Session 6: Streptococci: Streptococcus pyogenes Flashcards

1
Q

How will streptococci appear on blood culture?

A

As gram positive (purple)

In chains and each segment of the chains is globular

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2
Q

How can streptococci be classified?

A

By haemolysis
By based on cell wall antigens
By whether they are pyogenic, viridans, enterococcal or lactic streptococci

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3
Q

What are the different subgroups of classification of streptococci by haemolysis? Give the degree of haemolysis in each case.

A
Alpha haemolysis (partial haemolysis)
Beta haemolysis (complete breakdown)
Gamma haemolysis (no haemolysis)
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4
Q

Give an example of streptococci in each haemolytic group.

A

Alpha haemolysis: viridans streptococci like streptococci pneumoniae

Beta haemolysis: Streptococcus pyogenes

Gamma haemolysis: Enterococus faecalis

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5
Q

How can you tell whether the streptococcus is alpha, beta or gamma haemolytic?

A

By the use of a blood agar plate.

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6
Q

How will the appearance of the blood agar plate differ between the three haemolytic classifications?

A

Alpha: will appear somewhat green/brownish
Beta: Will appear much more white and the blood will disappear
Gamma: will barely have a shift of appearance, there might be pale silvery dots.

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7
Q

What are the virulence factors of streptococcus pyogenes?

A
Hyaluronic acid capsule
M proteins
Adhesins
Streptolysins
DNAses
Hyaluronidase
Streptokinase
Streptococcal pyrogenic exotoxins
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8
Q

Briefly explain the mechanism of action of: Hyaluronic acid capsule

A

Inhibits phagocytosis by neutrophils and macrophages and immune system doesn’t response as readily due to the similarity to human connective tissue hyaluronate.

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9
Q

Briefly explain the mechanism of action of: M protein

A

Resistance to phagocytosis by inhibition of activation of alternative complement pathways.
Multiple of nucleotide variants of M-gene meaning antibodies might not recognise them.

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10
Q

Briefly explain the mechanism of action of: Adhesins

A

Adherence of the bacteria for colonisation and infection

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11
Q

Briefly explain the mechanism of action of: Streptolysins

A

Lysis of erythrocytes, neutrophils and platelets

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12
Q

Briefly explain the mechanism of action of: DNAses

A

Degradation of DNA

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13
Q

Briefly explain the mechanism of action of: Hyaluronidase

A

Degradation of hyaluronic acid in connective tissue

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14
Q

Briefly explain the mechanism of action of: Streptokinase

A

Dissolution of thrombus by converting inactive plasminogen to active plasmin

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15
Q

Briefly explain the mechanism of action of: Streptococcal pyrogenic exotoxins

A

Active secretion of toxins

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16
Q

What is a common infection that is caused by Streptococcus pyogenes?

A

Streptococcal pharyngitis (sore throat)

17
Q

What patients are most susceptible to Strep pharyngitis?

A

5-15 years of age
Over-crowding places
People who have been treated with antibiotics regularly for Strep pharyngitis (no antibodies for it)

18
Q

Clinical features of Strep pharyngitis.

A

Abrupt onset of sore throat
Malaise, fever and headache
Lymphoid hyperplasia
Tonsillopharyngeal exudates

19
Q

How do you make a diagnosis of Strep pharyngitis?

A

Check for clinical features. Do a throat swab and then blood agar plate if needed.

20
Q

How do you treat Strep pharyngitis?

A

Usually you leave it to its own device. Antibiotics will work but will probably only make it better 1 or 2 days in advance.
The problem with treating with antibiotics is that they might not develop M-protein specific antibodies which means that they might get infection again and again.

21
Q

What are the complications of Strep pharyngitis?

A
Scarlet fever
Suppurative complications
Acute rheumatic fever
Acute post-streptococcal glomerulonephritis
Skin infections
Streptococcal toxic shock syndrome
22
Q

How is Strep pharyngitis transmitted?

A

Usually via coughs (droplets) airborne

23
Q

Briefly explain Scarlet fever. Mechanism of infection, spread of infection and clinical features.

A

Due to infection of Strep pharyngitis with streptococcal pyrogenic exotoxin strain of Strep. pyogenes.

It can be of local or haematogenous spread that results in high fever, sepsis, arthritis and jaundice.

24
Q

What are suppurative complications of Strep pharyngitis.

A

Such as peritonsillar cellulitis/abscess
Retropharyngeal abscess
Mastoiditis, sinusitis and otitis media
Meningitis and brain abscess in case of infection entering via carotid artery and haematogenous spread.

25
Q

Briefly explain acute rheumatic fever.

A
Inflammation of heart, joints and CNS.
From pharyngitis
Rheumatogenic M types are the cause.
Mechanisms such as:
Auto-immune
Sreum sickness
Binding of M protein to collagen
ASO, ASS induced injury
26
Q

Briefly explain post-streptococcal glomerulonephritis.

A

Acute inflammation of renal glomerulus
M type specific
Antigen-antibody complexes in glomerulus

27
Q

What are some common streptococcus pyogenes skin infections that can result from pharyngitis?

A

Impetigo
Erysipelas
Cellulitis
Necrotising fasciitis

28
Q

Briefly explain impetigo.

A

Childhood infection 2-5 years
Skin colonisation followed by intradermal inoculation
No acute renal failure but impetigo is most common cause of glomerulonephritis

29
Q

Briefly explain Erysipelas

A

Dermis infection with lymphatic involvement
Face and lower limbs
Facial lesions
Lower limb infections

30
Q

Briefly explain cellulitis

A

Skin and subcutaneous tissue infection
Impaired lymphatic drainage and illicit injecting drug use is an important risk factor.
Can also be caused by S. aureus

31
Q

Briefly explain necrotising fasciitis

A
Infection of deeper subcutaneous tissue and fascia
Rapid and extensive necrosis
Usually secondary to skin break
Severe pain
High fever and high mortality
32
Q

How do you necrotising fasciitis?

A

Usually by antibiotics and debridement of dead tissue.

33
Q

Explain mechanism of streptococcal toxic shock syndrome.

A
Group A strep enters into deeper tissue and bloodstream.
Strep. pyrogenic exotoxins stimulate T-cells though binding to mHC class II antigen presenting cells inducing monocyte cytokines and lymphokines.
M-protein fibrinogen complex formation occurs.

Adherence of leucocytes to endothelium where they perform respiratory burst. Endothelium gets damaged causing vascular leakage and hypercoagulability.

Hypotension, DIC and organ damage will ensue.