Bacterial infections of the skin
The resident flora of the skin
Many microorganisms live on the surface of the skin, most numerous in moist hairy areas.
Microorganisms are found in clusters in irregularities of stratum corneum & within hair follicles.
Resident flora ------harmless staphylococcus, micrococcus & diphtheroids.
Staph epidermidis & aerobic diphtheroids are present on skin surface
Anaerobic diphtheroids (propionibacteria) live deep in hair follicles.
Lipophilic yeast ---- part of the flora
Resident flora defends against outside pathogens through bacterial interference & antibiotic production.
St overgrowth of aerobic diphtheroids leads to disease.
Trichomycosisaxillaris:
Axillary hair becomes beaded with concretions made of colonies of diphtheroids.
Erythrasma:
Some diphtheroids produce porphyrins which results in coral-red fluorescence under Wood's light. Overgrowth leads to symptomless patches, red brown, chronic usu in intertrigenous areas e.g. Axilla groin.
Treat: topical antibiotic or antifungal.
Staphylococcal infections:
Staph aureus is not part of the resident flora except in a minority who carry it in their nostrils and perineum.
Usu infects diseased skin e.g. eczema.
Impetigo contagiosa:
Org: staph, strept or both.
Bullous impetigo is caused by staph
Non-bullous impetigo is caused by betahaemolyticstrept.
Clinical features:
Thin-walled, flaccid blister ----- puslule then ruptures to leave an area of exudation then a crust.
Usu children, usus face, contagious.
Complications: strept impetigo can trigger acute glomerulonephritis.
Management:
Swab for direct stain and culture.
Treatment: systemic antibiotic e.g. flucloxacillin, erythromycin or cephalosporin.
Topical antibiotic e.g. fusidic acid, mupirocin or bacitracin
Ecthyma:
Ulcer forms under a crusted surface infection
Usu neglected minor trauma or insect bites (poor hygiene)
Same bacteria as impetigo but heals with scar.
Furunclosis (boils):
Pustular infection of a hair follicle usu w. staph aureus.
Usu adolescents.
Clinical features:
Tender nodule later discharges pus and leaves a scar. St w. fever
Few pat have recurrent boils
Invest: swab for culture.
Treat: drainage by incision. Oral antibiotics.
Recurrent boils: treat carrier sites nostrils, groins with topical antibiotics for 6 weeks. St systemic antibiotics for 6 weeks.
Carbuncle:
Adjacent hair follicles become deeply infected with staph aureus leading to a swollen, painful area discharging pus from several points. Pain + systemic upset.
Exclude DM
Treat: incision & drainage, systemic antibiotics.
Scalded skin syndrome:
Wide area of skin is affected with erythema & tenderness followed by loosening and desquamation of the epidermis
Usu affects infants & children caused by staph infection elsewhere ( impetigo or conjunctivitis) the bacteria produce a toxin (exfoliatin) that causes a split through the epidermis
Treat: systemic antibiotic
Prognosis: good.
Toxic shock syndrome:
Caused by a toxin-producing staph
Clinical features:
Fever and rash ( usu wide-spread erythema)
St circulatory collapse.
1to 2 weeks later desquamation, generalized notable on fingers and hands.
Staph overgrowth in the vagina of women using tampons.
Treat: systemic antibiotics, irrigation
Streptococcal infections:
Erysipelas:
Starts with malaise, shivering then fever.
The affected area becomes red and swollen with well-defined edge. The organism gains entry through a split in the skin e.g. between the fingers or toes.
The disease can be fatal.
Treat: IV penicillin.
Recurrent erysipelas can lead to persistent lymphedema.
Cellulitis:
Infection is deeper than erysipelas. The subcutaneous tissue is involved. The area is more raised and swollen. Erythema is less well-marginated. Usufollows injury in area withdependent edema e.g.leg. The cause: strept, staph, other organisms
Treat: systemic antibiotic St IV
Necrotizingfasciitis:
Mixture of pathogens including strept & anaerobes
Rare, surgical emergency
Starts as a painful cellulitis but turns into an extending necrosis of the skin and subcutaneous tissue
Diagnosis by MRI
Treat: early surgical debridement + IV antibiotics
Prognosis: poor
Mycobacterial infection:
organism: Mycobacterium tuberculosis, Mycobacteriumbovis
Clinical types:
Lupus vulgaris:
Direct inoculation or through blood or underlying lymph nodes
Lesion occur mostly around the head and neck
Red-brown, scaly plaque, slowly grow over months or years
Can damage deeper tissues such as cartilage leading to ugly mutilations, scarring & contractures
Diascopy shows characteristic brow apple-jelly nodules.
Diagnosis: Biopsy + animal inoculation.
Scrofuloderma:
Skin overlying a Tb lymph node or joint becomes involved.
Clinical features: Irregular scars + fisulae + cold abscesses
Most commonly neck.
Tuberculides:
Presence of Tb focus leads to a distant skin eruptionin which Tb DNA is demonstrated by PCR in the eruptione.g. papulonecrotictuberculide.
e.g. erythema induratum (Bazin's disease): deep purple ulcerating nodules on the back of the lower legs usu women.
Treatment of skin Tb
Full course standard Tb therapy.
Leprosy (Hansen's disease):
Cause: Mycobacterium leprae
Epidemiology: becoming rare all-over the world.
Clinical features:Depends on the immune response of the patient.
High resistance develops pauci-bacillary, tuberculoid leprosy with low infectivity
Low resistance develops multi-bacillary, lepromatous leprosy with high infectivity
In between there is border-line leprosy.
Treatment of Leprosy:combinationof drugsincluding dapsone, rifampicin and clofazimine
Comparison between tuberculoid and lepromatous leprosy
tuberculoid lepromatous
involvement skin & nerves many tissues
number of lesions 1 or 2 face innumerable
wide-spread
morphology sharply marginated macules, papules
of lesions hypopigmented macules plaques, nodules
hairless, slightly raised border thickened face
(leonine face)
nerve involvement thick near lesion lesion not hyposthetic
hyposthesia, loss glove & stocking
sweating in lesion anesthesia,
trophic ulcers
muscle paralysis
other features none nasal crusting, epistaxis
saddle nose, keratitis
infectivity low high