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microbiology > oral bacteria B > Flashcards

oral bacteria B Flashcards

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1
Q

endo disease progression

A

carious lesion can infect or inflame pulp leading to abcess or inflammed ligament

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2
Q

Dentoalveolar infections

A

Pyogenic infections associated with the teeth and surrounding supporting structures

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3
Q

Bacteriology of root canal infections

A

Endodontic infections are endogenous infections that are opportunistic

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4
Q

most frequent spp of root canals

A

bacteroids and prevotella

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5
Q

Presentation of dentoalveolar infections

A
  • Abscess localized to tooth that initiated the infection
  • Diffuse cellulitis which spreads along fascial planes
  • Mixture of both
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6
Q

Dentoalveolar Abscess: routes of access to pulp/periapical tissue

A
  • Spread from carious lesion (1)
  • Tooth fracture/wear
  • Through periodontal membrane and accessory root canals (2)
  • Anachoresis (3) (via pulpal blood supply) during bacteremia from tooth extraction at different site
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7
Q

are dentoavleolar infections local or can they spread

A

Infection may remain localized or spread

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8
Q

O2 use of species commonly in abcesses

A

obligate or facultative anaerobes

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9
Q

spp commonly found at abcesses

A
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10
Q

Ludwigs Angina
spp involved?
risk?

A

A spreading, bilateral infection of the sublingual and submandibular spaces. Cellulitis of the fascial spaces rather than true abscess formation

Mixed endogenous infection:
Porphyromonas spp.
Prevotella spp.
Fusobacteria
Anaerobic streptococci

Airway obstruction - death by asphyxiation (without intervention)

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11
Q

Periodontal Abscess

species?

A

A localized collection of pus caused by acute or chronic destruction of the periodontium

Endogenous, subgingival plaque bacteria

Porphyromonas spp.
Prevotella spp.
Fusobacteria
Anaerobic streptococci

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12
Q

Suppurative Osteomyelitis of the Jaws

species

A

like abcess but involves bone

polymicrobial
Porphyromonas spp.
Prevotella spp.
Fusobacteria
Anaerobic streptococci
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13
Q

Cervicofacial Actinomycosis
presentation?
speceis?

A

endogenous, granulomatous disease
65% in cervicofacial region

Actinomyces (oral commensal)
visible granules in pus called sulphur granules = collections of bacteria

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14
Q

Oral manifestations of bacterial infections: diseases we have learned

A

syphilis
leprosy
tuberculosis

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15
Q

Syphilis oral manifestations

A

congenital: Hutchinson’s incisors, mulberry molars
primary and secondary syphilis lesions
gummas (granulomatous lesions)

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16
Q

Tuberculosis oral manifestations

A

– oral lesions in up to 5% of primary and secondary tuberculosis cases ulcers on palate and gingiva

17
Q

Leprosy oral manifestations

A

many

18
Q

Bacterial infections of salivary glands involves what spp often?

A

– often Staphylococcus

19
Q

Diseases or situations associated with

oral bacteria or their components:

A 
Infective endocarditis
Disseminated intravascular coagulation
Nephritis
Rheumatoid arthritis
Behçets disease (chronic inflammatory disorder with oral ulcers)
Atherosclerosis
Low-birth-weight infants
20
Q

how could oral bacteria cause infection elsewhere

A

altered metabolism/ gene expression when in a new environment, possible that a certain gene could be pathogenic elsewhere in body

21
Q

Infective endocarditis

spp

A

streptococci from oral
damaged heart valves will have platelets bound
streptococci posses PAAP/ adhesins to bind these platelets
PAAP induces additional platelets to adhere via cross linking with fibrinogen
leukocytes may accumulate on the septic thrombus and induce an inflammatory response

22
Q

Other possible associations between oral microbes and systemic disease

A

HSPs and Autorecognition induced by oral microorganisms

23
Q

Heat shock proteins (HSPs) and systemic disease

A

Microbial HSPs are very similar to human HSPs that are normally shielded within cells.

Antibodies elicited by bacterial HSPs can cross-react with exposed human HSPs (e.g. present in damaged tissue).

If immune complexes are deposited in the arterial wall (atherosclerosis), joints(arthritis), or mucous membranes (Behçets disease), HSP mimicry can contribute to systemic disease.

24
Q

Autorecognition induced by oral microorganisms and systemic disease

A

Streptococcus sanguinis express an epitope within PAAP which is similar to the arthritogenic epitope of type II collagen.

In a murine arthritis model, S. sanguinis infection exacerbates arthritis.

Interestingly, exposure of neonatal mice to PAAP+ S. sanguinis inhibited development of autoimmune arthritis in the adult (early exposure protective?).

25
Q

how local inflammation with oral microbes can cause systemic pathology

A

gram - bac produce toxins to/LPS to diffuse into gingiva causing local response
Macrophages take up these toxin and produce TNF a and IL-1B, enter sys circulation
this induces the liver to produce acute-phase proteins (CRP)
TNF and IL-1B can also act on atherscerltoic lesions, exacerbating them

26
Q

mucosal barrier for oral defense

A

Contains Toll-like receptors: TLRs recognize PAMPs

27
Q

TLR of oral mucosa

A

TLR 2, 4, 6, 10

28
Q

TLR2

A

peptidoglycan

29
Q

TLR4

A

LPS, lipoteichoic acid

30
Q

TLR6

A

LPS

31
Q

TLR10

A

LPS

32
Q

defensins of the oral surface (tooth/mucosa)
main one?
why bacteria would be susceptible?

A

Small peptides (proteins) that form pores in bacterial membranes, disrupting cells.

HBD-1 (human b-defensin 1) is the main defensin produced by epithelial cells.

Bacterial membranes are susceptibledue to their high phospholipid content.

33
Q

Adherent mucin layer or oral surfaces

A

Mucins attached to mucosal surface form a selectively permeable layer (a mucus coat analogous to a bacterial capsule).

Mucins are glycoproteins and carbo-hydrates portion form a sticky slippery gel.

MG1 and MG2 are mucins in oral cavity

34
Q

Commensal oral microbiota as a defense

A

tooth surfaces and mucosa
Endogenous bacteria keep out new bacteria, and the stimulate immune system. But
they can cause disease when the balance shifts.

35
Q

fluid of oral defense

main components

A

Fluid phase: saliva=0.5 - 1.5 liters per day secreted into the mouth

Mucins: MG1 and MG2 aggregate and clear oral microbes via lectin-like interactions.

Lysozyme: Degrades peptidoglycan by cutting bond between NAG and NAM (muramidase)

36
Q

Acquired specific immunity of oral cavity mediated by?

A

mediated by S-IgA

37
Q

Mucosal lymphocytes

A

Lamina propria lymphocytes = resting memory cells awaiting reexposure; their role upon
reexposure is mainly cytokine production

Intraepithelial lymphocytes: surveillance for pathogens and removal of stressed and infected
epithelial cells

38
Q

GCF

A

GCF flushes gingival crevice, removing microbes and products. Health vs inflammation: more
serum-like composition during inflammation (vs tissue-like composition)

IgG, IgA, and IgM

GCF is major source of leukocytes in oral cavity: 95% are neutrophils

microbiology (42 decks)

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