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Periodontology > Bacteria > Flashcards

Bacteria Flashcards

1
Q

bacterial complexes

A

the composition of the different color coded complexes is based on the frequency with which the organisms are encountered together

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2
Q

blue and purple complex

what are these considered?

A

consists of gram-positive cocci and rods

PRIMARY COLONIZERS

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3
Q

yellow complex

A

is compromised of gram-negative faculative cocci

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4
Q

green complex

A

contains gram-positive and negative rods and cocci- biut NON-motile species present

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5
Q

orange complex + importance

A

demonstrates a higher concentration of gram-negative rods and cocci, with some motile species present

what we see with perio patients

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6
Q

red complex and importance

A

is EXCLUSIVELY gram-negative , MOTILE anaerobes

what we see with perio patients

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7
Q

bacteria present in the red complex

A

P. gingivalis
T. denticola
T. forysthensis

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8
Q

bacteria present in green complex

A

A. actinomycetemcomitans

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9
Q

red and orange complex?

A

implicated in perio patients with higher
- patients will develop symptoms of perio in these complexes

you dont want these

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10
Q

will you ever find a patietn with just red and orange complex?

A

NO - they need the primary colonizers to adhere

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11
Q

transition from health to disease?

A

gram - positive, aerobic, non-motile —> gram-negative, anaerobic, motile

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12
Q

where does anaerobic bacteria thrive?

A

sulcus – attachment apparatus here

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13
Q

gingivitis association with complexes?

A

early colonizers are associated with mild, gingival inflammation (gingivitis)

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14
Q

shear mass of plaque is more geared toward what hypothesis?

A

non-specific plaque hypothesis

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15
Q

what does non-specific theory represent?

A

gingivitis

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16
Q

plaque hypothesis of periodontitis?

A

introduction of specific bacteria

-ecological plaque hypothesis – triggers some species to become more aggressive

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17
Q

late colonizers implication?

A

“red complex” – are associated with severe periodontal inflammtion

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18
Q

how does bacteria cause disease?

steps..7 total

A

when this sequence occurs…

  1. acquisition
  2. adherence or retention
  3. initial survival
  4. prosperity and long-term survival
  5. avoidance of elimination
  6. multiplication
  7. elaboration of virulence factors
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19
Q

vertical transmission

A

occurs at birth from parental and other environmental sources

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20
Q

endogenous organisms

A

those organisms already present within the host when the disease is developed

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21
Q

exogenous organisms

A

those acquired from other individuals or the environment which may initiate the disease process or enable its progression

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22
Q

main microbes in oral cavity and amount

A 
up to 10^3 bacteria per MILLIMETER. 
types 
- streptococci
- staphylococci
- Cornyebacteria
- Neisseria, 
-LActobacilli, 
- Candida -- note this is a fungus
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23
Q

important colonizer on the surface of teeth?what aids the growth of lactobacilli?

A

Streptococcus mutans is an important colonizer on the surface of the teeth (especially in those with a high sucrose diet)

when sugar is broken down – lactic acid— lowers pH in mouth and aids growth

  • usually above process done by streptococcus
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24
Q

streptococcus mutans importance in oral cavity and location?

A

mostly colonizers on the surface of the teeth and are more prevalent in patients that have a high sucrose diet and will break down this sugar and lactic acid will be produced– attacks surface

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25
Q

describe environment of sulcus

A

crevices – microenvironements with LOW levels or absnence of oxygen, thus favoring these anerobic microbes

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26
Q

normal oral flora

A

essential for life

  • collectively describes the various microbial types frequently found by culture or microscopy on the skin and mucous membranes and certain body cavities in normal healthy individuals
  • *****species and amount of flora vary in different areas of the body and at different stages of development

it is the foreign microbes that were responsible for infecting animals and humans and causing disease

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27
Q

when is oral cavity sterile?

A

during intrauterine life and at birth

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28
Q

within 4-12 hours of flora in development

A

lacotbacilli and streptocicci

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29
Q

first feeding implication on flora?

A

colonized from environment

see streptococcus salivarius, staphylococci, Niesseria, Moraxella eatarrhalis

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30
Q

what happens when switch to solid food?

A

microflora similar to parents

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31
Q

flora when teeth appear?

A

nondesquamating surface (so now a surface to attach to)

streptococci mutans, streptococcus parasanguis

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32
Q

flora in crevice area?

A

anaerobic species, yeasts

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33
Q

flora at puberty?

A

bacteroides, spirochetes

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34
Q

complexity of flora as you get teeth and change diet?

A

becomes more complex and more anaerobes become established

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35
Q

caries bacteria?

A

lactobaccilli

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36
Q

older age / loss of teeth effect on normal flora

A

flora becomes less complex

- less lactobacilli, strept mutans and yeast

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37
Q

when can you see an increase in yeast?

A

in complete dentures, and can also get an increase in strept mutans

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38
Q

bacterial flora around a dental implant?

A

bacterial flora around dental implants is similar to that found around natural teeth

39
Q

commensals?

A

describes the microorganisms present in the oral cavity

40
Q

physiological factors in a given area that effect flora?

A

Temperature
Moisture
Presence of nutrients

41
Q

3 main benefits of the normal oral flora

A
  1. occupy available colonization sites which makes it more difficult for other microorganisms (nonindigenous species) to become established (protective)
  2. host nutrition through the synthesis of vitamins and by contributing to immunity by inducing low levels of circulating and secretory antibodies that may cross react with pathogens
  3. production of fatty acids, peroxides, and bacteriocins which can exert microbial antagonism against other nonindigenous species)
42
Q

what do early colonizers produce? what does this allow/form?

A

EPS (exopolysaccharides) which will enable attachment / adherence
–> that will glue the cells to the surface and eventually form the biofilm matrix

43
Q

EPS composition?

A

Mainly polysaccharides but can also include proteins, nucleic acids, and plymeric lopiphilic compounds

represents the major structural component of biofilms

44
Q

biofilm function?

A

The development of a biofilm – ability for the prosperity/ long term survival

Responsible for the interaction of microbes with each other as well as with interfaces

bacteria in the biofilm are protected in this environment

think of these as ‘bacterial cities’

can get access to food and get rid of wastes

then ‘live in harmony’ with neighbors

45
Q

describe initial adherence between bacteria and non-living surfaces

A

mediated by non-specific – HYDROPHOBIC interactions

46
Q

describe adhesion to living surfaces

A

accomplished through specific molecular docking mechanisms

47
Q

adhesion/ retention during biofilm growth

A

mediated by specific ADHESINS – or cell surface modifications such as PILLI OR FIMBRAE

48
Q

coaggregation

A

development of mixed-species biofilms — genetically distinct bacteria together via specific molecules

49
Q

gingival crevicular fluid implication on survival of bacteria?

A

aids in initial survival

  • this fluid is a rich source of nutrients such as essential energy sources like GLUCOSE AND IRON.
  • also contains host-derived elements which can decrease bacterial survival such as antibodies and complement
50
Q

LPS is so important because?

A

essential for gram-negative bacteria to live

one of the most toxic substances we can administer to someone

51
Q

3 main
recognized by the AAP

NEED TO MEMORIZE

A
  1. Porphymonas gingivalis
  2. Tannerella forsythia (bacteriodes forsythus)
  3. Aggregatibacter (aa)

T. denticola – overwhelming evidence

52
Q

associated with bacteria chronic adult periodontisits

A

p. gingivalis is most known

53
Q

3 main
recognized by the AAP

NEED TO MEMORIZE

A
  1. Porphymonas gingivalis
  2. Tannerella forsythia (bacteroides forsythus)
  3. Aggregatibacter (aa) actinomycetemcomitans

T. denticola – overwhelming evidence

54
Q

p. ging. host invasion factors and produce?

A

aggressive and produce things that are toxic to host

acitvely attacking host tissues

produce gingipains

55
Q

Porphymonas gingivalis- describe colonization site

A

major site is subgingival pocket

  • surface adhesion molecules
  • some mobility

evidence that this causes chronic periodontitis

56
Q

Tannerella forsythia (bacteroides forsythus)

A

difficult to obtain from host (difficult to culture)

  • a gram - filament shaped, non-motile, non-pigmented oral bacterium
  • overall not well characterized

conversion of periodontally healthy sites into diseases sites and associated with ‘refractory’ periodontitis

57
Q

Tannerella forsythia (bacteroides forsythus)

A

difficult to obtain from host (difficult to culture)

  • a gram - filament shaped, non-motile, non-pigmented oral bacterium
  • overall not well characterized

conversion of periodontally healthy sites into diseases sites and associated with ‘refractory’ periodontitis

58
Q

refractory periodintitis

A

perio tx not working - like due to smoking and likely harbored larger amounts of Tannerella forsythia

59
Q

Aggregatibacter (aa) actinomycetemcomitans assoicated with?

A

AGGRESSIVE LOCALIZED PERIO

60
Q

aggressive localized perio main bacterium

A

Aggregatibacter (aa) actinomycetemcomitans

61
Q

what is unusual about Aggregatibacter (aa) actinomycetemcomitans complex/ profile

A

IT IS GREEN – not in the red orange complex

62
Q

what is unusual about Aggregatibacter (aa) actinomycetemcomitans complex/ profile

A

IT IS GREEN – not in the red orange complex

- growth is enhanced by the presence of CO2

63
Q

what does Aggregatibacter (aa) actinomycetemcomitans produce?

A

LEUKOTOXIN – so it actively attacks the white blood cells

64
Q

virulence factors of Aggregatibacter (aa) actinomycetemcomitans

A

major one is the leukotoxin

65
Q

T/F the oral flora is the usual cause of various oral diseases in humans, included abscesses, dental caries, gingivitis, and periodontal disease

A

TRUE

can even gain entrance into deeper tissues like bone, lung, brain, or extremities

66
Q

Quorum sensing

A

the ability to respond to products or signals from other biofilm organisms, or the host, and to use these to grow and prosper

  • contributing to the prosperity and long term survival of the bacteria
67
Q

what do you see in mature biofilms?

A

NICHES – complex architecture that provides niches with different physicochemical conditions, differing in oxygen availability, in concentration of diffusible substrates and metabolic side products, in pH, and in the cell density

  • cells in different regions of biofilm can exhibit different patterns of gene expression

-

68
Q

mixed species biofilms?

A

can contain niches with distinct groups of bacteria having metabolic cooperation

  • dynamic community with sharing of genetic matiera, competing, and cooperating
69
Q

key to avoidance of elimination? additional components to this

A

acterial capsules - facilitates this

+ some can undergo genetic drift and shift
so antigens mutate and antibodies can no longer recognize and bind to them

+sequester themselves within the host tissues

70
Q

use of antibiotics in chronic periodontitis?

A

counter- productive because by the time the active agent has penetrated the biofilm - its concentration is too low to be effective and resistant strains of bacteria can emerge

71
Q

multiplication for organisms? implication on survival?

A

essential for longer term survival

the pathogens need to reach a certain critical mass within the subgingival biofilm in order to survive

  • once this level is reached further multiplication beyond a certain threshold is required for disease to occur
72
Q

three categories of virulence factors

A
  1. enzymes
  2. metabolic waste products
  3. toxins
73
Q

definition of virulence?virulence correlates to what?

A

“full of poison”

    • molecules produced by a pathogen that SPECIFICALLY cause disease, or that influence their host’s function to allow the pathogen to thrive
    • ability of bacteria to cause disease in general terms of
      1. # of infecting bacteria
      2. route of entry into the body
      3. effects of host defense mechanisms
      4. intrinsic characteristics of the virulence factor

an organisms ‘power’ o produce disease

these are essential for the production of disease

74
Q

virulence factors are typically what structure?

coded for by?

A

proteins or molecules synthesized by enzymes of bacterial origin

proteins coded for by genes in chromosomal DNA bacteriophage DNA or plasmids

75
Q

virulence factor that is ‘constitutive’ vs?

A

expressed all the time vs others under specific environmental signals

76
Q

general methods by which pathogens cause disease

A
  1. adhesion
  2. colonization
  3. invasion
  4. immune response inhibitors – like producing proteins that bind to host antibodies
  5. toxins – proteins made by bacteria that poison host cells
77
Q

what allows for adhesion and colinixation

A
  1. fimbriae
  2. capsule
  3. microbial antagonisms/ synergy
78
Q

action of hyaluronidase

A

increases tissue permeability

79
Q

action of phospholipase A or C

A

induces prostaglandin - mediated bone resorption

80
Q

neurominidase action

A

enzyme that facilitates tissue spread of bacteria

81
Q

catalase action

A

decreases PMN peroxidase

82
Q

fibronylisis action

A

inhibits healing, allows tissue spread of bacteria

83
Q

what is responsible for odor and taste in periodontal disease

A

metabolic products of bacteria like

  1. hydrogen sulfide
  2. ammonia
  3. indole
  4. acids
84
Q

exotoxins

A

SOLUBLE PROTEIN EXCRETED BY A PATHOGEN

  • may be secreted or may be released during lysis of the cell
  • both gram negative and gram positive bacteria can produce these

causes damage to the host by destroying cells or disrupting normal cellular metabolism

85
Q

endotoxin definition?
differ from exotoxin?
in perio disease, endotoxins do what?

A

potentially toxic, natural compounds found inside pathogens

unlike an exotoxin – IS NOT SECRETED IN SOLUBLE FORM by live bacteria, but is a structural component in the bacteria which is released mainly when bacteria are lysed

in perio the endotoxin will

  • cause tissue damage
  • amplify the inflammatory response
86
Q

LPS in what? consists of ?

A

found in the OUTER MEMBRANE OF gram negative bacteria
- ENDOTOXIN - that can elicit a strong immune response

consists of lipid A and a polysaccharide (O-antigen) side chain joined by a covalent bond

the core is attached to lipid A

LIPID A is the key in the toxicity

87
Q

what do the the toxins stimulate in periodontal disease?

A

a chronic inflammatory response – which the body in essence turns on itself – attachment broken down and the epithelial attachment migrates APICALLY – forming pockets that are further colonized by bacteria

88
Q

what about P gingivalis is associated with eading/modulating the host response?
multiplying?
damaging and spreading?

A

Modulating –> Ig and complement proteases, LPS, capsule

Multiplying –> proteinases, hemolysins

Damaging host tissues and spreading –> proteinases - GINGIPAINS - collagenase, trypsin-like activity, fribrinolytic

89
Q

metabolic end products of p gingivalis?

A

include butyrate, propionate, and have low molecular weights which allows them to easily penetrate periodontal tissues and disrupt the hose cell activity

90
Q

Virulence of Tannerella forsythia

A

Virtually unknown

  • proteolytic enzymes, trypsin-like enzymes
  • sialidase (Neuraminidase)
91
Q

T.denticola?

A

commonly associated with periodontal disease with the other three
P. gingivalis
AA
Tannerella forsythia

92
Q

spirochetes

A

gram negative, anerobic, spiral, highly motile

associated with necrotizing periodontal disease and increased number of perio pockets

T. denticola is a common in diseased, SUBGINGIVAL SITES **

93
Q

Do periodontal bacteria physically invade host tissue in vivo?

A

controversal BUT NECROTIZING PERIODONTAL DISEASES has been comfirmed – invasion of spirochetes in NUG and NUP

Periodontology (20 decks)

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