Skin and soft tissue infection

Question 1

Cellulitis

Answer 1

Infection of the dermis and the subcutaneous tissue

Often seen around injury site or deep accesses

Question 2

Impetigo

Answer 2

Can be caused by staph A

School sores, quite harmless, crowed areas, humidity and unhygienic places

Question 3

Erysipelas

Answer 3

Typical group A strep disease

Looks like cellulitis but clear demarkation line

Question 4

Innate immune response

Answer 4

Non-specific generic response to pathogens
Immediate response
Does not confer long lasting protective immunity

Question 5

Overview of process of infection and inflammation

Answer 5

Infection leads to tissue damage and activation of mast cell
Release of heparin and histamine from mast cells
Innate immune mechanisms (PAMPs, complement) lead to activation of residential macrophages
Release of pro inflammatory cytokines and chemokine
Vasodilation and increased permeability of blood vessels (vascular leakage) swelling
Leukocyte extra vase from the blood and migrate to the site of infection
Migration is guided by the chemokine interleukin-8 (macrophages) and C5a (activated complement)

Question 6

What organisms cause SSTI (skin and soft tissue infections)

Answer 6

Streptococcus pyogenes 
Staphylococcus aureus 
Some other bacteria (vibrio vulnificus) 
Fungi (dermatophytic moulds and tinea)
Viruses (chicken pox)

Question 7

Describe strep bacteria

Answer 7

Gram positive spherical or oval cocci 
asymptomatic colonisation of the pharynx in 15-20% of the population catalase negative (in contrast to staph) 
Causes 
- SSTI 
- Severe systemic diseases 
- Pharyngitis/ tonsillitis 
- Acute rheumatic fever

Question 8

How are skin cells invaded with S.pyogenes

Answer 8

MSCRAMMS= microbial surface components recognising adhesive matrix molecules

• cell wall attached adhesions
• Specific binding to host extracellular matrix proteins (fibronectin, elastin, laminin, vitronectin, collagen)

Question 9

Ways S. pyogenes can evade bobs immune system

Answer 9

Hyaluronic acid capsule (prevents opsonisation and phagocytosis)
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)

Question 10

S. pyogenes spreading factors

Answer 10

Proteases
Lipases
Hyaluronidase
Streptokinase = an anticoagulant that activates plasminogen to plasmin which degrades fibrin (given to heart attack patients)

Question 11

Necrotising fasciitis (flesh eating disease)

Answer 11

Deep infection of the skin

Destruction of the tissue and fascia

Question 12

How to you diagnose a skin infection?

Answer 12

Swab or purulent material
Cultivate and identify causative organism in microbiology lab
Swab on intact skin (absence of pus) is not useful (commensal skin bacteria)
Hospitalised patients should also have blood cultures taken
Positive cultures (bacteremia) could lead to further complications (sepsis, streptococcal toxic shock syndrome)

Question 13

Treatment of bobs skin disease + what to do if strep or staph

Answer 13

Supportive care
Rest and elevation
Analgesia
Antimicrobial drugs
- S. pyogenes - give penicillin or derivative (amoxycillin)
- Staph. aureus give Beta- lactase resistant penicillin e.g. flucloxacillin (except for MRSA strains)

Question 14

How does penicillin work

Answer 14

Binds to the transpeptidase enzyme (aka penicillin binding protein)
Prevents formation of peptide cross links in bacterial cell wall
results in weak cell wall and cell lysis