Infectious Disease · Skin and Soft Tissue Infections
The facts most likely to be tested
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 and inpatient admission.
Erysipelas is distinguished from cellulitis by its superficial involvement, sharp demarcation, and bright red appearance, typically caused by Group A Streptococcus.
Diabetes mellitus, tinea pedis, and venous insufficiency are the most significant risk factors for the development of lower extremity cellulitis.
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, non-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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High yield triage
Etiology / Epidemiology
Acute spreading infection of the dermis and subcutaneous fat. Group A Strep is the most common pathogen.
Clinical Manifestations
Presents as erysipelas-like spreading erythema, warmth, edema, and tenderness without sharp borders.
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 in patients with puncture wounds or water exposure.
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 indicate severe infection requiring parenteral therapy.
Diagnosis
Diagnosis is clinical. Blood cultures have low yield and are reserved for patients with systemic toxicity or severe comorbidities. Imaging like ultrasound is only indicated to rule out an abscess if fluctuance is present.
Treatment
For non-purulent cellulitis, Cephalexin is the first-line agent. If MRSA is suspected or purulence is present, use Trimethoprim-sulfamethoxazole or Doxycycline. Contraindications include severe penicillin allergy (use Clindamycin). Parenteral Vancomycin is required for severe, systemic, or hospital-acquired cases.
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 without warmth/erythema
Stasis dermatitis: bilateral, chronic, associated with venous insufficiency
Necrotizing fasciitis: pain out of proportion, crepitus, rapid progression
Contact dermatitis: pruritic, history of allergen exposure