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microbiology > oral bacteria A > Flashcards

oral bacteria A Flashcards

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1
Q

Sampling oral bacteria- niches?

A

distinctive communities in different niches tongue, teeth, buccal mucosa, gingival crevice, etc.

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2
Q

sampling methods

A

collect saliva, tongue blade, scrape from tooth surface, wick fluid from deep pockets (endodontic paper)

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3
Q

for molecular ID what is often the main target

A

16s RNA genes which possess both variable and common regions

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4
Q

Identifying oral bacteria: Molecular techniques

A

PCR
hybridization assays
16S sequence analysis
microscopy

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5
Q

dental plaque

A
  • Biofilm on tooth surface

* One of the highest concentrations of bacteria in the body

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6
Q

colonizing bac of plaque interact with?

A

acquired pellicle

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7
Q

steps to plaque formation

A 
bac contact acquired pellicle / passive transport of bac to pellicle surface 
coaggregation 
supportive microenvironment 
glucan production
O2 drops 
some species detatch
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8
Q

acquired pellicle

A

A. Bacteria never come in contact with a clean tooth surface. Tooth surface is coated with an acquired pellicle
•film deposited on tooth surface
•film composition = molecules in saliva (predominant), material shed from bacterial cell surfaces, polymers from gingival crevicular fluid

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9
Q 
initial colonation/ passive transport
what species? 
what binds? 
binds to?
irreversible?
A 
Initial colonization is by Streptococcus species
Streptococcus gordonii
Streptococcus oralis
Streptococcus mitis
Streptococcus sanguis (now sanguinis)

Adhesins on bacterial surface bind to receptors in the pellicle.

Streptococcus: Antigen I/II are important adhesins

Bind human salivary glycoproteins, other bacteria and calcium
Pellicle receptors = polymers from saliva and bacteria

Adhesion is usually irreversible

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10
Q

coaggregation

mportant species at this stage?

A

Subsequent attachment of these species and other bacterial species occurs by coaggregation
•bacteria binding to other bacteria
•additional bacteria bind to early-binding bacteria and to each other
•multiple species coaggregate

Important species at this stage:
Actinomyces naeslundii
Actinomyces viscosus
Streptococcus gordonii

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11
Q

supportive microenvironment, strains supported by this?

A

D. Microenvironment created that supports additional species: Streptococcus mutans and Streptococcus sobrinus

Bacteria multiply in the developing biofilm

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12
Q

glucan production

A

Streptococci produce glucosyltransferases
•extracellular enzymes which polymerize the glucose moiety of sucrose into glucan polymers and other polysaccharides

Glucans = branched-chain polysaccharides
Alpha(1-6) linkage
Alpha(1-3) linkage

Glucans are like cement
Bacteria bind to glucans
Bacteria are bound to each other and to matrix of glucans

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13
Q

O2 dropping levels
allow what strains to colonize?
where does this occur especially?

A

Oxygen levels drop: Late colonizers include obligate anaerobes.

Prevotella melaninogenicus
Prevotella oralis
Veillonella spp.

Especially between teeth and dental gingival crevice

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14
Q

detatchment of some species, how they detatch

A

Get some detachment of bacteria and colonization of new sites

Some bacteria will shed or degrade their adhesins to facilitate release

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15
Q

Altered properties of bacteria in a biofilm

A
  1. Up-regulation of genes for extracellular polysaccharide synthesis
  2. Increased resistance to antimicrobial agents
  3. Metabolic interaction between closely spaced bacteria
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16
Q

Increased resistance to antimicrobial agents found in biofilm due to?

A

a. restricted penetration of agent into biofilm (due to polysac)
b. inactivation of agents by enzymes concentrated in biofilm
c. slow growth rate of bacteria in biofilm
d. expression of novel surface-associated phenotypes

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17
Q

Metabolic interaction between closely spaced bacteria of biofilm

A

Synergistic - degradation of complex nutrients

Antagonistic - bacteriocins (exclude susceptible strains)

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18
Q

plaque eventually reaches?

A

Plaque eventually reaches a microbial homeostasis = stability in bacterial composition

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19
Q

Breakdown of homeostasis will?

A

alters bacterial composition

can be due to:
•reduction in saliva flow
•increased consumption of sucrose

Caries can result

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20
Q

main bacterial strains of caries

A

Mutans streptococci:
Streptococcus mutans (mainly)
Streptococcus sobrinus

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21
Q

Fermentation in biofilm produces:

A

acids: lactic acid, will demineralize teeth

acid is produced from the metabolic activities of the bacteria using saccharides produced with GTF

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22
Q

metabolic acid effect on teeth, what molecule is affected?

result of increased pH?

A

Solubilizes calcium and phosphate (produced from hydroxyapatite)
Get reprecipitation when pH increases (becomes less acidic)

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23
Q

prolonged acidic environments created by?

causes?

A

Prolonged acidic environment created by regular snacking on high sucrose foods

demineralization > remineralization

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24
Q

enamel and dentin dissolving, results?

A

Enamel dissolves slowly
Dentin more easily attacked and colonized by bacteria
Dentin is protein rich/many different bacteria can grow: Then disease rapidly progresses
Root canal becomes invaded and Abscess form

25
Q

Age and root surface caries

likely causative strains?

A

Gingival recession occurs with age: This fact changes the microbial homeostasis
Cementum surface of the root is exposed and made vulnerable to bacterial colonization
60% of individual >60 years old have root caries

MS and lactobacilli likely pathogens, Actinomyces viscosus and Actinomyces naeslundii.

(Both of these Actinomyces species had been shown toproduce root surface caries in experimental animals)

26
Q

Pathogenic properties of cariogenic bacteria

A

Rapidly transport fermentable sugars/convert to acid

Production of extracellular and intracellular polysaccharides

Ability to maintain sugar metabolism under extreme conditions

27
Q

Rapid transport of fermentable sugars/convert to acid of cariogenic bacteria

A

•Rapidly transport fermentable sugars/convert to acid
Rapid compared to other plaque bacteria
Cariogenic bacteria have multiple sugar transporters
Including PEP-PTS systems (group translocation system)

Group translocation - molecule transported into the cell while being chemically altered

28
Q

Production of extracellular and intracellular polysaccharides of cariogenic bac

A

Glucans and Fructans (extracellular)
Intracellular storage - allows acid production even
when sucrose in not available

29
Q

how oral bac maintain sugar metabolism under extreme conditions of cariogenic bacteria?
spp?

A

Acidic conditions more tolerated by MS and lactobacilli (so they are both acid-producing and acid-tolerant)

a. maintain a favorable intracellular environment (pump out protons even into acidic surroundings) ATP usage is coupled to protons being pumped out (using ATP synthesized by glycolysis)
b. bacterial enzymes have more acidic pH optima
c. produce acid-stress response proteins to protect cell contents

30
Q

Notable property of noncariogenic bacteria

A

Alkali production
Urea and arginine are the major substrates for alkali production via the generation of
ammonia (NH3), using enzymes urease and arginine deiminase

31
Q

virulence factors of s mutans

A 
Ag I/II 
GTFs
GBPs
fructanse 
dextranase 
intracell polysac 
PEP-PTS
H-ATPase 
acid tolerance
32
Q

Ag I/II of s mutans

A

adherence to salivary pellicle

33
Q

GTFs of s mutans

A

production of glucan polymers from sucrose, used for adherence and accumulation

34
Q

GBPs of s mutans

A

binding to glucans, adherence

35
Q

fructanase of s mutans

A

hydrolysis of fructan polymers, produces acid

36
Q

dextranse of s mutans

A

cleavage of glucans/ relase glucose to be used= produces acid

37
Q

intracellular polysaccharides of s mutans

A

can be used when exogenous stores of saccharides are depleted

38
Q

PEP-PTS of s mutans

A

catalyzes high affinity uptake of multiple different sugars

39
Q

H-ATPase of s mutans

A

use of ATP to move protons out of cell in acidic environment

40
Q

Basis for periodontal disease, hypothesis?

A

non-specific plaque

specific plaque

41
Q

Non-specific plaque hypothesis of periodontitis

A

disease is due to the host response to non-specific growth of bacteria on tooth surfaces
(inflammatory disease)

Traditional view
Bacterial complexity of dental plaque
Non-specific mechanisms of generating inflammatory response: LPS and volatile fatty acids

42
Q

Specific plaque hypothesis of periodontitis

A

disease is due to a limited number of species which produce biologically active molecules that are proinflammatory or antigenic (infection)

43
Q

Non-specific plaque hypothesis treatment

failure?

A

Treatment dictates that flora be suppressed continuously or periodically

Sometimes traditional debridement fails leading to:
refractory periodontitis
give broad-spectrum antibiotics

44
Q

Specific plaque hypothesis Key illustrative examples:

A

Localized juvenile periodontitis

Acute necrotizing ulcerative gingivitis

45
Q

Localized juvenile periodontitis
strain?
mechanism?
treatment?

A

1-5 out of 1000 teenagers
Aggregatibacter actinomycetemcomitans can invade gingival tissues and produces a leukotoxin (LT) that inhibits neutrophils

locally delivered antimicrobial agents or systemic tetracycline treatment

46
Q

Acute necrotizing ulcerative gingivitis
strain?
treatment?

A

Trench mouth of World War I
Spirochetes and Fusobacterium nucleatum

controlled by antibiotic mouth rinses with oxidizing agents also systemic metronidazole (antibiotic) treatment

47
Q

Specific plaque hypothesis early and adult form considerations
important strains?

A

Consider both early-onset and adult forms of disease No single bacterial species uniquely involved= polymicrobial infection

Porphyromonas gingivalis
Tannerella forsythia
Treponema denticola (& other spirochetes)

48
Q

Porphyromonas gingivalis Virulence Factors and their functions

A

• Fimbriae allows adhesion to:
– Saliva-coated hydroxyapatite
– Human oral epithelial cells

  • Hemagglutinins
  • Capsule prevents phagocytosis

• 3 major proteolytic activities:
– Trypsin-like
– Collagenolytic
– Glycylprolyl peptidase activity

49
Q

Porphyromonas gingivalis as a “keystone pathogen”

A

Current model for periodontal disease, In between specific and nonspecific plaque hypotheses

Low-abundance bacteria with community wide effects that are critical for the
development of dysbiosis is now known as keystone pathogens, the best documented example of which is Porphyromonas gingivalis.

50
Q

Aggregatibacter actinomycetemcomitans important Virulence Factors

A 
leukotoxins 
invasins 
bacteriocin 
PLC
capsular polysac
51
Q

Leukotoxin of Aggregatibacter actinomycetemcomitan

A

Cytotoxic to human PMNs, monocytes, and T-lymphoctyes

52
Q

• Invasins of Aggregatibacter actinomycetemcomitan

A

– Aids in bacteria penetrating eukaryotic cells

53
Q

• Bacteriocin of Aggregatibacter actinomycetemcomitan, target spp?

A

• Inhibition of growth or killing of other bacterial species: streptococcus sanguis and actinomyces viscosus

54
Q

• Capsular polysaccharide of Aggregatibacter actinomycetemcomitan

A

• Capsular polysaccharide • Resistance to phagocytosis by PMNs, reduction in complement dependent response by PMNs, increase In bone resorption

55
Q

• Phospholipase C of Aggregatibacter actinomycetemcomitan

A

• Hydrolyzation of host cell membrane

56
Q

Fusobacterium nucleatum Virulence factors

A

capsule
• Hemolysin
• Leukocidin(leukotoxin)
• Superoxide dismutase

57
Q

Prevotella intermedia Virulence factors, actions?

A

• The brown or black pigment
§ metabolic end-product of hemin, acts as a defensive barrier that protects the bacteria from the toxic effects of oxygen

• Collagenase, hyaluronidase, and protease
§ Degrade host tissues and cleave other host derived molecules

• Hemolysin
§ Enhanced by the action of proteases
§ Favors the acquisition of iron, which is an essential nutrient to their metabolism and their survival

58
Q

Modified Koch’s postulates

A
  1. Association of microorganism with periodontitis
  2. Elimination of bacteria reduce the disease
  3. Evidence of host response to pathogen
  4. Ability of pathogen to cause disease in animal model
  5. Evidence that pathogen produces virulence factors that contribute to disease.

microbiology (42 decks)

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