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GI- Week 1 > Zimmer: Microbiology of the Upper GI > Flashcards

Zimmer: Microbiology of the Upper GI Flashcards

1
Q

What are Peyer’s Patches?

A

Small masses of lymphatic tissue found throughout the ileum region of the small intestine

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2
Q

How many bacteria are in the mouth?

A

FEW! Until the teeth erupt

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3
Q

What is the normal flora of the esophagus, stomach and small intestine?

A

Spare–less than 10^4 organisms/ ml of inestinal secretions

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4
Q

How many phyla are found in the stomach?

A

Four:

Proteobacteria
Firmicutes
Actinobacteria
Bacteroidetes

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5
Q

What is the normal flora of the large intestine?

A

Microbe rich, “microbiome”!

Anaerobes
Gram-negative rods
Enterococcus – can survive wide range of stressors and enviromental conditions
Spirochetes

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6
Q

What is caries?

A

infectious disease that causes tooth decay>

Pain, tooth loss, spread of infection

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7
Q

What are RFs for caries?

A

high-sugar diet, poor oral hygiene, reduced amount of saliva, smoking, periodontal disease

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8
Q

How does caries happen?

A

Microbial proliferation in the right environment!

Fermentable sugars + acid producing bacteria in a LOW pH–> demineralization

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9
Q

What is the treatment for dental caries?

A

Drill out decayed area of tooth and put in filling

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10
Q

What is periodontal disease?

A

Gingivitis (irritation, redness, swelling of gums)

Infectious disease that destroys supporting structures of teeh

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11
Q

What is periodontitis?

A

Infection of underlying tissues and bones–> localized loss of attachment

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12
Q

Periodontitis can be associated w/:

A

Heart attack
Stroke
Lung disease
Premature birth or having a baby with low birth weight, in women

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13
Q

What increases the risk of periodontal disease?

A

Diabetes

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14
Q

What is the MOA of gingivitis and periodontitis?

A

host immune response causes illness!

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15
Q

What is essential for dental diseases?

A

plaque/biofilm

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16
Q

What does a biofilm consist of?

A

two or more species of bacterial microcolonies enclosed in glycocalyx

Proteins
DNA

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17
Q

What is glycocalyx?

A

polysaccharides

50-95% of biofilm

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18
Q

How is a biofilm formed?

A

weak adherence of cells to a surface>
stronger adhesion (co adhesion mediated)>
multiplication of cells>
polysaccharide formation>
change in microbial composition over time

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19
Q

Why do bacteria like to life 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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20
Q

Is plaque bad?

A

Not if it’s removed regularly, but if not it can trend towards a pathological community

(low pH, sugar rich diet, low saliva flow)

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21
Q

What bugs are associated with good plaque vs. bad plaque?

A

Bad plaque = s. mutans, lactobacilli

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22
Q

What microbes are normally present in the mouth?

A

Anerobic organisms

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23
Q

What species play an important role in protecting against dental caries and periodontitis and produce hydrogen peroxide inhibiting growth of other bacteria?

A

Oral Streptococci

S. sanguinis
S. mitis

  • gram positive lactobacilli are also prominent as well as spirochetes
  • bacteria associated w/ infection are present but are commensals
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24
Q

Microbes that cause caries are often locate in plaques on tooth surfaces between the crevices of teeth and are usually gram….

A

POSITIVE

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25
Q

Microbes that cause peridontal disease do their destruction…..

What type of bacteria are they?

A

BELOW the gum line in the subgingival space

Gram NEGATIVE

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26
Q

Why is it complicated to identify the BAD oral streptococci that can cause peridontal disease?

A

many oral streptococci are naturally transformable and readily exchange DNA with one another so it makes it harder to conduct a 16s rRNA analysis

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27
Q

What is s. Mutans?

A 
Gram +
cocci
cat -
facultative anaerobic
alpha hemolytic
opt resistant
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28
Q

What is the difference between a toxin and a VR?

A

VF: Properties (i.e., gene products) enabling a microorganism to ESTABLISH ITSELF on or within a host and enhance its potential to cause disease. Virulence factors include BACTERIAL TOXIN

Toxin: Microbial toxins PROMOTE INFECTION and disease by directly damaging host tissues and by disabling the immune system.

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29
Q

What are the VF of mutans streptococci?

A
  1. Adhesin like surface proteins (AgI/II family) that bind to receptors in the pellicle
  2. Gtfs (extracellular glucosyltransferases) constituents of the pellicle, synthesize GLUCANS in situ from sucrase. Glucans provide additional S. mutans binding sites
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30
Q

What streptococci represent most of the normal mouth bacteria?

A

s. mitis

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31
Q

What streptococci represent most of the bacteria involved in tooth decay?

A

Mutans

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32
Q

What are keystone/red group pathogens?

A

Not present in large numbers, but the ratio of these bacteria to others is what allows them to be identified

Low-abundance microbes that can orchestrate destructive periodontal inflammation by remodeling a normally symbiotic microbiota into a dysbiotic state”

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33
Q

What are three keystone pathogens?

A

treponema denticola = spirochete

tannerella forsythia= anaerobic gram negative

Porphyromonas gingivalis**

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34
Q

What gram - rod relates to the severity of a periodontal disease?

A

Aggregatibacter (formerly Actinobacillus) actinomycetemcomitans

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35
Q

porphyromonas gingivalis

A 
gram -
bacillus
anaerobic
assaccharolytic
black pigmented colonies on blood agar
bacitracin resistant
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36
Q

P. gingivalis
Capnocytophaga gingivalis
Prevotella denticola

are all….

A

Microbes involved in periodontal disease

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37
Q

How do you prevent caries and periodontal disease?

A
  1. Less sugar in diet – less chance of existing biofilm becoming more pathogenic
  2. Brush and floss frequently – removes plaque, less chance of harboring bacteria that trigger inflammatory responses
  3. Fluoride
    for remineralization to counteract the effects of demineralization under low pH conditions
    Inhibits bacterial glycolysis and pH maintenance enzymes
  4. 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
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38
Q

Is gingivitis reversible?

A

Yes

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39
Q

What is the treatment for gingivitis?

A

prevention!

good cleaning and oral care

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40
Q

What is the tx for periodontitis?

A

Thoroughly clean all surfaces and pockets around teeth to prevent bone damage or prevent further bone damage

41
Q

How do you treat a milder case of periodontitis?

A
  1. Scaling to remove tartar and bacteria
  2. Root planing: discourage further bacterial growth
  3. Antibiotics
    - Topical is typical
    - Oral antibiotic may be necessary in cases of persistent periodontitis despite conventional treatment, when bacteria remain in tissues
42
Q

What antibiotics may be used to treat a mild case of periodontitis?

A

amoxicillin

metronidazole

43
Q

How do you treat severe cases of periodontitis?

A

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

44
Q

What disease MC occurs in babies, elderly, immunocompromised?

A

candida albicans (oral candidiasis)

45
Q

What disease MC occurs in HIV +

A

EBV (hairy leukoplakia)

46
Q

What disease MC is a copmlication of severe tooth infection/periodontal disease?

A

Bacterial: alpha-hemolytic streptococci, staphylococci and bacteroides groups

Ludwig’s angina

47
Q

What is the difference between thrush and diptheria/strep throat?

A

Corynebacterium diptheriae- diptheria

s. pyogenes- strep throat

48
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.

49
Q

A pt presents w/ breathing difficulty, confusion, fever, neck pain, neck swelling, NECK REDNESS. What does he have?

A

Ludwig’s angina

50
Q

How does candida albicans usually grow?

A

Yeast-like fungus

Grows as yeast/filamentous cells

Can form spores under right conditoins

51
Q

A pt present w/ creamy white lesions on the tongue and inner cheeks.

A

Candidiasis

52
Q

What form of candidiasis is dangerous?

A

esophageal

53
Q

How do you diagnose candidiasiss

A

sxs

can scrape on microscope slide to look for HYPHAE

54
Q

How do you treat candidiasis?

A

antifungal

*usuallly topical like clotrimazole or nystatine (swish and swallow)

55
Q

How do you treat unresponsive cases of candidiasis?

A

systemic antifungal

FLUCANOZOLE

56
Q

If someone has candidiasis taht WONT go away how do you treat them?

A

IV administration of amphotericin B

57
Q

What can lead to invasive candidiasis?

A

Untreated candidiasis infections

58
Q

Candida albicans

A 
fungus
hypae forms
bacilli
non-spore forming
non motile
59
Q

Where does c. albicans usually present?

A

TONgue!

60
Q

Where does s. pyogenes usually present?

A

back of throat

61
Q

Where does c. diptheriae usually present?

A

pseudomembarne

62
Q

What causes leukoplakia?

A

“white plaque”

smoking/chewing tobacco, other irritations

NOT microorganism

63
Q

What causes hairy leukoplakia?

A

EBV in a pt that is almost always HIV +

64
Q

If a pt presents w/ a fuzzy white patch on the side of their tongue that CANNOT be scraped away.

A

Hairy leukoplakia

65
Q

EBV

A 
Herpesviridae
DS
Linear
DNA
env
HHV- 4
66
Q

What is the major player in stomach infections?

A

helicobacter pylori

67
Q

How is helicobacter pylori normally transmitted?

A

fecal oral transmission (50% adults are infected)

68
Q

helicobacter pylori

A 
Bacteria
gram -
flagellated helix shaped rod
microaerophilic
catalase and oxidase +
69
Q

Does H. Pylori always cause infections?

A

No! only sometimes

50% of adults are infected, but in the third world almost all are

Yet estimated that H. pylori-positive patients have only a 10 to 20% lifetime risk of developing ulcer disease and a 1 to 2% risk of developing distal gastric cancer

70
Q

Why are pts infected w/ h. pylori usually assymptomatic?

A

Strains of H. pylori are more or less virulent (pathogen genetics)

Individuals respond immunologically in different ways (host response/host genetics)

Gastric microbiome (a recent concept)**

71
Q

What can a h. pylori infection cause?

A

Asymptomatic gastritis that can lead to:

symptomatic gastritis
ulcer
carcinoma
lymphoma

72
Q

How does h. pylori cause disease?

A

Toxin production

Host immune response

73
Q

What causes these sxs?

Gnawing or burning ache in upper abdomen. May become either worse or better with eating

Nausea
Vomiting
A feeling of fullness in your upper abdomen after eating

A

Gastritis!

Inflammation of the gastric mucosa (transient/chronic)

74
Q

A pt presents w/ BURNING ABDOMINAL PAIN…

they also have:

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

A

Gastric ulcer

Sore that develops on the inside stomach lining

*Felt anywhere from navel to breastbone

75
Q

How do h. pylori cause disease?

A

VacA
Adhesins
TFSS and CagA

76
Q

How do h. pylori survive in the stomach?

A

Inhibit phagocytic uptake
Inhibit adaptive immune response
Evade killing by reactive oxygen species and nitric oxide
Evade recognition by pattern recognition receptors

77
Q

How does being able to produce urease help h. pylori to survive in the stomach?

A

raises the local pH from 2 to about 6 creating some transient buffering

78
Q

What allows h. pylori to enter the low pH layer?

A

flagella based motility

79
Q

What keeps most of the h. pylori swimming in the higher pH zone immediately on top of the epithelial cells?

A

CHEMOTAXIS based on pH gradient and motility

80
Q

Why is it important that h. pylori has a subset of cells that adhere to the epithelial cells?

A
  1. Adherence allows some cells to avoid mechanical clearance
  2. Promote invasion and persistence
  3. Activity of adhesins contributes to inflammation
81
Q

What are the two main VFs of h. pylori?

A

VacAa

Cag pathogenicity island= Cag A

82
Q

What is VacA?

A

Pore forming cytotoxin that allows leakage of Ca from epithelial celll

83
Q

What is CagA?

A

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. The entire system is also highly proinflammatory

84
Q

How do you cause an ulcer?

A
  1. Attract inflammatory cells
  2. Inflammatory cells cannot kill easily
  3. Host damages itself by continual, ineffective immune response!
85
Q

How do you diagnose h. pylori?

A

Endoscopy + culture
Breath Test
Stool test
Blood test

86
Q

How do you treat h. pylori?

A

A week of ‘TRIPLE THERAPY’

clarithromycin + amoxicillin to REMOVE h. pylori

PPI to aid in HEALING of ulcer

87
Q

What is the gold standard diagnostic technique for h. pylori?

A

Endoscopy

Guided biopsy>
rapid urease testing, histology, culture

very expensive!

88
Q

How does a rapid urease test detect h. pylori?

A

Detects the urease enzyme of h. pylori

89
Q

How does a breath test detect h. pylori?

A

Detects radioactive CO2
Good for dx and can confirm cure

Requires a skilled technician

90
Q

How does a blood test detect h. pylori?

A

h. pylori Antibodies

* initial diagnosis only, can’t confirm cure

91
Q

How does a stool ag test detect h. pylori?

A

Differentiate btwn active and latent infection (serology can only detect exposure)

92
Q

Why is a stool antigen test great?

A

easy
good for diagnosis
good for confirming a cure

93
Q

What cancer are associated w/ h. pylori?

A

MALT lymphoma

Gastric carcinoma

94
Q

What is MALT?

A

Mucosa associated lymphohid tissue caused by LONG TERM INFLAMMATION>

indigestion, heartburn/stomach pain

95
Q

MALT is a tumor of…

A

B cells

96
Q

What is part of the tx strategy for MALT?

A

antibiotics

97
Q

What is Gastric carcinoma?

A

long term inflammation>
indigestion, heartburn>
cancer of the stomach lining (epithelial cells)

98
Q

H. pylori is a RF in what percentage of gastric carcinoma?

A

65-80%

GI- Week 1 (12 decks)

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