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PH-SD22

Purulent skin infections

Skin infections sorted by the layer they reach: impetigo in the epidermis, boils down the hair follicle, erysipelas and cellulitis in the dermis, necrotising fasciitis along the fascia, and the staphylococcal toxin that splits the epidermis.

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  • 6 steps · 10 questions
  • 3D anatomy, affected parts marked

By the end, you can

  • Relate each purulent skin infection to the layer of skin it involves, from the stratum corneum to the fascia.
  • Compare how Staphylococcus aureus and Streptococcus pyogenes use toxins and enzymes to stay localised or to spread.
  • Explain how exfoliative toxin splits the epidermis in bullous impetigo and in scalded skin syndrome, and why the two differ.
  • Explain why necrotising fasciitis causes pain out of proportion to the skin and spreads so fast.
  • Recognise the classic appearances, classifications and tests of skin infections, and explain how drainage, antibiotics and debridement act on the mechanism.

What it is

Purulent (pyogenic) skin infections are bacterial infections of the skin and the soft tissue beneath it, caused mostly by Staphylococcus aureus and Streptococcus pyogenes (group A streptococcus). They are best understood by depth: impetigo lies in the epidermis; folliculitis, furuncles and carbuncles follow the hair follicle; abscesses collect in the dermis and subcutis; erysipelas and cellulitis spread through the dermis and fat; and necrotising fasciitis runs along the fascia. Some of their toxins act far from the infection itself.

4 types to tell apart
Superficial (epidermal)
Impetigo, non-bullous or bullous, confined to the epidermis and healing without a scar; ecthyma is its deeper, ulcerating form.
Purulent (localised)
Folliculitis, furuncle, carbuncle and skin abscess: pus collects and is walled off. Mostly S. aureus, including MRSA.
Non-purulent (spreading)
Erysipelas, most cellulitis and necrotising fasciitis: infection spreads through tissue with little pus. Mostly streptococci; necrotising fasciitis can also be a mixed infection.
Toxin-mediated
Staphylococcal scalded skin syndrome and toxic shock syndrome: toxins from a small or hidden focus act on the whole skin or the whole body.

Normal function

Skin layers as barriers, and the gaps between them

Each layer of the skin resists bacteria in its own way. The is a dry, slightly acidic wall of dead, keratin-filled cells that is constantly shed. Beneath it the living keratinocytes of the and layers are riveted together by desmosomes, whose adhesion proteins include desmoglein 1, most abundant in the upper epidermis, and desmoglein 3, mainly in the lower layers.

The and hold blood vessels, lymphatics and resident immune cells. Below lies the , crossed by that carry vessels and nerves up from the deep fascia over the muscles. Each layer is a plane along which infection can spread once it gets in.

The barrier has natural gaps. Every is a warm, moist, oily pocket of epidermis reaching deep into the dermis, where bacteria can settle. Many healthy people carry S. aureus in the nose and on the skin, and streptococci live on the skin and in the throat. Infection usually needs a break in the barrier: a scratch, an insect bite, eczema, a fungal crack between the toes or a leg ulcer.

Point to it on the model
Skin infections by depthSchematic
FeatureLayer involvedUsual organismHallmark
Non-bullous impetigoBeneath the stratum corneumS. aureus, S. pyogenes or bothHoney-coloured crusts
Bullous impetigoSplit at the granular layerS. aureus making exfoliative toxinFlaccid blisters containing bacteria
EcthymaThrough the epidermis into the dermisStreptococci, staphylococciPunched-out ulcers that scar
FolliculitisUpper hair follicleS. aureus; Pseudomonas after hot tubsPustule pierced by a hair
Furuncle and carbuncleDermis round one follicle; several linked through the fatS. aureusA pointing nodule; several draining openings
ErysipelasUpper dermis and its lymphaticsS. pyogenes (group A)Raised, shiny plaque with a sharp edge
CellulitisDeeper dermis and subcutaneous fatStreptococci; S. aureus if purulentFlat redness with an ill-defined edge
Necrotising fasciitisSubcutaneous fat and the fascia beneathMixed (type I) or group A streptococcus (type II)Pain out of proportion; dusky skin
Staphylococcal scalded skin syndromeGranular layer everywhere, via the bloodS. aureus exfoliative toxinTender skin that shears off; sterile blisters

Schematic; organisms overlap, and deeper infections tend to cause more systemic illness.