1Skin andSoft Tissue InfectionsElizabeth D. Hermsen, Pharm.D.Infectious Diseases Research FellowUniversity of MinnesotaCollege of PharmacySpring 2004 PHAR 6124 2Objectives• Discuss three classification variables involvedin the evaluation of skin and soft tissueinfections (SSTI’s).• Identify five host defense mechanisms thatmay prevent SSTI’s.• List three predisposing factors for SSTI’s.• Differentiate between the various SSTI’s– Identify pathogens commonly encountered witheach type– Suggest antimicrobial therapy for common SSTI’sSpring 2004 PHAR 6124 3Introduction• SSTI’s are common and vary widely inseverity• Multiple classification systems– Uncomplicated vs. complicated– Single pathogen vs. mixed infection– Acute vs. chronic– Local vs. diffuse– Systemic signs• Important to have an idea of what theinfecting organism is appropriate empiricantimicrobial therapy when necessary2Spring 2004 PHAR 6124 4Mandell’s Atlas of Infectious Diseases CD-ROMSpring 2004 PHAR 6124 5Host Defenses• Multi-layered construction of skin– Stratum corneum, epidermis, dermis, subcutaneousfat, superficial fascia• Skin is dry• Limited epithelial cell adherence by pathogens• Intact stratum corneum• Low skin pH• Host immune system• Resident skin floraSpring 2004 PHAR 6124 6Predisposing Factors• Systemic– Peripheral neuropathy, vascular insufficiency– Increased age, smoking, poor nutrition, obesity– Comorbidities– Immunosuppression• Local– Type, site, size, and depth of wound– Edema– Tissue ischemia– Excessive moistureBowler PG et al. Clin Microbiol Rev. 2001;14:244-69.3Spring 2004 PHAR 6124 7Classification of SSTI’sPrimary(Uncomplicated)• Folliculitis, furuncles,carbuncles• Erysipelas• Impetigo• Cellulitis• Necrotizing fasciitisSecondary(Complicated)• Diabetic foot infections• Pressure sores• Bite wounds• Burn wounds• Cellulitis• Necrotizing fasciitisSpring 2004 PHAR 6124 8Importance of Etiology• Single pathogen– Usually uncomplicated/primary– Commonly gram-positive• Mixed infection– Aerobes – usually open wounds– Aerobes and anaerobes –• Most likely deeper infections• Microbial synergy – severityBowler PG et al. Clin Microbiol Rev. 2001;14:244-69.Spring 2004 PHAR 6124 9Bacteria CommonlyAssociated with SSTI’sGram-positive• S. aureus, S.epidermidis• Streptococci spp.• Enterococcus spp.Gram-negative• E. coli, Klebsiella,Proteus• P. aeruginosa• Pasteurella multocidaAnaerobes• Eikenella corrodens• Other oral anaerobes• Clostridium spp.• B. fragilis4Spring 2004 PHAR 6124 10Acute vs. ChronicAcute• External damage tointact skin– Cuts– Trauma– Bites– Burns– Surgical woundsChronic• Endogenousmechanism andpredisposingconditions– Leg/foot ulcers– Pressure soresBowler PG et al. Clin Microbiol Rev. 2001;14:244-69.Spring 2004 PHAR 6124 11Folliculitis• Pathogenesis– Superficial infection around hair follicles– Most common on hairy areas of the body– Can occur with insufficient chlorine levels in hottubs/swimming pools• Clinical findings– Pruritic, erythematous papules– ~48 hours after exposure– Evolve to pustules– Heals in several daysSpring 2004 PHAR 6124 12Folliculitis (cont.)• Etiology– S. aureus– P. aeruginosa (hot tub)• Treatment– Warm compress– May need topical antimicrobials(clindamycin, erythromycin)5Spring 2004 PHAR 6124 13Furuncles and Carbuncles• Pathogenesis– Furuncles• Extension of folliculitis –inflammation involvesdermis• Usually on hairy areassubject to friction andmoisture (perspiration)– Carbuncles• Extension of furuncle –extends to subcutaneoustissue• Clinical Findings– Furuncles• Firm, tender, rednodule• Painful, pustulant• Discrete lesions– Carbuncles• Similar to furuncle,but coalesced lesions• Fever, chills, malaise• May spread to othertissuesSpring 2004 PHAR 6124 14Furuncles and Carbuncles (cont.)• Etiology– S. aureus• Treatment– Small furuncles -- moist heat– Large furuncles/ Carbuncles• Dicloxacillin 250mg po QID x 10d• PCN allergy – clindamycin 150-300mg po QIDor erythromycin 250-500mg po QID x 10d• Surgical incision for non-draining lesionsSpring 2004 PHAR 6124 15Erysipelas• Pathogenesis– Superficial cellulitis– Bacteria gain access via small break in skin(insect bite, abrasion)• Clinical Findings– Most common in infants, young children, andelderly– Most common on lower extremities– Bright red, edematous, indurated, painful– Sharply surrounded by a raised border– Fever and WBC common6Spring 2004 PHAR 6124 16Erysipelas (cont.)• Etiology– S. pyogenes– Group B streptococci in newborns– Rarely S. aureusSpring 2004 PHAR 6124 17Erysipelas (cont.)• Treatment– Mild to moderate• procaine PCN G 600,000 U IM BID• PCN VK 250-500mg po QID x 10d• PCN allergy – erythromycin 250-500mg po QID x 10d– Serious• Aqueous PCN G 2-8 MU qd IV– Infection may appear to worsen shortly aftertreatmentSpring 2004 PHAR 6124 18Impetigo• Pathogenesis– Most common in hot, humid weather– Bacteria gain access via minor trauma (insect bites)– Most common in children– Highly communicable – spread through closecontact/poor hygiene• Clinical Findings– Small, fluid-filled vesicles develop into pus-filledblisters– Purulent discharge dries to form “honey crusts”– Pruritis is common7Spring 2004 PHAR 6124 19Impetigo (cont.)• Etiology– S. aureus– S. pyogenesSpring 2004 PHAR 6124 20Impetigo (cont.)• Treatment (7-10 days)– Warm water soak– PenVK 250-500mg po QID– Cephalexin 500mg po QID– Cefaclor 500mg po TID– Benzathine PCN G 1.2 MU IM x 1– PCN allergy – erythromycin 250-500mg po QID– Prophylaxis – mupirocin ointment TID x 7dSpring 2004 PHAR 6124 21Cellulitis• Pathogenesis– Acute; spreads to involve subcutaneous tissues– Previous trauma (laceration, puncture) or otherskin lesion (furuncle, ulceration) predisposes tocellulitis– Propensity to spread to bloodstream• bacteremia present in ~30% cases– Other complications• local abscess and osteomyelitis8Spring 2004 PHAR 6124 22Cellulitis (cont.)• Clinical Findings– Can occur within hours or days of initial trauma– Local tenderness, pain, erythema,• Rapidly intensifies– Fever, chills, malaise with severe cellulitis– Feels warm to touch, appears swollen, poorlydemarcated– Regional lymphadenopathy– Cultures usually not