Pedia: Skin & Soft Tissue Infection

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SKIN AND SOFT TISSUE INFECTIONS (Overview)

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Localized clusters of vesicles:  Shingles  Herpes simplex  Impetigo

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Painless nodules:  Warts  Molluscum contagiosum  Large lesion

By Lester A. Deniega, MD (Pedia2 Module4/ Lecture Date: June 15, 2006) NORMAL SKIN • Skin - host to variety of microorganisms • As a habitat, skin has various climatic zones: o Moist intertriginous areas - increased bacterial population o Dry, exposed skin - decreased bacterial flora • Areas rich in sebaceous secretions - increased bacterial flora

Reference: Lecture notes on Infectious Diseases; Mandal

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SKIN FLORA • Resident flora o regularly present on the skin; nonpathogenic o example: S. epidermidis, micrococci, anaerobic and aerobic diphtheroids • Transient flora o pathogenic or nonpathogenic o removed easily from normal but not from diseased skin

ERYSIPELAS

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o STREPTOCOCCAL AND STAPHYLOCOCCAL INFECTIONS •

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Usually caused by direct invasion of the organisms. They may also cause disease by releasing toxins, some of which may act as superantigens o Whereas conventional antigens stimulate only a small subset of T cells which have specific receptors, superantigens bind to a part of the T cell receptor which is shared by many T cells and thus stimulate massive T cell proliferation and cytokine release.

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Streptococcal infections

MODE Direct

Toxinmediated

Postinfectious

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DISEASE Tonsillitis Otitis media Pneumonia mpetigo Cellulitis Osteomyelitis Septicemia Meningitis Scarlet fever Erysipelas

Glomerulonephritis Rheumatic fever Arthritis Erythema nodosum

MECHANISM By release of proteases and attachment to host cells

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In many infections, the dominant clinical features are confined to the skin, with or without deeper soft tissue involvement. These conditions can be conveniently grouped under two broad headings o Infections associated with a widespread rash which may be maculopapular, erythematous, purpuric/hemorrhagic or papulo-vesicular e.g. Measles, Rubella etc o Infections associated with a localized involvement of the skin with or without deeper tissue involvement

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CONDITIONS ASSOCIATED WITH LOCALIZED INVOLVEMENT OF THE SKIN: o

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Streptococcal pyrogenic exotoxins (also called “erythrogenic toxins”). These toxins cause T cell proliferation & cytokine release. Immunological response to primary infection may cause host damage

SKIN AND SUBCUTANEOUS INFECTION

Erythematous, tender, indurated lesions:  Erysipelas  Cellulitis  Erythema nodosum

Epidemiology  Neonate and elderly  Preschool or school age children – lesions in lower extremities  Surgical wounds Portal of entry: surgical wounds, umbilicus in NB or any break in skin Etiology – GABHS Etiopathogenesis  Caused by streptococcal toxin infiltrating the skin from a small primary focus, which may be invisible.

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In contrast to staphylococcal infection of the skin, which often generates localized pusproducing lesions, S. pyogenes tends to cause spreading lesions due to the production of a variety of extracellular toxins which destroy fibrin, cellular proteins and hyaluronic acid. This facilitates the spread of infection through the tissues. Clinical Manifestations  Rapidly enlarging, deeply erythematous plaque with sharply demarcated, slightly elevated advancing margin  Involved skin: tender, indurated, peau d’ orange, with occasional large tension bullae  Lesions advance rapidly and may involve entire trunk or extremities w/in 12 hrs  Signs of toxicity- fever and chills Diagnosis  Aspirate or advancing margin of infected area and C/S  Blood culture Management

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Standard: Aqueous penicillin x 10 days Alternative: Phenoxymethyl Penicillin x 10 days or Erythromycin

OTHER LOCALIZED SKIN INFECTIONS THAT MAY BE CAUSED BY GABHS: IMPETIGO

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Epidemiology  Mainly seen in children  Most common in warm, humid climates  Bullous impetigo less common than classical; may occur in nursery epidemics

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Etiology  Classical – GABHS, S. aureus  Bullous – S.aureus (epidermolytic toxin) Clinical Manifestations  Classical

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Erythematous papules/vesicles in traumatized areasà evolve into honeycolored crusted plaques surrounded by discrete erythematous margin Associated with regional lymphadenopathy May lead to acute post-streptococcal glomerulonephritis

ECTHYMA o Pyoderma involving both epidermis and dermis o Characteristic lesion deep-seated with small ulcer formation o Painful and heal with scarring o Caused by S. aureus or GABHS o Widespread infection treated with PenicillinaseResistant penicillin and Mupirocin or Fusidic acid locally

CELLULITIS (NONFACIAL)

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dental abscess – anaerobes Local skin trauma – S.aureus

Epidemiology  May occur at any site and all ages  Risk factors – trauma, immunocompromised state Etiology  Coagulase + Staphylococcus  GABHS  H. influenzae

NECROTIZING CELLULITIS

Ecthyma gangrenosum •

ERYSIPELAS AND CELLULITIS

CELLULITIS

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ERYSIPELAS

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• Diffuse spreading infection of deep dermis without sharp demarcation

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Superficial infection with raised and sharply demarcated edge

CELLULITIS (BUCCAL/FACIAL)

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Necrotizing Fasciitis; Acute Streptococcal hemolytic gangrene; synergistic necrotizing cellulitis; gangrenous necrotizing erysipelas Etiology  Aerobes – GABHS;S. aureus; Gram – enteric organisms  Anaerobes – anaerobic streptococcus; bacteroides spp

CASE 1: “ SKINNY DIPPING” History o Baby A is a 1 year very active boy who was brought to the OPD because of an infected insect bite of the left lower leg. o The lesion was described as a red indurated thickening of the skin which began as a small lesion that marginally spread for 5 days. The margins had a raised, firm, tender, palpable border. o The lesion was associated with fever, irritability and incessant crying upon touching the extremity. Diagnosis: Erysipelas /3na

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Epidemiology  Buccal • Uncommon, infection occur between ages 6 mo to 5 yrs • No identified portal of entry - ? Direct seeding of buccal mucosa from bloodstream or lymphatic extension from otitis media  Facial • Older patient • From direct extension from dental infection or local trauma Etiology  Buccal – almost always HiB; S. pneumoniae (occasional)  Facial (depends on portal of entry):