GI Micro Flashcards

1
Q

GI System Defenses

A

General –> epithelium, mucous, peristalsis
Mouth –> saliva and normal flora
Stomach –> acidity and normal flora??
Intestines –> peyer’s patches and normal flora

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2
Q

Normal flora in mouth???

A

Mouth is very clean until teeth come in –> then lots of normal flora

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3
Q

Upper GI normal flora

A

sparse in stomach and small intestine

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4
Q

Lower GI normal flora

A

MICROBIOME

  • anaerobes
  • gram (-) rods
  • Enterococcus
  • Spirochetes
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5
Q

Caries

A

Dental infection –> tooth decay
Pain, tooth decay, and spread of infection
Risks => high sugar diet, poor oral hygiene, decreased saliva, smoking, periodontal disease
Common worldwide
Occurs by microbial overgrowth –> decrease in pH –> demineralization of teeth

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6
Q

Treatment of dental caries

A

drill out tooth that is infected and replace

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7
Q

Periodontal Disease

A

Gingivitis –> infectious disease destroying supporting structures of teeth
Mild –> irritation, redness, swelling

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8
Q

Periodontitis

A

Infection of underlying tissue and bone
- associated with MI, stroke, lung disease, premature birth
Occurs because of host immune response to infection

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9
Q

What is essential for dental disease?

A

Plaque formation –> BIOFILMS

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10
Q

Biofilm

A
2 or more species of bacterial microcolonies enclosed in a glycocalyx (polysaccharides, DNA, protein)
Formation
1. weak adherence
2. strong adherence
3. multiplication
4. polysaccharide formation
5. changing of composition over time
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11
Q

Advantages of living in biofilm

A
adherence
protection from immune system
protection against antibiotics
symbiotic relationships 
better pH
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12
Q

Normal microbes of mouth

A

ANAEROBIC ORGANISMS
‘mitis’ group of strep species –> protect against dental caries
- also gram (+) lactobacilli and spirochetes

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13
Q

Microbes that cause caries

A

Usually located on tooth/plaque surface –> usually gram (+)

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14
Q

Microbes that cause periodontal disease

A

Usually located in subginival space –> usually gram (-)

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15
Q

Streptococcus mutans

A

gram (+) –> cocci –> catalase (-) –> anaerobic –> alpha hemolytic –> optochin resistant
VF
1. adhesion-like surface proteins (AG I/II) –> bind to pellicle
2. extracellular glucosyltransferases (Gtfs) –> become part of pellicle and pump out glucans –> additional binding sites

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16
Q

Keystone pathogens of periodontal disease

A

“red group” pathogens –> hard to detect
BIG 3
Treponema denticola –> spirochete
Tanerella forsythia –> anaerobic, gram (-)
Porphyromanos gingivalis –> best studied

17
Q

Aggergatibacter actinomycetemcomitans

A

extreme aggressive gram (-) rod of periodontal disease

18
Q

Porphyromonas gingivalis

A

Gram (-) –> bacillus –> anaerobic –> asaccharolytic –> black-pigmented colonies on blood agar –> bacitracin resistant

19
Q

Prevention of periodontal disease

A

less sugar in diet
brush and floss regularly
fluoride
increased saliva –> gum

20
Q

Gingivitis Treatment

A

Same as prevention –> good cleaning and oral care

21
Q

Periodontitis Treatment

A

clean all surfaces and pockets

  • topical empiric antibiotics = mild cases
  • surgery = severe cases
22
Q

Ludwig’s Angina

A

skin infection on floor of mouth from untreated dental infections –> swelling of infected area may block airway
REDNESS OF NECK

23
Q

Candidia albicans

A

yeast-like fungus –> pleomorphic
oral thrush –> creamy white lesion on tongue or cheeks
esophageal form = DANGEROUS
diagnosis made on clinical symptoms
Tx with anti-fungal –> azole/amphotericin

24
Q

Helicobacter pylori

A

Gram (-) –> flagellated helix-shaped rod (spirilli) –> microaerophilic –> catalase and oxidase (+) –> urease +
- 50% of U.S. infected –> only 10% have ulcer (some strains more virulent)

25
Q

H. pylori infections

A

symptoms and disease result from host immune response

26
Q

Gastritis

A

caused by H. pylori –> inflammation of gastric mucosa
Symptoms
- gnawing or burning ache in upper abdomen
- N/V
- feeling of fullness in abdomen

27
Q

Gastric ulcer

A
caused by H. pylori --> open sores that develop on inside of stomach lining
Symptoms
- felt anywhere from navel to breastbone
- worse when stomach empty
- flares at night
- relieved by eating foods
- disappear and reappear within days
28
Q

Virulence Factors of H. pylori

A
  • Inhibits phagocytic uptake, inhibits immune response, evades killing by ROS and NO, evades recognition of receptors
  • Urease –> raises pH (ammonia) –> needs to break through low pH layer
  • Flagella –> move through pH layer
  • Chemotaxis –> based on pH gradient
  • Adherence
29
Q

Toxins produced

A

VacA –> pore forming cytotoxin that allows leakage to Ca from cell
CagA –> T4SS, travels through needle into cytosol and affects proliferation, adhesion –> HIGHLY proinflammatory

30
Q

How to cause ulcers

A
  1. Attract inflammatory cells
  2. Inflammatory cells cannot kill easily
  3. Host damages itself by continual ineffective immune response
31
Q

Diagnosis of H. pylori

A

Endoscopy –> gold standard
Breath test –> detects radioactive CO2 as a result of urease (+)
Stool test –> direct antigen test –> good for diagnosis and confirming cure
Blood test –> detects H. pylori antibodies –> not useful for confirming cure

32
Q

Treatment of H. pylori

A

“Triple Therapy”
Antibiotics –> clarithromycin and amoxicillin
Proton Pump Inhibitor

33
Q

Gastric MALT

A

Indigestion, heart burn
Long term inflammation is culprit
Tumor of B cells
Antibiotics still part of strategy

34
Q

Gastric Carcinoma

A

Indigestion, heart burn
Long term inflammation is culprit
Cancer of stomach lining
H. pylori is risk factor