Residency · Residency · Dermatology

Bacterial Skin Infections: From Impetigo to Necrotizing Fasciitis

Overview

Bacterial skin and soft tissue infections (SSTIs) represent a spectrum from superficial, self-limited conditions like impetigo to life-threatening emergencies such as necrotizing fasciitis. Staphylococcus aureus and Streptococcus pyogenes (group A streptococcus, GAS) are the predominant pathogens. The emergence of community-acquired methicillin-resistant S. aureus (CA-MRSA) has significantly altered empiric treatment strategies.

Superficial Infections

Impetigo

Impetigo is the most common bacterial skin infection in children. Non-bullous impetigo accounts for 70 percent of cases and is caused by S. aureus (most common) or GAS. It presents with honey-colored or golden crusts on an erythematous base, favoring the face (perioral and perinasal) and extremities, and is highly contagious through direct contact. Bullous impetigo accounts for the remaining 30 percent and is caused exclusively by S. aureus phage group II, which produces exfoliative toxins A and B. It presents as flaccid bullae with clear to cloudy fluid that rupture to leave a varnish-like crust, primarily in neonates and young children, representing a localized form of staphylococcal scalded skin syndrome.

Treatment for limited disease involves topical mupirocin 2% or retapamulin 1%. Widespread disease requires oral antibiotics such as cephalexin or dicloxacillin, with TMP-SMX or doxycycline if MRSA is suspected. An important complication is post-streptococcal glomerulonephritis from nephritogenic GAS strains; however, rheumatic fever does not follow skin streptococcal infections.

Ecthyma

Ecthyma represents deeper extension of impetigo through the epidermis into the dermis, presenting as punched-out ulcers with adherent crust and raised violaceous borders, usually on the lower extremities. It is caused by GAS and sometimes S. aureus, heals with scarring, and requires systemic antibiotics.

Folliculitis

Folliculitis is a superficial infection of hair follicles presenting as small pustules centered on follicular ostia with surrounding erythema. S. aureus is the most common cause. Hot tub folliculitis, caused by Pseudomonas aeruginosa from chlorinated water exposure, is typically self-limited. Gram-negative folliculitis complicates long-term antibiotic use for acne and involves Klebsiella, Enterobacter, or Proteus. Pityrosporum (Malassezia) folliculitis produces pruritic, monomorphic papules and pustules on the trunk and is not bacterial. Treatment consists of topical antibiotics for mild disease, oral antibiotics for recurrent or extensive cases, and benzoyl peroxide wash for prevention.

Furuncles and Carbuncles

A furuncle (boil) is a deep follicular abscess extending into the subcutis, presenting as a painful, fluctuant nodule. A carbuncle is a coalescence of multiple furuncles draining through multiple sinus openings, often on the posterior neck. S. aureus, including CA-MRSA, is the predominant pathogen. The primary treatment is incision and drainage, with antibiotics reserved for surrounding cellulitis, systemic symptoms, or immunosuppressed patients. Recurrent furunculosis should prompt MRSA decolonization with mupirocin nares, chlorhexidine washes, and household decontamination.

Deeper Infections

Erysipelas

Erysipelas involves the superficial dermis and lymphatics and is caused almost exclusively by GAS (rarely group B, C, or G streptococci). It presents as a well-demarcated, raised, bright red, indurated plaque with an advancing border and "peau d'orange" (orange peel) texture from dermal edema. Classic locations include the face (butterfly distribution) and lower extremities. Fever and systemic symptoms are common, and onset is rapid. Treatment consists of penicillin or amoxicillin, as GAS remains universally penicillin-susceptible, with cephalosporins for penicillin-allergic patients.

Cellulitis

Cellulitis is an infection of the deeper dermis and subcutaneous fat, most commonly caused by GAS and S. aureus. It presents as poorly demarcated, spreading erythema with warmth, edema, and tenderness, most commonly on the lower extremities (often unilateral). Risk factors include lymphedema, venous insufficiency, tinea pedis (serving as a portal of entry), obesity, and prior cellulitis. Cellulitis is not purulent, distinguishing it from abscess.

Treatment depends on the presentation: non-purulent cellulitis is treated with cephalexin or dicloxacillin targeting streptococci and MSSA, while purulent cellulitis or abscess is treated with incision and drainage plus TMP-SMX or doxycycline targeting CA-MRSA. Severe cases require IV vancomycin plus piperacillin-tazobactam. Recurrent cellulitis may benefit from prophylactic penicillin V or erythromycin along with treatment of predisposing conditions. The differential includes stasis dermatitis (bilateral, chronic, with brown discoloration), DVT, contact dermatitis, and lipodermatosclerosis.

Perianal Streptococcal Dermatitis

This condition presents as well-demarcated perianal erythema in children, caused by GAS and diagnosed by perianal culture. Symptoms include pain with defecation and rectal bleeding, treated with oral penicillin or amoxicillin for 14 to 21 days.

Toxin-Mediated Diseases

Staphylococcal Scalded Skin Syndrome (SSSS)

SSSS is caused by exfoliative toxins A and B produced by S. aureus phage group II. These toxins cleave desmoglein 1 (the same target as pemphigus foliaceus antibodies), causing a cleavage within the granular layer of the epidermis (intragranular split). Clinically, it presents as diffuse erythema followed by superficial desquamation with a positive Nikolsky sign. Perioral crusting and radial fissuring are characteristic. SSSS primarily affects neonates and young children who lack anti-toxin antibodies and have immature renal clearance, while adult cases are rare and occur in renal failure or immunosuppression.

The key distinction from TEN is that SSSS has an intragranular split (superficial) while TEN has a subepidermal split (full-thickness epidermal necrosis). Frozen section biopsy can rapidly distinguish these two conditions. Treatment consists of IV anti-staphylococcal antibiotics (nafcillin, oxacillin), gentle wound care, and no corticosteroids. Prognosis is excellent in children (less than 5 percent mortality) but carries high mortality in adults.

Scarlet Fever

Scarlet fever results from GAS pharyngitis combined with erythrogenic toxin (streptococcal pyrogenic exotoxin). It presents with diffuse erythema with a sandpaper texture, accentuation in flexures (Pastia lines), circumoral pallor, and strawberry tongue, followed by desquamation during convalescence. Treatment is penicillin.

Necrotizing Soft Tissue Infections

Overview

Necrotizing soft tissue infections are rapidly progressive, life-threatening infections involving fascia and/or muscle. They represent a surgical emergency, with mortality of 20 to 40 percent even with treatment, and delays in surgery dramatically increase mortality. | Type | Microbiology | Typical Setting |

Type I (polymicrobial/synergistic) involves mixed aerobic and anaerobic organisms, typically in diabetics, immunocompromised, or post-surgical patients. Type II (monomicrobial) is usually caused by GAS ("flesh-eating bacteria") and can occur in young healthy individuals. Type III involves gas gangrene from Clostridium species (C. perfringens) with myonecrosis. Marine-associated types include Vibrio vulnificus from saltwater or raw shellfish exposure and Aeromonas from freshwater.

Clinical Features

"Hard signs" requiring urgent surgery include pain out of proportion to examination (the most important early sign), rapidly spreading erythema with dusky or violaceous color change, bullae or hemorrhagic bullae, crepitus (subcutaneous gas), skin anesthesia from nerve destruction, systemic toxicity (fever, tachycardia, hypotension, altered mental status), and failure to improve on appropriate antibiotics. "Soft signs" that should heighten suspicion in early disease include edema extending beyond the erythema margin, severe pain with minimal skin findings, fever with elevated WBC, CRP, and lactate, and rapid clinical deterioration.

Diagnosis

This is a clinical diagnosis, and surgery should not be delayed for imaging. The LRINEC score (Laboratory Risk Indicator for Necrotizing Fasciitis), which incorporates CRP, WBC, hemoglobin, sodium, creatinine, and glucose, raises concern at a score of 6 or above, but sensitivity is imperfect. CT or MRI may show fascial thickening, gas, or fluid collections, but normal imaging does not exclude necrotizing fasciitis. The "finger test" involves a bedside incision to the fascia, where dishwater-gray necrotic fascia with lack of bleeding confirms the diagnosis.

Management

Management requires immediate surgical debridement to viable tissue, often with multiple returns to the operating room. Broad-spectrum IV antibiotics include vancomycin plus piperacillin-tazobactam plus clindamycin (which inhibits toxin production), adjusted based on culture results. ICU admission with aggressive fluid resuscitation is necessary. IVIG may be considered for streptococcal toxic shock syndrome. Hyperbaric oxygen is controversial with limited evidence and should never delay surgery.

MRSA Considerations

CA-MRSA, predominantly the USA300 strain, produces Panton-Valentine leukocidin (PVL) and is associated with purulent SSTIs including abscesses, furuncles, and carbuncles, and rarely causes necrotizing pneumonia. It is susceptible to TMP-SMX, doxycycline, and clindamycin (though the D-test should be performed to check for inducible resistance). The decolonization protocol for recurrent MRSA infections includes mupirocin 2% nasal ointment twice daily for five days, chlorhexidine 4% body wash daily for five days, decontamination of household fomites, and simultaneous treatment of household contacts.

<image>Clinical photograph panel showing the spectrum of bacterial skin infections: (A) non-bullous impetigo with honey-colored crusts on a child's face, (B) bullous impetigo with flaccid bullae and denuded skin, (C) cellulitis of the lower leg showing poorly demarcated erythema with edema, (D) early necrotizing fasciitis showing dusky erythema with hemorrhagic bullae and skin necrosis. Show on diverse skin tones.</image>

<image>Cross-sectional anatomic diagram showing the depth of different bacterial skin infections: impetigo (epidermis), ecthyma (into dermis), erysipelas (superficial dermis and lymphatics), cellulitis (deep dermis and subcutis), necrotizing fasciitis (fascia), and myonecrosis (muscle). Label each layer and the typical organisms at each level.</image>

<image>Flowchart for the emergency evaluation of suspected necrotizing fasciitis: clinical assessment (pain out of proportion, crepitus, bullae, systemic toxicity), LRINEC score calculation, imaging if stable (CT showing fascial gas), and decision pathway leading to emergent surgical debridement. Emphasize that imaging should NOT delay surgery when clinical suspicion is high.</image>

Key Clinical Pearls

Pain out of proportion to examination is the single most important early sign of necrotizing fasciitis, and maintaining a high index of suspicion is essential to avoid delays in surgical consultation. SSSS and TEN can be distinguished by frozen section biopsy: SSSS shows an intragranular split (superficial) while TEN shows full-thickness epidermal necrosis, a distinction with critical treatment implications. Non-purulent cellulitis is usually streptococcal while purulent SSTIs (abscesses, furuncles) are usually staphylococcal, and antibiotic selection should be tailored accordingly. Tinea pedis is the most common portal of entry for lower extremity cellulitis, and treating interdigital tinea reduces cellulitis recurrence. Post-streptococcal glomerulonephritis can follow skin (impetigo) or pharyngeal GAS infection, but rheumatic fever follows only pharyngeal infection. Recurrent furunculosis in a patient or household should prompt MRSA decolonization of the index patient and close contacts.

References

• Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the IDSA. Clin Infect Dis. 2014;59(2):e10-e52.
• Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the IDSA for the treatment of MRSA infections in adults and children. Clin Infect Dis. 2011;52(3):e18-e55.
• Baddour LM. Cellulitis and erysipelas. UpToDate. 2024.
• Wong CH, Khin LW, Heng KS, et al. The LRINEC score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections. Crit Care Med. 2004;32(7):1535-1541.

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