GI 1 Flashcards

(53 cards)

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
MOA botulism toxin
acts at neuromuscular nerve junctions, blocks ach release, thus muscle stimulation is blocked
26
home-canning
clostridum botulinum
27
treatment clostridium botulinum
- supportive therapy | - IV anti-toxin administration
28
complications of clostridium botulinum
lingering weakness, dyspnea, up to 1 year after primary disease
29
floppy baby syndrome
clostridum botulinum
30
MOA infant botulism
germination of c. botulinum spores in intestines -> growth -> toxin production - often when infant ingest honey
31
when can you feed baby honey?
after 1 year, the permeability of the intestinal mucosa decreases and changes
32
- 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
clostridiym perfringens
33
etiology of clostridium perfingens
c. perfringens enterotoxin which mediates membrane permeability -> efflux of water
34
- gram-postive rods, spore forming | - onset of vomiting, nausea and abdominal cramps 1-8 hrs after ingestion of preformed heat stable enterotoxin
emetic form of bacilus cereus
35
associated with improper storage of cooked rice
bacillus cereus food poisoning - spores survive cooking -> bac multiply -> produce heat stable enterotoxin
36
- gram positive rod, spore forming - onset of diarrhea, nausea and abdominal cramps 8-16 hrs post ingestion - production of heat liable enterotoxin in intestine
diarrheal form of bacillus cereus food poisoning
37
gram negative curved rod - microaerophilic - ulcers and chronic gastritis
helicobacter pylori
38
virulence factors of heliobacter pylori
- flagella - urease - cytotoxin- vacA - adhesins
39
ulcers are caused by stress, smoking and spicy foods
false gastric ulcers are mostly caused by helicobacter pylori
40
mechanism of h. pylori ulcers
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
diagnosis of h. pylori
radioactive urea breath test | or biopsy
42
treatment of h. pylori
- antibiotics and proton pump inhibitor
43
- gram positive rod pairs - intracellular faculative anaerobe - cold loving and salt and pH resistant
listeria monocytogenes
44
large outbreaks concerning ready to eat meats and raw vegetables
listeria monocytogenes
45
fever malaise chills with no obvious focus
bacteremia from listeria monoctogenes in immunocompromised pateient
46
fever, persistent headache, stiff neck, vomiting and confusion
meningitis and encephalitis from listeria monocytogenes in immunocompromised patient
47
what should you do if a patient presents with a fever with no obvious infection
blood culture
48
granulomatosis infantiseptica
pyogenic granulomas distributed all over the body | symptom of neonatal infection with listeria monocytogenes (see 2-3 wks after birth)
49
MOA of listeria monocytogenes
- 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
where besides GI does listeria monocytogenes infect
liver spleen CNS
51
how does listeria mono. spread?
sheer motility via ActA mediated actin polymerization allows them to push through membranes and spread to blood stream and neighboring cells
52
cold enrichment selection | also weak B hemolysis and motility test
listeria monocytogenes
53
treatment listeria mono.
beta lactam or trimethoprim-sulfamethoxazole