Lecture 14: Skin and soft tissue infection Flashcards
What is impertigo?
Risk factors?
- Infection of upper layer of the skin
- Vesicles form
- Risk factors:
- Crowding
- Poor hygiene
- High temperatures
How you differentiate between erysepelas and cellulitis?
-Clear demarcation line in erysipelas
Cellulitis is an infection in which layer of skin?
Lower dermis and subcutaneous tissue
*note that often seen around injury site or deep abcess
Erysepelas is an infection of what layers of the skin?
-Upper dermis and also superficial lymphatics
What is the predominant causative organism for erysipelas?
Group A beta haemolytic streptococci e.g. S Pyrogenes
How do macrophages recognise bacteria?
- PAMPs on bacterial surface
- Macrophages have pattern recognition receptors
General innate immune response to bacteria?
- Platelets form blood clots
- Mast cells cause vessel vasodilation (heparin, histamine)
- Macrophages secrete cytokines
- More vasodilation (leakage, sweeling)
- Neutrophils pass through leaky vessels (diapedesis) and phagocytose bacteria
Which two substances guide leucocyte migration?
- Macrophages
- Complement
- IL8 (macrophages)
- C5a (activated complement)
What are the 3 complement pathways involved in innate immunity?
- Classical
- Lectin
- Alternative
At which step do the 3 complement pathways merge?
Conversion of C3 to C3a and C3b
What organisms causes SSTI?
- Strep pyogenes
- Staph. aureus
- some other bacteria e.g Vibrio vulnificus
- Fungi e.g dermatophytic moulds, tinea
- Viruses e.g chicken pox
General features of streptococcus pyogenes
-GRAM POSITIVE
-Spherical or ovoid cocci (0.5-1 micron)
-Often an asymptomatic colonisation in 15-20% of people
-Are Catalase negative (in contrast to staphylococci)
-Has the group A antigen
Synonomous with group A streptococcus
What are four complications of streptococcus infection?
- Skin/soft tissue infection
- Severe systemic disease (TSS)
- Pharyngitis/tonsillitis
- Acute rheumatic fever
Through what mechanism does group A streptococcus colonise the skin?
MSCRAMMS on bacteria cell wall bind to host ECM proteins
What are three methods of immune evasion by group A strep?
- Hylauronic acid capsule prevents opsonisation and phagocytosis
- M protein binds with factor H, prevents opsonisation with C3b
- Toxins Streptolysins, C5a peptidase (no chemotaxis), DNAases (degrdae neutrophil extracellular traps) and SpyCEP (destroys IL-8)