GI 1 Flashcards

1
Q

what GI host defenses can trigger the expression of bacterial virulence factors (2)

A

1) mucus

2) bile

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2
Q

inflammation of the stomach

A

gastritis

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3
Q

inflammation of the stomach and intestines

A

gastroenteritis

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4
Q

frequent loose and fluid filled stools

A

diarrhea

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5
Q

inflammatory disorder of the GI associated with

  • diarrhea with blood and pus
  • pain, fever, abdominal cramps
A

dysentery

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6
Q

dysentery v. diarrhea

A

dysentery: usually disease of the large intestine
diarrhea: disease of the small intestine

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7
Q

inflammation of the intestines, especially small

A

enteritis

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8
Q

inflammation of the mucosa of the small and large intestine

A

enterocolitis

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9
Q

inflammation of the large colon

A

colitis

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10
Q

inflammatory GI bacteria (7)

A

1) campylocater jejuni
2) c. difficile
3) EHEC
4) EIEC
5) Shigella spp.
6) vibrio paraheaemolyticus
7) yersinia enterocolitica

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11
Q

more likely to see fecal occult or visible blood

more likely to see fecal leukocytes

A

inflammatory GI bacteria

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12
Q

bacteria passing through the intestine or adherent to the intestinal epithelium

A

non-inflammatory GI bacteria

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13
Q

non-inflammatory GI bacteria (4)

A

1) EPEC
2) ETEC
3) Vibrio cholerae
4) listeria monocytogenes

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14
Q

preformed toxin

A

1-8 hrs. after ingestion

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15
Q

production of toxin after ingestion

A

8-16 hr after ingestion

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16
Q

adherence, growth, and virulence factor production

A

16+ hr after ingestion

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17
Q
  • staph. aureus
  • bacillus cereus (emetic)
  • clostridium botulinum
A

preformed toxin

1-8 hr after ingestion

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18
Q
  • bacillus cereus (diarrheal)
  • clostridum perfringens
  • clostridium botulinum
A

production of toxin after ingestion

8-16 hr

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19
Q
  • shigella spp.
  • salmonella spp.
    listeria monocytogenes
  • EHEC, EPEC, ETEC, EIEC
  • campylobacter
  • vibrio spp.
A

16+ hours after ingestion

adherence, growth and virulence factor production

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20
Q

two types of bacterial food poisoning

A
  1. preformed toxins in the food
  2. large numbers of spores ingested, germinate in intestine, produce toxins without colonization or adherence to GI tract
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21
Q
  • diarrhea, vomiting or both
  • NO FEVER
  • 1-8 hrs or 8-16 hrs after ingestion
A

symptoms of bacterial food poisoning

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22
Q

four bacterial causes of food poisoning

A
  1. staph aureus
  2. clostridium botulinum
  3. clostridium perfringens
  4. bacilus cereus
23
Q
  • gram positive cocci in clusters
  • not spore forming
  • ingestion of a preformed,heat-stable toxin
  • severe vomiting, diarrhea, and abdominal pain within 1-8 hrs of consumption
A

staph. aureus food poisoning

24
Q
  • gram positive rod
  • spore forming
  • early: vomiting, diarhea, abdominal pain 1-8hr after ingestion if preformed toxin, 8-16 hrs if spores
  • late: flaccid paralysis
A

bacterial food poisoning with clostridum botulinum

25
Q

MOA botulism toxin

A

acts at neuromuscular nerve junctions, blocks ach release, thus muscle stimulation is blocked

26
Q

home-canning

A

clostridum botulinum

27
Q

treatment clostridium botulinum

A
  • supportive therapy

- IV anti-toxin administration

28
Q

complications of clostridium botulinum

A

lingering weakness, dyspnea, up to 1 year after primary disease

29
Q

floppy baby syndrome

A

clostridum botulinum

30
Q

MOA infant botulism

A

germination of c. botulinum spores in intestines -> growth -> toxin production
- often when infant ingest honey

31
Q

when can you feed baby honey?

A

after 1 year, the permeability of the intestinal mucosa decreases and changes

32
Q
  • gram positive rod
  • spore forming
  • meat products held at below recommended tempreratures
  • onset of diarrhea and abdominal cramps 8-16 h post-ingestion and lasts 24 hr
A

clostridiym perfringens

33
Q

etiology of clostridium perfingens

A

c. perfringens enterotoxin which mediates membrane permeability -> efflux of water

34
Q
  • gram-postive rods, spore forming

- onset of vomiting, nausea and abdominal cramps 1-8 hrs after ingestion of preformed heat stable enterotoxin

A

emetic form of bacilus cereus

35
Q

associated with improper storage of cooked rice

A

bacillus cereus food poisoning

  • spores survive cooking -> bac multiply -> produce heat stable enterotoxin
36
Q
  • gram positive rod, spore forming
  • onset of diarrhea, nausea and abdominal cramps 8-16 hrs post ingestion
  • production of heat liable enterotoxin in intestine
A

diarrheal form of bacillus cereus food poisoning

37
Q

gram negative curved rod

  • microaerophilic
  • ulcers and chronic gastritis
A

helicobacter pylori

38
Q

virulence factors of heliobacter pylori

A
  • flagella
  • urease
  • cytotoxin- vacA
  • adhesins
39
Q

ulcers are caused by stress, smoking and spicy foods

A

false

gastric ulcers are mostly caused by helicobacter pylori

40
Q

mechanism of h. pylori ulcers

A

1- h. pylori penetrates mucous layer attract to hemin and urea
2- h. pylori recruits and activates inflammatory cells and released urease which produces NH3 to neutralize the acid
3- h. pylori cytotoxin and NH3 destroy mucous cells and expose the underlying tissue to stomach acid

41
Q

diagnosis of h. pylori

A

radioactive urea breath test

or biopsy

42
Q

treatment of h. pylori

A
  • antibiotics and proton pump inhibitor
43
Q
  • gram positive rod pairs
  • intracellular faculative anaerobe
  • cold loving and salt and pH resistant
A

listeria monocytogenes

44
Q

large outbreaks concerning ready to eat meats and raw vegetables

A

listeria monocytogenes

45
Q

fever
malaise
chills with no obvious focus

A

bacteremia from listeria monoctogenes in immunocompromised pateient

46
Q

fever, persistent headache, stiff neck, vomiting and confusion

A

meningitis and encephalitis from listeria monocytogenes in immunocompromised patient

47
Q

what should you do if a patient presents with a fever with no obvious infection

A

blood culture

48
Q

granulomatosis infantiseptica

A

pyogenic granulomas distributed all over the body

symptom of neonatal infection with listeria monocytogenes (see 2-3 wks after birth)

49
Q

MOA of listeria monocytogenes

A
  • adherence and uptake mediated by internalin A
  • intenalized into vacuole
  • acidification of vacuole triggeres listeriolysisn O to allow escape into cytosol
  • replicates in host cell cytoplasm
50
Q

where besides GI does listeria monocytogenes infect

A

liver spleen CNS

51
Q

how does listeria mono. spread?

A

sheer motility via ActA mediated actin polymerization allows them to push through membranes and spread to blood stream and neighboring cells

52
Q

cold enrichment selection

also weak B hemolysis and motility test

A

listeria monocytogenes

53
Q

treatment listeria mono.

A

beta lactam or trimethoprim-sulfamethoxazole