L12. Skin and Soft Tissue infection Flashcards
What are the signs and symptoms of skin infection (4,3 systemic) and what are the fungi and viruses that can cause it
Erythema, Warmth, Tenderness/Pain, Purulence
Systemic: fever, increased HR, WBC
Fungi: eg. tinea,
Viruses: eg. chicken pox
What are the 3 non-purulent skin/soft tissue infection (ssi) and compare their presentation, layer of skin affected and main bacterial agent: strep A (pyogenes) / staph. aureus
- Cellulitis:
- Infection of the dermis and subcutaneous tissue
- Oedema and pain, with poorly demarcated erythema.
- Often around wound/abscess
- Can be Strep pyogenes or Staph a. - Erysipelas:
- Infection of the upper dermis and superior lymphatics
- Oedema, well demarcated erythema, Fever
- Mainly strep pyogenes - Necrotising fasciitis
- Infection that destroys tissue from epidermis to the fascia surrounding muscle.
- Evolves rapidly, excruciating pain, fever and systemic erythematous rash
- Has potential for sepsis due to easy spread to blood so high mortality
- Mainly Strep pyogenes
What are the 2 purulent skin/soft tissue infection (ssi) and compare their presentation, layer of skin affected and main bacterial agent
- Impetigo
- infection of the epidermis
- painless, erythematous base with honey-crusted exudate
- highly infectious,
mainly caused by Staph. a but can also be caused by Strep pyogenes - Carbuncle:
- multiple furuncles ( deep bacterial folliculitis within the dermis)
- tender, red, pustule centred on hair follicles.
- mainly caused by Staph A.
What are the steps involved in inflammatory response of bacteria entering a skin wound
- what is the role of cytokines and complement in this innate immune response
- Bacteria enters a wound -causing tissue damage via toxins or direct
- Platelets from blood release fibrinogen to make a blood clot and seal the bloodstream from bacteria
- Mast cell secrete immune modulators heparin and histamine to increase the delivery of blood, plasma and cells to the injured area
- Macrophages secrete pro-inflam chemokine and cytokines - leaky vessels, increase e-selectins/integrins to help neutrophils extravasate from blood to the site.
Chemotactic factors are IL8 and C5a.
- also helps to initiate repair - Neutrophils and macrophages phagocytose bacteria: helped by opsonisation with C3b which they have a receptor for.
- Inflammation continues until the wound is repaired and foreign material eliminated - macrophages help to clean up the pus.
What triggers the macrophage to secrete cytokines (activate) and give example
PAMPS - eg. LPS on gram - bacteria binds to Toll-like receptor 4.
This starts a signalling cascade which results in the production of cytokines IL8, Tnf-a, IL-1B. (pro-inflam)
What type of bacteria is Streptococcus pyogenes/ Group A strep: gram stain, shape.
What is its colonisation/transmission like
Gram positive spherical/ovoid cocci. It is catalyse negative (unlike staph)
There is transient colonisation of the skin, helped by breaks in the skin but mostly assymptomatic colonisation of the oropharynx in 15-20% of the population.
Transmission is by human contact - (coughing due to aerosol in oropharynx)
so higher rates in kindergarten/overcrowded house
What are the molecular mechanisms that help S. pyogenes colonisation of the skin
S. pyogenes has specific
Microbial surface components recognising adhesive matrix molecules (MSCRAMM)
that bind to host ECM proteins eg. fibronectin, elastin, laminin.
They also have fimbriae protruding through capsule which is important for adhering to epithelial cells- they have M protein associated
What are the ways that S. pyogenes can evade the immune system
- hyaluronic acid capsule which is immunological inert, preventing opsonisation and phagocytosis
- M protein (MSCRAMM) which binds host factor H in the blood - which is usually used by own cells to prevent opsonisation with C3b. different M proteins associated with
- Secretes toxins:
- Streptolysin to lyse immune cells
- C5a peptidase to destroy C5a +
- SpyCEP which destroys IL8 for neutrophil chemotaxis
-DNases which degrade neutrophil extracellular traps
What are factors secreted by S. pyogenes to help it spread into deeper tissue (2) and cause SSTIs like necrotising fasciitis and which is used clinically
Unspecific enzymes to cleave tissue: proteases, lipases, hyaluronidase
Streptokinase used to activate plasminogen to cleave fibrin clot to stop containment of the bacteria.
Is used clinically as an anticoagulant to prevent thrombosis
What are the steps to diagnosing S. pyogenes infection
- Get sample
a) Swab purulent material - intact skin not useful as only has commensal bacteria.
b) hospitilised patients which systemic symptoms should also get blood culture to determine bacteremia - View under microscope to check morphology
- confirm with catalyse test shape to differentiate streptococcus with staphylococcus.
- S pyogenes has negative test. S aureus has + test with bubbles bc of H2O2 conversion to O2 and H2O - Check haemolysis on blood agar. S pyogenes is B-haemolytic
- Check bacitracin susceptibility - antibiotic used for lab diagnosis
- S pyogenes won’t grow, but other eg. s. agalactiae will
What are the main treatments for S. pyogenes SSTI and mechanism of the antimicrobial
and compare to staph aureus treatment
- Supportive care: rest and elevation, analgesia
- Antimicrobial drugs: Penicillin/ derivative eg. amoxycillin,
Cephalosporin or Carbapenems
All b-lactam antibiotics which binds to transpeptidase enzyme and prevents formation of peptide cross-links in the bacterial cell wall, leaving weak cell wall and vulnerable to cell lysis
90% of S, aureus is not susceptible to penicillin so needs to be treated with b-lactamase resistant antibiotic except for MRSA strains
