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Infection * > S11 Streptococci > Flashcards

S11 Streptococci Flashcards

1
Q

What type of gram stain is Streptococci?

A

Gram positive cocci (in chains)

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2
Q

How are Streptococci classified by haemolysis?

A
  • alpha haemolysis e.g. Strep. pneumoniae (partial breakdown - greenish zone)
  • beta haemolysis e.g. Strep. pyogenes (full breakdown - clear zone)

(* non-haemolytic gamma e.g. Enterococcus faecalis)

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3
Q

What is the Lancefield (1993) classification of Streptococci?

A

Serological classification of beta-haemolytic streptococci - based on cell wall antigens

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4
Q

What does Sherman (1937) classify Streptococci based on?

A

4 classes:

  • pyogenic
  • viridans (alpha-haemolytic)
  • enterococcal
  • lactic streptococci
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5
Q

What is the Lancefield antigen for S. pyogenes?
For S. agalactiae?
For S. dysglactiae?

A

A
B
C

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6
Q

How do most people experience S. pyogenes?

A

Sore throat - tonsillitis

Necrotising fasciitis

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7
Q

How do most people experience S. galactiae?

A

Usually symptom free - often carried as part of woman’s normal vaginal flora - so can cause infections in newborns - bacteria into vagina and into amniotic cavity, causing infection whilst baby is still in-utero or as baby passes through birth canal - becomes colonised with bacteria which can then invade

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8
Q

How do most people experience S. dysgalactiae?

A

Sore throats and skin infections

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9
Q

How do most people experience S. pneumoniae?

A

Pneumonia

If capsulated:
Meningitis
Endocarditis
Peritonitis

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10
Q

What is the S. milleri group main characteristic? What Sherman group is it?

A

Cause abscesses

Viridans

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11
Q

You have Lancefield, Sherman and haemolysis classifications for Strep. bacteria, what is the last and most recent?

A

DNAsequencing (16S ribosomal RNA sequences)

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12
Q

What are the virulence factors for Streptococcus pyogenes?

A
  • hyaluronic acid capsule
  • M protein
  • adhesins
  • streptolysins O and S
  • Dnases A, B, C and D
  • hyaluronidase
  • streptokinase
  • streptococcal pyogenic exotoxins
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13
Q

What is the action of the hyaluronic acid capsule?

Streptococcus pyogenes

A

Inhibits phagocytosis by neutrophils and macrophages (has similarities to human CT so not much immune response to it)

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14
Q

What is the action of M protein? (Streptococcus pyogenes)

A

Resistance to phagocytosis by inhibiting activation of alternative complement pathways on bacterial cell surface.

There are many different antigenically different stereotypes of M protein

(Fuzzy around cell)

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15
Q

What is the action of adhesins? (Streptococcus pyogenes)

A

Helps with adherence (which is the first step in colonisation/infection)

E.g. lipoteichoic acid, M protein, fibronectin binding proteins

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16
Q

What is the action of streptolysins O and S? (Streptococcus pyogenes)

A

Lysis of erythrocytes, neutrophils and platelets

17
Q

What is the action of Dnases A, B, C and D? (Streptococcus pyogenes)

A

Degradation of DNA

18
Q

What is the action of hyaluronidase? (Streptococcus pyogenes)

A

Degradation of hyaluronic acid in CT

19
Q

What is the action of streptokinase? (Streptococcus pyogenes)

A

Break down of clots through conversion of plasminogen to plasmin

20
Q

What is the action of streptococcal pyrogenic exotoxins? (Streptococcus pyogenes)

A

Cleaves IgG bound to Group A strep

Fever producing toxin

21
Q

What is Streptococcal pharyngitis - what is it caused by, who does it occur most in, how is it spread, why is there an argument to leave untreated?

A

Caused by Streptococcus pyogenes

Mostly occurs in children (5-15 years)

Spread by droplets e.g. coughing
Associated with overcrowding

untreated patients develop an M protein specific antibody - if treated they don’t have an immune response

22
Q

What are the clinical features of Streptococcal pharyngitis?

A
  • abrupt onset sore throat
  • malaise, fever, headache
  • lymphoid hyperplasia
  • tonsillopharyngeal exudates

A throat swab will show Group A strep

23
Q

What are the complications of streptococcal pharyngitis?

A
  • scarlet fever - if have streptococcal pyrogenic exotoxin, local/haematogenous spread , high fever, sepsis, arthritis and jaundice
  • suppurative (pus) complications - peritonsillar cellulitis/abscess, retropharyngeal abscess, mastoiditis, sinusitis, otitis media, meningitis and brain abscess
  • acute rheumatic fever - inflammation of heart, joints and CNS
  • acute post-streptococcal glomerulonephritis - acute inflammation of renal glomerulus (specific M types lead to this)
24
Q

What are the possible mechanisms of acute rheumatic fever (following pharyngitis)?

A
  • autoimmune
  • serum sickness
  • binding of M protein to collagen - certain types of M protein are linked to rheumatic fever
  • ASO, ASS induces tissue injury
25
Q

What are 4 types of streptococcus pyogenes skin infections?

A
  • impetigo
  • erysipelas
  • cellulitis
  • necrotising fasciitis
26
Q

What is impetigo?

A

A childhood infection (2-5 years)

Initial skin colonisation followed by intradermal inoculation

Common cause of glomerulonephritis

27
Q

What is erysipelas?

A

A dermis infection with lymphatic involvement, usually occurs on face and lower limbs

On the face - usually preceded by pharyngitis
On the lower limbs - usually secondly to invasion of skin via trauma, skin disease or a local fungal infection

28
Q

What is cellulitis?

A

A skin and subcutaneous tissue infection

Risk factors of cellulitis are: impaired lymphatic drainage and illicit injecting drug use

29
Q

What is necrotising fasciitis?

A

An infection of the deeper subcutaneous tissues and fascia - it involves rapid extensive necrosis

It’s usually secondary to a skin break

Results in severe pain even before there are any clinical changes, high fever and has a high mortality rate

30
Q

What is streptococcal toxic shock syndrome, clinically and pathologically?

A

A deep tissue infection with Strep. pyogenes
And bacteraemia, vascular collapse and organ failure

(Health to death in hours)

It involves the entry of group A strep into deeper tissues and the bloodstream - strep pyrogenic exotoxins stimulate T-cells by binding to MHC class II APCs, this induces cytokines and lymphokines.
M-proteins bind to fibrinogen forming a complex.

Degranulation, respiratory burst and endothelial damage occur

Infection * (18 decks)

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