Lecture 4: Skin and Soft tissue infection Flashcards
What are cellulitis and erysipelas?
Cellulitis is an infection of the dermis and subcutaneous tissue, often seen around an injury site or deep abcess. Can be caused by a number of bacteria including streptococcus pyogenes.
Erysipelas is an acute infection of the upper dermis and superficial lymphatics caused by strep pyogenes exclusively. Has a demarcation line unlike cellulitis.
Inflammation in response to bacterial infection?
- Bacteria and other pathogens enter the wound
- Platelets from blood release blood-clotting proteins at wound site to contain pathogens (out of BV)
- mast cells secrete vasoactive factors
- neutrophils secrete factors that kill and degrade pathogens
- Neutrophils and marophages remove pathogens
- macrophages secrete cytokines that attract immune cells and active tissue repair cells
- Inflammatory response continues till foreign material is gone and wound is repaired
Innate immune responses are? mediated by?
- Non-specific, generic responses to pathogens
- immediate response with no long-lasting immunity
- due to conserved/common pathogen features known as PAMPs = pathogen-associated molecular patterns - signal the expression of pro-inflammatory cytokines
Pro-inflammatory cytokine role in BV endothelium?
- Increase the expression of E-selectin on the endothelium to slow down neutrophils so they roll along and come to a stop
- They open up the gaps between the endothelium cells
- Known as leukocyte extravasation (diapedesis)
- Neutrophils then follow a chemotactic gradient (eg. IL-8 and C5a)
Major bacteria that cause SSTI?
Streptococcus pyogenes
Staphylococcus aureus
Some other bac: (eg. Vibrio vulnificus)
Fungi: (eg deratophytic moulds, tinea)
Viruses: (eg. chicken pox)
Transmission of GAS?
Group A Strep is exclusively found in humans and can:
- Asymptomatically colonise the oropharynx (15-20% population)
- Transient colonisation of skin
- Transmission by human contact
- High infection rates in overcrowded houses, schools etc.
Why is GAS exclusively in humans?
MSCRAMMS : (Microbial surface components recognising adhesive matrix molecules) = large protein family
- cell wall-attached adhesions
- specific binding ti host extracellular matrix proteins
How does S. Pyogenes evade the immune system?
- Hyaluronic acid capsule - prevents opsonisation and phagocytosis by appearing as ‘self’
- M Protein - Binds factor H, which prevents opsonisation with C3b)
- Secretion of toxins - streptolysins (lyse immune cells), C5a peptidase (destroys C5a to prevent neutrophil chemotaxis), DNAses (degrade neutrophil extracellular traps - NETs), SpyCEP (destroys IL-8 to prevent neutrophil chemotaxis)
- Spreading Factors: Proteases, Lipases, Hyaluronidase, Streptokinase - Anticoagulant that activates plasminogen to plasmin which degrades fibrin
Necrotising Fasciitis? Diagnosis of causitive bacteria?
- Deep infection of the skin, destruction of tissue and fascia
- Often development into severe systemic disease with high mortality
- Swab purulent material and cultivate and identify in the lab
- Blood culuture can be useful in hospitilised patients
Diagnositic tests?
Catalse test: add H2O2 and bubbles in strep due to hyaluronic acid but not in staph
Hemlysis on blood agar: B-hemolytic like strep , partially hemolytic will go green colour
Bacterial susceptability: Strep is very susceptable to bacitracin
Treatment of staph and strep?
S. Pyogenes: Penecillin or dervative (eg. amoxycillin)
Staphylococcus aureus: B-lactamase resistant penecillin (eg. fluoxacillin) - EXCEPT for MRSA
How does penecillin work?
Penecillin binds to transpeptidase (aka penecillin-binding protein) and prevents formation of peptide cross-links in bacterial cell wall resulting in a weak cell wall and and cell lysis.
