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Microbiology > Oral Bacteria B > Flashcards

Oral Bacteria B Flashcards

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1
Q

Dentoalveolar infections

A

Pyogenic infections associated with the
teeth and surrounding supporting
structures

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2
Q

Bacteriology of root canal infections

A

Endodontic infections are endogenous infections

that are opportunistic

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3
Q

Dentoalveolar Abscess (4)

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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4
Q 
bacteria commonly isolated from dentoalveolar abscesses
Facultative anaerobes (2)
Obligate anaerobes (4)
A

Streptococcus
Actinomyces spp.

Peptostreptococcus spp.
Porphyromonas gingivalis
Prevotella
Fusobacterium nucleatum

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5
Q

Ludwigs Angina (2)

A

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

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6
Q

Mixed endogenous infection: (4)

A

Porphyromonas spp.
Prevotella spp.
Fusobacteria
Anaerobic streptococci

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7
Q

Airway obstruction -

A

death by asphyxiation

without intervention

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8
Q

Periodontal Abscess

A

Localized collection of pus caused by acute or chronic destruction of periodontium
Endogenous, subgingival plaque bacteria
polymicrobial

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9
Q

polymicrobial (4)

A

Porphyromonas spp.
Prevotella spp.
Fusobacteria
Anaerobic streptococci

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10
Q

Suppurative Osteomyelitis of the Jaws

A

Same organisms as above but involves bone

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11
Q

Cervicofacial Actinomycosis

A 
endogenous, granulomatous disease
65% in cervicofacial region
Actinomyces (oral commensal)
visible granules in pus
sulphur granules
= collections of bacteria
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12
Q

Syphilis –

A

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

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13
Q

Tuberculosis –

A

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

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14
Q

Leprosy -

A

For leprosy just know there are

many oral manifestations

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15
Q

Bacterial infections of salivary glands – often

A

Staphylococcus

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16
Q

Diseases or situations associated with

oral bacteria or their components: (7)

A 
Infective endocarditis
Disseminated intravascular coagulation
Nephritis
Rheumatoid arthritis
Behçets disease (chronic
inflammatory disorder with oral
ulcers)
Atherosclerosis
Low-birth-weight infants
17
Q

Infective endocarditis

A

FIGURE 4 Platelet streptococcal interactions in infective endocarditis. Circulating
platelets adhere to collagen exposed on damaged heart valves. During polymicrobial
bacteremia, oral streptococci bind to the activated adherent platelets through expressed
adhesins and PAAP. PAP activates and induces additional platelers to aggregate on the
heart valve. Aggregation requires the cross-linking of platelets to one another by fibrin-
gen molecules. The fibrinogen molecules are polymerized into fibrin by thrombin,
forming an insoluble thrombus or platelet clot. Released plateler granules contain
innate antimicrobials, including platelet microbicidal protein, which may limit the
valvular infection by sensitive bacteria. Leukocytes accumulate on the exterior of the
septic thrombus as an inflammatory response is initiated.
PAP = platelet aggregation-associated protein = Streptococcal surface protein (adhesio)

18
Q

Other possible associations between oral microbes

and systemic disease (2)

A

Heat shock proteins (HSPs)

Autorecognition induced by oral microorganisms

19
Q

Heat shock proteins (HSPs)

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.

20
Q

Autorecognition induced by oral microorganisms

A

Streptococcus sanguinis express an epitope within PAAP (plateletaggregation associated protein), 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?)

21
Q

Inflammation -
a link between local
dental disease and
systemic pathology?

A

FIGURE 5 How oral microbes produce local inflammation to influence systemic
pathology. In the gingival sulcus, bacteria and their PA.MPs such as LPS affect under-
lying tissues, causing local inflammation. High levels of the inflammatory mediators
TNF-a and IL-1ß may enter the circulation and induce the liver to produce acure-
phase reactants, such as CRP. IL-1ß and TNF-a may also act on monocytes in exist-
ing atherosclerotic plaques, causing exacerbation of existing disease.
(PAMPs = pathogen associate molecular patterns)

22
Q

Innate host defenses

A

Oral surfaces
The mucosal barrier
Contains Toll-like receptors

23
Q

TLRs recognize

A

PAMPs (PathogenAssociated Molecular Patterns)

24
Q

TLR2

A

peptidoglycan

25
Q

TLR4

A

Lipopolysaccharide, lipoteichoic acid

26
Q

TLR6

A

Lipopolysaccharide

27
Q

TLR10

A

Lipopolysaccharide

28
Q

Innate host defenses
Oral surfaces
Defensins

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 susceptible
due to their high phospholipid content.
29
Q

Innate host defenses: Oral surfaces

Adherent mucin layer

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.
30
Q

Innate host defenses: Oral surfaces

Commensal oral microbiota (including on tooth surfaces)

A

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

31
Q

Innate host defenses

Fluid phase: saliva

A

0.5 - 1.5 liters per day secreted into the mouth

32
Q

Innate host defenses
Fluid phase: saliva
Mucins

A

MG1 and MG2 aggregate and clear oral

microbes via lectin-like interactions.

33
Q

Innate host defenses
Fluid phase: saliva (continued)
Lysozyme

A

Degrades peptidoglycan by cutting bond

between NAG and NAM (muramidase)

Microbiology (42 decks)

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