Lecture 16: Skin and soft tissue infection Flashcards
What are the signs and symptoms of Skin and Soft Tissue Infections (SSTIs)?
- Erythema (redness)
- Warmth
- Tenderness
- Pain (dep. on type as to degree)
- Fever (deeper -> systemic inf.)
- Purulence (pussy)
- Fever
- Increased HR, WBC
Relate depth of infection to skin layers:
Inf of epidermis = Erysipelas impetigo
Inf of dermis = Cellulitis
Inf of epidermis -> Fascia = Necrotizing soft tissue infection
Infection of fascia = Necrotizing fascitis
What organisms cause SSTI?
Mainly:
Streptococcus pyogenes
Staphylococcus aureus
Some other bacteria i.e vibrio vulnificus, clostridium perfringens
Fungi: Tinea
Viruses i.e chicken pox
What are some examples of non-purulent SSTI?
Cellulitis
Erysipelas
Necrotising fasciitis
What are purulent SSTI?
Carbuncle
Impetigo
What are some notes on cellulitis presentation:
Cellulitis
- Edema, pain
- Poorly demarcated erythema (no clear boundary b/w healthy and unhealthy)
- Often around wound/abscess i.e cellulitis around abscess
Write some notes on erysipelas:
Swelling/redness
Well demarcated erythema
Fever
Write some notes on necrotising fasciitis
Evolves rapidly, excruciating pain, fever, systemic erythematous rash
Write notes on impetigo:
Could be staph or strep pyogenes or polymicrobial
Painless, erythematous base with honey crusted exudate
Whats a carbuncle?
Big abscess following folliculitis
Staph aureus only
Whats the function of innate immune response?
- Non-specific, generic response to pathogens
- Immediate response
What recognize PAMPS?
Pattern recognition receptors (on macrophages, secrete pro-inflam cytokines upon binding)
PAMPS - highly conserved structures
How does infection relate to inflammation?
- Infection leads to tissue damage and activation of mast cells
- Release of heparin and histamine from mast cells
- Innate immune mechanisms (PAMPS, complement) lead to activation of resident macrophages
- Vasodilation, increased permeability of blood vessels. (vascular leakage, swelling)
- Leukocyte extravasation
- Migration via chemokine (IL8) and C5a
Write some notes on streptococcus:
- Gram positive spherical or oval cocci
- Catalase negative (compared to staphylococci)
Causes:
- SSTI
- Severe systemic diseases (streptococcal toxic shock syndrome)
- Pharyngitis/tonsilitis (SPECIFIC for STREPT)
- Acute rheumatic fever
What is the lancefield classification?
Uses sero typing i.e specific antibody against group A antigen isolate S pyogenes
i.e Further classification
Is GAS commensual to humans?
Group A streptococcus
- Exclusively found in humans
- Asymptomatic in many
- Transient colonization of skin
- Transmission by human contact
- High infection rates in overcrowding
How does S pyogenes infect skin?
MSCRAMMS (microbial surface components recognizing adhesive matrix molecules)
- Cell wall attatched adhesions
- Specific binding to host ECM proteins
i.e M protein
MSCRAMMS are found in ALL pathogenic GRAM POSITIVE bacteria
How can S pyogenes evade the immune system?
- Hyaluronic acid capsule (prevents opsonization and phagocytosis)
- M protein = Binds factor H, which prevents opsonisation with C3b.
- Secretes toxins i.e
-> Streptolysins (lyse immune cells)
-> C5a peptidase (preventing neutrophil chemotaxis)
-> SNases (Degrade neutrophil EC traps (nets))
-> SpyCEP (Destroys IL8 to prevent neutrophil chemotaxis)
What virulence factors allow S pyogenes to invade deeper tissues?
Spreading factors:
- Proteases
- Lipases
- Hyaluronidase
- Streptokinase (anticoagulant that activates plasminogen to plasmin, degrading fibrin)
How can S pyogenes be diagnosed?
- Swab of purulent material
- Identified in microbiology lab
- If in hospital then blood culture should be taken. (bacteremia could lead to sepsis or streptococcal toxic shock syndrome)
How can S pyogenes be identified diagnostically?
Gram +ive cocci
-> Catalase test
-> Grow on blood agar (hemolysis)
-> Bacitracin susceptible
= S pyogenes
How can S-pyogenes be treated?
- Supportive care
- Rest and elevation
- Analgesia
- Antimicrobial drugs (penicillin)
What do you give for staph aureus?
- Beta lactamase resistance penicillin i.e flucoxacillin (except for MRSA strains)
How does penicillin work?
Penicillin 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
What are the three main classes of beta lactam antibiotics?
- Penicillins -> Pen g, Pen V and amoxycillin
- Cephalosporins
- Carbapanems
How effective is penicillin?
All s. pyogenes are susceptible to penicillin but only 10% of staph aureus are
