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SMP - MIM Part 2 > Lecture 9 - Streptococcal Respiratory Infections > Flashcards

Lecture 9 - Streptococcal Respiratory Infections Flashcards

1
Q

5 characteristics of streptococci?

A
  1. Gram-positive cocci (cells may be ovoid or bullet-shaped) that grow in chains
  2. Catalase-negative: important in distinguishing them from staphylococcus genus (also gram + cocci)
  3. Widely distributed in nature: found in milk, dairy products, water, dust and vegetation
  4. Normal inhabitants of the upper respiratory tract and intestinal tract and other mucosal surfaces of man and various animal
  5. Majority of streptococci are saprophytic and nonpathogenic but some are opportunistic or overt pathogens
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2
Q

How to culture streptococci?

A
  1. 24-48 h incubation at 37°C in 5% CO2 in air = capnophilic
  2. Ferment a variety of carbohydrates producing lactic acid as the major fermentation end-product = homolactic fermenters, even if O2 in the environment
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3
Q

What are the 3 types of hemolyses produced by streptococcal colonies growing on blood agar

A
  1. Incomplete hemolysis: alpha (α) hemolysis
  2. Complete hemolysis: beta (β) hemolysis
  3. Not hemolytic: “gamma” (γ) hemolysis
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4
Q

4 groups of streptococci?

A
  1. Pyogenic group: produce pus
  2. “Viridans” group: alpha-hemolytic
  3. Enterococcus group => its own genus
  4. Lactic group: used in dairy industry => actually their own lactococcus genus
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5
Q

3 ways of classifying streptococci? Which is most reliable?

A
  1. Hemolysis type
  2. 4 groups
  3. ***Lancefield system based on the antigenic characteristics of the group-specific ‘C substance’ (Lancefield group A, B, C, D, etc.) which are cell wall polysaccharides or teichoic acids
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6
Q

Envelope composition of streptococci?

A

Thick cross-linked peptidoglycans

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7
Q

What is the principle virulence factor of GAS (Group A streptococci)?

A

M protein

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8
Q

How many different immunologically distinct types of M proteins? What does this mean? What to note?

A

Over 200 => highly immunologically variable

NOTE: immunity is M type specific (memory immunity will only be to the one type of M protein that you have been exposed to)

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9
Q

Describe the M protein. Role?

A

α-helical coiled-coil fibrillar protein that has a domain-like structure with the AA sequence of the extracellular portion highly variable => involved in immune evasion (antiphagocytic and degrades complement component C3b) and adhesion

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10
Q

2 classes of M proteins? Describe each.

A
  1. Class I: share extracellular epitopes but strains do not produce opacity factor
  2. Class II: lack shared epitopes, but strains produce opacity factor
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11
Q

Which M proteins cause rheumatic fever?

A

Class I only

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12
Q

What are 2 diseases resulting from local infection with GAS and their products? What can each progress to?

A
  1. Mucosal infection: streptococcal sore throat scarlet fever rash from erythrogenic toxin (bacteriophage encoded) => may proceed to ARF or AGN
  2. Skin infection: streptococcal pyoderma => may proceed to AGN
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13
Q

What are 4 diseases resulting from invasion of GAS?

A
  1. Erysipelas: skin infection, typically on lower limbs with blistering and sharp demarcations
  2. Puerperal fever: uterus infection
  3. Sepsis from traumatic or surgical wounds infections
  4. Toxic-shock syndrome and necrotizing infections/fasciitis
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14
Q

3 M protein types involved in toxic-shock syndrome and necrotizing infections/fasciitis?

A

M1, M3, M5

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15
Q

What is post-streptococcal disease?

A
  1. Pharyngeal infections => rheumatic fever OR glomerulonephritis
  2. Skin infections => only acute glomerulonephritis
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16
Q

What is acute glomerulonephritis from post-streptococcal disease characterized by? Cause?

A
  1. Edema
  2. HT
  3. Hematuria
  4. Proteinuria

Cause: deposition of immune complexes in the renal glomeruli (Type III immunopathology)

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17
Q

Onset of acute glomerulonephritis from post-streptococcal disease?

A

~10 days following a skin infection

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18
Q

How does acute glomerulonephritis from post-streptococcal disease heal?

A

Spontaneous healing over weeks to months

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19
Q

What can progressive course of acute glomerulonephritis from post-streptococcal disease lead to?

A

Renal failure, congestive heart failure, and death

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20
Q

What is rheumatic fever from post-streptococcal disease characterized by?

A
  1. Valvulitis
  2. Pericarditis
  3. Myocarditis
  4. Erythema marginatum
  5. Arthritis/arthralgias
  6. Aschoff nodules (subcutaneous)
  7. PANDAS = pediatric autoimmune neurologic disorder associated with streptococci (CNS)
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21
Q

Describe molecular mimicry of GAS.

A

The group A carbohydrate and M protein are the main cross-reactive antigens with:

HEART

  1. Myocardium and valve endothelium
  2. Myosin, laminin, keratin

BRAIN

  1. Lysoganglioside and tubulin
  2. Dopamine D2 and D1 receptors
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22
Q

5 M types associated with rheumatic fever?

A

M3, M5, M18, M19, M24

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23
Q

5 M types associated with glomerulonephritis?

A

M49, 57, M59-61

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24
Q

Describe antibodies against GAS?

A

Anti-M antibodies are opsonic (promote phagocytosis)

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25
Q

What is the most common form of bacterial pneumonia?

A

Streptococcus pneumoniae

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26
Q

Reservoir of Streptococcus pneumoniae?

A

Nasopharynx

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27
Q

Carrier rate of Streptococcus pneumoniae? What to note?

A

May be as high as 60%

NOTE: as individuals get older the periods of carriage become shorter and intervals in between become longer

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28
Q

Are all Streptococcus pneumoniae capsule types equally invasive?

A

NOPE

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29
Q

Is Streptococcus pneumoniae usually a primary infection? What does this mean?

A

NOPE

Usually infects a respiratory tree primarily infected by a viral infection

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30
Q

What is the major line of defense against Streptococcus pneumoniae? What to note?

A

PMNs

NOTE: opsonic antibodies are important as well

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31
Q

Describe antibodies against Streptococcus pneumoniae.

A

Capsule-type specific (up to ~ 100 types of capsules )

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32
Q

What does the enzyme catalase do?

A

Breaks down hydrogen peroxide to O2 and H2O

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33
Q

What does saprophytic mean?

A

Deriving its nourishment from dead or decaying organic matter

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34
Q

Other name for alpha hemolysis?

A

Greening hemolysis

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35
Q

Group of streptococci that conduct alpha hemolysis?

A

“Viridans” group

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36
Q

Hemolysis type of Streptococcus pneumoniae?

A

Alpha hemolytic

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37
Q

Hemolysis type of GAS?

A

Beta hemolytic

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38
Q

Most important Lancefield groups in humans?

A

A, B, C, D, and G

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39
Q

Which streptococci species can be classified in the Lancefield system?

A

Only non- and beta-hemolytic streptococci

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40
Q

Proper name of GAS?

A

Streptococcus pyogenes

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41
Q

Other name for Streptococcus pneumoniae?

A

Pneumococcus

42
Q

4 tests to identify GAS? Which is determinative?

A
  1. Gram stains => should be +
  2. Catalase test => should be -
  3. Bacitracin antibiotic test on blood agar plate => should be + with clear zone surrounding the disk
  4. ***Antibodies against Lancefield antigen: latex beads coated with antibodies to which a drop of specimen is added in suspension => if positive latex beads will cross-link when binding to antigen => agglutination
43
Q

How does the catalase test work?

A

Take tiny piece of colony and smear on microscope slide, then add a drop of hydrogen peroxide => immediate fizzing/bubbling is a positive test

44
Q

Most common cause of bacterial pharyngitis? What to note?

A

GAS infection

NOTE: almost all pharyngites are viral though

45
Q

Incubation time for bacitracin test for GAS?

A

48 h

46
Q

When testing for GAS, if the Lanfield antigen antibody test is negative, what should you do?

A

Bacitracin antibiotic test on blood agar plate

47
Q

Treatment for GAS infections?

A

Penicillin

48
Q

Envelope composition of GAS?

A
  1. Capsule: hyaluronic acid with low immunogenicity

2. Cell wall: protein antigens M, T, R, and E

49
Q

Do both GAS and Streptococcus pneumoniae have a capsule?

A

YUP

50
Q

What are the 14 virulence factors of GAS?

A
  1. Capsule
  2. Lipoteichoic acid
  3. M protein
  4. M-like proteins
  5. F protein
  6. Pyrogenic exotoxins
  7. Streptolysin S
  8. Streptolysin O
  9. Streptokinase
  10. DNase
  11. C5a peptidase
  12. Opacity factor
  13. G3PD
  14. Enolase
51
Q

How is the GAS capsule virulent?

A

Antiphagocytic and complement inactivating

52
Q

How is the GAS lipoteichoic virulent?

A

Binds to epithelial cells

53
Q

How is the GAS F protein virulent? What does it stand for?

A

Mediates adherence to epithelial cells

Fibernectin protein

54
Q

Do GAS express all 14 virulence factors at all times?

A

NOPE

55
Q

How are the GAS M-like proteins virulent?

A

Bind immunoglobulins M and G and alpha2-macroglobulins (protease inhibitors)

56
Q

How are the GAS pyrogenic exotoxins virulent? 6

A
  1. Mediate pyrogenicity
  2. Enhancement of delayed hypersensitivity and susceptibility to endotoxin,
  3. Cytotoxicity
  4. Nonspecific mitogenicity for T cells (all CD4 T cells = superantigens)
  5. Immunosuppression of B-cell function
  6. Production of scarlatiniform rash
57
Q

3 examples of GAS pyrogenic exotoxins? How many total?

A

SpeA, SpeB, SpeC

May be as many as 13

58
Q

How the GAS streptolysins S and O virulent? 3

A
  1. Lyse leukocytes, platelets, and erythrocytes
  2. Stimulate release of lysosomal enzymes
  3. Immunogenic
59
Q

How is the GAS steptokinase virulent? 2

A
  1. Lyses blood clots

2. Faciliates spread of bacteria in tissues

60
Q

How is the GAS DNase virulent? 2

A
  1. Depolymerizes cell-free DNA in purulent material

2. Interferes with NETs = neutrophil extracellular traps

61
Q

How is the GAS C5a peptidase virulent?

A

Degrades C5a, which is the most important chemokine of the complement cascade

62
Q

How is the GAS opacity factor virulent? What is it? 2

A

Lipoproteinase

  1. Increases opacity of serum
  2. Binds fibronectin
63
Q

How is the GAS G3PD virulent? Where is it located?

A

Acts as an adhesin

Located at cell surface

64
Q

How is the GAS enolase virulent? Where is it located?

A

Binds plasminogen

Located at cell surface

65
Q

What do both GAS G3PD and enolase have in common?

A

Both in glycolytic pathway

66
Q

What happens if you knock down GAS M protein?

A

GAS is essentially non-virulent

67
Q

4 types of pathogeneses of GAS infections?

A
  1. Diseases resulting from local infection with GAS and their products
  2. Diseases resulting from invasion of GAS
  3. Infective endocarditis
  4. Post-streptococcal disease
68
Q

Clinical manifestation of streptococcal sore throat scarlet fever rash? 2

A
  1. Strawberry colored tongue with pale color around mouth = circumoral pallor
  2. Sand-paper like rashes on trunk and limbs
69
Q

Other name for streptococcal pyoderma?

A

Impetigo

70
Q

5 M types of streptococcal pyoderma?

A

M types 49, 57, 59-61

71
Q

Common co-infection with streptococcal pyoderma?

A

With staphylococcus aureus

72
Q

Population at risk of streptococcal pyoderma?

A

Kids starting school

73
Q

Clinical manifestation of streptococcal pyoderma?

A

Honey-crusted lesions

74
Q

Which skin infection is deeper in the dermis: impetigo or erysipelas?

A

Erysipelas

75
Q

Other name for puerperal fever?

A

Childbed fever

76
Q

Other bacteria that cause puerperal fever?

A

GBS

77
Q

Why can invasive GAS infections lead to toxic-shock syndrome?

A

Due to the superantigenicity of the pyrogenic exotoxins produced by GAS

78
Q

Why do certain patients that have GAS pharyngitis develop acute rheumatic fever?

A

Some individuals are susceptible to this because of the particular T cell repertoire they have and their particular MHCs that enable them to recognize certain peptides

79
Q

Disease type of acute rheumatic fever?

A

Musculoskeletal disease

80
Q

Does acute rheumatic fever affect all layers of the heart?

A

YUP

81
Q

Pathogenesis of acute rheumatic fever?

A

Antibodies against streptococcus are cross-reacting with host tissues

82
Q

Gell and Coombs classification for acute rheumatic fever?

A

Type II

83
Q

How to make an acute rheumatic fever diagnosis?

A

Test blood for high titers of antibodies against streptolysin O => > 250 units indicates recent or repeated infections

84
Q

Long-term effect of acute rheumatic fever? Implication?

A

Permanent cardiac scarring, especially the valves => more susceptible to be colonized by any bacteria in the blood

85
Q

Long-term effect of acute glomerulonephritis?

A

NONE

86
Q

Immunity against the erythrogenic toxins in GAS infections? What to note?

A

Neutralized by antitoxins

NOTE: no effect on infection

87
Q

What GAS immunity follows infection?

A

Antibodies against streptolysin O

88
Q

GAS infection diagnostic tool?

A

Anti-DNAse antibodies

89
Q

How to make an acute glomerulonephritis diagnosis?

A

Anti-DNAse antibodies

90
Q

Transmission of GAS infections?

A

Transmission from one infected person to the other (horizontal transfer), as it is not carried asymptomatically

91
Q

Can Streptococcus pneumoniae be asymptomatic?

A

YUP

92
Q

3 tests to identify Streptococcus pneumoniae?

A
  1. Gram stains => should be +
  2. Catalase test => should be -
  3. Optochin (detergent = O-disk) OR bile test on blood agar plate => cell wall undergoes lysis due to activation of cell wall transpeptidases (autolysins) => should be + with clear zone surrounding the disk
93
Q

Specimen to send to lab for testing for Streptococcus pneumoniae?

A

Sputum sample

94
Q

What is special about the Streptococcus pneumoniae capsule?

A

It is produced on blood agar plate (not usually the case) => colonies have a mucoid appearance

95
Q

How to differentiate Streptococcus pneumoniae from all of the viridans streptococci that are residents in the oralpharynx? Why?

A

O-disk/bile disk because all of them are resistant to optochin/bile

96
Q

Most important virulence factor of Streptococcus pneumoniae?

A

Cps = polysaccharide capsule

97
Q

Why are virulence factors not as relevant in Streptococcus pneumoniae? Implication?

A

Because the virulence is caused by the immune response against the pathogen: pathogen + detergents => lysis releasing pro-inflammatory molecules associated with the gram + cell wall (e.g. proteoglycans, lipoteichoic acid, wall teichoic acid), which are PAMPs

Implication: naturally acquired immunity is high with opsonic antibodies, which are capsule specific

98
Q

3 diseases caused by Streptococcus pneumoniae?

A
  1. Pneumonia
  2. Middle ear infections = otitis media
  3. Meningitis
99
Q

What is special about Streptococcus pneumoniae immunity?

A

Immunity transferred from mother to neonate with IgGs for 3-5 weeks postpartum, which is important while the newborn ramps up his own immune system

100
Q

2 vaccines for Streptococcus pneumoniae? What to note?

A
  1. Polyvalent conjugated capsular polysaccharide with proteins that are virulent factors for other bacteria (e.g. exotoxins) = T-dependent antigen (13 capsule types)
  2. 23 capsule types (most virulent ones) protecting against 90% of pneumococcal infections

NOTE: #2 does not work in neonates and the elderly because polysaccharide antigens are T-independent (Ti2) and induce IgMs, which newborns/elderly cannot handle

SMP - MIM Part 2 (13 decks)

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