Pathogenesis of Streptococci Flashcards

1
Q

How are Streptococci Identified?

A

Through lancefield grouping

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2
Q

List the different groups of strep with an example, area of infection and disease caused

A

Group A: S pyogenes, Skin/throat, many
Group B: S algalactiae, Female GT/GIT, Neonatal meningitis
Group D: Enterococcus, Oral/GIT/Female GT, UTI/endocarditis

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3
Q

What form of haemolysis is Group A strep? what are some characteristics

A

B Haemolytic
Pyogenic (pus forming)
Sensitive to bacitracin

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4
Q

What are 2 examples of respiratory infections and skin infections caused by Strep

A

Respiratory infections:
Acute pharyngitis (strep throat)
Scarlet fever

Skin infections:
Impetigo
Erysipelas
Cellulitis
necrotising fascilitis
Toxic shock syndrome
Acute rheumatic fever
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5
Q

Explain sequelae of skin or throat infections with strep

A

Acute glomerulonephritis may occur which may result in kidney failure

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6
Q

Explain what hyaluronic acid capsules are and their purpose (strep)

A
  • causes bacteria to look mucoid in appeatance
  • varies slightly strain to strain
  • anti-phagocytic properties (interference with the interaction of bound C3b complement with phagocytes, non-immunogenic)
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7
Q

How are M-proteins able to bind to many mammalian proteins (strep)

A
  • Fibrogen (adhesion by forming complex to adhere to platelet
  • Serum albumin (masking of bacteria, bacteria looks like host protein, able to bind to Fc region of IgG)
  • Factor H (regulatory protein for alternative complement pathway, complement C3b mediator and degrades it, prevents completion of complement cascade)
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8
Q

What does an M-protein look like under an electron micrograph (strep)

A

Appears as har like structures

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9
Q

What are the 3 regions of M-proteins (strep)

A
  • A repeat (high variability)
  • B repeat (High variability)
  • C repeat (Highly conserved)
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10
Q

How many M-protein sero-types are there? How are they defined (strep)

A
  • > 80

- Based on difference in A and B regions

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11
Q

Not all M proteins exhibit the same function, which M proteins bind fibronectin and which do not? (strep)

A
  • M3 binds fibronectin

- M5 and M24 do not bind Fibronectin

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12
Q

What gene encodes M proteins (strep)

A
  • Emm genes
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13
Q

How many bp and amino acid residues are in M1? (strep)

A
  • 1452 bp

- 482 amino acid residues

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14
Q

Explain the gene structure of M proteins (strep)

A
  • 1-3 emm proteins in tandem
  • 4 subfamilies (SF1-SF4) with 3’ end conserved
  • 5 pattern (A-E) (content and arrangement)
  • Serotype determinant (5’ end variable region, Emm types >150)
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15
Q

What are the 3 steps in basic mechanisms of pathogenesis (strep)

A
  1. Invade and spread through tissue
  2. Production of toxins
  3. Provoke an autoimmune response
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16
Q

Explain how Strep invades tissue

A
  • bind to extracellular matric components or specific receptors
  • M protein attaches to keratinocytes in skin infection, delete C1 and C2 repeats, membrane cofactor protein CD46 is the receptor for M protein
  • Many other adhesions
17
Q

Explain how strep evades phagocytic cells

A
  • evades recognision through proteases
    • protect strep from interacting with phagocytic cells by using C5a peptidase (serine protease which degrades C5a, a complement component that recruits and activates phagocytic cells)
18
Q

How does Strep spread in tissue?

A
  • secrete digestive enzymes
  • Pus from strep is thin and runny because DNA and gibrin are degraded
  • Streptokinase activates protein plasminogen to plasmin which dissolves fibrin clots. 2 types (SLO and SLS), SLO is oxygen sensitive and enhances haemolysis under anaerobic conditions, SLS is oxygen stable and is non immunogenic
19
Q

What are the hallmarks of toxin mediated disease?

A
  • Damage at sites distinct from primary site of infection
20
Q

How can strep produce toxin mediated disease?

A
  • exotoxins (Strep pyrogenic exotocins SPE, Spe A-J excluding D,E,I)
  • superantigens stimulate T cell proliferation (up to 20%)
  • also induce release of cytokines leading to inflammation and septic shock
  • responsible for the rash in scarlet fever as it has a direct effect on the capillary bed
21
Q

What are the hallmarks of autoimmune based disease

A
  • unrelated disease post infection e.g. rheumatic fever
22
Q

How can strep produce autoimmune based disease?

A
  • antigenic mimicry (strep antigens hsare epitopes with human tissues, antibodies cross react with host tissue leading to damage)
23
Q

Explain autoimmunity and molecular mimicry in regards to rheumatic fever (strep)

A
  • autoantibodies against the heart is associated with rheumatic fever
  • Monoclonal antibodies identifies myosin as the autoantigen in the heard
  • M protein antibodies cross react with myosin: M5, M6
24
Q

Explain molecular mimicry in glomerulonepghritis (strep)

A
  • less certain of its role
  • glomerular basement membrane shares antigen with M12 protein
  • Mab against glomeruli reacted with M12 protein