Infection - Streptococci Flashcards

(27 cards)

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
What is cellulitis?
Infection of skin and subcutaneous tissue. Impaired lymphatic drainage and illicit drug injection are important risk factors
26
What is necrotising fasciitis?
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
What is streptococcal toxic shock syndrome?
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