L4- skin and soft tissue infection Flashcards

1
Q

what is Cellulitis

A

infection of the dermis and subcutaneous tissue

- often seen arounf injury site or deep abscess

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2
Q

eryipelas definitions

A

impetigo - common acute superficial s.pyogenes skin infection of dermis and the lymphatics

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3
Q

how does the innate immune system recognise the pathogens?

A

recognises pathogen associated molecular patterns (PAMPS) by pattern recognition receptors.

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4
Q

binding of PAMPS to the pattern recognising receptors causes..

A

propagation of action potential –> causes transcription for cytokine reelase (IL8)

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5
Q

what effect does cytokine release have on the endothelial cells?

A

causes expression of E-selectin on endothelial cell

- binds to neutrohils (slows down)

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6
Q

what is diapedesis?

A

neutrophils squeeze through the endothelial barriers (leukocyte extravasation)

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7
Q

what are the main organisms that cause SSTIs?

A

s. pyogenes
s. aureus
other bacteria/ fungi
viruses

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8
Q

characterstics of streptococcus?

shape, what can it cause?

A
gram positive spherical/cocci
- SSTI
- Toxic shock
- pharyngitis
acute rheumatic fever
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9
Q

how to test for streptococcus?

A

known antibody is added to the agar plate sample, should bind to antigen –> cuause agglutination

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10
Q

what is the route of infection of GAS?

- mode of transmission

A

asymptomatic colonisation of the oropharynx (relatively common)

  • they are opportunistic
  • transmitted by human contact
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11
Q

how does the s. pyogenes recognise teh host cell?

A

has MSCRAMMS on their cell surface (microbial surface components recognising adhesive matrix molecules)
- helps them bind to components of the host cell (fibronectin, elastin and collagen etc)

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12
Q

How does s. Pyogenes evade immune responses?

what are the 3 structures that prevent it from being detected by the immune system?

A

hyaluronic acid
M protein
secretion of toxins

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13
Q

what is the function of hyaluronic acid in avoiding the immune response

A

prevents opsonisation and phagocytosis

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14
Q

role of M protein for S. pyogenes

A

binds to factor H (regulates the complement system)- prevents with C3b opsonisation

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15
Q

3 examples of toxins released by s.pyogenes to prevent immune responses

A

streptolysins (lyse immune cells)

C5a pepetidase (prevents neutrophil chemotaxis)

DNases (destroys neutrophils)

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16
Q

what is necrotising fasciculitis?
what is the prognosis?
treatment?

A

deep infection of the skin causing destruction of the tissue and fascia.

  • often develops into severe systemic disease (high mortality)
  • remove necrosed layers, pump with IV antibiotics and amputations.
17
Q

how are skin infections diagnosed?

A

swab the pus –> microbiology

18
Q

explain the order of testing process to differentiate gram positive bacteria the microbial cause of infection?

A

catalase test

haemolysis test

bacitracin susceptibility

19
Q

how does the catalase test work?

- negative/positive test results differentiate what?

A

if the bacteria has the catalase enzyme it will convert H2O2 into O2 (see bubbles)

  • negative (strep)
  • positive (staphylococci)
20
Q

haemolysis testing- procedue and result inrterpretation

A
not haemolytic (gamma)
partial haemolytic (alpha)
complete haemolysis (beta)
21
Q

bacitracin susceptibility

- sensitive/insensitive indications

A

sensitive - pyogenes

resistant - other forms of strep

22
Q

what is the treatment for SSTI?

how does this differ between s.pyogenes and s aureus

A

supportive care
analgesia
antimicrobial drugs
- pyogenes - penicillin or amoxiillin

staph- b-lactamase resistant penicillin

23
Q

what is the mechanism of penicilllin?

A

bacterial cell wall consists of 2 types of sugar complexes (NAM and NAG)
- bound by transpeptidase enzyme (this is inhibited by penicillin) = prevented by penicillin so weaker cell wall