Infectious Disease · Skin and Soft Tissue Infections
The facts most likely to be tested
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Cellulitis is a non-necrotizing infection of the deep dermis and subcutaneous fat characterized by erythema, edema, and warmth without sharp demarcation.
Group A Streptococcus (Streptococcus pyogenes) is the most common causative pathogen in non-purulent cellulitis.
Staphylococcus aureus is the primary pathogen associated with purulent cellulitis, often presenting with fluctuance or purulent drainage.
Systemic signs of infection, such as fever, tachycardia, or hypotension, necessitate intravenous antibiotics, with inpatient admission reserved for hypotension, immunocompromise, suspected deep or necrotizing infection, or failure of outpatient therapy.
Erysipelas is distinguished from cellulitis by its superficial involvement, sharp demarcation, and bright red appearance, typically caused by Group A Streptococcus.
Lymphedema and disruption of the cutaneous barrier (classically tinea pedis with toe-web fissuring) are the strongest risk factors for lower extremity cellulitis, followed by venous insufficiency, chronic leg edema, and obesity.
Empiric antibiotic therapy for non-purulent cellulitis must cover beta-hemolytic streptococci using agents like cephalexin or penicillin.
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A 54-year-old male with a history of type 2 diabetes presents to the urgent care clinic with a 3-day history of increasing pain and redness in his left lower leg. Physical examination reveals a diffuse, blanching, erythematous plaque extending from the ankle to the mid-calf with ill-defined borders and local warmth. The patient is afebrile, and there is no evidence of fluctuance, crepitus, or purulent drainage. His white blood cell count is 9,500/mm³.
What is the most appropriate first-line outpatient antibiotic treatment?
Cephalexin
The patient presents with classic non-purulent cellulitis, which is most commonly caused by Group A Streptococcus; therefore, a first-generation cephalosporin like cephalexin is the treatment of choice.
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Etiology / Epidemiology
Acute spreading infection of the dermis and subcutaneous fat. Group A Strep is the most common pathogen.
Clinical Manifestations
Presents as spreading erythema, warmth, edema, and tenderness with indistinct, non-elevated borders — unlike erysipelas, which is sharply demarcated and raised.
Diagnosis
Primarily a clinical diagnosis. Blood cultures are rarely indicated unless the patient is immunocompromised.
Treatment
First-line for non-purulent: Cephalexin. For purulent/MRSA suspicion: Trimethoprim-sulfamethoxazole.
Prognosis
Monitor for sepsis or progression to necrotizing fasciitis. Most cases resolve with 5-10 days of therapy.
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Epidemiology & Etiology
Common in patients with skin barrier disruption such as tinea pedis, venous stasis, or lymphedema. Group A Streptococcus (*S. pyogenes*) is the primary cause, followed by *Staphylococcus aureus*. Consider Pseudomonas after plantar puncture wounds through footwear; after water exposure, consider Aeromonas (fresh water) or Vibrio vulnificus (salt water/shellfish).
Pertinent Anatomy
Involves the deep dermis and subcutaneous fat. Unlike erysipelas, which is superficial and well-demarcated, cellulitis involves deeper tissues leading to indistinct, non-palpable borders.
Pathophysiology
Entry occurs via minor trauma or skin fissures, allowing bacteria to proliferate in the interstitial space. The host inflammatory response triggers vasodilation and capillary leak, manifesting as the classic rubor, calor, tumor, and dolor. Rapid spread is facilitated by bacterial enzymes like hyaluronidase.
Clinical Manifestations
Patients present with unilateral, poorly demarcated erythema and localized pain. Red flags include crepitus, bullae, skin necrosis, or rapid progression, which suggest necrotizing fasciitis. Systemic signs like fever and tachycardia define moderate infection requiring parenteral therapy; severe infection additionally requires hypotension, immunocompromise, failed oral therapy, or concern for a necrotizing process.
Diagnosis
Diagnosis is clinical. Blood cultures have low yield and are reserved for patients with systemic toxicity or severe comorbidities. Bedside ultrasound is most useful when the exam is equivocal, because it detects occult abscess that is not clinically fluctuant; pooled sensitivity is about 95% and specificity about 85% for distinguishing abscess from cellulitis, and it correctly changes management in roughly 10% of cases.
Treatment
For non-purulent cellulitis, Cephalexin is the first-line agent. If purulence or an abscess is present, incision and drainage is the primary intervention; add MRSA coverage with Trimethoprim-sulfamethoxazole or Doxycycline. Contraindications include severe penicillin allergy (use Clindamycin). Moderate non-purulent cellulitis (systemic signs) is treated with parenteral cefazolin, ceftriaxone, or penicillin; parenteral vancomycin — usually with broad-spectrum coverage such as piperacillin-tazobactam — is reserved for severe infection: hypotension, immunocompromise, failure of oral therapy plus SIRS, penetrating trauma, injection drug use, or known MRSA colonization.
Prognosis
Most patients respond to oral antibiotics within 48-72 hours. Failure to improve suggests abscess formation or resistant organisms. Complications include bacteremia, osteomyelitis, and endocarditis.
Differential Diagnosis
Erysipelas: well-demarcated, raised borders
DVT: unilateral swelling and calf tenderness; may be warm but usually lacks the confluent advancing erythema of cellulitis — confirm with compression ultrasound
Stasis dermatitis: bilateral, chronic, associated with venous insufficiency
Necrotizing fasciitis: pain out of proportion, crepitus, rapid progression
Contact dermatitis: pruritic, history of allergen exposure