What is the pathophysiology of cellulitis?

Pathophysiology of Cellulitis

Cellulitis is primarily an infection of the dermis and subcutaneous tissue that occurs when bacteria enter through breaches in the skin barrier, with streptococci being the most common causative organisms, followed by Staphylococcus aureus. 1, 2

Pathogenic Mechanism

• Cellulitis develops when microorganisms penetrate disruptions in the cutaneous barrier, invading the dermis and subcutaneous tissues 1
• The infection spreads through the tissue planes, causing rapidly expanding areas of inflammation characterized by edema, erythema, warmth, and tenderness 1
• Streptococci (particularly group A, but also groups B, C, and G) are the predominant causative organisms, with Staphylococcus aureus less frequently involved except in cases with prior penetrating trauma 1

Entry Points and Predisposing Factors

• The disrupted skin barrier may result from:

  • Trauma (often minor and clinically inapparent) 1
  • Preexisting skin infections (impetigo, ecthyma) 1
  • Ulceration 1
  • Fissured toe webs from maceration or fungal infection 1
  • Inflammatory dermatoses such as eczema 1

• Conditions that increase susceptibility include:

  • Obesity 3
  • Previous cutaneous damage 1
  • Edema from venous insufficiency 1
  • Lymphatic obstruction 1
  • Diabetes 3
  • Advanced age 3

• Surgical procedures that disrupt lymphatic drainage increase risk:

  • Saphenous venectomy 1
  • Axillary node dissection for breast cancer 1
  • Operations for gynecologic malignancies involving lymph node dissection 1

Microbiology

• Most cellulitis cases (approximately 85%) are nonculturable, making identification of the causative organism difficult 2

• In the 15% of cases where organisms are identified:

  • β-hemolytic Streptococcus species are most common 2
  • Staphylococcus aureus is the second most common pathogen 2
  • The source of streptococci in lower extremity infections is often macerated or fissured interdigital toe spaces 1
  • Other reservoirs may include the anal canal or vagina (especially for group B streptococci) 1

• Special circumstances may involve other pathogens:

  • Pasteurella species or Capnocytophaga canimorsus following cat or dog bites 1
  • Aeromonas hydrophila after freshwater exposure 1
  • Vibrio species (particularly V. vulnificus) after saltwater exposure 1
  • Rarely, Streptococcus iniae or Erysipelothrix rhusiopathiae 1

Inflammatory Response

• The infection triggers a robust inflammatory response in the affected tissues 1
• This results in the classic signs of inflammation: erythema, edema, warmth, and tenderness 1
• The skin surface may develop a peau d'orange appearance due to superficial cutaneous edema surrounding hair follicles 1
• Vesicles, bullae, and cutaneous hemorrhage may develop in the inflamed skin 1
• Systemic manifestations (fever, tachycardia, confusion, hypotension, leukocytosis) can occur, sometimes preceding visible skin changes 1

Tissue Damage and Complications

• Each episode of cellulitis causes lymphatic inflammation and potentially permanent damage 1
• Severe or repeated episodes may lead to lymphedema, sometimes substantial enough to cause elephantiasis 1
• The inflammatory process can worsen after initiating antibiotic therapy due to the sudden destruction of pathogens releasing enzymes that increase local inflammation 1

Distinguishing Features from Other Infections

• Erysipelas affects the upper dermis and superficial lymphatics, while cellulitis involves the deeper dermis and subcutaneous fat 1
• Unlike cellulitis, necrotizing fasciitis tracks along fascial planes and extends beyond superficial signs of infection 1
• A distinguishing feature of necrotizing fasciitis is the wooden-hard feel of subcutaneous tissues, whereas in cellulitis, the tissues remain yielding 1

Understanding the pathophysiology of cellulitis is essential for proper diagnosis and management, as many clinical conditions can mimic its presentation, including venous stasis dermatitis, contact dermatitis, deep vein thrombosis, and panniculitis 4.