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Infection and Immunity > 26 Staphylocci and Streptococci > Flashcards

26 Staphylocci and Streptococci Flashcards

1
Q

how many are in the staphylococci genus

A

approx 50 different species

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2
Q

what is the most common/important species causing human disease -staph

A

Staphylococcus aureus

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3
Q

what is the second most important species in humans - staph

A

Staphylococcus epidermidis

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4
Q

what gram is staph

A

positive

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5
Q

what morphology is staph

A

cocci form in clusters of cells

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6
Q

examples of staphylococcus aureus infections/syndromes include

A
  • impetigo
  • sepsis
  • food poisoning
  • TSS
  • septic arthritis
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7
Q

what are the infections of staph like

A

Many of these infections are relatively minor and superficial – skin and soft tissue infections

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8
Q

what are some staph infections like

A

associated with entry into the bloodstream to cause more serious disease in deeper tissues
Some S.aureus diseases are associated with production of specific toxins

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9
Q

where is staph aureus present

A

Around 50% of population carry it
- permanently
- intermittently in back of nose
Also carried in armpits (axillae), groin and gut

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10
Q

what type of bacteria is staph

A

usually commensal

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11
Q

when is staph harmful

A

S. aureus penetrates skin and find way into other body sites can cause disease = opportunistic pathogen

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12
Q

what are endogenous infections

A

infect self, own S. aureus by transfer from nose, axillae or groin to site of tissue damage e.g. cut, surgery

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13
Q

what are exogenous infections

A

S. aureus transferred from another infected individual, carrier or from environment to site of tissue damage

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14
Q

how can staph aureus survive in environment

A

S. aureus resists desiccation = can survive in environment in dust and surfaces

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15
Q

what immune responses are triggered due to S. aureus

A

Innate and acquired immune responses

phagocytosis

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16
Q

when is phagocytosis triggered in staph infection

A

Phagocytosis after opsonisation by AB and complement important for controlling infection

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17
Q

what is used to prevent staph aureus infection

A

no vaccine available

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18
Q

how good is the immune system at removing staph infection

A

not always able to eliminate infection or prevent re-infection with staphylococci

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19
Q

what are the staph virulence factors associated with

A

production of a large number of surface proteins, toxins and immune evasion factors

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20
Q

what are the virulence factors - surface proteins

A

Surface proteins act as adhesins for colonisation, receptors for nutrient uptake and protect against immune responses

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21
Q

how can staph aureus isolates exchange genes

A

by horizontal gene transfer e.g. on plasmids, transposons, bacteriophage…

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22
Q

Virulence factors promoting invasion and tissue damage include

A
  • enterotoxins
  • proteases
  • lipases
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23
Q

Virulence factors promoting colonisation include

A
  • clumping factors
  • protein A
  • adhesins
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24
Q

what is staph aureus adhesins important for

A

Adhesion important in initial infection stage – colonisation

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25
Q

what does the staph aureus adhere to

A

mammalian cells e.g. nasal epithelial cells, also biomaterial surfaces e.g. catheters

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26
Q

example of a staph aureus adhesin family

A

MSCRAMMs

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27
Q

what is MSCRAMMs

A

Microbial Surface Components Recognising Adhesive Matrix Molecules

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28
Q

what do MSCRAMMs do

A

Bind to mammalian extracellular matrix (ECM) proteins e.g. fibronectin, fibrinogen collagen etc.

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29
Q

what are MSCRAMMs involved in

A

Involved in initial tissue colonisation e.g:

  • FnbA/B - Fibronectin binding proteins
  • Cna - Collagen binding protein
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30
Q

examples of staph aureus toxins

A 
Panton Valentine leucocidin 
Alpha-hemolysin 
Phenol soluble modulins 
Exfoliative toxins A and B 
Toxic shock syndrome toxin 
Enterotoxins
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31
Q

what does PVL do

A

lyses neutrophils

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32
Q

what does alpha-hemolysin do

A

lyses RBC, inhibits neutrophil chemotaxis

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33
Q

what do phenol soluble modulins do

A

cytotoxic peptides which are active against leukocytes – induce chemotaxis, induce IL-8 production and cause neutrophil lysis (intracellular)

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34
Q

what do ETA/B do

A

cause symptoms of scalded skin syndrome by splitting the dermis from the epidermis in skin

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35
Q

what does TSST-1 do

A

TSS by acting as a superantigen to non-specifically trigger excessive cytokine production by T cells

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36
Q

what do enterotoxins do

A

cause food poisoning (intoxication) can also act as superantigens causing TSS

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37
Q

Examples of S.aureus virulence factors that affect immune function

A

Antibody function
Complement activation or function
Antibody and Complement functions

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38
Q

what is the AB function in S.aureus virulence factors that affect immune function

A

Protein A and Staphylococcal binder of immunoglobulin (Sbi) are proteins that interfere with opsonisation by AB

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39
Q

what is the complement activation in S.aureus virulence factors that affect immune function

A

staphylococcal complement inhibitor (SCIN) interact with bacterial bound C3 convertases which facilitate C3b binding to bacterial surface – normally promotes opsonisation and phagocytosis

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40
Q

what is the AB and complement functions in S.aureus virulence factors that affect immune function

A

Staphylokinase activates plasminogen to make active protease – plasmin, can degrade complement opsonin C3b and Fc component of immunoglobulins

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41
Q

where is staphylococcus epidermis found

A

Member of normal skin flora

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42
Q

what are the Staphylococcus epidermis infection causes

A

tend to be less acute than those caused by S. aureus – infection is subacute or chronic

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43
Q

what is most important about staph epidermis in infections

A

Most important as cause of biomaterial related infection

- infections associated with medical device use

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44
Q

what makes biofilms

A

S.epidermidis and S.aureus can both form biofilms on biomaterials such as catheters

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45
Q

how does a biofilm form

A

Bacteria are encased in a matrix consisting of bacterial polysaccharides and extracellular DNA released from dead bacterial cells

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46
Q

what is a biofilm

A

Bacteria grow attached to the catheter surface to form a three dimensional aggregate

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47
Q

how are biofilms treated

A

Bacteria growing in biofilms may be more difficult to treat with antibiotics

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48
Q

are biofilms easy to killl

A

Bacteria in biofilms are more difficult for phagocytic cells to ingest and kill

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49
Q

how many species does the streptococci genus contain

A

around 40 species

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50
Q

what are most streptococci like

A

many Streptococci are commensal bacteria – but may act as opportunistic pathogens

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51
Q

what are some streptococci

A

Some Streptococci are primary pathogens – able to cause disease in fit, healthy people

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52
Q

what gram are streptococci

A

Gram positive

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53
Q

what is the morphology of streptococci

A

cocci which form chains or pairs of cells

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54
Q

Streptococci – main pathogens

A

Streptococcus pyogenes Streptococcus pneumoniae

Streptococcus mutans, Streptococcus mitior etc

55
Q

what does Streptococcus pyogenes cause

A

things including: Sore throat, scarlet fever, skin infection, bacteraemia, toxic shock

56
Q

what does Streptococcus pneumoniae cause

A

things including: Pneumonia, sinusitis, meningitis

- A vaccine is available to prevent S.pneumoniae infection

57
Q

what does Streptococcus mutans, Streptococcus mitior etc cause

A

things including: Dental caries, Infective endocarditis

58
Q

what does Streptococcus pyogenes infect

A

only humans

59
Q

what is the source of strap pyogenes infection

A

other infected individuals

60
Q

what Lancefield Group is strep pyogenes

A

Group A (Group A Strep – GAS)

61
Q

what is lancefield grouping

A

Lancefield typing system differentiates streptococci based on differences in their surface polysaccharide antigens

62
Q

what is characteristic of strep pyogenes

A

b- haemolytic makes haemolysin – Streptolysin S – which breaks down red blood cells

63
Q

what is used to prevent strep pyogenes infections

A

Currently no vaccines are available to prevent S.pyogenes disease

64
Q

what are some of the non-invasive diseases that strep pyogenes causes

A

Pharyngitis
Scarlet Fever
Skin infections

65
Q

where do non-invasive diseases infect

A

Upper respiratory tract commonest site of infection and entry to the body

66
Q

who carries strep pyogenes

A

People recovering from infection may carry S.pyogenes in the throat
Few healthy adults carry S.pyogenes but in young school children >10% may carry the organism

67
Q

what does pharyngitis cause

A
  • Sore throat, fever, malaise and headache

- Enlarged tonsils

68
Q

what is pharyngitis known as

A

“Strep sore throat”

69
Q

what does scarlet fever cause

A
  • Causes a diffuse rash on the skin and mucous membranes

- Eventually the tongue goes red - “Strawberry tongue”

70
Q

what causes scarlet fever

A

Follows throat infection by some strains of S.pyogenes that produce erythrogenic toxins

71
Q

examples of skin infections

A
  • Impetigo

- Erysipelas

72
Q

what is erysipelas

A

more serious –affects superficial skin layers – may lead to cellulitis and spread to bloodstream to cause bacteraemia

73
Q

what is sequalae of S.pyogenes infections

A

In some people, additional symptoms develop 1-5 weeks after the initial infection
“sequalae” are thought to be due to immune reactions to S.pyogenes which induce an autoimmune response against host tissues

74
Q

what is an example of sequale - strep pyogenes

A

e.g Rheumatic fever after Strep sore throat

75
Q

what is acute post-Strep glomerulonephritis

A

Immune complex mediated disease affecting the kidneys

76
Q

what is an Invasive S.pyogenes disease

A

Infection spreads into deeper soft tissues

77
Q

what are invasive S.pyogenes diseases associated with

A

These infections are frequently associated with bacteraemia

78
Q

who is at risk to invasive diseases

A

Invasive disease may occur in healthy people but people with chronic illnesses are at increased risk
e.g patients with cancer, diabetes, dialysis patients, patients on steroids

79
Q

examples of invasive diseases - strep pyogenes

A

Necrotising fasciitis
Strep TSS
bacteraemia

80
Q

what does Necrotising fasciitis cause

A
  • Infection destroys fat and muscle fascia – skin may not be affected
  • Infection is progressive, and bacteraemia leads to systemic shock
81
Q

what causes Strep TSS

A

by release of streptococcal toxins into the bloodstream

82
Q

what causes bacteraemia

A

S.pyogenes grows very rapidly in the bloodstream

83
Q

what can bacteraemia cause

A

acute endocarditis

84
Q

what is the mortality rate for bacteraemia

A

40%

85
Q

what allows S.pyogenes to cause infection - disease

A

Disease causation involves adhesion, avoidance of components of the immune system and toxin production

86
Q

why is s. pyogenes able to cause range of diseases

A

S.pyogenes produces a range of virulence factors which contribute to these functions

87
Q

how can genes encoding virulence factors for S. pyogenes by transferred

A

Genes encoding virulence factors may be transferred horizontally by bacteriophage

88
Q

where does S.pyogenes binds to

A

connective tissue protein fibronectin in the pharynx and on the skin

89
Q

where do the adhesins anchor - s. pyogenes

A

anchors the bacterium into that location so it is able to persist

90
Q

what mediates s. pyogenes adhesins

A

Adhesion is mediated by the F protein which also mediates internalisation of S.pyogenes into cells

91
Q

what is involved in adhesion

A

M protein

lipoteichoic acid

92
Q

what do M proteins form

A

fibrillar structures on the bacterial surface

93
Q

how many M proteins are there

A

over 80

94
Q

why is recurrence of strep pyogenes common

A

Antibody against one M protein won’t affect function of a different type

95
Q

what is the effect of M protein presence

A

prevent phagocytosis

96
Q

what do M proteins bind to

A

host proteins such as fibrinogen, plasminogen and IgG and IgA to their surfaces which can mask the bacterium from immune system

97
Q

what is factor H

A

causes destabilisation of major complement opsonin C3b = bacterium may not be recognised by phagocytic cells so is able to persist in the tissues

98
Q

what does s. pyogenes make

A

makes C5a peptidase

99
Q

what does C5a peptidase do

A

degrades C5a, a product of the complement system

100
Q

what do some s. pyogenes strains contain

A

capsule – made of hyaluronic acid

101
Q

what is the effect of hyaluronic acid capsule of s. pyogenes

A

Capsule is anti-phagocytic because it is made of the same hyaluronic acid polymer which forms part of the connective tissue in humans
= immune system does not recognise the capsule as “foreign” no immune response is induced

102
Q

what are the s. pyogenes toxins

A

Streptolysins

Pyrogenic exotoxins

103
Q

what are the streptolysin toxins

A

Streptolysin O

Streptolysin S

104
Q

what is streptolysin O

A

secreted exotoxin

105
Q

what does streptolysin O cause

A

acute effects on heart muscle – lethal in animals

106
Q

what is streptolysin s

A

surface bound

107
Q

what does streptolysin S cause

A

beta-haemolysis

108
Q

what are the pyrogenic exotoxins

A

SPEA, SPEB, SPEC and others

109
Q

what is the effect of pyrogenic exotoxins

A

lethal in animals

110
Q

what do the pyrogenic toxins cause

A

rash seen in scarlet fever

111
Q

what are pyrogenic toxins known as

A

superantigens

112
Q

what does a superantigen cause

A

antigen-independent activation of T cells

113
Q

what is the result of superantigen

A
  • over production of pro-inflammatory cytokines such as IL-1 and TNF – a
  • inflammation, tissue damage, shock and organ failure – may be lethal
114
Q

what does hyaluronidase do

A

S.pyogenes virulence factors

enzyme degrades hyaluronic acid in connective tissue

115
Q

what is streptokinase

A

S.pyogenes virulence factors

enzyme activates a host protease precursor (plasminogen) to produce an active protease called plasmin

116
Q

what does the plasmin do made from streptokinase

A

degrades fibrin clots which may form around the site of tissue damage and infection

117
Q

what does the streptokinase allow

A

S.pyogenes to escape and spread into surrounding tissue

118
Q

what is streptokinase used to treat

A

used therapeutically in patients who have had heart attacks to break down fibrin clots

119
Q

what is Streptococcus pneumoniae

A

member of the normal oropharyngeal flora of between 5 and 70% of the human population

120
Q

what can Streptococcus pneumoniae cause

A

e.g influenza, bronchitis, diabetes

121
Q

what is streptococcus pneumoniae

A

a - haemolytic Streptococcus

122
Q

what does streptococcus pneumoniae make

A

produces hydrogen peroxide which reacts with haemoglobin to produce methaemoglobin resulting in a characteristic greening around bacterial growth on blood agar

123
Q

what is S.pneumoniae meningitis

A

Among the leading causes of bacterial meningitis

124
Q

where does the S.pneumoniae move in infection

A

Bacterium moves from the pharynx into the bloodstream and crosses blood-brain barrier to reach meninges

125
Q

what can s. pneumoniae cause

A

sepsis

126
Q

what does s. pneumoniae make

A

polysaccharide capsule which is a major virulence determinant

127
Q

what is the effect of S.pneumoniae virulence factors - anti-phagocytic

A

inhibits complement deposition and phagocytosis in the absence of type specific antibody

128
Q

what is the effect of S.pneumoniae producing a capsule

A

produce particular capsule type will induce antibody production against the capsule, but this antibody will not protect against re-infection with S.pneumoniae carrying a different capsule type

129
Q

what vaccine is there for s. pneumoniae

A

vaccine based on the polysaccharide capsule antigens from 23 different serotypes has been used for a number of years

130
Q

what does IgA1 protease do

A

Cleaves IgA1 – the main antibody type found in the upper respiratory tract mucosa
Prevents the antibody from binding to the bacterium

131
Q

what is Pneumolysin

A

intracellular, membrane damaging toxin which is released from S.pneumoniae when it undergoes autolysis

132
Q

what does pneumolysin cause

A

Inhibits neutrophil chemotaxis, phagocytosis and the respiratory burst involved in killing of phagocytosed bacteria

133
Q

what is autolysin

A

enzyme produced by S.pneumoniae which breaks down the bacterial peptidoglycan in the cell wall

134
Q

what does autolysin release

A

pneumolysin and fragments of peptidoglycan from the bacterial cells

Infection and Immunity (29 decks)

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