Streptococci

Question 1

Streptococci

Answer 1

“A string of pearls” - all streptococci are chains

Gram positive cocci in chains

Question 2

There are lots of streptococci species - can classify them in different ways

Answer 2

1 way is to see how good they are breaking down RBC in blood agar.

Reason blood is used as it contains many nutrients that the bacteria can use to grow - the main one is iron - in agar the iron is hidden away in RBC, so those bacteria that can break RBC to access the iron will grow better, therefore we can distinguish between them

The clear ß shape - shows ß haemolysis - which is complete breakdown of RBC (due to enzyme called haemolysin)

The green alpha shape = shows alpha haemolysis - which is the partial breakdown of RBC (viridans streptococci)

Streptococci, classification schemes
Lancefield, 1933

Question 3

Streptococcus progenies virulence factors

Answer 3

Cause a wide range of diseases - such as sore throats to rapidly fatal disease

What determines they type of disease you get with these organisms depends on the virulence factors that these bacterial strains may or may not possess

Hyaluronic acid capsule - inhibits phagocytosis by neutrophils and macrophages as they struggle to digest it - because its very similar to native molecules in human connective tissue, therefore theres not much of a new response to it as it looks the same as us, so it protects bacteria from host mechanisms

M protein - resistance to phagocytosis by inhibiting activation of alternative complement pathway on bacterial cell surface, there are >150 antigenically differnet serotypes as a consequence of nucleotide variant as of emm gene

Adhesins (including lipoteichoic acid, M protein, fibronectin binding proteins) - adherence is first step in colonisation/infection

Streptolysins O and S - lysis of erythrocytes, neutrophils and platelets

Dnases A, B, C and D - degradation of DNA

Hyaluronidase - Degradation of hyaluronic acid in connective tissue

Streptokinase - dissolution of clots through conversion of plasminogen to plasmin

Streptococcal pyrogenic exotoxins - Cleaves Ig G bound to Group A strep. Member of superantigenic Spe family

Question 4

Streptococcal pharyngitis

Answer 4

Caused by Streptococcus pyogenes
Peak incidence 5-15 years
Droplet spread

Association with over- crowding
Untreated patients develop M protein specific antibody

Clinical features - Abrupt onset sore throat Malaise, fever, headache Lymphoid hyperplasia Tonsillopharyngeal exudates
Throat swab -> Group A strep

Complications of streptococcal pharyngitis:

Scarlet fever - Due to infection with streptococcal pyrogenic exotoxin strain of S.pyogenes
Local or haematogenous spread
High fever, sepsis, arthritis, jaundice

Question 5

Streptococcus pyogenes skin infections - more characteristically what we see with strep

Answer 5

Impetigo
Childhood infection, 2-5 years
Initial skin colonisation, followed by intradermal innoculation
No ARF but impetigo is most common cause of glomeruonephritis

Erysipelas
Dermis infection with lymphatic involvement
Face, lower limbs
Facial lesions frequently preceded by pharyngitis
Lower limb infection usually secondary to invasion of skin via trauma, skin disease or local fungal infection

Cellulitis
Skin and subcutaneous tissue infection
Impaired lymphatic drainage and illicit injecting drug use important risk factors

Necrotising fasciitis
Infection of deeper subcutaneous tissues and fascia.
Rapid, extensive necrosis
Usually secondary to skin break
Severe pain, even before gross clinical changes
High fever, fulminant course, high mortality (20-70%)

Question 6

Streptococcal toxic shock syndrome

Answer 6

Deep tissue infection with Strep pyogenes 
AND 
Bacteraemia 
AND 
Vascular collapse 
AND 
Organ failure 

From health to death in hours

Entry of group A strep into deeper tissues and bloodstream 
Streptococcal pyrogenic exotoxins stimulate T-cells through binding to MHC class II antigen-presenting cells and V-β region of T-cell receptor, inducing monocyte cytokines (TNF-α, IL-1β, IL-6) and lymphokines (TNF-β, IL-2, IFN-γ). 
M-protein fibrinogen complex formation

Pathogenesis of streptococcal toxic shock syndrome - Group A strep invades the blood

M protein is shed from its surface and forms a complex with fibrinogen

Its thought that m protein fibrogen complex binds to integrins on the surface of polymorphonuclear leukocytes activating these cells

Once activated, these leukocytes adhere to endothelium and degranulate, which releases a wide range of hydrolytic enzymes and produces a respiratory burst

The resulting damage to the underlying endothelium leads to vascular leakage and hypercoagulability which in turn cause the hypertension, disseminated intravascular coagulation and organ damage which is seen in strep toxic shock syndrome