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Dermatology > Bacterial Virulence > Flashcards

Bacterial Virulence Flashcards

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Dermatology Board Prep flashcards
1
Q

What do virulence factors contribute to?

A

The microbes ability to cause pathology

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2
Q

What is the function of adhesin?

A

Enables the binding of the organism to host tissue

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3
Q

What is the function of invasion?

A

Enables the organism to evade a host cell/tissue

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4
Q

What is the function of impedin?

A

Enables the organism to avoid host defence mechanism

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5
Q

What is the function of aggressin?

A

Causes damage to the host directly

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6
Q

What is the function of modulin?

A

Induces damage to the host indirectly

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7
Q

What are the factors responsible for the variation in virulence within and between species?

A

Adhesin
Impedin
Aggressin

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8
Q

What are the infections of the skin most commonly?

A

Gram +ve staphylococcus and streptocuccus

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9
Q

What differentiates staph aureus and staph epidermidis?

A

Coagulase test

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10
Q

Where is staph aureus common?

A

Anterior nares and perineum

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11
Q

Where is staph aureus contracted?

A

Nosocomial and community

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12
Q

What is MRSA defined by?

A

Flucloxacillin resistance

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13
Q

Who gets MRSA and where?

A 
Nosocomial
Elderly and immunocompromised 
ICU
surgical patients
IV lines
Dialysis patients
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14
Q

Where is staph epidermidis common?

A

Skin and mucous membrane

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15
Q

Who gets staph epidermis?

A

Nosocomial infection in immunocompromised

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16
Q

What is staph epidermidis associated with?

A

Foreign devices e.g. catheters

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17
Q

What does superficial staph aureus look like?

A

Lesions- boils to abscesses

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18
Q

What is the toxinoses risk with S. aureus?

A

Toxic shock, scared skin syndrome

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19
Q

What is the role of fibrinogen binding protein in staph aureus?

A

Adhesin

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20
Q

What is the role of coagulase in staph aureus?

A

Clots plasma

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21
Q

What is the role of leukocidin (PVL) in staph aureus?

A

Kills leukocytes

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22
Q

What is the role of TSST-1 in staph aureus?

A

Shock, rash, desquamation

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23
Q

What is the progression and symptoms of TSST-1?

A

Rapid progression (48hrs)

High fever

vomiting

diarrhoea

sore throat

muscle pain

24
Q

What is the progression and symptoms of staphylococcal food poisoning?
enterotoxin SeA, SeB, SeC

A

intoxication
1-5hrs
vomiting diarrhoea

25
Q

Describe SSS

A

> exfoliation toxins, often neonatal, face, axilla and groin

>ETA & ETB toxins target Desmoglein-1 (DG-1)

26
Q

What is a super antigen?

A

activate 1 in 5 T cells (normally 1:10,000)

Antigen is not processed by PMN and binds directly to MHCII complex outside of conventional binding groove

27
Q

What is the result of super antigen activation?

A

Massive release of cytokines and inappropriate immune response

28
Q

What are the diagnostic criteria for TSS?

A

-Fever >39
-Diffuse macular rash and desquamation (diffuse macular erythroderma- suburn)
-hypotension =90mmHg in adults
->/=3 organ systems involved
liver, muscular, blood, renal, mucous, GI , CNS

29
Q

What are adhesins?

A

Extracellular matrix molecules are present on epithelial, endothelial surfaces as well as a component of blood clots

30
Q

Name three adhesins

A

Fibrinogen binding (ClfA ClfB)

Collagen binding (CNA)

Elastin binding protein (EbpS)

31
Q

What is Panton-Valentine Leukocidin?

A

PVL bicomponent toxin (lukS and lukF)

Specifically toxic to leukocytes

32
Q

What is PVL associated with?

A

Severe skin infections

e.g. recurrent furunculosis, sepsis/necrotizing fasciitis

33
Q

What are PVL and alpha toxin linked to?

A

CA-MRSA responsible for necrotising pneumonia and contagious severe skin infections

34
Q

What is necrotising pneunomia?

A

Preceding influenza like syndrome, neutralising haemorrhagic pneumonia

35
Q

Describe the presentation of necrotising pneumonia?

A

Rapid progression

ARDS

Deterioration in pulmonary function

Refractory hypoxaemia

Multi-organ failure despite antibiotic therapy

36
Q

Describe streptococcus pyogenes?

A

Gram +ve cocci in chains

Catalase negative
B haemolysis

37
Q

What infections does streptococcus pyogenes cause?

A

Impetigo
Cellulitis
Necrotising faciitis

38
Q

What is the lancefield system,?

A

Serotyping of cell wall carbohydrates

39
Q

How many major lancefield serotypes are there?

A

A-H and K-V (20)

40
Q

How are group a lancefield further divided?

A

M protein antigens

  • M1 & M3 major serotype
  • M3 & M18 severe invasive disease
  • emm typing and emm89 epidemic
41
Q

What are the GAS skin diseases?

A

Impetigo
Cellulitis
Erysipelas

42
Q

Describe impetigo

A

Highly contagious through contact with discharge on the face. infection immediately below surface (stratum corneum-keratin layers)

43
Q

Describe cellulitis

A

deeper skin infections in the dermis

not associated with necrosis

44
Q

Describe erysipelas

A

Fever, riggers, nausea

45
Q

What are the iGAS diseases?

A

Invasive group A streptococci

  • cellulitis
  • necrotising fasciitis
46
Q

Describe necrotising fasciitis

A

> Type I, clostridia spp

> invasive streptococcus A strains penetrate mucous membrane and develop in lesion

> rapidly destroys connective tissue

47
Q

What proteins are responsible for tissue/cell destruction?

A

Haemolysins

Streptolysin S

48
Q

What is the role of SLS?

A

Pore forming cytolysis

Toxic to PMN, organelles, platelets, important in animal models

49
Q

What are the virulence factors of Streptococcus pyogenes?

A

Superantigenic towns

Haemolysins

Capsule

M-protein binds;
>factor M
>fibrinonectin
>fibrinogen
>albumin
50
Q

Describe TSLS (toxic shock like syndrome)

A 
Pyogenic exotoxin
-complication of invasive infections
-30% mortality
-hours to days
hypotension to organ failure 
-SpeB, SpeC
51
Q

What is a pyrogen

A

Agent that causes a raise in body tissue

52
Q

Describe S.aureus toxic shock

A
  • localised infection
  • no bacteraemia
  • menstrual TSST-1
  • non-menstrual SEB or SEC
  • pyrogenic toxin
53
Q

Describe S. pyogenes toxic shock

A
  • invasive disease (pharyngitis
  • SpeA and SpeC most common toxin
  • pyrogenic toxin
54
Q

What do S. aureus and s. pyogenes toxic shock have in common?

A

Virulence factor: Superantigen

55
Q

What are the stages of horizontal gene transfer between bacteria?

A

a. bacterial transformation
b. bacterial transduction
c. bacterial conjugation

Dermatology (15 decks)

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