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Human Microbial Diseases Block 1 > Group A Streptococcus > Flashcards

Group A Streptococcus Flashcards

1
Q

What do alpha-haemolytic streptococci do on blood agar?

A

Incompletely breaks down blood and so have a greenish hue around the colonies

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2
Q

What do beta-haemolytic streptococci do on blood agar?

A

Completely breakdown blood and so have a zone of clearance around colonies

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3
Q

What do gamma-haemolytic streptococci do on blood agar?

A

They don’t breakdown blood

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4
Q

Is Streptococcus pyogenes alpha, beta or gamma haemolytic?

A

Beta haemolytic

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5
Q

What is the main disease caused by Streptococcus pyogenes?

A

Uncomplicated pharyngitis

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6
Q

What type of pathogen is a group A Streptococcus?

A

Strict human pathogen

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7
Q

What are the non-invasive GAS infections?

A
  • Pharyngitis
  • Scarlet fever
  • Impetigo
  • Otitis media
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8
Q

What are the severe invasive GAS infections?

A
  • Meningitis
  • Puerperal fever
  • Septicaemia
  • Necrotising faciitis
  • Toxic shock syndrome
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9
Q

Describe necrotising faciitis

A
  • Post pharyngitis or direct inoculation
  • Toxin mediated
  • Rampant unfettered tissue damage, vascular dissemination and systemic disease
  • High morbidity and mortality
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10
Q

Describe acute rheumatic fever

A
  • Non-suppurative sequelae
  • Potential sequelae to pharyngitis
  • 4-8 weeks post infection
  • Inflammation of the heart and joints
  • Leading cause of preventable heart disease in IUDCs
  • Can recur and cause permanent damage to heart valves
  • Caused by rheumatogenic strains
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11
Q

Describe acute glomerulonephritis

A
  • Non-suppurative sequelae
  • Post pharyngitis or skin infection
  • Few weeks post infection
  • Get haematuria, proteinuria, hypertension and impaired renal function
  • Complications are rare and not usually recurrent
  • Most people thought to make a full recovery however, a risk factor for chronic kidney disease and end stage renal failure
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12
Q

How is GAS transmitted?

A

Primarily transmitted person to person but there have been numerous reports of food-borne cases

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13
Q

Where are GAS carried?

A
  • Nasopharyngeal mucosa -> challenging niche
  • Skin
  • Vaginal tract
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14
Q

What are the primary reservoir of GAS?

A

Humans

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15
Q

Is carriage required for disease?

A

No

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16
Q

What do GAS rely on to survive in saliva?

A

Amylase as saliva is a carbohydrate-limited environment

17
Q

Describe the adherence mechanism of GAS

A
  • Lipoteichoic acid establishes weak attachment between bacteria and host
  • Long surface attachment mediated by longer pili like structures and other surface fibronectin binding proteins and the M protein
  • Allows higher affinity attachment by numerous protein adhesins that permit bacterial interactions with multiple host components allowing GAS to colonise diverse tissue sites in the human body
  • Many of the cell surface adhesions are also involved in internalisation into epithelial cells
18
Q

How does M protein act as a virulence factor of S. pyogenes?

A
  • Enables GAS to resist complement-mediated killing by polymorphonuclear leukocytes and macrophages -> protects against phagocytosis
  • Required for attachment of the GAS to keratinocytes -> critical role in infections initiated at the skin surface
  • Causes GAS to aggregate when they attach to tonsillar epithelial cells -> critical role in initiation of colonisation of the respiratory mucosa
19
Q

What virulence factors are involved in spread and avoidance?

A
  • Hyaluronidase is involved in spread as it digests connective tissue as well as its own capsule
  • Streptokinase is involved in spread and possibly colonisation of the nasopharynx
  • Streptococcal pyrogenic exotoxin B degrades host and GAS factors and degrades host antimicrobial peptides
  • DNase degrades host protective neutrophil extracellular traps
  • Capsule disguises GAS and is antiphagocytic
  • M protein is antiphagocytic and anticomplement
  • Streptococcal inhibition complement is involved in avoidance
  • Streptococcal C5a peptidase is involved in avoidance
  • Mac1/IdeS is involved in avoidance
20
Q

What virulence factors are involved in resisting the immune system?

A
  • M protein inhibits complement binding
  • Capsule shields bacteria by molecular mimicry, blocks antibody access, inhibits complement deposition and enhances survival of NETs
  • Secreted proteases inhibit phagocyte recruitment, blocks phagocytosis and impairs recruitment by degrading cytokines
  • Antimicrobial peptide resistance is mediated by the capsule, SIC binding and SpeB
  • Degradation of NETs is mediated by Sda1 DNase
  • Lysis and apoptosis of neutrophils and macrophages is mediated by the cytolysins SLS and SLO
21
Q

What virulence factors cause damage?

A
  • Streptolysins (SLS) and SLO are pore forming cytotoxins
  • Spe A, B and C are superantigens
  • Secreted streptococcal carboxylic esterase contributes to invasive disease
  • Streptococcal pyogenes cell envelope proteinase cleaves cytokines
  • SlaA is a phospholipase
  • SSE and SlaA are secreted and diffusely damage heart tissue
  • SLS, SLO, Spe A, B and C and SpyCEP are cell localised
22
Q

What happens in toxic shock syndrome?

A
  • Release of elevated levels of inflammatory cytokines
  • Cytokine storm
  • Vascular leakage
  • Coagulation
  • Circulatory collapse
  • Organ failure
23
Q

What are superantigens?

A

Potent immuno-stimulatory molecules

24
Q

What do superantigens activate?

A

Bind TCR irrespective of its antigenic specificity and so activates a large number of T cells of different antigenic specificity

25
Q

Describe rheumatic fever

A
  • Associated with rheumatogenic strains
  • Molecular mimicry
  • Cross reactive immune response to Streptococcal antigen and cardiac tissue
  • Driven by a superantigen?
26
Q

What type of reaction is post streptococcal acute glomerulonephritis fever?

A

Type III hypersensitivity reaction

27
Q

What is the evidence that post streptococcal acute glomerulonephritis fever is a type III hypersensitivity reaction?

A
  • Occurs 1-6 weeks post GAS infection
  • High antibody titres
  • Deposits of IgG complexes containing GAS antigens

Human Microbial Diseases Block 1 (7 decks)

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