(B) Lecture 19: Streptococcus pyogenes Flashcards

1
Q

Streptococci

A
  • gram-POSITIVE
  • coccus shaped
  • grows in chains (bent or twisted)
  • hemolysis on blood agar
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2
Q

Alpha hemolysis

Streptococci

A
  • green colour
  • PARTIAL hemolysis of blood
  • S. pneumoniae

Viridans group includes:
- S. viridans: endocarditis (invades blood + causes heart problems)
- S. mutans: tooth decay
- S. thermophilus: dairy foods

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3
Q

Beta hemolysis

Streptococci

A
  • COMPLETELY lysing hemoglobin
  • S. pyogenes (Group A streprococcus)
  • S. agalactiae (Group B streptococcus)
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4
Q

Gamma hemolysis

Streptococci

A

NO hemolysis

  • Enterococcus species (Group D streptococcus)
  • Lactococcus lactis (Group N streptocous) - another dairy organism
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5
Q

Lancefield classification

A

classified on basis of surface carbohydrate antigens

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6
Q

Streptococcus pyogenes

A
  • human-specific pathogen
  • 5-15% asymptomatic carriage
  • extracellular pathogen (pyo = pus)
  • major cause of scarlet fever, puerperal sepsis and wound infections
  • today a common cause of pharyngitis (strep throat) + impetigo
  • also causes severe invasive streptococcal disease and streptococcal toxic shock syndrome (“flesh-eating”)
  • important cause of “post infection sequelae” like acute rheumatic fever
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7
Q

S. pyogenes virulence factors

A
  • M protein
  • Hyaluronic acid capsule
  • Hemolysins
  • Superantigens
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8
Q

M protein

S. pyogenes

A
  • main hallmark
  • PROTECTS BACTERIA FROM COMPLEMENT SYSTEM
  • anti-phagocytic cell surface protein
  • binds C4 binding protein of host = protects bacteria from complement
  • however, if you have antibodies to a specific M protein serotype, you will opsonize + kill the bacteria
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9
Q

Hyaluronic acid capsule

S. pyogenes

A
  • polysaccharide
  • hyaluronic acid is major component of host tissue - bacteria looks like self
  • can’t make a vaccine against it b/c it would target self cells
  • can also block opsonization through C3b
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10
Q

Hemolysins

A

S. pyogenes makes 2 hemolysisn

Streptolysins: O and S
- streptolysin S produces beta hemolysis
- streptolysin O is O2 sensitive

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11
Q

Streptolysin S

A

produces beta hemolysis

makes capsule and clears around itself using hemolytic toxin

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12
Q

Superantigens

A
  • secreted exotoxins
  • Streptococcal Pyrogenic Exotoxins (Spe’s) = induces fevers
  • act as potent T cell activators
  • can result in cytokine storm and lead to toxic shock syndrome
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13
Q

Pharyngitis

A
  • most common in school-aged children and teenagers
  • fevers and severe sore throat
  • absence of cough
  • swollen cervical lymph nodes
  • tonsillar exudate (pus)
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14
Q

Diagnosis and treatment of pharyngitis

A

Diagnosed by rapid strep test
- looking for group A carb antigen
- positive test = strep throat –> antibiotics
- negative test –> throat culture

Treated with antibiotics
- beta-lactams (no documented resistance) – ex. amoxicillin
- erythromycin (resistant strain) - for ppl allergic to penicillin

Untreated pharyngitis = acute rheumatic fever

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15
Q

Impetigo

A
  • common among children
  • caused by Staphylococcus aureus
  • superficial skin infection
  • red sores that form crusts, usually on face
  • highly contagious thru direct contact
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16
Q

Scarlet Fever

A
  • rash develops during strep throat
  • high fever, strawberry/red tongue
  • rash - small red bumps (rough sandpaper feel)
  • toxin-mediated caused by scarlet fever toxins (same toxins as S. pyogenic exotoxins)
17
Q

Rheumatic Fever

A
  • “post-infection” sequelae
  • caused by AUTOIMMUNE response
  • 2-3 weeks after infection
  • autoimmunity caused by antibody cross-reactivity w/ M protein
  • acute rheumatic fever = initial inflammation can cause swollen joints
  • rheumatic heart disease = damaged heart valves

Rare in high-income countries but endemic in low resource settings

18
Q

Invasive streptococcal disease

A

Invasive: able to isolate organism from usually sterile site

  • rare in developed countries
  • blood isolation –> bacteremia

Flesh eating disease
- soft tissue involved = necrotizing fasciitis
- muscle involved = necrotizing myositis
- streptococcal toxic shock syndrome

19
Q

Risk factors for invasive streptococcal disease

A
  • tissue injury (bruise or penetrating)
  • chicken pox in kids (lesions allow entry)
  • postpartum
  • lack of immunity to superantigens and M protein
  • MHC class II haplotypes (superantigen receptors) - wrong set of MHC class II and superantigen binding well = more likely to develop
20
Q

Treatment of invasive streptococcal disease

A
  • antibiotics (protein synthesis inhibitors)
  • debridement/amputation
  • IVIG (neutralize superantigen activity + opsonizes S. pyogenes)
21
Q

Superantigen-mediated T cell activation

A

Superantigen is not processed by APC like conventional binding

Superantigen wedges receptor apart
- T cell can’t recognize antigen and becomes independent of antigen
- superantigen causes activation of huge number of T cells = cytokine storm
- superantigen binds directly to MHC class II and not APC

22
Q

Mouse model of S. pyogenes

A

S. pyogenes is human-specific pathogen

Superantigens do NOT bind well to mouse MHC class II

Without SpeA = barely infect
Without all superantigens = bacteria can’t infect

23
Q

Induced rheumatic heart disease

A
  • Mitral valve is mostly targeted w/ rheumatic heart disease
  • Left ventricle pumps most blood

Control = no infection

WT (fully-loaded pathogen) = heart impaired
- drop in EF and raise in E/A ratio
- LV can’t push out as much blood

No M protein = no infection

24
Q

Ejection fraction

A

how much blood heart can pump out every LV contracts

25
Q

Important contributors to S. pyogenes

A
  • MHC Class II
  • Superantigens act as colonization factors (should be considered for vaccines)
  • M protein is an important virulence factor for experimental rheumatic heart disease
26
Q

Important virulence factors of Rheumatic heart disease

A

M protein is an important virulence factor

M protein knocked out = no reduction in EF and no increase in E/A ratio
- nor as effective at infection