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  • The importance of an intact epidermis was once summed up with great brevity by a mentor:
  • ‘You need skin, it holds your insides in’. ...
  • BJ Currie, JR Carapetis - Australasian Journal of Dermatology, 2000


Bacterial skin infections

Skin layer Infection Common causes
Epidermis Impetigo Strep pyogenes and/or Staph aureus
Dermis Erysipelas (dermal lymphatics, fever, rare sepsis) Strep pyogenes
Hair follicles Folliculitis, boils, carbuncles (like boils but with multiple heads; tend to be more serious, and painful) Staph aureus
Subcutaneous fat Cellulitis (can spread by lymphatics to bloodstream) Strep pyogenes, staph aureus
Fascia Necrotising fascitis (treated by amputation) Anaerobes and microaerophiles (need 5-10% CO2 with a little O2)
Muscle Myenecrosis gangrene Clostridium perfringens
  • Strain = minor genetic differences within a species. These often relate to virulence - and make the infection more severe. Includes both plasmid and chromosomal material.
  • Clostridium are spore formers (includes Clostridium tetanii as well). They form spores in the environment where they can't reproduce
    • If blood flow is compromised, then the area becomes anaerobic so that the organism can grow + reproduce
  • Clostridium perfringens produces gas - hence gas gangrene
    • Need to amputate


  • An infection of the skin usually the result of a bacterial invasion

Staphylococcus aureus

  • Gram positive coccus
  • Most common cause of skin infections
  • Minor infections
    • Boils, Abcesses, Folliculitis, Carbuncles, Impetigo (bullous)
  • More serious infections
    • Post operative wound infections
    • Antibiotic resistance common

Acquisition of Staph aureus

  • Self-inoculation
    • Carrier of Staph aureus
      • Nose and/or skin
  • Contact with exogenous source
    • Usually another person

Wash hands both before and after working with a patient.

Diagnosis & treatment of Staph aureus associated skin infections

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

Antibiotic therapy for Staph aureus associated skin infections

Review the 2-hour lecture on antibiotics. Get the Therapeutic Guidelines for Antibiotics (keeps up with resistance information). Also in Mims Microbiology.

  • Boils, Folliculitis, Carbuncles
  • Staph aureus commonly resistant to Penicillin (covers gram positives; Neisseria gonorrhea and Neisseria meningitis)
    • beta lactamase production (Enzyme degrades Penicillin)
      • Penicillin not used unless sensitivity proven (there are very high penicillin resistance rates)
  • methicillin has exactly the same spectrum of activity as penicillin (but it has a beta lactamase inhibitor)
  • Methicillin sensitive Staph aureus (MSSA)
    • Di/Flucloxacillin orally
  • Hypersensitivity to Penicillins (not immediate)
    • Cephalexin orally; 10% cross hypersensitivity between the penicillins and the cephalosporins
  • Immediate hypersensitivity: Clindamycin (angioedema, anaphylaxis)
    • Belongs to lincosamides; they cover gram positives
  • Impetigo
    • If required - as for Boils, Folliculitis Carbuncles

Antibiotic therapy for Staph aureus associated skin infections

  • Mild Cellulitis and Erysipelas
    • Di/Flucloxicillin orally
    • Hypersensitivity (not immediate) to Penicillins - Cephalexin
  • Severe cellulitis
    • Di(flu)cloxicillin intravenously (IV)
    • Hypersensitivity (not immediate)
      • Cephalothin IV or Cephazolin IV
    • Immediate Penicillin hypersensitivity
      • Clindamycin or Lincomycin IV OR vancomycin IV (vancomycin is second line therapy; to prevent resistance; acts on cell wall, but not on beta lactam)

Antibiotic therapy for skin infections caused by Staph aureus resistant to Di(flu)cloxacillin)

  • Community associated Staph aureus (CA-MRSA) - generally only resistant to methicillin
    • Treatment should be guided by susceptibility testing
    • Generally susceptible to
      • Clindamycin, Trimethoprim+Sulfamethoxasole or Doxycycline
  • Hospital associated Staph aureus (HA-MRSA) - generally resistant to methicillin and others
    • Generally multi-resistant
    • Treatment should be guided by susceptibility testing
      • Possible treatments include
        • Vancomycin, Rifampicin + Sodium fusidate, Teicoplanin (another glycopeptide, like vancomycin)
  • Vancomycin is a glycopeptide

Streptococcal skin infections

  • Major pathogen
    • Streptococcus pyogenes
      • (Group A streptococci); beta hemolytic, bacitracin sensitive
  • (Also associated with throat infections)
    • note that viruses cause 90% of throat infection; other bacterial causes are Neisseria Gonorrhoea, Candida albicans
  • Gram positive coccus
    • Exclusively human pathogens under natural conditions


  • Causative agents
    • Strep pyogenes (more common in developing countries)
      • (NB:Staph aureus - more common in developed countries)
  • Develops independently of Group A Streptococcus pyogenes (GAS) upper respiratory infections


  • Up to 35% patients carry the same strain of Strep pyogenes in their nose or throat
    • ? Throat colonisation occurs after skin is infected


  • Acquisition of GAS
  1. Contact with other people with skin lesions
  2. Initial colonisation and multiplication on intact skin
  3. Invasion through minor breaks in the epithelium
  4. Lesions

Clinical features of impetigo

  • Develop within 24-48 hrs of skin invasion
  • Marked inflammatory response
    • Limited to the epidermis
  • Yellow crusted lesions (at the beginning, they're water-filled blisters, then become crusted)
  • May occur on any part of the body
  • Spread of lesions common

Three virulence factors of GAS, M protein, Streptokinase and Hyaluronidase contribute to infection

  • M protein
    • Binds fibrinogen from serum
    • Blocks binding of complement to underlying peptidoglycan
      • Allows survival of organism by inhibiting phagocytosis by neutrophils & macrophages (no opsonisation)
  • Streptokinase
    • Converts plasminogen of human plasma into plasmin --> digestion of fibrin and other proteins
      • Allows organisms to spread through tissues
  • Hyaluronidase
    • Aids spread through connective tissue


  • Diagnosis
    • Made on clinical grounds
  • If severe
    • Collection of swab of pus from vesicles
    • Put it in Stewart's transport medium
  • Microbiology laboratory
    • Gram stain of pus
    • Culture of pus (e.g. Horse blood agar)
    • Identification of pathogen
    • Antibiotic sensitivity testing

Treatment of impetigo

  • Small number of lesions
    • Soap and water topically, 8-hourly to soften crusts
      • NB. Crusts should be sponged off (not torn --> scarring) and hands washed after handling lesions
    • Mupirocin (good against GP organisms) 2% ointment or cream topically to any crusted areas (after washing)
  • Large number lesions OR failure to resolve
    • Antibiotic therapy

Antibiotic therapy for impetigo

  • Strep pyogenes (very sensitive to penicillin)
    • Bathing of lesions (as previously discussed)
    • +
    • Phenoxymethyl Penicillin (oral) -10 days
    • OR
    • Benzathine Penicillin (Intramuscular [IM]) - Single dose; good idea but people are scared
    • OR
    • Roxythromycin (oral) - 10 days (Penicillin allergy)
      • Roxythromycin is a macrolide (like erythromycin)
  • Staph aureus primary pathogen Dicloxacillin (oral) 10 days

Epidemiology of GAS

  • Industrialized countries
    • Commonly causes pharyngitis & tonsillitis
      • Common in children 5-15 years
        • Less commonly causes pyoderma
  • Non-industrialized countries
    • Most commonly associated with pyoderma
      • Majority of children in a community infected
      • Multiple strains may be circulating
  • Australian Indigenous populations
    • Prevalence pyoderma in communities up to 70%
    • Sore throat uncommon
      • Throat carriage of Group A Streptococci (<5%)

Predisposing factors to pyoderma

  • Overall:
    • Crowding
    • Hot weather
    • Water supply
    • Humidity
    • Hygiene
  • Scabies - mite infection
  • Dermatophytes
    • Scabies and dermatophytes both break the skin
  • Pyoderma predisposes to acute post streptococcal glomerulonephritis and acute rheumatic fever

Prevalence of scabies in the Aboriginal community

  • High prevalence
    • Present in up to 50% children
    • Present in up to 25% adults
  • Underlies
    • 50-70% of Streptococcal pyoderma


  • Aetiology
    • Infestation of skin by arthropod mite
      • Sarcoptes scabei
  • Scabies
    • Common infestation
    • Occurs worldwide
    • Affects all races and social classes
  • Highest prevalence
    • Children < 15 years
  • Sarcoptes scabei
    • Intimate contact with host
  • Lives in burrows within skin Usually hands or wrists
  • Female lays eggs in burrows
  • Infection can spread over large areas of body
  • Mites do not survive> 48-72 hours away from human body
  • Adult female mite can live up to a month on their host

*Naive individuals

    • Asymptomatic for up to 4-6 weeks
  • Scabies lesions
    • Roughly symmetrical
  • Location
    • Hands often first part body to demonstrate cutaneous lesions Eczema of hands may occur
  • Lesions also found on
    • skin folds, under the wrist, elbow, knee, penis, breasts, shoulder blades, abdomen

Symptoms of scabies

  • Characteristic itchy rash
    • Secondary infections follow scratching
  • Very heavy infections can occur in
    • Immunosuppressed
    • Individuals with poor hygiene
  • Norwegian scabies
    • Mite population high due to poor host response
    • Extensive thickening and crusting of skin

Diagnosis of Scabies

  • Aboriginal populations
    • Generally diagnosed clinically
  • Industrialized countries
    • Skin scrapings may be collected in a jar to aid in diagnosis
    • Dilute KOH mixed with skin scrapings
    • Aids in clearing thick layers of skin cells
    • Examined microscopically
      • Mites, eggs or faeces.

Transmission of scabies

  • Spread from infested person to another
    • Prolonged OR close personal contact
  • Predisposing factors
    • Overcrowding, associated poverty and poor hygiene transmission
  • Spread facilitated by
    • Prolonged hand-holding
    • Sleeping together in same bed
    • Sexual intercourse
  • Commonly spread to
    • family members, playmates, inmates of institutions and dormitories

Treatment of Scabies

  • Permethrin 5% cream topically
    • Applied to whole body including face and hair
    • Leave on for minimum 8 hours but may leave overnight
  • If patient allergic to Permethrin
    • Benzyl benzoate 25% emulsion in water
    • Leave on for 24 hours
  • NB: Must treat family members and close contacts as scabies may take several weeks to develop
  • Moderate to severe infection
    • Repeat treatment in 7-14 days
  • Norwegian scabies
    • Ivermectin orally
      • Length of treatment depends on severity

Dermatophyte infections

  • Cutaneous Mycoses
    • Infections of the skin, hair and nails
      • Invade keratinized layers
  • Clinical conditions
    • Ringworm
    • Tinea
  • Causative agents
    • Members of the Dermatophyta
      • Epidermiphyton
      • Trichophyton Fungi
      • Microsporum

Tinea corporis

  • Tinea corporis caused by T. rubrum in Australian Aborigines living near Darwin in the Northern Territory.
  • Need to take scraping from edge of the lesion (where it's proliferating)

Tinea pedis

  • Moccasin distribution with inflammation
  • Tinea pedis with marked erythema of the first and second toes
  • Tinea pedis with toe-web maceration and minimal inflammation.
  • Tinea can be transmitted from feet through desquamated skin scales shed in carpet and matting

Diagnosis of Fungal Infections

  • Identification of Dermatophytes
  • Based on presence/absence of conidia, their size, shape & location

Treatment of Dermatophyte infections

  • Tinea corporis, pedis and cruris
    • Terbanafine OR Bifonazole OR Clotrimazole OR Miconazole OR Econazole OR Ketoconazole Administered as a topical cream
  • If unresponsive
    • Terbanifine orally (2-6 wks) OR Itraconazole orally (1-3 wks) OR Fluconazole (4-6 weeks)
  • Tinea capitis OR widespread Tinea
    • Fluconazole OR Ketoconazole OR Terbanifine orally (4-8 wks)

Tinea capitis - start with oral treatment (so they don't lose their hair)

Sequalae associated with Streptococcal skin infections

  • Acute rheumatic fever (ARF)
    • Generally associated with GAS throat infections HOWEVER
    • In Aboriginal population often associated with GAS skin infection
  • Acute Glomerulonephritis (AGN)
    • Occurs more often after skin infections than throat infections

Acute rheumatic fever (ARF)

  • Leading cause of preventable pediatric heart disease worldwide
  • Occurs 2-4 weeks after Group A Streptococcal (GAS) sore throat (or pyoderma in Australian Aboriginals)
  • Occurs in approx 3% of patients with GAS
  • Genetic susceptibility?

Epidemiology acute rheumatic fever

  • Developed countries
    • Prevalence reduced dramatically over past decades
    • 0.014/1000 population
      • Improved socioeconomic conditions, rapid diagnosis and treatment
  • Developing countries
    • Prevalence high
      • up to 24 per 1000 population (same as 80 years ago in developing world)
  • Occurs most frequently among children and adolescents ( 5 to 18 years)
  • Coincides with age distribution of highest prevalence of streptococcal infections

Diagnosis of ARF Based on the Revised Jones Criteria

  • Firm diagnosis requires that two major or one major and two minor criteria are satisfied, in addition to evidence of recent streptococcal infection.

Major Criteria

  • 1. Carditis:All layers of cardiac tissue may be affected (pericardium, epicardium,myocardium, endocardium). Patient may have a new or changing

murmur, with mitral regurgitation being the most common, followed by aortic insufficiency.

  • 2.Polyarthritis: Migrating arthritis that typically affects the knees, ankles, elbows and wrists. Joints are very painful and symptoms very responsive to anti-inflammatories
  • 3.Chorea (Syndenham ́s chorea, or "St. Vitus ́ dance”): Abrupt, purposeless movements. May be only manifestation of ARF. Presence is

diagnostic. May also include emotional disturbances and inappropriate behavior.

  • 4.Erythema marginatum: A non-pruritic rash that commonly affects the trunk and proximal extremities, but spares the face. The rash typically migrates from central areas to periphery, and has well-defined borders.
  • 5. Subcutaneous nodules: Usually located over bones or tendons, these nodules are painless and firm.

Minor Criteria

  • 1. Fever (39C; in Aborigines/developing it's 38C)
  • 2. Arthralgia
  • 3. Previous rheumatic fever or rheumatic heart disease
  • 4. Acute phase reactants: Leukocytosis, elevated erythrosedimentation rate (ESR) & C-reactive protein (CRP)
  • 5. Prolonged P-R interval on electrocardiogram


Evidence of preceding streptococcal infection

  • Any 1 of following is adequate evidence of infection
    • Increased streptococcal antibodies (S. pyogenes)
      • Most commonly used antibody assays
        • Antistreptolysin O (ASO)
        • Anti-deoxyribonuclease B (anti-DNase B)
          • Elevated titers may persist for weeks to months
      • ASO titers rise & fall more rapidly than anti-DNase B
      • Anti-DNase B titers may remain elevated for months
  • Throat culture +ve for Group A beta-hemolytic Strep
  • Positive rapid Group A strep carbohydrate Ag test
  • Recent scarlet fever (caused by strep pyogenes, with erythrogenic toxin)

Aetiology of ARF relates to M surface proteins of GAS

  • M surface proteins
    • Most studied virulence factor of GAS
    • Used for bacterial typing of GAS strains
      • > 100 antigenic types
    • Antigenic variation due primarily to single amino acid substitutions.
  • Antigenic epitopes of M protein
    • Mimic those of mammalian muscle and connective tissue
  • Acute Rheumatic fever
    • Most commonly associated with M types (1,3,5,16,18) however many serotypes implicated

Aetiology of rheumatic fever

  • Antibodies stimulated to M protein in Streptococcal cell wall
  • Antibodies cross-react with
    • Tissue glycoproteins in
      • Heart, joints and Other tissues
        • Focal inflammatory lesions
  • Heart --> Carditis
  • Joints --> Polyarthritis
  • Basal ganglia neurons --> Chorea

Chronic rheumatic heart disease

  • Most important consequence ARF
    • Rheumatic heart disease
  • May occur following initial ARF or following repeated attacks of GAS infection with different M types (usually associated with skin infection )
  • Infection leads to damage to heart valves
  • Major public health problem in developing countries and Australian Aboriginals
  • Associated pathology
    • Valves thickened
    • Small vegetations occur on deformed valves-->Infective endocarditis

Acute Glomerulonephritis

  • M Protein of GAS also associated with Glomerulonephritis
  • Glomerulonephritis can follow
    • Pharyngitis (commonly M-types 1,4,12,15) OR
    • Impetigo
      • (M-types 49,52,55,59-61)
  • Restricted to small number of "nephritogenic" strains

Acute post Streptococcal Glomerulonephritis

  • Antibodies to streptococcal antigens combine to form immune complexes
    • -->Circulating immune complexes
  • Complexes deposited in glomeruli
  • Auto-antibodies to glomerular components may also be involved
  • Activation of complement and coagulation systems activated
    • -->Local inflammation
      • Glomerulonephritis

Antibiotic Prophylaxis against GAS

  • Acute rheumatic fever
    • Antibody response to GAS provides immunity to a particular M type but NOT other types
      • Thus GAS infection can occur repeatedly --> Rheumatic heart disease
      • Continuous antibiotic prophylaxis recommended against GAS for patients with well documented history of ARF
        • Benzathine Penicillin (IM) monthly
        • Phenoxymethylpenicillin orally (12 hourly)
  • Acute glomerulonephritis
    • Repeated infection with nephrogenic M types is uncommon
      • No prophylaxis required