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?
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
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.