, haematobium, and japonicum
104
Schistosomiasis- spread
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
Schistosomiasis- virulence
Mature organisms incorporation of host proteins into their own membranes (antigenic mimicry). Ova are highly immunogenic, causing granulamatous inflammation, fibrosis, and even allergy.
106
Schistosomiasis- presentation
Intestinal, liver, bladder, and skin penetration site symptoms
107
Schistosomiasis- treatment
Antihistamines, corticosteroids for snail fever. Praziquantel.
108
Traveler's diarrhea- bloody diarrhea species
Shigella, salmonella, EHEC, EIEC, campylobacter
109
Most common nematode infection worldwide
Ascariasis
110
Ascariasis- spread
Contact with contaminated soil or ingestion of eggs (fecal-oral route)
111
Ascariasis- presentation
Abdominal pain, nausea/vomiting, cough/wheezing/dyspnea, jaundice, peripheral eosinophilia. May cause small bowel obstruction.
112
Enteropathogenic E. coli- presentation
Noninflammatory diarrhea in infants in developing countries
113
Enteropathogenic E. coli (EPEC)- virulence
Adherence to M cells, rearrangement of actin and effacement of brush border villi
114
Shiga-like toxin mechanism
N-glycosylation of the 28S rRNA, inhibiting the 60S ribosomal subunit. AKA "verotoxin"
115
Echinococcus granulosus- spread
Cestode, usually ingested as eggs from dog feces in rural settings
116
Echinococcus granulosus- presentation
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
Echinococcus granulosus- treatment
Surgical intervention (may cause anaphylaxis) or albendazole
118
Schistosoma mansoni and japonicum venous location and presentation
mesenteric veins and portal veins, causing portal hypertension leading to cirrhosis and even liver failure
119
Schistosoma haematobium venous location and presentation
Veins of bladder, leading to hematuria and bladder cancer
120
Schistosoma mansoni O&P findings
Egg with large lateral spine
121
Schistosoma japonicum O&P findings
Egg with small spine, round
122
Schistosoma haematobium
Egg with large terminal spine
123
Clonorchis sinesis- spread
Trematode. Snails are intermediate hosts. Larvae are ingested by humans from undercooked fish. Worms mature and reside in biliary system.
124
Clonorchis sinesis- presentation
Biliary tract fibrosis, pigmented gallstones, choleangiocarcinoma
125
Clonorchis sinesis- O&P findings
Operculated eggs
126
Clonorchis sinesis- treatment
Praziquantel
