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Skin infections

  • Healthy skin
    • Protects underlying tissues
    • Provides defense against invading microbes
  • Number of bacteria on the skin - quite low
    • 100-1000/cm2
      • Dry areas
    • 10x10^3 /cm2
      • Moist areas

Properties of skin that limit microbial colonisation

  • Limited moisture
  • Acid pH of normal skin
  • Surface temperature <optimum for many pathogens
  • Excreted chemicals such as sebum, fatty acids and urea
  • Competition between different species

Normal flora of the skin

  • Staphylococcus epidermidis
  • Corynebacteria
  • Some anaerobic bacteria eg Propionibacteria and Peptococcus
    • Deeper follicles in dermis
  • Yeasts
  • Some people may also carry Staph aureus as part of their normal flora (25-35%; more in HCW)

Bacterial skin infections

  • Skin infections caused by direct entry into the skin
    • Folliculitis, Boils, Carbuncles
      • Abscesses
    • Impetigo
    • Erysipelas
    • Cellulitis
    • Necrotising fasciitis
    • Myenecrosis (gangrene)


  • Superficial pustule or inflammatory nodule surrounding a hair follicle.
  • Infected hairs fall out new pustules develop
  • Most commonly found on face, scalp, areas rubbed by clothing
    • eg.thighs and groin
  • Causative agent
    • Stapylococcus aureus
      • Gram-positive coccus
        • Catalase positive (to differentiate from diplococcus)
        • Coagulase positive (to differentiate from S. epidermidis)
  • Also causative agent of Boils and Carbuncles
  • Pseudomonas aeruginosa (much less common)
    • Associated with use of hot tubs and spas
    • Boils, carbuncles and folliculitis

Boils (furuncles)

  • Clinical picture
    • Superficial infection in and around hair follicles
    • Boil occurs 2-4 days following inoculation with Staph aureus
  • Course of infection
    • Bacteria relatively protected from host defenses
    • Allows rapid multiplication and local spread
    • Inflammatory response
      • Influx PMN
      • Fibrin deposition
    • Walling off of the site
    • Continue to expand slowly
    • eventually erode overlying skin
    • pus builds up under skin (yellow stuff under skin)
      • Boil bursts
    • If drainage inward occurs seeding of underlying body sites can occur
  • Treatment - lance the boil to release the pus (so it's not walled off)


  • Boil with >1 focus of infection
  • Caused by bacterial invasion of hair follicles or sebaceous gland ducts
  • several follicles or ducts involved
  • More common in men due to extensive body hair

Source of Staph aureus

  • Self-inoculation
    • Carrier of Staph aureus
      • Nose and/or skin
    • Carriers of Staph aureus may suffer recurrent boils
  • Contact with exogenous source
    • Usually another person e.g. contact sports
  • In absence of a wound or foreign body >10^6 organisms required for infection

Diagnosis & treatment

  • Boils, Folliculitis, Carbuncles
  • Diagnosis
    • Generally made on clinical grounds
  • Treatment
    • Drainage of pus
      • Usually sufficient for minor lesions
    • More severe lesions associated with fever
      • Antibiotic therapy also required

Antibiotic therapy

  • Boils, Folliculitis, Carbuncles
  • Staph aureus commonly resistant to Penicillin
    • β lactamase production (Enzyme degrades Penicillin)
    • Penicillin not used unless sensitivity proven
  • Methicillin sensitive Staph aureus (MSSA)
    • Dicloxacillin/flucloxacillin orally
  • Recurrent infections in nasal carriers
    • Antibiotic creams (Mupiricin)


  • Superficial cutaneous infection
    • Effects the epidermis only
  • Common in children 5-15 years
  • Causative agents
    • a) Streptococcus pyogenes (More common in developing countries)
    • b) Staphylococcus aureus (More common in affluent communities)
  • Acquisition
    • (a) Contact with infected skin lesions
    • (b) Contact with carriers of Staph aureus
  • May first colonise normal skin and multiply
    • Invasion occurs via breaks in skin (even very small)
  • Characterised by crusted lesions, exudate filled vesicles with marked red border

Clinical features

  • Acute infection
    • Develops within 24-48 hours of invasion
    • Triggers marked inflammatory response
    • Can spread through tissue
  • Lymphatic involvement common
    • Lymphadenitis (Inflammation of one or more lymph nodes)
    • Lymphangitis (Inflammation of one or more lymphatic vessels)

Bullous impetigo

  • Rarer variant of impetigo
    • Characterized by fragile fluid-filled \vesicles and flaccid blisters
  • Always caused by Staph aureus
    • BI --> SA
    • SA -/-> BI

Diagnosis of impetigo

  • Diagnosis made on clinical grounds
  • If severe
    • Collection of swab of exudate from vesicles
  • Microbiology Laboratory
    • Gram stain of fluid or exudate
    • Culture of pus (eg. Horse blood agar)
    • Identification of pathogen
    • Antibiotic sensitivity testing

Treatment of impetigo

  • Small number of lesions
    • Crusts should be sponged off (don't pull off or it will scar, and wash your hands after doing it)
    • Saline OR soap and water OR aluminium acetateOR potassium permanganate solution
    • AND:
    • Mupiricin (topical agent active against Staphylococci & Streptococci)
  • Large number lesions OR failure to resolve
    • Antibiotic therapy + sponging of the crusts
    • Strep pyogenes confirmed: Penicillin; Staph aureus: Di/flucloxacilin
    • NB: Hands must be washed after handling lesions


  • Localised superficial cellulitis
    • Demarcated cellulitis, affecting dermal lymphatics
  • Signs
    • Erythema
    • Oedema
    • Raised, definite margin
    • Constitutional upset
      • High fever, chills, and a general feeling of illness (malaise).
  • Classically involves the face
    • May also occur on lower legs
  • Major causative agent
    • Streptoccus pyogenes
    • Staph aureus co-infection may occur
  • Clinical picture
    • Rapid onset
    • Rapidly spreading
    • Affects superficial skin layers and dermal lymphatics


  • Clinical picture
    • Involves subcutaneous tissues, usually fat
    • Acute inflammation
    • Rapid spread
    • Minor injury --> septicaemia in 24-48 hrs
  • Signs variable
    • Erythema, induration, some tenderness: ill-defined margins; often no pus
  • Symptoms may include
    • Lymphadenitis
    • Systemic symptoms: fever, chills, malaise
  • Area of erythema
  • Indurated (hardening or thickening of tissue)
  • Boundaries often not well defined
  • Causative agent
    • Strep. pyogenes (>90% cases)
      • Staph aureus may also be involved
      • Haemophilus influenzae (children) (Gram negative cocco-bacillus)
      • Pasteurella multocida after animal bites
      • Aeromonas or Vibrio species (water related infections)
  • Diagnosis
    • Often based on clinical appearance - can sometimes see sneaky streaky red lines following lymph vessels
  • Laboratory investigations
    • Swab from leading edge of lesion
    • Often few organisms in tissue
      • Difficult to culture
    • Due to risk of septicaemia
      • Blood cultures essential
  • Treatment
    • Based on clinical diagnosis
    • Must cover both Staph and Strep
  • Antibiotic therapy
    • Di(flu)cloxacillin
    • If abdominal wound or “dirty” area
      • Metronidazole added to cover anaerobes
  • NB: Other bacterial causes require alternative antibiotic therapies

Necrotising infections

  • Clinical syndromes that can lead to rapidly progressing necrotising skin infections eg. Necrotizing fasciitis and necrotizing cellulitis
  • Characterized by death of infected tissue (necrosis).
  • Clinical features of necrotising skin infection
    • Severe constant pain
    • Skin necrosis (can be really bad underneath)
    • Wooden-hard feel of subcutaneous tissue
    • Oedema beyond margin of erythema
    • Systemic toxicity - fever
    • Gas in soft tissues (esp necrotising cellulitis)
    • Leucocytosis, High C-reactive protein (CRP)
    • Rapid spread

Necrotising fasciitis

  • Acute highly toxic infection
  • Widespread necrosis undermining of surrounding tissues
  • Spreads extremely rapidly along fascial planes
  • Underlying destruction more widespread than skin lesion
  • Most commonly caused by Strep pyogenes
    • “Flesh eating bacteria”
    • NB not all Strep pyogenes are the same (there are different strains with different virulence factors). SP can cause scarlet fever as well, and strep throat. It can be a sneaky chameleon.
  • Patients deteriorate rapidly
    • 60-80% mortality
  • Radical excision of all necrotic fascia essential
  • Early IV antibiotics (Penicillin plus Clindamycin or Lincomycin)
  • Necrotising fasciitis -area aggressively debrided
  • 30-year-old man - rapidly progressive painful erythema and edema of the right foot following a bee sting
    • Often ends up in amputation

Synergistic necrotizing fasciitis

  • May develop in areas of traumatised and devitalised tissue eg. Surgical or traumatised wounds
  • Mixed infections
    • Anaerobes plus
    • facultative anaerobes
      • Streptococci
      • Enterococci
      • Gram-ve enteric bacteria
      • Anaerobic rods
  • Causative organisms depends on site of trauma
    • eg. infection in lower body often involve faecal flora

Ischaemic ulcers

  • Common in diabetics
    • Due to impaired blood supply
    • High [glucose] impairs immune responses
    • Neuropathy means they won't feel it or notice it
  • Ulcers may not be infected
    • If no erythema, oedema, pus, fever or lymphangitis
      • Infection unlikely (may be colonisation, but no infection)
  • Ulcer infected
    • Spreading cellulitis, fasciitis, myonecrosis
    • Usually mixed infections
    • Aerobes and anaerobes
    • Acute: s. aureus or streptococci
    • Chronic: polymicrobial
  • Treatment (if sepsis present)
    • Surgical debridement of necrotic tissue
    • Antibiotic therapy (broad spectrum)

Gas gangrene (Clostridial myenecrosis)

  • Causative agent
    • Clostridium perfringens
    • Strict anaerobe, spore former
  • Spores in soil, human and animal faeces
  • Gains access to traumatised tissue
    • Crush injuries
    • Deep wounds
    • Ischaemic ulcers
      • Anaerobic environment
      • Overwhelming gas gangrene

Course of disease

  • Organisms multiply in subcutaneous tissue
    • Produce gas and an anaerobic cellulitis
    • Invade deeper into muscle
      • necrosis, bubbles of gas
  • Infection proceeds rapidly
    • Acute pain
  • Damage due to an α−toxin (lecithinase)
    • Hydrolyses lipids in cell membranes
  • Presence of dead and dying tissue further compromises blood supply (even better environment for organism)

Diagnosis and treatment

  • Diagnosis
    • Clinical
  • Requires aggressive treatment:
    • Surgical debridement of devitalised tissue
    • Amputation may be required
    • Hyperbaric oxygen in severe infections
  • Systemic antibiotics
    • Penicillin IV
    • Hypersensitive to Penicillin- Metronidazole

Propionibacterium acnes and acne

  • Acne associated with hormonal changes at puberty
    • Increased response to androgenic hormones
      • Increased sebum production
      • Increased keratinisation and desquamation in pilosebaceous ducts
    • Blockage of ducts
      • Bacteria multiply in blocked ducts
        • Propionibacterium acnes
        • Micrococci
        • Yeasts
        • Staphylococci
      • Inflammation
  • Treatment
    • One of the tetracycline or erythromycin antibiotics

Fungal skin infections

  • Fungal skin infections
    • Superficial mycose
  • Superficial infections of skin e.g. Pityriasis versicolour
    • Causative agent: Malassezia furfur (yeast)
  • Usually confined to trunk or proximal area of limbs
  • Diagnosis: Direct microscopy of skin scrapings
    • Mainly causes cosmetic problem

Cutaneous mycoses, caused by Dermatophytes

  • Typical annular lesions
  • Scaly with raised edges
  • Itchy
  • Hyphae with sneaky stalk that produces more spores
    • Get annular lesions where the spores fall off on the outside, lesions increasing in size.
  • Clinical name often relates to location
    • (e.g. tinea corporis, tinea pedis)
  • Three main genera involved
    • Epidermophyton
    • Trichophyton
    • Microsporum


  • Acquired from a range of sources
    • Humans, animals, soil
  • Invade skin, hair and nails
  • Spread by arthrospores
    • Adhere to keratinocytes
    • Germinate and invade
  • Damage caused by inflammatory response to fungal antigens
  • Put it on Sabaroud's plate
  • Whole lot of hyphae together are called mycellia (look at the appearance of the mycellia for diagnosis)
  • Tinea can be transmitted from feet through desquamated skin scales shed in carpet and matting or in showers
  • Diagnosis: appearance, microscopy and culture

Viral infections of the skin

  • Cold sores
    • Causative agent
      • Herpes simplex virus 1 (HSV-1)
      • Less commonly HSV-2
    • Initial infection
      • Often occurs at young age
      • > 90% adults sero-positive
    • Transmission
      • Close personal contact with a person who has an active infected with HSV-1 or HSV2

Primary HSV-1 Infectious course

  • Primary HSV-1
    • 2-12 day incubation period
    • Patient may experience mild febrile illness
    • Lesions may occur on or around mouth (cold sores)
      • (May be unnoticed by some patients)
    • Primary lesions clear up in 2-3 weeks
      • Virus transported to the dorsal root (trigeminal) ganglion - virus remains latent
    • Latent virus remains for life
      • Can cause recurrent infections characterized by cold sores

Recurrent infection: infectious course

  • Reactivation signaled by
    • Pain, burning or itching where a lesion may appear
    • Generally occurs around junctions of nose and skin or mouth and skin
  • Lesions scab over after approx 1 week
  • Virus returns to latency
  • Recurrence
    • Triggered by number of factors
      • Other viral infections, direct sunlight, stress, menstruation, immunocompromised state NOTE
  • Treatment - Zovirax (can prevent sores developing)
  • NOTE: Reactivation more severe in immunocompromised hosts - potentially harmful complications


  • Common Warts
    • Found in exposed and frequently rubbed areas eg. hands and knees.
    • Warts raised and rough
  • Flat or Plane Warts
    • Common in children
    • Located on arms, knees and face
    • Smaller and less rough than other warts
  • Plantar warts
    • Painful, deep warts found on bottom of foot
  • Causative agent
    • Human papilloma viruses
    • Icosahedral double stranded DNA virus
  • Course of infection
    • Virus enters body via surface abrasions


  • Virus infects lower basal layer of stratified epithelium

Treatment of warts

  • Salicylic acid (15-25%)
    • Painted onto warts appears to have therapeutic effect cheap, can be bought over counter
  • Cryotherapy
    • Effectiveness similar to use of paints
    • Paints cheaper, simpler to use and safer