microbiol 2 Flashcards

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1
Q

Name some oral defences we have

A
  1. Saliva2. GCF3. Epithelial barrier 4. Neutrophils
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2
Q

What does saliva contain that makes it part of our oral defence system?

A
  1. IgA2. Mucins 3. Lysozymes 4. Lactoferrin5. Histatins 6. Defensins 7. Protease
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3
Q

What does GCF contain that makes it part of our oral defence system?

A
  1. IgG2. IgA3. IgD4. Complement 5. PMNs 6. Defensins
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4
Q

How is our epithelial barrier an oral defence mechanism?

A

Epithelial barrier cells detect invading pathogens

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5
Q

Describe neutrophils

A

Neutrophils have many nuclei & many granules stuffed with antimicrobials

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6
Q

What happens when neutrophils die?

A

If neutrophils die (lysed by bacteria) they release granules that cause damage to bacteria & host

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7
Q

What do organism on the tooth surface produce when they die?

A

They produce enzymes, metabolites, cell constituents when die These activate signalling pathways releasing pro inflammatory cytokines, chemokines and antimicrobials

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8
Q

In disease why does destruction occur?

A

Destruction occurs due to uncontrolled response to enzymes when tooth surface organisms die

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9
Q

Go through the stages of microbial pathogenesis

A
  1. Entry2. Attachment3. Multiplication 4. Avoiding host defences5. Causing host damage6. Releasing & spreading
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10
Q

What are virulence factors

A

Virulence factors are molecules produced by bacteria, viruses, fungi, and protozoa that add to their effectiveness to incur damage on the host cell

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11
Q

Name the 5 bacterial virulence factors associated with periodontal disease

A
  1. Adhesins 2. Invasins 3. Impedin4. Agressin 5. Modulin
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12
Q

What do adhesins do?

A

Enables binding to host tissues

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13
Q

What do invasins do?

A

Enables invasion of host cell/ tissue

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14
Q

What do modulins do?

A

Induces indirect damage by perturbing regulation of host defences

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15
Q

What do aggressins do?

A

causing direct damage to host

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16
Q

What so impedins do?

A

Enables avoidance of host defence mechanism(s)

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17
Q

Name some cellular virulence factors

A
  1. Capsule 2. Fimbriae/pilli 3. Flagellum
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18
Q

How does the capsule act as a cellular virulence factors?

A

Acts as K antigen: the Immune response stimulated against capsule Capsules help with adhesionCapsule incur resistance to killing by neutrophils & complement

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19
Q

How does the frimbriae act as a cellular virulence factors?

A

Act as receptors (adhesive characteristics)| Promotes gene transfer (resistance genes)

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20
Q

How does the flagellum act as a cellular virulence factors?

A
  1. Act as an H antigen which leads to an Immune response stimulated against Flagellum2. Allows mobility of the bacterium
21
Q

Describe the cell wall of a gram positive bacteria

A

Has a thick peptidoglycan layer, teichoic and lipoteichoic acid associate with this layer

22
Q

How does the thick peptidoglycan layer (Teichoic/lipoteichoic acids) in gram positive cell walls help it to invade the host?

A
  1. Helps in adhesion 2. Induces cytokine release3. Acts in aiding resistance to host defences
23
Q

What do gram negative bacteria have that gram positive bacteria don’t ?

A

Has lipopolysaccharide in its cell wall that have a variety of virulence factors

24
Q

What does the lipopolysaccharide act as in gram negative bacteria?

A

Acts as an O antigen

25
Q

How does the lipopolysaccharide in gram negative cell walls help it to invade the host?

A
  1. Stimulates cytokine release and inflammatory response 2. Resistant to host defences 3. Mediates adhesion 4. Promotes bone loss 5. Kills macrophages
26
Q

What is increased inflammation associated with?

A
High GCF flow Bleeding Raised pH Raised temperature Low Eh (redox potenital)
27
Q

Which enzymes do bacteria produce to damage the host?

A
  1. Proteases2. Collagenases 3. Fibrolysin, Hyaluronidase, Heparinise 4. IgA & IgG proteases
28
Q

What does bacteria produced proteases do?

A

Causes direct damage to tissue or host defences

29
Q

What does bacteria produced collagenase do?

A

Breaks down the PDL

30
Q

What does bacteria produced Fibrolysin, Hyaluronidase and Heparinise do?

A

Breaks down host proteins

31
Q

What do bacteria produced IgA and IgG proteases do?

A

Breaks down immunoglobulins

32
Q

Name some extracelluar virulence factors?

A
  1. Enzymes 2. Leukotoxins 3. Cyrotoxins
33
Q

What do Leukotoxins do?

A

Kill neutrophils

34
Q

What do cytotoxins do?

A

They are specific toxins that are released by bacteria that can lead to cell death

35
Q

Name the bacteria associated with localised aggressive periodontitis?

A

Aggregatibacter actinomycetemcomitans

36
Q

What do Aggregatibacter actinomycetemcomitan target?

A

The target neutrophils and causes functional abnormalities in them

37
Q

How do Aggregatibacter actinomycetemcomitans cause functional abnormalities in neutrophils?

A
  1. It affects the signal pathways promoting responses of neutrophils 2. Decreases the number of chemotaxis so neutrophils don’t move to the site 3. They increase the number of superoxide radical causing tissue damage
38
Q

What type of Aggregatibacter actinomycetemcomitans is most common in localised periodontitis out of the 6 ?

A

Serotype B

39
Q

What are some virulence factors of Aggregatibacter actinomycetemcomitans ?

A
  1. Potent leukotoxin which are toxic to neutrophils2. Cytolethal descending toxin which are toxic to lymphocytes 3. Produce a range of adhesions 4. Lipopolysaccharide and cell material which lead to bone resorption 5. Produces Collagenase which breaks down the PDL
40
Q

Describe Porphyromonas Gingivalis

A

It is an obligate anaerobe| It is a gram negative bacteria
Black-pigmented

41
Q

What are some of the virulence factors of Porphyromonas Gingivalis?

A
  1. Arg Gingipain & Lys Gingipain2. Lipopolysaccharide and Fimbriae present which acts as an adhesin3. Has a capsule the helps resist host defences 4. Produces Haemagglutinin which causes red blood cells to stick5. Has extracellular vesicles which is packed with enzymes
42
Q

How does Porphyromonas Gingivalis manipulate the host defences?

A
  1. Results in s local chemokine paralysis in the epithelium so neutrophils are not attracted 2. It inhibits a particular receptor (E-Selectin) which Affects neutrophil migration 3. Inhibits complement activation 4. Disrupts the immune regulation5. Causes Subversion of Toll like receptors (particular TLR 2 & TLR 4) 5. Causes Direct cytotoxicity6. Causes Citrullination which Changes the immune response
43
Q

What is citrullination?

A

Results in the altering of protein shape by adding small group

44
Q

How does P. Gingivalis act as a keystone periodontal pathogen?

A

P. Gingivalis elevates the virulence of the whole community by communicating with streptococci It impairs the Host immune system & the dysbiotic community inc in number, eventually disrupts tissue homeostasis causing perio tissue destruction

45
Q

What is Homeostatic balance between in health?

A

immunostimulatory and immunosuppressive commensal organisms

46
Q

Toll like receptors

A

Receptors on/in epithelial cells and immune cells, which detect microbial components and initiate cellular response pathways

47
Q

What does A. actinomycetemcomitans leukotoxin and cytolethal distending toxin cause?

A

local “immune paralysis” and allow overgrowth of other organisms that increase in prevalence with disease.

48
Q

Functions of P. gingivalis GINGIPAINS

A

Ø Cleavage of host defence peptides, complement, Ig
Ø Cleavage of cell receptors e.g. CD14
Ø Degradation of cytokines, chemokines, plasma protease inhibitors
Ø Activation of Protease Activated Receptors, ­ IL-6 (cytokine)
Ø Activation of matrix metallo-proteinases (MMPs) and degradation of tissue inhibitors of MMPs (TIMPs)
Ø Immune evasion
Ø Nutrition (especially haem release from haemoglobin)

49
Q

Allocate each of the following to category/categories of virulence factor (adhesin, invasin, impedin, aggressin, modulin)

A

• Collagenase- aggressin
• IgG protease- impedin, modulin
• Capsule- adhesin, impedin
• Lipopolysaccharide- adhesin, impedin, modulin
• Leukotoxin- aggressin, impedin, modulin