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Bacterial Virulence Flashcards

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1
Q

What is the importance of virulence factors?

A

They contribute to microbes ability to cause pathology

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2
Q

What do adhesins do?

A

Enable binding of the organism to the host tissue

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3
Q

What does invasion do?

A

Allows the organism to invade a host cell/tissue

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4
Q

What is the function of impedin?

A

Lets the organism avoid host defence mechanisms

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5
Q

What does aggressin do?

A

Causes damage to the cell directly

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6
Q

What is the function of modulin?

A

Induces damage to the cell indirectly

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7
Q

What are virulence factors?

A

The factors responsible for variation in virulence within and between species

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8
Q

What does SSTI stand for?

A

Skin and Soft Tissue Infection

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9
Q

What microbiology causes SSTIs?

A

Natural flora, gram +/-, Staphylococcus, Streptococcus, Propionibacterium, Corynebacteria, Yeast

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10
Q

What are the two common species of staphylococci involved in skin infections?

A

S.epidermidis and S.aureus

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11
Q

Where is S. epidermidis found?

A

Skin and mucous membranes, 100% colonisation (nosocomial infection/immunocompromised)

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12
Q

What is S.epidermidis associated with?

A

Foreign devices

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13
Q

What is the percentage colonisation of S.aureus?

A

20-60%

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14
Q

Where is S.aureus found?

A

Anterior nares and perineum (nasal strain can protect), nosocomial and community

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15
Q

How is MRSA defined?

A

By resistance to flucloxacillin (mainly nosocomial)

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16
Q

Who gets MRSA?

A

Elderly and immunocompromised, ICU and burns patients, patients with IV lines and on dialysis

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17
Q

How does S.aureus infection present?

A

Superficial lesions (boil-abscesses), systemic manifestations (life threatening), toxinoses (toxic shock)

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18
Q

What are some examples of toxinoses?

A

TSST-1, Staphylococcal food poisoning, Scalded skin syndrome

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19
Q

What are toxinoses?

A

Illnesses caused by bacterial toxins alone

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20
Q

What are some features of TSST-1?

A

Rapid progression (48hrs), high fever, vomiting, diarrhoea, sore throat, muscle pain

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21
Q

What are some features of Staphylococcal food poisoning?

A

Intoxication, 1-5 hrs, vomiting, diarrhoea

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22
Q

What causes Staphylococcal food poisoning?

A

Enterotoxin SeA, SeB and SeC

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23
Q

What causes Scalded skin syndrome?

A

Exfoliatin toxins, ETA and ETB toxins target desmoglein-1 (DG-1)

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24
Q

Who gets scalded skin syndrome and where does if occur?

A

Often neonatal; occurs in face, axilla and groin

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25
How do superantigens work?
Activate 1 in 5 T cells, antigen is processed by PMN and binds directly to MHC II complex, causes massive release of cytokines and inappropriate immune response
26
What is TSST-1 associated with in particular?
Toxic shock syndrome
27
What are the diagnostic criteria for toxic shock syndrome?
Fever=39C Diffuse macular erythroderma and desquamation Hypotension = 90 mmHg (adults) >/= 3 organ systems involved (liver, blood, renal etc)
28
What are adhesins involved in?
Attachment/colonisation
29
Where are extra cellular matrix molecules present?
Epithelial and endothelial surfaces as well as a component of blood clots
30
What are some methods that viruses use to evade host defences?
Protein A, Proteases, Superantigens, Lipases, Phospholipases, Esterase, Coagulase
31
What does PVL stand for?
Panton-Valentine Leukocidin
32
What are the two bicomponent toxins present in PVL?
lukS and lukF
33
What does PVL have a specific toxicity for?
Leukocytes
34
Name some conditions associated with PVL?
Recurrent furunculosis, sepsis/ necrotising fasciitis
35
What have PVL and the a-toxin linked with CA-MRSA been associated with?
Necrotising pneumonia and contagious severe skin infections
36
What precedes necrotising pneumonia?
Influenza-like syndrome
37
Is necrotising pneumonia haemorrhagic?
Yes
38
How does necrotising pneumonia progress?
Acute respiratory distress, deterioration in pulmonary function, refractory hypoxaemia, multi-organ failure despite antibiotic therapy
39
What are some ways virulence factors impact on clinical care?
Next generation sequencing, molecular techniques (PCR, antibodies), diagnosis (understanding pathology/risk), epidemiology, vaccines/anti-infectives, novel approaches (e.g replacement therapy)
40
What are some features of Streptococcus pyogenes?
Gram + cocci, chains, catalase negative, GAS (beta haemolysis)
41
How is Streptococcus pyogenes classified?
Using the Lancefield system (surface antigen), serotyping of cell wall carbohydrate, C polysaccharides extracted from cell wall
42
What are the major serotypes of Streptococcus pyogenes?
A-H and K-V (20 types), group A further divided according to M proteins (M1 and M3 are major serotypes, M3 and M18 cause severe invasive diseases)
43
What are the two kinds of viral capsule?
Mucoid and microcapsule
44
What are some conditions linked to Streptococcus pyogenes?
Impetigo, Cellulitis, Necrotising fasciitis, Toxic shock like syndrome (TSLS)
45
Where does the infection of Impetigo take place?
Usually the face, infection is immediately below surface
46
Is Impetigo contagious?
Yes-highly contagious through contact with discharge on the face
47
What is cellulitis?
General term for a deeper infection in the dermis that isn't associated with necrosis, range of spreading subcutaneous skin infections
48
What is the primary infection/trauma of cellulitis associated with?
Associated with the organism spreading through the blood and seeding cellulitis
49
What is Erysipelas?
Localised cellulitis-fever, rigors, nausea
50
What causes necrotising fasciitis?
Invasive Strep.A strains penetrate mucous membrane and develop in lesion, rapidly destroys connective tissue, may have TSLS
51
What bacteria causes Type 1 necrotising fasciitis?
Clostridia spp.
52
What does iGAS stand for?
Invasive Group A Strep.
53
What causes TSLS?
Pyrogenic exotoxins
54
What are some features of TSLS?
Complication of invasive infections, 30% mortality, hours-days, hypotension to organ failure, SpeA/B/C/F
55
How do haemolysins cause cell destruction?
Second soluble oxygen labile haemolysin SLO contributes to tissue destruction
56
What is Streptolysin S (SLS)?
Pore forming cytolysin, toxic to PMN and organelles as well as platelets, causes tissue and cell destruction
57
What are some of Strep. pyogenes virulence factors?
Superantigenic toxins, capsule, Haemolysins SLO/SLS cause tissue damage and ulcers
58
What does the M protein in the Strep. pyogenes capsule bind to?
Factor M, fibronectin, fibrinogen, albumin
59
What are the features of toxic shock caused by S.aureus?
Localised infection, no bacteremia, menstrual TSST-1, non-menstrual SEB/SEC, pyrogenic toxin
60
What are the features of toxic shock caused by Strep. pyogenes?
Invasive disease (pharyngitis), SpeA/SpeC most common toxin, pyrogenic toxin
61
What is the virulence factor involved in toxic shock caused by both S.aureus and Strep. pyogenes?
Superantigens
62
What are the toxic shock toxins of S.aureus?
TSST-1, SEA, SEB
63
What are the toxic shock toxins of Strep.pyogenes?
SpeA, SpeC
64
How does virulence vary?
Strain evolution through mobile genetic elements encoding virulence determinants?
65
What are some mobile genetic elements that encode for virulence determinants?
Plasmids, bacteriophage, transposons and IS, pathogenicity islands (PI)
66
What do opportunistic infections and toxinoses depend on?
Genotype and expression of virulence proteins
67
Where is Strep. pyogenes normally found?
In the pharynx (also adheres to skin)
68
How can toxic shock be produced by more than one organism?
Due to production of similar exo-proteins, common virulence factors and disease mechanisms
69
Is S.aureus coagulase positive or negative?
Coagulase positive
70
Is S.epidermidis coagulase positive or negative?
Coagulase negative
71
What are some examples of adhesins?
Fibrinogen-binding (ClfA/B), Fibronectin-binding (FnbpA/B), Collagen binding (CNA), Elastin binding protein (Ebps)

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