Infection - Streptococci Flashcards

1
Q

How does streptococci appear on a gram stain?

A

Gram positive (purple) cocci in chains

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2
Q

What are the three possible reactions after adding streptococci to a blood plate?

A
  • non-haemolytic (gamma) do nothing
  • viridans streptococci turn it green (alpha haemolysis)
  • streptococcus pyogenes turn it yellow (beta haemolysis)
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3
Q

True or false - encapsulated bacteria are much more pathogenic than non-encapsulated?

A

True - the capsule protects them

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4
Q

Why is streptococcus pyogenes called ‘pyogenes’?

A

Because it forms pus

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5
Q

How are different strains of streptococcus identified?

A

They are reacted with different antibodies. If it reacts with antibody A then it will be group A etc.

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6
Q

What type of strep is group A usually?

A

Streptococcus pyogenes

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7
Q

What kind of strep is group B usually?

A

Streptococcus agalactiae - important cause of neonatal sepsis due to being normal vaginal flora

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8
Q

What are the four Sherman groups of streptococci?

A

Pyogenic, viridans, enterococcal and lactic

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9
Q

What is the best way of identifying bacteria?

A

Looking at the 16S ribosomal RNA sequence

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10
Q

How does the hyaluronic acid capsule benefit strep pyogenes?

A
  • inhibits phagocytosis by neutrophils and macrophages

- poor immunogenicity due to similar to human connective tissue

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11
Q

How do M proteins help strep pyogenes?

A
  • resistant to phagocytosis as they inhibit activation of alternative complement pathway on bacterial cell surface
  • over 150 different stereotypes so difficult to become immune to them
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12
Q

What do adhesins do to help strep pyogenes?

A

They allow adherence, which is the first step in colonisation/infection

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13
Q

How do streptolysins O and S help strep pyogenes?

A

They cause lysis of erythrocytes, neutrophils and platelets

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14
Q

What is the function of DNAses A, B C and D?

A

They degrade DNA, so it can be expelled and used as a net

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15
Q

What is the function of hyaluronidase?

A

Degradation of hyaluronic acid in connective tissue

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16
Q

What is the role of streptokinase?

A

Dissolution of clots through conversation of plasminogen to plasmin

17
Q

What is the function of streptococcal pyrogenic exotoxins?

A

They cleave IgG bound to group A strep. They are a member of superantigenic Spe family

18
Q

Which type of strep causes streptococcal pharyngitis?

A

Strep pyogenes

19
Q

What are the clinical features of strep pharyngitis?

A
  • abrupt onset sore throat
  • malaise, fever, headache
  • lymphoid hyperplasia
  • tonsillopharyngeal exudates
20
Q

Someone with streptococcal pharyngitis develops high fever, sepsis, arthritis and jaundice. What have they now contracted?

A

Scarlet fever

21
Q

Give some complications of streptococcal pharyngitis

A
  • peritonsular cellulitis/abscess
  • retropharyngeal abscess
  • mastoiditis, sinusitis, otitis media
  • meningitis, brain abscess
  • acute rheumatic fever
  • acute post-streptococcal glomerulonephritis
22
Q

Give some skin infections caused by streptococcus pyogenes

A
  • impetigo
  • erysipelas
  • cellulitis
  • necrotising fasciitis
23
Q

What is impetigo?

A

Very superficial childhood infection (usually 2-5 years), where strep pyogenes has an initial skin colonisation followed by it entering to intradermal area. Can lead to glomeruonephritis

24
Q

What is erysipelas?

A

Dermis infection with lymphatic involvement of face and lower limbs by strep pyogenes. Usually preceded by pharyngitis

25
Q

What is cellulitis?

A

Infection of skin and subcutaneous tissue. Impaired lymphatic drainage and illicit drug injection are important risk factors

26
Q

What is necrotising fasciitis?

A

Infection of deeper subcutaneous tissues and fascia leads to rapid, extensive necrosis. Usually secondary to skin break and causes severe pain. High fever, fulminant course, high mortality

27
Q

What is streptococcal toxic shock syndrome?

A

Deep tissue infection with strep pyogenes and bacteraemia leading to vascular collapse and organ failure. Streptococcal pyrogenic exotoxins stimulate T-cells through binding to MHC class II antigen-presenting cells and T cell receptors, inducing monocytes cytokines and lymphokines. M-protein fibrinogen complexes form