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 – Impetigo, erysipelas, folliculitis, carbuncles  Infections secondary to pre-existing conditions – 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 – Staph aureus, epidermidis  Intriginous/perineal – 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

GN Anaerobes

Deep Other Specific Skin Infections

Epidemiology Common Pathgen(s) Therapy

Cat/Dog Bites P. multocida; Amox/clav (Doxy; FQ or SXT + Capnocytophaga Clinda)

Human bites Mixed flora Hand Surgeon; ATB as above

Fresh water injury Aeromonas FQ; Broad Spectrum Beta- lactam

Salt water injury Vibrio vulnificus FQ; Ceftazidime (warm)

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. File MD 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 – Less resistant to non-beta-lactam agents – Often susceptible to TMP-SMX, clinda, tetracyclines, +/- fluoroquinolones – Panton-Valentine leukocidin (PVL) – virulence factor  Risk Factors – 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 C. perfringes – Hydrolyzes cell membranes 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 C- section – 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 E. Faecalis in blood culture  Bacteroides 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) Questions?