38.1 Bacterial Skin Infections: Impetigo, Cellulitis & Cutaneous Abscesses

Spectrum of Bacterial Skin & Soft Tissue Infections

Bacterial skin and soft tissue infections (SSTIs) constitute one of the most frequent reasons for acute outpatient visits and hospital admissions in primary care. Accurate management requires clinicians to systematically distinguish superficial epidermal infections from deep dermal and subcutaneous processes, recognize surgical emergencies such as necrotizing fasciitis, and apply rigorous antimicrobial stewardship to avoid overprescribing antibiotics for uncomplicated drained abscesses while providing timely coverage for community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) and Streptococcus pyogenes (Group A Streptococcus [GAS]).

              ANATOMICAL DEPTH OF BACTERIAL CUTANEOUS INFECTIONS

  Skin Layer             Pathology                     Dominant Pathogens
  ─────────────────────────────────────────────────────────────────────────────
  Epidermis (Subcorneal)  Impetigo (Non-bullous/Bullous) S. aureus, S. pyogenes
  ─────────────────────────────────────────────────────────────────────────────
  Deep Epidermis/Dermis  Ecthyma (Ulcerative impetigo)  S. pyogenes, S. aureus
  ─────────────────────────────────────────────────────────────────────────────
  Upper Dermis &         Erysipelas                    S. pyogenes (GAS)
  Superficial Lymphatics (Sharply demarcated, raised)
  ─────────────────────────────────────────────────────────────────────────────
  Deep Dermis &          Non-Purulent Cellulitis       GAS, Groups B/C/G Strep,
  Subcutaneous Fat       (Poorly demarcated, flat)     MSSA
  ─────────────────────────────────────────────────────────────────────────────
  Hair Follicle & Dermis Folliculitis / Furuncle /     CA-MRSA, MSSA
                         Carbuncle / Cutaneous Abscess
  ─────────────────────────────────────────────────────────────────────────────
  Deep Fascia & Muscle   Necrotizing Fasciitis         Polymicrobial (Type I)
                         (SURGICAL EMERGENCY!)         GAS monomicrobial (Type II)

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Impetigo & Ecthyma

Impetigo is a highly contagious, superficial bacterial infection of the epidermis, occurring predominantly in children aged 2 to 5 years, though individuals of any age can be affected in warm, humid conditions or settings of close physical contact (e.g., daycare centers, sports teams).

1. Non-Bullous Impetigo

• Epidemiology & Etiology: Accounts for approximately 70% of all impetigo cases. The primary causative organisms are Staphylococcus aureus (most common) and Streptococcus pyogenes (Group A beta-hemolytic Streptococcus [GAS]), either alone or in combination.
• Pathogenesis: Bacteria inoculate through microscopic breaks in the epidermal stratum corneum caused by minor abrasions, insect bites, varicella lesions, or atopic dermatitis. Autoinoculation occurs rapidly via scratching and fingers.
• Clinical Presentation:
  • Initial lesions are transient, thin-walled microvesicles or pustules that rapidly rupture.
  • The hallmark physical exam finding is superficial, moist erosions covered by thick, adherent, golden, honey-colored ("meliceric") crusts.
  • Lesions characteristically cluster on the face, particularly around the nares and perioral region, as well as exposed extremities.
  • Pruritus is common, but systemic symptoms (fever, malaise, toxicity) and marked regional lymphadenopathy are typically absent in mild-to-moderate disease.
• Complications: Untreated streptococcal impetigo can precipitate post-streptococcal glomerulonephritis (PSGN), which typically develops 3 to 6 weeks after cutaneous infection. Crucial Board Pearl: Antimicrobial treatment of impetigo prevents secondary transmission and heals cutaneous lesions, but does NOT prevent the development of post-streptococcal glomerulonephritis! In contrast to pharyngeal GAS infections, cutaneous GAS infections are not associated with acute rheumatic fever.

2. Bullous Impetigo

• Epidemiology & Etiology: Accounts for approximately 30% of impetigo cases, occurring most commonly in neonates, infants, and young children. It is caused exclusively by toxin-producing strains of Staphylococcus aureus.
• Pathogenesis: S. aureus produces exfoliative toxin A (ETA), a serine protease that specifically targets and cleaves desmoglein-1, a key desmosomal cell-cell adhesion protein located exclusively in the superficial epidermis (stratum granulosum). Cleavage of desmoglein-1 results in intraepidermal acantholysis, blistering, and bullae formation without inflammatory cellular infiltrate.
• Clinical Presentation:
  • Begins as small vesicles that enlarge rapidly to form large, flaccid, clear-to-turbid fluid-filled bullae (1 to 2 cm in diameter) on previously intact skin of the trunk, intertriginous folds, face, or buttocks.
  • Because the blister roof is thin superficial epidermis, the bullae easily rupture, leaving shiny, red, moist, shallow erosions surrounded by a characteristic thin, delicate rim or "collarette" of scale.
  • In contrast to non-bullous impetigo, honey-colored crusting is minimal or absent.
  • Bullous impetigo represents a localized manifestation of the same exfoliative toxin responsible for generalized Staphylococcal Scalded Skin Syndrome (SSSS) in neonates and young infants with immature renal toxin clearance.

3. Ecthyma

• Pathogenesis & Depth: Ecthyma represents an ulcerative, deeper variant of impetigo that penetrates through the full-thickness epidermis and extends into the deep dermis.
• Etiology: Caused predominantly by Streptococcus pyogenes, frequently with secondary S. aureus superinfection. Predisposing factors include poor hygiene, malnutrition, tropical climates, excoriations, homeless populations, and immunocompromised states.
• Clinical Presentation:
  • Presents as painful, "punched-out" round or oval deep cutaneous ulcers with raised, indurated, violaceous borders.
  • The ulcers are covered by a thick, hard, tightly adherent, yellowish-black crust or eschar.
  • Removal of the crust reveals a raw, purulent, granulating ulcer base.
  • Lesions occur most commonly on the lower extremities (shins, dorsum of feet).
  • Because the dermal basement membrane and papillary dermis are breached, ecthyma heals slowly and invariably resolves with permanent scar formation.

Evidence-Based Treatment Algorithm for Impetigo & Ecthyma

[!TIP] PEDIATRIC IMPETIGO PEARL: For mild, localized non-bullous impetigo involving only a few crusted lesions around the nose and mouth, topical mupirocin 2% ointment is equal in clinical efficacy to oral cephalexin, avoids systemic adverse effects (such as gastrointestinal upset and diarrhea), and minimizes selective pressure for broad antimicrobial resistance. Crusts should be gently soaked with warm soapy water before ointment application to facilitate topical penetration.

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Cellulitis vs. Erysipelas

Differentiating erysipelas from non-purulent cellulitis is a classic clinical challenge in primary care. Although both represent acute spreading bacterial infections of the skin, their anatomical depth, microbiology, and physical features differ substantially.

                   ERYSIPELAS vs. NON-PURULENT CELLULITIS

  Feature                ERYSIPELAS                   NON-PURULENT CELLULITIS
  ─────────────────────────────────────────────────────────────────────────────
  Anatomic Depth         Upper dermis & superficial   Deep dermis & subcutaneous
                         lymphatics                   fat
  ─────────────────────────────────────────────────────────────────────────────
  Primary Etiology       Streptococcus pyogenes       Beta-hemolytic Strep (GAS,
                         (GAS >90%)                   GBS, GCS, GGS) & MSSA
  ─────────────────────────────────────────────────────────────────────────────
  Onset & Toxicity       Acute, abrupt onset;         Subacute onset (over days);
                         high fever, shaking chills   mild-moderate systemic signs
  ─────────────────────────────────────────────────────────────────────────────
  Clinical Appearance    Fiery bright red, shiny,     Dull pink-red, flat, poorly
                         indurated, raised border     demarcated, ill-defined
                         SHARPLY DEMARCATED           edges blend into normal skin
  ─────────────────────────────────────────────────────────────────────────────
  Classic Locations      Lower extremities, Face      Lower leg (unilateral),
                         (malar butterfly rash)       extremities, abdominal wall
  ─────────────────────────────────────────────────────────────────────────────
  Initial Outpatient Rx  Oral Penicillin VK or        Oral Cephalexin 500 mg QID
                         Amoxicillin or Cephalexin    or Cefadroxil 500 mg-1 g daily

1. Erysipelas

• Pathogenesis & Depth: Involves the upper papillary dermis and superficial cutaneous lymphatics. The superficial anatomical localization accounts for the intense dermal edema, prominent lymphangitis, and conspicuous clinical demarcation.
• Etiology: Overwhelmingly caused by Group A beta-hemolytic Streptococcus (Streptococcus pyogenes); rarely caused by Group B, C, or G streptococci.
• Clinical Presentation:
  • Rapid, dramatic, explosive onset over a few hours.
  • High fever (often ≥38.5°C to 39.5°C), rigor, tachycardia, and prominent systemic toxicity preceding the skin changes by several hours.
  • Physical Findings: An area of bright, fiery red, shiny, hot, tense, indurated plaque with a raised, sharply demarcated, elevated advancing border that is palpably distinct from surrounding healthy skin.
  • Superficial skin involvement may produce an "orange peel" (peau d'orange) appearance due to cutaneous lymphatic obstruction surrounding hair follicles.
  • Locations: Lower extremities are most common (~80%), followed by the face (~15-20%). Facial erysipelas classically presents with a bilateral butterfly-shaped malar distribution, but characteristically spares the nasolabial folds (involvement of the nasolabial folds suggests seborrheic dermatitis or contact dermatitis rather than erysipelas).
• First-Line Therapy:
  • Mild Outpatient Erysipelas: Oral Penicillin VK 500 mg PO QID, Oral Amoxicillin 500 mg PO TID, or Oral Cephalexin 500 mg PO QID for 5 days (extend to 7-10 days if clinical response is slow).
  • Severe / Toxic / Hospitalized Patients: Intravenous Cefazolin 1 g to 2 g IV every 8 hours or IV Aqueous Penicillin G 2 to 4 million units IV every 4 to 6 hours.
  • Penicillin-Allergic: Oral Clindamycin 300 to 450 mg PO TID.

2. Non-Purulent Cellulitis

• Pathogenesis & Depth: Involves the deeper reticular dermis and subcutaneous adipose tissue.
• Etiology: Primarily caused by beta-hemolytic streptococci (S. pyogenes, Group B S. agalactiae, Group C, and Group G streptococci) in >75% of cases, followed by methicillin-susceptible Staphylococcus aureus (MSSA). Methicillin-resistant S. aureus (MRSA) is an infrequent cause of typical non-purulent cellulitis in the absence of penetrating trauma, purulent drainage, or systemic risk factors.
• Clinical Presentation:
  • Subacute onset progressing over several days.
  • Localized cardinal signs of inflammation: erythema, warmth, edema, and tenderness.
  • In contrast to erysipelas, the erythema is flat and poorly demarcated, with indistinct, ill-defined margins that gradually merge into adjacent normal skin.
  • Fever and systemic toxicity may be present but are generally less acute and dramatic than in erysipelas.
  • Predisposing Risk Factors: Tinea pedis (especially interdigital maceration serving as the microscopic portal of bacterial entry), chronic venous insufficiency, lymphedema, obesity (BMI ≥30), prior saphenous vein harvest for coronary bypass, and prior episodes of cellulitis.
• Diagnostic Stewardship:
  • Uncomplicated cellulitis is a clinical diagnosis.
  • Swabbing intact, non-broken skin or sending superficial skin cultures is useless and clinically misleading (grows colonizing skin flora).
  • Blood cultures are positive in <5% of immunocompetent outpatients and are not recommended for routine, uncomplicated cellulitis.
  • Blood cultures are indicated ONLY in patients with systemic toxicity, underlying immunosuppression, hematologic malignancy, animal bites, water immersion injuries, or failure to respond to initial empiric therapy.
  • Marking the border: The leading edge of erythema should be outlined with a surgical skin marker to track clinical response.
• Treatment of Typical Non-Purulent Cellulitis:
  • First-Line Oral Outpatient Therapy: Targets beta-hemolytic streptococci and MSSA:
    • Oral Cephalexin 500 mg PO QID for 5 to 7 days;
    • Oral Cefadroxil 500 mg to 1 g PO daily or divided BID for 5 to 7 days;
    • Oral Dicloxacillin 500 mg PO QID for 5 to 7 days.
  • Penicillin/Cephalosporin Allergy (non-severe): Oral Clindamycin 300 to 450 mg PO TID.
  • Duration of Therapy: High-quality randomized controlled trials confirm that 5 to 6 days of oral therapy is just as effective as 10 to 14 days for uncomplicated cellulitis that has shown clinical improvement by day 5. Prolonged antibiotic courses increase adverse drug events and C. difficile colitis without reducing treatment failure.
  • Non-Pharmacologic Adjuncts: Elevation of the affected extremity above the level of the heart is critical to promote lymphatic and venous drainage, accelerating clinical resolution. Interdigital tinea pedis must be actively identified and treated with topical antifungals to eliminate the primary portal of bacterial entry and prevent cellulitis recurrence.

Clinical Mimics & Red Flags: Recognizing Necrotizing Fasciitis

                      CELLULITIS vs. CLINICAL MIMICS

  Diagnosis              Distinguishing Physical & Clinical Characteristics
  ─────────────────────────────────────────────────────────────────────────────
  Venous Stasis          BILATERAL lower leg involvement, chronic pitting edema,
  Dermatitis             hemosiderin brown pigmentation, lipodermatosclerosis
                         ("inverted champagne bottle"), absent fever or leukocytosis;
                         improves with elevation; responds to compression therapy.
  ─────────────────────────────────────────────────────────────────────────────
  Deep Vein Thrombosis   Unilateral calf pain and asymmetric edema; lacking bright
  (DVT)                  superficial warmth and advancing erythema border;
                         diagnosed via Wells score + D-dimer / duplex ultrasound.
  ─────────────────────────────────────────────────────────────────────────────
  NECROTIZING            PAIN OUT OF PROPORTION to physical findings, rapid spread,
  FASCIITIS              crepitus (gas), bullae (especially hemorrhagic), skin
  (SURGICAL EMERGENCY!)  necrosis/anesthesia, severe systemic toxicity, hypotension;
                         EMERGENT SURGICAL DEBRIDEMENT + broad-spectrum IV antibiotics.

[!CAUTION] RED FLAG CLINICAL WARNING: NECROTIZING FASCIITIS Necrotizing soft tissue infection (NSTI / necrotizing fasciitis) is a rapidly fatal surgical emergency involving the deep muscular fascia and subcutaneous fat. It may initially resemble benign cellulitis, but rapid progression occurs within hours. Hallmark warning signs include:

1. Excruciating pain out of proportion to physical examination findings;
2. Failure to respond to standard broad-spectrum antibiotics within 12 to 24 hours;
3. "Hard" physical signs: cutaneous anesthesia (due to thrombosis of cutaneous microvessels and necrosis of dermal sensory nerves), tense wooden edema extending beyond erythema, subcutaneous crepitus (gas in soft tissues), bullae (particularly violaceous or hemorrhagic bullae), and frank skin ecchymosis or gangrene;
4. Systemic toxicity: high fever, refractory hypotension, tachycardia out of proportion to fever, tachypnea, altered mental status, and marked leukocytosis with bandemia (LRINEC score ≥6);
5. Immediate Management: DO NOT DELAY SURGICAL EXPLORATION FOR IMAGING! Urgent operative debridement with direct visualization of "dishwater pus" and lack of fascial resistance to probing is both diagnostic and life-saving. Empiric medical resuscitation requires broad-spectrum IV antimicrobials: IV Vancomycin (for MRSA) + IV Piperacillin-tazobactam (for Gram-negative bacilli and anaerobes) + IV Clindamycin (inhibits bacterial ribosome synthesis, shutting down streptococcal pyrogenic exotoxin A/B and staphylococcal toxic shock syndrome toxin synthesis).

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Purulent Skin Infections: Folliculitis, Furuncles, Carbuncles & Cutaneous Abscesses

Purulent SSTIs are overwhelmingly caused by Staphylococcus aureus, with Community-Associated MRSA (CA-MRSA) accounting for the majority of purulent skin infections presenting to ambulatory clinics and emergency departments across North America.

Spectrum of Purulent Pathologies

1. Folliculitis: Superficial bacterial infection localized strictly to the hair follicle ostium. Presents as tiny, 1 to 2 mm, erythematous papules or central pustules pierced by a hair shaft. Typically self-limiting; managed with warm compresses and topical mupirocin 2% or topical clindamycin 1% lotion. Hot tub folliculitis is caused by Pseudomonas aeruginosa (contaminated whirlpools/hot tubs), presenting with pruritic, tender papulopustules in bathing-suit distribution, resolving spontaneously in 7-10 days.
2. Furuncle ("Boil"): A deep, tender, inflammatory, circumscribed nodule centered on a hair follicle that extends into the deep dermis and subcutaneous tissue, terminating in central necrosis and purulence. Often arises from pre-existing folliculitis.
3. Carbuncle: A coalescence of multiple neighboring furuncles into a single, large, deeply indurated, extremely painful inflammatory mass. Features multiple loculations and draining follicular orifices ("sieve-like" draining sinus tracts). Commonly located on the posterior neck, upper back, or thighs, and frequently accompanied by systemic symptoms (fever, chills, leukocytosis).
4. Cutaneous Abscess: A localized collection of pus within the dermis and deeper subcutaneous tissue, presenting as an erythematous, warm, exquisitely tender, fluctuant mass, frequently with a surrounding rim of erythematous induration.

CA-MRSA Virulence & The "Spider Bite" Fallacy

• CA-MRSA isolates (predominantly the USA300 pulsotype, carrying the staphylococcal cassette chromosome mec [SCCmec] type IV or V element) carry specific virulence determinants, notably the Panton-Valentine leukocidin (PVL) gene.
• PVL is a pore-forming bicomponent cytotoxin that targets human polymorphonuclear leukocytes and monocytes, causing rapid leukocyte necrosis, deep tissue destruction, and profound inflammatory purulence.
• Classic Board & Clinical Pearl: Patients with acute, necrotizing, purulent furuncles or abscesses frequently present insisting they were "bitten by a spider." In non-endemic areas (outside brown recluse spider habitats in the south-central US), virtually all acute necrotic "spider bites" are CA-MRSA cutaneous abscesses.

Definitive Abscess Management: The Incision & Drainage Standard

                    CUTANEOUS ABSCESS MANAGEMENT ALGORITHM

   Patient Presents with Fluctuant, Tender, Erythematous Subcutaneous Mass
                                     │
                                     ▼
             PRIMARY DEFINITIVE THERAPY: INCISION & DRAINAGE (I&D)
             • Adequate local anesthesia (field block / freezing spray)
             • Linear incision along skin tension lines (Langer lines)
             • Blunt breakdown of internal loculations with hemostat
             • Copious normal saline irrigation; loose wick if >3-5 cm
                                     │
                                     ▼
               ARE ADJUNCTIVE ORAL ANTIBIOTICS INDICATED?
                 Assess for specific high-risk criteria:
                 [1] Surrounding cellulitis extending >2 cm from edge
                 [2] Systemic signs (T >38°C, HR >90, tachypnea, WBC >12k)
                 [3] Multiple abscesses or multiloculated complex collection
                 [4] Immunocompromised host (poorly controlled DM, HIV, chemo)
                 [5] Extremes of age (infants <6 months, frail elderly)
                 [6] High-risk sites (face/danger triangle, hands, genitalia)
                 [7] Failure of prior drainage alone
                                ╱         ╲
                             NO             YES
                            ╱                 ╲
                           ▼                   ▼
           NO ORAL ANTIBIOTICS REQUIRED      ADD EMPIRIC ORAL MRSA REGIMEN:
           • Warm compresses                 • TMP-SMX (1-2 DS tabs BID) OR
           • Follow-up in 48 hours           • Doxycycline (100 mg BID) OR
           • Wound checks & dressing change  • Clindamycin (300-450 mg TID; D-test)
                                             • Duration: 5 to 7 days

Antibiotic Stewardship in Simple Abscesses

• The Rule: For simple, isolated, uncomplicated cutaneous abscesses successfully drained in immunocompetent patients, routine adjunctive oral antibiotics are NOT indicated and provide no clinically meaningful benefit in cure rates or recurrence prevention!
• Evidence: Multiple landmark randomized controlled trials have confirmed that complete mechanical evacuation of pus and disruption of loculations is the definitive curative intervention.
• Indications for Adjunctive Oral Antibiotics Post-I&D:
  1. Extensive surrounding cellulitis extending >2 cm beyond the abscess perimeter;
  2. Systemic inflammatory response syndrome (SIRS): Oral temperature >38.0°C (100.4°F), resting heart rate >90 beats/min, respiratory rate >20 breaths/min, or abnormal white blood cell count (>12,000/mcL or >10% bands);
  3. Multiple abscesses or extensive multiloculated collections;
  4. Immunocompromised host: Poorly controlled diabetes mellitus, active chemotherapy, organ transplantation, advanced HIV/AIDS, or chronic systemic immunosuppressive medications;
  5. Extremes of age: Neonates and infants <6 months of age, or frail elderly patients;
  6. Critical / High-Risk Anatomical Locations:
     • Central face ("Danger triangle of the face"): Bounded by the corners of the mouth and the nasal bridge; venous drainage via facial and angular veins communicates directly with the ophthalmic veins and the cavernous sinus, creating high risk for septic cavernous sinus thrombosis;
     • Hands and digits: Risk of purulent tenosynovitis and fascial space infection;
     • Perineum and genitalia: Risk of Fournier gangrene;
  7. Lack of clinical response or rapid recurrence following initial incision and drainage alone.

Empiric Outpatient Oral Antibiotic Regimens for CA-MRSA

1. Trimethoprim-Sulfamethoxazole (TMP-SMX):
   • Dose: 1 to 2 Double-Strength (DS: 160 mg TMP / 800 mg SMX) tablets PO BID for 5 to 7 days.
   • Spectrum: Outstanding activity against CA-MRSA (>95% susceptibility).
   • Important Limitation: Poor, unreliable activity against Group A Streptococcus! If an abscess is accompanied by significant surrounding non-purulent cellulitis (where streptococcal co-infection is suspected), TMP-SMX must be combined with a beta-lactam such as Cephalexin 500 mg PO QID.
   • Adverse Effects & Precautions: Sulfa allergy, hyperkalemia (especially with concurrent ACE inhibitors/ARBs), acute kidney injury, bone marrow suppression, hemolysis in G6PD deficiency, and severe dermatologic reactions (Stevens-Johnson syndrome). Contraindicated in pregnancy at term (kernicterus) and infants <2 months.
2. Doxycycline:
   • Dose: 100 mg PO BID for 5 to 7 days.
   • Spectrum: Excellent activity against CA-MRSA; limited/variable streptococcal activity.
   • Precautions: Contraindicated in pregnancy (second and third trimesters; bone/tooth dysgenesis) and breastfeeding; pill-induced esophagitis (must take with a full glass of water and remain upright for 30 minutes); phototoxicity.
3. Clindamycin:
   • Dose: 300 mg to 450 mg PO TID for 5 to 7 days.
   • Spectrum: Unique advantage of providing monotherapy coverage against both CA-MRSA and Streptococcus pyogenes, plus potent inhibition of staphylococcal toxin synthesis (PVL and TSST-1).
   • The D-Test (Double-Disk Diffusion): In staphylococcal isolates that test resistant to erythromycin but susceptible to clindamycin, an inducible erm gene (erythromycin ribosome methylase) may mediate resistance under clindamycin exposure. A positive D-test indicates inducible clindamycin resistance, rendering clindamycin ineffective in vivo. Clindamycin should only be used if the D-test is negative.
   • Major Risk: Potent risk factor for Clostridioides difficile colitis.

Recurrent Furunculosis / CA-MRSA Decolonization Protocol

Patients presenting with recurrent furuncles or abscesses (defined as ≥2 episodes within 6 months) often harbor persistent staphylococcal colonization in mucosal and cutaneous reservoirs (anterior nares, axillae, groin, perineum). Once active infections have resolved, an evidence-based decolonization regimen should be implemented:

1. Intranasal Mupirocin: Apply mupirocin 2% nasal ointment to both anterior nares twice daily for 5 consecutive days.
2. Chlorhexidine Body Washes: Daily full-body washing with chlorhexidine gluconate 4% solution from the neck down (leave on skin for 2 minutes before rinsing) for 5 to 14 days.
3. Environmental & Household Measures: Decontaminate personal hygiene items; do not share towels, washcloths, or razors; launder all sheets, towels, and undergarments in hot water (>60°C / 140°F) with detergent and tumble dry on high heat; evaluate and simultaneously decolonize symptomatic household contacts.