What do alpha-haemolytic streptococci do on blood agar?
Incompletely breaks down blood and so have a greenish hue around the colonies
What do beta-haemolytic streptococci do on blood agar?
Completely breakdown blood and so have a zone of clearance around colonies
What do gamma-haemolytic streptococci do on blood agar?
They don’t breakdown blood
Is Streptococcus pyogenes alpha, beta or gamma haemolytic?
Beta haemolytic
What is the main disease caused by Streptococcus pyogenes?
Uncomplicated pharyngitis
What type of pathogen is a group A Streptococcus?
Strict human pathogen
What are the non-invasive GAS infections?
- Pharyngitis
- Scarlet fever
- Impetigo
- Otitis media
What are the severe invasive GAS infections?
- Meningitis
- Puerperal fever
- Septicaemia
- Necrotising faciitis
- Toxic shock syndrome
Describe necrotising faciitis
- Post pharyngitis or direct inoculation
- Toxin mediated
- Rampant unfettered tissue damage, vascular dissemination and systemic disease
- High morbidity and mortality
Describe acute rheumatic fever
- 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
Describe acute glomerulonephritis
- 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
How is GAS transmitted?
Primarily transmitted person to person but there have been numerous reports of food-borne cases
Where are GAS carried?
- Nasopharyngeal mucosa -> challenging niche
- Skin
- Vaginal tract
What are the primary reservoir of GAS?
Humans
Is carriage required for disease?
No
What do GAS rely on to survive in saliva?
Amylase as saliva is a carbohydrate-limited environment
Describe the adherence mechanism of GAS
- 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
How does M protein act as a virulence factor of S. pyogenes?
- 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
What virulence factors are involved in spread and avoidance?
- 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
What virulence factors are involved in resisting the immune system?
- 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
What virulence factors cause damage?
- 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
What happens in toxic shock syndrome?
- Release of elevated levels of inflammatory cytokines
- Cytokine storm
- Vascular leakage
- Coagulation
- Circulatory collapse
- Organ failure
What are superantigens?
Potent immuno-stimulatory molecules
What do superantigens activate?
Bind TCR irrespective of its antigenic specificity and so activates a large number of T cells of different antigenic specificity
