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GI Week 2 - WLB > Microbiology of the Upper GI - Zimmer > Flashcards

Microbiology of the Upper GI - Zimmer Flashcards

1
Q

What are the three general GI system defenses?

A
  1. epithelium
  2. mucus,
  3. peristalsis
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2
Q

What are the 2 major defenses in the mouth?

A
  1. saliva (lysozyme, IgA, etc)
  2. normal flora
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3
Q

What are the 2 major defenses in the stomach?

A
  1. acid
  2. normal flora
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4
Q

What are the 2 major defenses in the intestines?

A
  1. Peyer’s patches
  2. normal flora
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5
Q

When do we have a really “clean” mouth?

A

Before we get teeth.

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6
Q

What are the four major normal flora microorganisms in the Esophagus, Stomach, Small Intestine?

A
  • Four phyla in stomach:
    1. Proteobacteria
    2. Firmicutes
    3. Actinobacteria
    4. Bacteroidetes
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7
Q

What does the normal flora in the large intestine consist of?

A
  • Microbe rich, “microbiome” studied here
  • Anaerobes
  • Gram-negative rods (Proteobacteria, etc)
  • Enterococcus – gram-postitive cocci
  • facultative anaerobes can survive wide range of stressors and enviromental conditions
  • Spirochetes
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8
Q

What are dental caries?

A

Infectious disease that causes tooth decay

Results in → pain, tooth loss, spread of infection

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9
Q

What are the risk factors for dental caries?

A
  • Risk factors:
    • high-sugar diet
    • poor oral hygiene
    • reduced amount of saliva
    • smoking
    • periodontal disease
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10
Q

What is the major mechanism that causes dental caries?

A
  • Microbial proliferation and invasion – growth and spread of microbes that causes damage that is significant in illness.
  • Fermentable sugars + Acid-producing bacteria => decreased pH ==>
    • DEMINERALIZATION OF TEETH
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11
Q

What is the treatment for dental caries?

A
  • ***Drill out decayed area of tooth and put in a filling
    • Do not want to let caries grow
    • Can involve the whole tooth, infection
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12
Q

What is Periodontal Disease?

A
  • Infectious disease destroying supporting structures of teeth
    • underlying tissues/bones
  • Mild and common form: gingivitis
    • Involves the gums
    • Irritation
    • Redness
    • Swelling
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13
Q

What conditions are associated with Periodontal Disease?

A
  • Heart attack
  • Stroke
  • Lung disease
  • Premature birth or having a baby with low birth weight, in women
  • Diabetes
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14
Q

What is the major mechanism that causes Gingivitis and Periodontitis?

A
  • Host immune response
    • response of host to microbe that causes illness
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15
Q

What microbial structure composes plaque?

A

Biofilm

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16
Q

What is a biofilm?

A
  • Biofilms consist of two or more species of bacterial microcolonies that are enclosed in a glycocalyx.
    • Glycocalyx is composed of polysaccharides and constitutes up to 50-95% of the biofilm
    • Other components of the biofilm include proteins and DNA
    • Can be hundreds of species in a biofilm
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17
Q

How is a biofilm formed?

A
  1. Weak adherence of cells to a surface
  2. Stronger adherence, likely co-adhesion mediated
  3. Multiplication of cells
  4. Polysaccharide formation
  5. Changing of microbial composition over time
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18
Q

Why is it beneficial for bacteria to live in a biofilm?

A
  • Adherence
  • Protection from the immune system
  • Protection from antibiotics
  • Symbiotic (but also anti-symbiotic) relationships
  • Local conditions of pH, etc, in a normally inhospitable environment
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19
Q

Is all plaque bad?

A
  • Some can be neutral:
    • Undisturbed dental plaque exists in a relatively stable microbial homeostasis.
  • Perturbations to the microbial balance are triggered by environmental or host factors:
    • excessive sugar intake in the case of caries
    • inflammatory response to subgingival plaque in the case of periodontitis
  • Subsequently, the microbial population within dental plaque shifts toward a more pathological community => DISEASE
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20
Q

What species of oral streptococci play important roles in protecting against dental caries and periodontitis?

A
  • S. sanguinis
  • S. oralis
  • S. gordonii
  • S. mitis – the “mitis group” produce hydrogen peroxide which inhibits the growth of other oral bacteria
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21
Q

Where do microbes that cause dental caries live in the mouth?

A
  • usually located in plaques on tooth surfaces
    • often in crevices or between teeth

Tip: they’re often gram positive

22
Q

Where do microbes that cause periodontal disease live?

A
  • below the gumline – in the subgingival space
  • Tip: they’re often gram negative
23
Q

What type of Streptococci are involved in dental caries?

A
  • Streptococcus mutans
    • The “bad” oral steptococci are key players
    • identification of streptococci to the species level is complicated by the fact that many oral streptococci are naturally transformable and readily exchange DNA with one another.
24
Q

What virulence factors of Streptococcus mutans allow it to cause disease?

A
  • adhesin-like surface-associated proteins (e.g. AgI/II family)
    • capable of binding to receptors in the pellicle
  • extracellular glucosyltransferases (Gtfs) are constituents of the pellicle
    • capable of synthesizing glucans (a type of polysaccharide) in situ from sucrose
    • Glucans provide additional S. mutans binding sites, as it binds avidly and in large numbers to these polymers
25
Q

What are “Keystone pathogens” (aka = “red group” pathogens) in periodontal disease?

A
  • low-abundance microbes can orchestrate destructive periodontal inflammation by remodeling a normally symbiotic microbiota into a dysbiotic state
26
Q

What are some examples of “Keystone pathogens”?

A
  • Treponema denticola – a spirochete
  • Tannerella forsythia – anaerobic, gram negative
  • Porphyromonas gingivalis – best studied because it can be cultured
  • Aggregatibacter (formerly Actinobacillus) actinomycetemcomitans
    • is related to the severity of the periodontal disease – gram(-) rod
27
Q

How do you prevent dental caries and periodontal disease?

A
  • Less sugar in diet – less chance of existing biofilm becoming more pathogenic
  • Brush and floss frequently – removes plaque, less chance of harboring bacteria that trigger inflammatory responses
  • Fluoride
    • remineralization to counteract the effects of demineralization under low pH conditions
    • Inhibits bacterial glycolysis and pH maintenance enzymes
  • Increased Saliva flow →sugar free gum
    • Introduces components of host response
    • Increases buffering capacity and removes sugars
    • Return biofilm pH more quickly to resting levels
28
Q

Is gingivitis reversible or irreversible?

A

REVERSIBLE

Treatment is the same as prevention: good cleaning and oral care.

29
Q

What is the treatment for periodontitis?

A
  • Thoroughly clean all surfaces and pockets around teeth to prevent bone damage or prevent further bone damage
  • Milder cases:
    • Scaling to remove tartar and bacteria
    • Root planing: discourage further bacterial growth
    • Antibiotics
      • Topical is typical
      • Oral antibiotic may be necessary in cases of persistent periodontitis despite conventional treatment, when bacteria remain in tissues empirical use of antibiotics, such as a combination of amoxicillin and metronidazole
  • Severe cases:
    • Centers around surgical treatments to fix permanent damage
    • Flap surgery
    • Soft tissue grafts
    • Bone grafts where underlying bone structure is affected
    • New techniques on the horizon
30
Q

What is the link between Diabetes and Periodontal Disease?

A
  • Diabetes has risk of periodontitis up to 3-fold
    • increased inflammatory markers/cytokines
  • Periodontal Disease has a negative effect on glycemic control
31
Q

What is Ludwig’s Angina?

A
  • Skin infection on floor of the mouth, usually results from untreated dental infections.
  • Swelling of infected area may block the airway or prevent swallowing of saliva.
  • Symptoms include:
    • Breathing difficulty
    • Confusion or other mental changes
    • Fever
    • Neck pain
    • Neck swelling
    • ***Redness of the neck
    • Weakness, fatigue, excess tiredness
32
Q

What pathogens cause Ludwig’s Angina?

A
  • alpha-hemolytic streptococci
  • staphylococci
  • bacteroides groups
33
Q

What microorganism causes Hairy Leukoplakia?

A

caused by a virus = EBV

Patient is almost always HIV(+)

34
Q

What are the morphological characteristics of EBV?

  • Genome
  • SS/DS structure
  • Non/Enveloped
A
  • Herpesviridae
  • Double stranded Linear DNA
  • enveloped
  • Epstein-barr virus (human herpesvirus 4)
35
Q

What is the treatment for Candidiasis?

A
  • Must treat with prescription antifungal
  • Most commonly a topical treatment:
    • clotrimazole lozenge
    • nystatin suspension (swish and swallow)
  • Unresponsive cases:
    • systemic antifungal such as fluconazole
  • Worst case:
    • IV administration of amphotericin B (significant side effects)
  • Untreated infections can lead to an invasive candidiasis.
36
Q

What is the difference between Leukoplakia and Hairy Leukoplakia?

A
  • Leukoplakia:
    • not caused by a microorganism, thought to be caused by smoking and chewing tobacco – or other irritations
  • Hairy Leukoplakia:
    • caused by a virus (EBV)
    • Patient is almost always HIV(+).
    • Fuzzy white patches on side of tongue.
    • Unlike thrush, it cannot be wiped away
37
Q

What is the major pathologic micoorganism of the stomach?

A

Helicobacter pylori

38
Q

What are the morphological features of H. pylori?

  • Gm +/-
  • Shape
  • Catalase +/-
  • Oxidase +/-
  • Urease +/-
A
  • Gram (-)
  • Flagellated helix-shaped rod (spirilli)
  • Microaerophilic
  • Catalase and oxidase (+)
  • Urease (+)
39
Q

What happens after Helicobacter pylori colonization in the stomach?

A
  • Asymptomatic Gastritis first
    • then can progress to any of the following:
      • Symptomatic Gastritis
      • Ulcer
      • Carcinoma
      • Lymphoma
40
Q

What mechanisms of H. pylori colonization help cause disease?

A
  • Toxin production –
    • bacteria release toxin that causes illness
  • Host immune response –
    • response of host to microbe that causes illness
41
Q

What are the symptoms of gastritis?

A
  • Inflammation of the gastric mucosa (transient or chronic)
  • Gnawing or burning ache in upper abdomen
  • Pain may become either worse or better with eating
  • Nausea/Vomiting
  • A feeling of fullness in your upper abdomen after eating
42
Q

What are the symptoms of Gastric Ulcers?

A
  • Most common = burning abdominal pain felt anywhere from navel to breastbone
    • Worse when stomach is empty
    • Flare at night
    • Often temporarily relieved by eating foods that buffer stomach acid
    • Disappear and then return for a few days or weeks
  • Less common: The vomiting of blood —
    • may appear red or black
    • Dark blood in stools or stools that are black or tarry
    • Nausea or vomiting
    • Unexplained weight loss
    • Appetite changes
43
Q

What are the major virulence factors that help H. pylori colonize the GI?

A
  • Immune Evasion:
    • Inhibit phagocytic uptake Inhibit adaptive immune response
    • Evade killing by reactive oxygen species and nitric oxide
    • Evade recognition by pattern recognition receptors (PAMPs)
  • Urease +:
    • Raises local pH Urea + Urease => CO2 + Ammonia (basic, raises pH)
    • Helps bacteria make it through buffering mucous layer
  • Flagella:
    • Allows bacteria to get through the lower pH layer
  • Chemotaxis:
    • Can sense pH gradient to help guide motility in preferred directions
  • Toxins:
    • VacA = Pore forming cytotoxin that allows leakage of Ca+ from epithelial cell
    • CagA = Type 4 secretion system (TFSS) is a needle through which CagA travels into the host cytosol and affects the proliferative activities, adhesion, and cytoskeletal organization of epithelial cells.
      • highly proinflammatory
      • known to interact with at least ten host proteins.
44
Q

How does H. pylori cause an ulcer?

A
  1. Attract inflammatory cells (host cells)
  2. Inflammatory cells cannot kill bacteria easily
  3. Host damages itself by continual, ineffective immune response!
45
Q

How is H. pylori diagnosed?

A
  • Diagnosis: A variety of methods are available, know the principles behind each test
    • Endoscopy + culture = GOLD STANDARD
      • rapid urease testing included
    • Breath Test = detects radioactive CO2
    • Stool test = direct antigen test (detects active vs. latent)
    • Blood test = detects H. pylori antibodies
46
Q

How is H. pylori treated?

A
  • week of “Triple therapy” is currently used:
  • Antibiotics will be necessary
    • often clarithromycin and amoxicillin
  • Proton pump inhibitor (3rd arm of triple therapy)
    • to aid in the healing of ulcer
47
Q

What type of lymphoma can be caused by H. pylori?

A
  • Mucosa-associated lymphoid tissue (MALT lymphoma or MALToma) in the stomach is termed “gastric MALT” (Tumors of B cells)
48
Q

What type of carcinoma can be caused by H. pylori?

A

Gastric carcinoma

49
Q

What are the symptoms of Gastric MALT?

A
  • Indigestion
  • Heartburn (stomach pain)
  • Long term inflammation
  • Antibiotics are still part of the treatment strategy
50
Q

What are the symptoms of Gastric Carcinoma?

A
  • Indigestion
  • Heartburn (stomach pain)
  • Long term inflammation
  • H. pylori a risk factor in only 65-80% of gastric carcinoma

GI Week 2 - WLB (11 decks)

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