Skin and Soft Tissue Infections Masoud Mardani MD, MPH,FIDSA Prof of Infectious Dis Shahid Beheshti Medical University
Usual Skin Flora Skin flora consists of those microbes able to adapt to the high salt concentration and drying effects of the skin Permanent Transient Offers protection from pathogens and UV rays
Types of Usual Skin Flora Coagulase-negative Staphylococcus is permanent resident Staphylococcus aureus is transient colonizer Diphtheroids Propionibacterium acnes Corynebacterium xerosis Yeasts Candida Pityrosporum Gram negative rods
Bacterial Skin and Soft Tissues Infections Primary Pyoderma Infections secondary to pre-existing conditions Impetigo, erysipelas, folliculitis, carbuncles Surgical wounds, trauma, bites, decubitus infections, diabetic foot infections Necrotizing infections Polymicrobial Monomicrobial (Gp A. Strep; Clostridium)
impetigo Ecthyma Erysipelas Cellulitis Panniculitis Necrotizing fasciitis
Primary Pyoderma
Impetigo Most often caused by: Streptococcus pyogenes/ Group A S. aureus- Exfoliative toxin Vesicles rupture, creating a thick, yellow, encrusted appearance Lesions are superficial and painless but pruritic and easily spread by scratching Highly contagious
Impetigo Treatment: topical mupirocin Numerous lesion or unreponsive to topical agents: Cloxacilin Cepalexin Erythromycin Clindamycin Co-Amoxiclave
Cellulitis Diffuse inflammation and infection of superficial skin layers Localized, mildly painful, swelling with poorly demarcated margins Streptococcus pyogenes & Staphylococcus aureus common pathogens
Cellulitis Pathophysiology Adults Staph/Strep spp. most common Children H. influenza most common Diabetics consider Enterobacteriaceae Most bacterial organism cleared from body with 12 hours. Majority of symptoms are from host immune response
Cellulitis Clinical Local inflammation, tenderness, warmth, erythema, induration Lymphangitis uncommon concerning Bacteremia uncommon in healthy hosts
Cellulitis Oral regimen: 1-Doxycycline plus Cephalexin or Amoxicillin 2-TMP/SMX plus Amoxicilin 3-Clindamycin Parentral regimen: 1-Clindamycin 600 mg qhs (mild disease) 2-Vancomycin (mod. To severe disease or nosocomial aquisition
Pyogenic Cellulitis
Erysipelas Deeper form of cellulitis that infects underlying dermis and lymphatic channels Painful, raised, crimson color with sharp demarcated border Usually affects face and lower extremities
Erysipelas Superficial cellulitis with lymphatic involvement Usually from Group A Streptococcus Antecedent trauma / bite or dermatoses Lower extremities now most common
Erysipelas Clinical Abrupt onset High fever, chills, malaise and nausea prodrome Area of erythema with burning develops over next 2 days Red, shiny, hot plaque, sharply demarcated
Erysipelas Treatment usually inpatient Pen G IV Nafcillin Rocephin Augmentin Imipenem in severe
Erysipelas
Folliculitis Inflammation & infection of hair follicles. Usually found in areas of points of friction S. aureus most common agent, but P. aeruginosa implicated from swimming pools and whirlpools
Furuncles Furuncle (boil) when the infection extends from the follicle/gland into surrounding tissues -results in localized redness, swelling, tenderness, and pain -suspected organism: S.areus including MRSA
Carbuncles larger, deeper lesion resulting from the aggregation and interconnection of multiple furuncles - results in the above furuncle symptoms plus several sites of draining pus - suspected organism: S.areus including MRSA
Carbuncle S. aureus
Folliculitis,Furuncles and Carbancles Treatment A-Folliculitis: -Warm compress -No antibiotics B-Furuncles and Carbancles -I&D -Antibiotiics, if fever and/or surrounding cellulitis presents
Cutaneous Abscesses Pathophysiology Requires loss of skin integrity Usually caused by common colonizers Scalp/trunk/extremities Intriginous/perineal Staph aureus, epidermidis E. coli, P. mirabilis Axilla P. mirabilis
Cutaneous Abscesses Clinical Swelling, tenderness, erythema Fluctuance, induration, drainage Systemic spread unusual in healthy Lymphadenitis, fever
Cutaneous Abscesses Specific abscesses Bartholin gland abscess Paronychia and felons Hidradenitis suppurativa Infected sebaceous cyst Perirectal abscess Pilonidal abscess
Cutaneous Abscesses Staphylococcal abscesses Continuum of severity Folliculitis Furuncle (boil) Carbuncle
Cutaneous Abscesses Treatment Incision and drainage Antibiotics Always in high risk groups (immunocompromised) In healthy persons if: Surrunding cellulitis Systemic symptoms Multiple lesions gangrene
What can you expect? superficial Gram Positives Anaerobes Deep GN
Other Specific Skin Infections Epidemiology Common Pathgen(s) Therapy Cat/Dog Bites P. multocida; Capnocytophaga Amox/clav (Doxy; FQ or SXT + Clinda) Human bites Mixed flora Hand Surgeon; ATB as above Fresh water injury Aeromonas FQ; Broad Spectrum Betalactam Salt water injury (warm) Vibrio vulnificus FQ; Ceftazidime Meat-packing Erysipelothrix Penicillin Cat scratch Bartonella Azithromycin IDSA Guidelines. Stevens D. et al. Clin Infect Dis 2005; 42:1379-406
Pyoderma-Antimicrobial Therapy S. pyogenes Beta-lactams; Others: macrolides (resistance 5-10%), clindamycin, doxycycline, minocycline S. aureus MSSA: antistaphylococcal penicillins (ie dicloxacillin, nafcillin, oxacillin); cephalosporins; clindamycin; macrolides; doxycycline, minocycline, TMP-SMX MRSA Hospital acquired: Vancomycin, linezolid, daptomycin Community-associated: Trimethoprim-sulfamethoxazole; doxycycline/minocycline; clindamycin (if D Test negative) Modified from IDSA Guidelines. Stevens D et al. Clin Infect Dis 2005;42:1379-406
Community-associated MRSA 65 y/o female with a boil unresponsive to 3 days of cephalexin Photo courtesy of T.
CDC Definition of CA-MRSA Diagnosis of MRSA made in the outpatient setting or by a culture positive for MRSA within 48h of hospital admission Patient has no medical history of MRSA colonization or infection Patient has no medical history in the past year of: Hospitalization(recent or reccurent prolonged hospitalization) Admission to a nursing home, skilled nursing facility or hospice, IDU Dialysis Surgery The patient has no indwelling catheters or medical devices that pass through the skin
Community-Associated (CA) MRSA Increasing cause of community skin infections Genotypically and phenotypically unique from nosocomial MRSA Risk Factors Less resistant to non-beta-lactam agents Often susceptible to TMP-SMX, clinda, tetracyclines, +/fluoroquinolones Panton-Valentine leukocidin (PVL) virulence factor Athletes, inmates, military recruits, men who have sex with men, injection drug user, prior antibiotic use Increases need to culture.
Necrotizing Soft Tissue Infections Gas gangrene (Clostridial myonecrosis) Gas gangrene (Nonclostridial myonecrosis) Streptococcal myositis Necrotizing fasciitis (polymicrobial) Necrotizing fasciitis ( Group A Streptococcus) Necrotizing cellulitis
Gas Gangrene (Clostridial) Epidemiology About 1000 cases reported to CDC yearly Pathophysiology Seven sp Clostridium C. perfringes 80-95% Soil, GI tract, Female GU Release endotoxins Cardiodepressant Hydrolyzes cell membranes C. perfringes
Gas Gangrene (Clostridial) Clinical Incubation: 3 days Pain out of proportion Heaviness of affected part Edema, brown discoloration +/- crepitance Serosanguineous discharge Bullae Fever, tachycardia Confusion, sepsis Uterine myonecrosis after Csection Deepest of the necrotizing soft tissue infections
Gas Gangrene (Clostridial) Clinical X-Ray/CT: gas Treatment Resuscitation Antibiotics Pen G + Clindamycin Augmentin Imipenem Unasyn Surgical debridement Hyperbaric oxygen therapy (HBO)
Gas Gangrene (Nonclostridial) Pathophysiology Mixed infections Aerobic / anaerobic Bacteria by prevalence: Enterococcus Staphylococcus Alpha-Streptococci E. coli Klebsiella Proteus Bacteroides E. Faecalis in blood culture
Gas Gangrene (Nonclostridial) Clinical Similar to Clostridial except: Pain at onset less Delayed presentation (2-10 days) Mortality 43%
Gas Gangrene (Nonclostridial) Treatment Broad spectrum antibiotics Aerobic gram + / Anerobes Unasyn Timentin Zosyn Imipenem Floroquinolone added if fresh water infection suspected Surgical debridement HBO
Streptococcal Myositis Rare muscle infection Group A Streptococcus Usually S. pyogenes flesh eating bacteria Epidemiology Age 20-50 Otherwise healthy
Streptococcal Myositis Clinical Difficult to distinguish from other myonecrosis No gas production High rate of bacteremia Toxic shock syndrome ~ 4-6 hours after admission Mortality: 80-100%
Streptococcal Myositis Treatment Aggressive management of shock Early vasopressors in shock Antibiotics IV Pen G / Clindamycin IVIG 2g/kg Neutralizes exotoxins Surgical debridement
Necrotizing Fasciitis (Polymicrobial) Necrosis of subq and fascia Does not spread to muscle as clostridial / nonclostridial myonecrosis Also grouped into tabloid term flesh eating bacteria
Necrotizing Fasciitis (Polymicrobial) Epidemology 10-20 cases per 100,000 people DM, PVD, IVDA, smoking Pathophysiology Mixed aerobic / anerobic Average 4.4 organisms per infection Usually antecedent trauma / bite Bacteremia 25-30% Mortality 25-50%
Necrotizing Fasciitis (Polymicrobial) Clinical Pain out of proportion Erythematous / edematous Discoloration, vesicles Fever, tachycardia May progress rapidly Crepitus as late finding Finger test
Necrotizing Fasciitis (Polymicrobial) Treatment Aggressive resuscitation Avoidance of vasopressors Antibiotics as in myonecrosis Surgery HBO
Necrotizing Fasciitis (Group A Streptococcus) Epidemiology 10-20 cases per 100,000 Mortality 20-60% Increased risk with: Varicella lesions NSAID use
Necrotizing Fasciitis (Group A Streptococcus) Clinical Same as polymicrobial except: No gas formation More rapid progression More prone to bacteremia Toxic shock more common
Necrotizing Fasciitis (Group A Streptococcus) Treatment Initial broad spectrum Abx Narrowed to PCN and Clindamycin after culture Clindamycin Synergistic to PCN Suppresses toxin formation Promotes phagocytosis Suppresses PCN binding protein HBO of little use (aerobic organism)
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