Lecture 14 Flashcards

(44 cards)

1
Q

Axenic organs of the GI tract

A

Esophagus, stomach, and duodenum are almost free of microbes

- peristalsis prevents long term colonization of GI tract

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2
Q

Plaque (formation and causative agent)

A
  • Streptococcus mutans (initial colonizer) will attach to surface of tooth
  • other bacteria come and attach to already attached bacteria using lectins (lectins bind to sugar, act as adhesin)
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3
Q

Dextran

A
  • enzyme that uses sugar to:
  • create biofilm for plaque
  • fermentation produces acid
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4
Q

3 things required for dental caries

A
  1. Buildup of plaque
    - place for bacteria to persist
  2. Dietary sucrose
    - food for bacteria
  3. Acidogenic bacteria
    - by-product of fermentation that deteriorates teeth
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5
Q

Cavities prevention

A

Regular dental hygiene

Block binding of bacteria/ formation of plaque

  • -Use polymers to cover teeth
  • -Use antibacterial coating for teeth

Fluoride

  • -Fluoride works by displacing the hydroxyl ions in hydroxyapatite
  • -Reduces the solubility of tooth enamel
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6
Q

Periodontal Disease (causative agent)

A
Porphyromonas gingivalis, Leptotrichia buccalis (Gram-negative rods)
Treponema vincentii (Gram-negative spirochete)
  • not flossing (b/c these bacteria colonize the anaerobic pockets between teeth and gums)
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7
Q

Staphylococcal Food Poisoning (causative agent)

A

Staphylococcus aureus, G (+) cocci

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8
Q

Staphylococcal Food Poisoning (transmission)

A
  • Part of normal flora in nose, on skin

- Introduced to food by sneezing, coughing, contact w/ boils or abscesses

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9
Q

Staphylococcal Food Poisoning (symptoms)

A
  • very fast acting, symptoms show within 1-6 hours

- abdominal cramps, nausea, vomiting, diarrhea

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10
Q

Staphylococcal Food Poisoning (pathogenixcity)

A
  • enterotoxins
    • resistant to high temp and low pH
    • able to survive in stomach and pass through
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11
Q

Staphylococcus aureus (identification)

A

mannitol salt agar

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12
Q

Cholera (causative agnet)

A

Vibrio cholerae

Gram-negative curved rod

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13
Q

Cholera (transmission)

A

Water or food (raw oysters) contaminated with feces

  • usually transmitted through human feces
  • must consume high dosage b/c most die in stomach
    • in high dosage, a few are able to pass through stomach and colonize intestines
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14
Q

Cholera (symptoms)

A
  • rice water stool” Diarrhea (1L/hour) –> good diagnostic factor
  • Dehydration, cramps
  • Blood thickens (from lack of water), resulting in shock and eventually, coma
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15
Q

Cholera (pathogenicity/virulence factor)

A
  • Cholera toxin stimulates fluid loss (diarrhea)
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16
Q

How does cholera toxin functions?

A
  • this is an AB toxin
  • B triggers endocytosis
  • A triggers cAMP that pump electrolytes out of the cell and into lumen
    • water follows salts (due to osmosis)
    • b/c there is a hypotonic solution outside of cell
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17
Q

Cholera (treatment)

A
  • replenish lost water and salts
  • usually with gatorade
  • antibiotics wont work well b/c everything is getting pumped out due to cholera toxin
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18
Q

Salmonellosis (causative agent)

A
  • Salmonella enterica G (-) rods
19
Q

Salmonellosis (transmission)

A
  • uncooked poultry
    • chicken, eggs
  • cutting board (where chicken was then veggies were cut)
20
Q

Salmonellosis (symptoms)

A
  • incubation 1-2 days

- Nausea, fever, vomiting, diarrhea (possible dehydration), abdominal cramps, possible intestinal ulceration

21
Q

Salmonellosis (pathogenicity/virulence factor)

A
  • type III secretion system (T3SS)
  • inject toxins into cells, and triggering endocytosis
    • pathogen is now able to replicate in cell (kills cell and escapes, which causes symptoms)
22
Q

Salmonellosis (Diagnosis/treatment)

A
  • diagnosed by stool sample, and symptoms

- treated with replacing fluid loss with with water and electrolytes

23
Q

Typhoid Fever (causative agent)

A

Salmonella enterica serotype Typhi, G (-) rod

  • tough pathogen, able to survive harsh environment, need a small dose for infection
24
Q

Typhoid Fever (pathogenicity)

A

Same as salmonellosis but…

  • Blood invasion
    • pathogen gets into blood and makes its way to other organs (gal bladder)
  • A2B5 toxin
    • causes: fever and delirium (typhos), rose spots on abdomen (hemorrhaging)
25
Typhoid Fever (Treatment)
- fluid, electrolytes, ciprofloxacin (flouroquineolones) - Gallbladder removal for carriers - vaccine (not very good, wears off after a while)
26
Traveler’s Diarrhea (causative agent)
Escherichia coli – G (-) rod -- Live in intestinal tract of animals E. coli O157:H7 highly virulent (Enterohemorrhagic)
27
Traveler’s Diarrhea (Transmission)
- Improperly cooked ground meats | - Inadequately washed fruits and vegetables
28
Traveler’s Diarrhea (Symptoms)
- Hemorrhagic colitis (bloody diarrhea) - Can result in hemolytic uremic syndrome (HUS)-kidney failure, coma, seizure, heart attack (hemorrhaging and bleeding in kidney)
29
Traveler’s Diarrhea (Pathogenicity/virulence factors)
- T3SS (type III secretion system) - Shiga-like toxin - - kills host cell tissue
30
Traveler’s Diarrhea (treatment)
- antibiotics and rehydration
31
Campylobacter Diarrhea (causative agent)
- Campylobacter jejuni - G-, polar flagella - Found in 81% of chickens - - similar to salmonella
32
Campylobacter Diarrhea (diagnosis)
bacteria presence in stool
33
Campylobacter Diarrhea (treatment)
azithromycin
34
Antimicrobial-Associated Diarrhea (causative agent)
- Clostridium difficile | - G+, anaerobic spore-forming
35
Antimicrobial-Associated Diarrhea (symptom)
- development of pseudomembrane lesions - - bumpy colon - bloody stool
36
Antimicrobial-Associated Diarrhea (pathogenicity)
- C. difficile Toxins A (TcdA) and B (TcdB
37
Antimicrobial-Associated Diarrhea (treatment)
- avoid unnecessary use of antimicrobial drugs - Vancomycin - Fecal transplant – restore normal microbiota
38
Antimicrobial-Associated Diarrhea (diagnosis)
- Bacteria in stool | - colonoscopy
39
Peptic Ulcer Disease (causative agent)
- Helicobacter pylori | - G (-) curved rod, microaerophilic
40
Peptic Ulcer Disease (symptoms)
- Abdominal pain - Gastritis - Peptic ulcers
41
Peptic Ulcer Disease (transmission)
- through contaminated food and water
42
Peptic Ulcer Disease (pathogenicity/virulence)
- urease raises pH in stomach - allows for colonization of helicobacter - flagella allows it to move into the stomach lining
43
Peptic Ulcer Disease (diagnosis)
- Urea Breath Test – radiolabeled urea converted to ammonia and CO2 by H. pylori urease, resulting in radiolabeled CO2 in patient’s breath
44
Peptic Ulcer Disese (treatment)
- Biaxin (clarithromycin, a macrolide) and Prilosec (omeprazole) - combination of antibacterial and drugs that inhibit acid production