Medsci 202 - Streptococci And Diseases

Front 1

Characteristics of Streptococci

Back 1

→ gram positive cocci bacteria = grow in chains (0.5-1.0 μm)
→ some strains produce capsules
→ susceptible to penicillin = no β-lactamase gene

Front 2

Types of Streptococci

Back 2

→ around 20 groups
→ medically relevant = Lancefield Groups (classified by serologic specificity of cell wall group specific carbohydrates)
→ Group A: S. pyogenes (only member)

Front 3

Streptococci Diagnostic

Back 3

→ negative in catalase test (no catalase enzyme)
→ β-hemolysis = bacitracin; GAS or GBS
→ α-hemolysis = optochin; Viridans Strep. or S. pneumoniae
→ y-hemolysis = bile esculine agar; GDS enterococcus or further tests

Front 4

Epidemiology of S. pyogenes

Back 4

→ asymptomatic colonisations of upper respiratory tract (20% carrier population)
→ resistant to dessication
→ person to person spread (air borne respiratory droplets)
→ higher Maori and Pacific islander prevalence than Europeans

Front 5

Streptococci Adhesins

Back 5

→ MSCRAMMS (Microbial surface components recognizing adhesive matrix)
→ bind to host ECM = tissue colonization
e.g. M proteins (fibronectin, fibrinogen)
F proteins (fibronectin)
Cpa (collagen-binding protein)

Front 6

Streptococci Pili

Back 6

→ hair like cells from cell surface
→ allows cell wall anchorage, host cell binding and formation of biofilms
→ tip of pili has adhesin tip

Front 7

Streptococci Cytolysins

Back 7

→ Streptolysin O (oxygen-liable) = SLO high antigenic (forms pores on host membrane) = haemolysis
→ Streptolysins S (oxygen stable) = SLS lyses leukocytes, erythrocytes and platelets via β-hemolysis
→ SLO is highly antigenic

Front 8

Streptococci Spreading Factors

Back 8

→ the same as staphylococci
→ lipases, nucleases, hyalurodinases, proteases, streptokinase (fibrinolysin)

Front 9

Streptococci Superantigens

Back 9

→ related to staphylococci SAgs but don't cause food poisoning
→ Streptococcal pyogenic exotoxins (SPE-A)
→ Streptococcal mitogenic exotoxins Z (SMEZ)
→ they trigger pro-inflammatory cytokines (TNF-α and TNF-y) = systemic inflammation + multi organ involvement

Front 10

Streptococci Immune Evasions

Back 10

→ capsule = made of hyaluronic acid; prevent opsonisation and inhibits phagocytosis (only some strains)
→ M-proteins = adhesins property, prevents complement factors C3b from opsonisation and phagocytosis
→ C5a peptidase = cleaves complement factor C5a (neutrophil chemotaxis), prevents neutrophil migration to site of infection

Front 11

Impetigo (Non Invasive - S. pyogenes)

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→ localised cutaneous infections with pus filled vesicles (young children)

Front 12

Pharyngitis (Non Invasive - S. pyogenes)

Back 12

→ develops 2-4 days after exposure to S. pyogenes
→ sore throat, fever, reddened pharynx, tonsillitis

Front 13

Scarlet Fever (Non Invasive - S. pyogenes)

Back 13

→ pharyngitis complications = systemic disease
→ caused by strains that produce super antigen pyrogenic exotoxin A (SPE-A) = 'scarlet fever toxin'

Front 14

Cellulitis (Non Invasive - S. pyogenes)

Back 14

→ infection of the skin which involves subcutaneous tissue, acute rapidly spreading infection (hyaluronidase, DNAse)

Front 15

Necrotising Fasciitis (Invasive - S. pyogenes)

Back 15

→ deep infection of the skin involving destruction of muscles via exposed tissue, viral infections
→ supported by spreading factors = develops into severe systemic disease with high mortality (TSS)

Front 16

Streptococcal TSS (Invasive - S. pyogenes)

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→ follows necrotising fasciitis and sepsis
→ high mortality rate 30-70%
→ massive release of pro-inflammatory cytokines in response to SAgs = systemic inflammation
→ symptoms = fever, headache, multi organ failure, shock

Front 17

Rheumatic Heart Disease (Post Streptococcus Disease)

Back 17

→ develops after untreated sore throats due to S. pyogenes = inflammation of endocardium, myocardium, pericardium results in thickened and deformed heart valves and granulomas in myocardium (starts from arthritis)

Front 18

Rheumatic Fever (Post Streptococcus Disease)

Back 18

→ an AUTOIMMUNE disease triggered by 'molecular mimicry'
→ an antibody cross-reaction where antibodies generated against the M protein also bind to host proteins triggering 'type II hypersensitivity immune response'

Front 19

S. agalactiae Physiology (Group B Streptococcus)

Back 19

→ gram positive coccus that grows in long chains
→ either β-haemolysis or non-haemolytic and carries Lancefield group B specific carbohydrates

Front 20

S. agalactiae Epidemiology (Group B Streptococcus)

Back 20

→ asymptomatic colonisation of upper respiratory and genitourinary tract (mostly neonatal diseases)
→ most infections are acquired from mother during pregnancy or at time of birth

Front 21

Viridans Streptococci

Back 21

→ asymptomatic colonisation of oropharynx, gastrointestinal and genitourinary tract
→ less virulent than S. pyogenes
→ cause dental caries, bacterial endocarditis and septic shock

Front 22

Streptococcus Pneumonia

Back 22

→ lancet shaped diplococcic (short chains), most have outer capsules
→ spread endogenously via pharynx, lungs, sinuses, ears
→ antiphagocytic and produce pneumolysin (cytolysin that destroys epithelial cells)
→ cause pneumonia (60% of cases), meningitis, bacteremia