Cellulitis & Erysipelas
Cellulitis and erysipelas are serious acute bacterial infections of the dermis and subcutaneous tissue. Both start when bacteria get in through a break in the skin barrier (an ulcer, cracked skin between the toes, an insect bite), but they differ clearly in depth, appearance and the main organisms involved. Erysipelas is the more superficial of the two, involving the upper dermis and its lymphatic network; it has a sharply defined, raised border and is mostly caused by group A beta-hemolytic streptococci (Streptococcus pyogenes). Cellulitis, by contrast, extends deeper into the lower dermis and subcutaneous fat, has an indistinct border, and is usually caused by Staphylococcus aureus or streptococci. Persistent tissue swelling not only causes throbbing pain but also compresses small blood vessels, which can lead to tissue necrosis and acute sepsis. At Haute-Derma, we provide urgent clinical assessment, marking of the affected area, Doppler ultrasound to screen for complications, and a systemic antibiotic regimen at the optimal dose.
How the infection develops at the cellular and immune level:
- Bacterial entry and the skin barrier:
- Bacteria enter through tiny breaks in the epidermis (micro-fissures), such as cracks between the toes caused by athlete's foot (tinea pedis), venous ulcers or scrapes.
- Bacterial exotoxins such as streptolysin, hyaluronidase and DNase break down collagen fibers and hyaluronic acid in the extracellular matrix, allowing the bacteria to spread rapidly through the tissue.
- Intense inflammation and tissue swelling:
- Bacterial PAMPs stimulate the endothelial cells lining the blood vessels, releasing a surge of pro-inflammatory cytokines (TNF-alpha, IL-1beta, IL-6) that cause widespread vasodilation and marked vascular leakage.
- Plasma leaks into the tissue, producing firm swelling that presses on nerve endings and causes severe pain, while also obstructing local lymphatic drainage.
- Neutrophil response and the risk of tissue necrosis:
- Neutrophils flood into the area and release elastase and reactive oxygen species (ROS) to kill the bacteria.
- However, this overreaction also causes secondary necrosis of subcutaneous fat cells and connective tissue, which can progress to a deep abscess or necrotizing fasciitis if not treated promptly.
Clinical Features
| Condition | Typical Skin Findings | Main Causative Organisms |
|---|---|---|
| Erysipelas | Bright red, raised plaque with a very sharp border and a tense, shiny, orange-peel surface, with sudden high fever and chills. | Streptococcus pyogenes (group A streptococcus). |
| Cellulitis | Red, swollen, warm, painful area with a vague, indistinct border; the surface is flat or slightly pitting, and the redness keeps spreading. | Staphylococcus aureus (including MRSA) and Streptococcus spp. |
| Bullous cellulitis | Large red swollen area with blood-filled blisters that rupture easily, leaving erosions. | Toxin-producing strains of S. aureus, or Vibrio vulnificus (after seawater exposure). |
| Recurrent cellulitis | Repeated episodes of red swelling on a limb with chronic lymphedema; the skin becomes progressively thicker and harder. | Group A, G and C streptococci in the setting of chronic lymphedema. |
Erysipelas vs. Cellulitis vs. Deep Vein Thrombosis (DVT)
| Erysipelas | Cellulitis | Deep Vein Thrombosis (DVT) |
|---|---|---|
| Sharp border, clearly raised above normal skin | Vague, diffuse border, not raised | No skin border; the whole limb is swollen |
| Bright red, very hot to the touch | Dark red or pink, warm | Pale or dusky purple skin, slightly warm |
| High fever and chills very early on | Mild to moderate fever, appearing later | Usually no fever (unless complicated by pulmonary embolism) |
| Orange-peel surface (peau d'orange) | Redness spreads beyond the pen-marked border | Positive Homans sign (calf pain on dorsiflexion of the foot) |
| Increased dermal blood flow, no vessel blockage | Subcutaneous edema in a "cobblestone" pattern | Clot prevents the deep vein from compressing |
Our Approach
At Haute-Derma, patients with suspected cellulitis or erysipelas are assessed quickly and accurately to rule out life-threatening complications:
- Marking the border (pen-marking test):
- The exact edge of the red, swollen area is traced with a medical skin marker as soon as the patient arrives.
- It is rechecked every 6–12 hours: if the redness keeps spreading beyond the line, the antibiotic regimen is not working or the bacteria are resistant.
- Duplex Doppler and soft tissue ultrasound:
- Looks for the characteristic cobblestone appearance of edema in the subcutaneous fat.
- Vascular ultrasound is mandatory to rule out coexisting deep vein thrombosis (DVT) and to detect deep abscesses that need drainage.
- Microbiological and systemic tests:
- Blood cultures (if there is high fever with chills) and cultures from the entry point (fluid from toe-web fissures or ulcers).
- Inflammatory markers – white blood cell count (WBC), procalcitonin and CRP – to assess the risk of sepsis.
Treatment Options at Haute-Derma
Treatment at Haute-Derma centers on prompt systemic antibiotics, local symptom control and eliminating the bacteria's point of entry:
- Oral or intravenous systemic antibiotics:
- Erysipelas or mild cellulitis (no systemic symptoms): oral antibiotics covering Streptococcus and MSSA, such as cephalexin, amoxicillin-clavulanate or clindamycin, for 7–10 days.
- Suspected MRSA or rapidly progressing infection: trimethoprim-sulfamethoxazole, doxycycline or intravenous vancomycin.
- Symptom control and drainage support at Haute-Derma:
- Elevation of the affected limb: keeping the leg raised above heart level is essential to improve venous and lymphatic drainage, lower hydrostatic pressure and noticeably reduce pain.
- Gentle cool compresses with saline or hypochlorous acid (HOCl) to soothe the local burning sensation.
- Closing the entry point and preventing recurrence:
- Thorough treatment of athlete's foot (tinea pedis) with terbinafine cream to remove the bacteria's way in.
- Management of underlying conditions such as lymphedema, chronic venous insufficiency and diabetes to prevent further episodes.
