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Dermatology > Bacterial Virulence > Flashcards

Bacterial Virulence Flashcards

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Dermatology Board Prep flashcards
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
Q

How do superantigens work?

A

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

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26
Q

What is TSST-1 associated with in particular?

A

Toxic shock syndrome

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27
Q

What are the diagnostic criteria for toxic shock syndrome?

A

Fever=39C
Diffuse macular erythroderma and desquamation
Hypotension = 90 mmHg (adults)
>/= 3 organ systems involved (liver, blood, renal etc)

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28
Q

What are adhesins involved in?

A

Attachment/colonisation

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29
Q

Where are extra cellular matrix molecules present?

A

Epithelial and endothelial surfaces as well as a component of blood clots

30
Q

What are some methods that viruses use to evade host defences?

A

Protein A, Proteases, Superantigens, Lipases, Phospholipases, Esterase, Coagulase

31
Q

What does PVL stand for?

A

Panton-Valentine Leukocidin

32
Q

What are the two bicomponent toxins present in PVL?

A

lukS and lukF

33
Q

What does PVL have a specific toxicity for?

A

Leukocytes

34
Q

Name some conditions associated with PVL?

A

Recurrent furunculosis, sepsis/ necrotising fasciitis

35
Q

What have PVL and the a-toxin linked with CA-MRSA been associated with?

A

Necrotising pneumonia and contagious severe skin infections

36
Q

What precedes necrotising pneumonia?

A

Influenza-like syndrome

37
Q

Is necrotising pneumonia haemorrhagic?

A

Yes

38
Q

How does necrotising pneumonia progress?

A

Acute respiratory distress, deterioration in pulmonary function, refractory hypoxaemia, multi-organ failure despite antibiotic therapy

39
Q

What are some ways virulence factors impact on clinical care?

A

Next generation sequencing, molecular techniques (PCR, antibodies), diagnosis (understanding pathology/risk), epidemiology, vaccines/anti-infectives, novel approaches (e.g replacement therapy)

40
Q

What are some features of Streptococcus pyogenes?

A

Gram + cocci, chains, catalase negative, GAS (beta haemolysis)

41
Q

How is Streptococcus pyogenes classified?

A

Using the Lancefield system (surface antigen), serotyping of cell wall carbohydrate, C polysaccharides extracted from cell wall

42
Q

What are the major serotypes of Streptococcus pyogenes?

A

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
Q

What are the two kinds of viral capsule?

A

Mucoid and microcapsule

44
Q

What are some conditions linked to Streptococcus pyogenes?

A

Impetigo, Cellulitis, Necrotising fasciitis, Toxic shock like syndrome (TSLS)

45
Q

Where does the infection of Impetigo take place?

A

Usually the face, infection is immediately below surface

46
Q

Is Impetigo contagious?

A

Yes-highly contagious through contact with discharge on the face

47
Q

What is cellulitis?

A

General term for a deeper infection in the dermis that isn’t associated with necrosis, range of spreading subcutaneous skin infections

48
Q

What is the primary infection/trauma of cellulitis associated with?

A

Associated with the organism spreading through the blood and seeding cellulitis

49
Q

What is Erysipelas?

A

Localised cellulitis-fever, rigors, nausea

50
Q

What causes necrotising fasciitis?

A

Invasive Strep.A strains penetrate mucous membrane and develop in lesion, rapidly destroys connective tissue, may have TSLS

51
Q

What bacteria causes Type 1 necrotising fasciitis?

A

Clostridia spp.

52
Q

What does iGAS stand for?

A

Invasive Group A Strep.

53
Q

What causes TSLS?

A

Pyrogenic exotoxins

54
Q

What are some features of TSLS?

A

Complication of invasive infections, 30% mortality, hours-days, hypotension to organ failure, SpeA/B/C/F

55
Q

How do haemolysins cause cell destruction?

A

Second soluble oxygen labile haemolysin SLO contributes to tissue destruction

56
Q

What is Streptolysin S (SLS)?

A

Pore forming cytolysin, toxic to PMN and organelles as well as platelets, causes tissue and cell destruction

57
Q

What are some of Strep. pyogenes virulence factors?

A

Superantigenic toxins, capsule, Haemolysins SLO/SLS cause tissue damage and ulcers

58
Q

What does the M protein in the Strep. pyogenes capsule bind to?

A

Factor M, fibronectin, fibrinogen, albumin

59
Q

What are the features of toxic shock caused by S.aureus?

A

Localised infection, no bacteremia, menstrual TSST-1, non-menstrual SEB/SEC, pyrogenic toxin

60
Q

What are the features of toxic shock caused by Strep. pyogenes?

A

Invasive disease (pharyngitis), SpeA/SpeC most common toxin, pyrogenic toxin

61
Q

What is the virulence factor involved in toxic shock caused by both S.aureus and Strep. pyogenes?

A

Superantigens

62
Q

What are the toxic shock toxins of S.aureus?

A

TSST-1, SEA, SEB

63
Q

What are the toxic shock toxins of Strep.pyogenes?

A

SpeA, SpeC

64
Q

How does virulence vary?

A

Strain evolution through mobile genetic elements encoding virulence determinants?

65
Q

What are some mobile genetic elements that encode for virulence determinants?

A

Plasmids, bacteriophage, transposons and IS, pathogenicity islands (PI)

66
Q

What do opportunistic infections and toxinoses depend on?

A

Genotype and expression of virulence proteins

67
Q

Where is Strep. pyogenes normally found?

A

In the pharynx (also adheres to skin)

68
Q

How can toxic shock be produced by more than one organism?

A

Due to production of similar exo-proteins, common virulence factors and disease mechanisms

69
Q

Is S.aureus coagulase positive or negative?

A

Coagulase positive

70
Q

Is S.epidermidis coagulase positive or negative?

A

Coagulase negative

71
Q

What are some examples of adhesins?

A

Fibrinogen-binding (ClfA/B), Fibronectin-binding (FnbpA/B), Collagen binding (CNA), Elastin binding protein (Ebps)

Dermatology (31 decks)

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