6-33: Infectious Erythemas

General Considerations

Erysipelas is a superficial form of cellulitis that is caused by beta-hemolytic streptococci.

Clinical Findings

A. Symptoms and Signs

The symptoms are pain, malaise, chills, and moderate fever. A bright red spot appears and then spreads to form a tense, sharply demarcated, glistening, smooth, hot plaque. The sharp margin characteristically makes noticeable advances in days or even hours (Figure 6–27). The lesion is edematous with a raised edge and may pit slightly with the finger. Vesicles or bullae occasionally develop on the surface. The lesion does not usually become pustular or gangrenous and heals without scar formation. The disease may complicate any break in the skin that provides a portal of entry for the organism. On the face, erysipelas begins near a fissure at the angle of the nose. On the lower extremity, tinea pedis with interdigital fissuring is a common portal of entry.

B. Laboratory Findings

Leukocytosis is almost invariably present; blood cultures may be positive.

Differential Diagnosis

Erysipeloid is a benign bacillary infection by Erysipelothrix rhusiopathiae that produces cellulitis of the skin of the fingers or the backs of the hands in fishermen and meat handlers.

Complications

Unless erysipelas is promptly treated, death may result from bacterial dissemination, particularly in older adults.

Treatment

Intravenous antibiotics effective against group A beta-hemolytic streptococci and staphylococci should be considered, but outpatient treatment with oral antibiotics has demonstrated equal efficacy. Oral regimens include a 7-day course with penicillin VK (250 mg), dicloxacillin (250 mg), or a first-generation cephalosporin (250 mg) four times a day. Alternatives in penicillin-allergic patients are clindamycin (250 mg twice daily orally for 7–14 days) or erythromycin (250 mg four times daily orally for 7–14 days), the latter only if the infection is known to be due to streptococci.

Prognosis

With appropriate treatment, rapid improvement is expected. The presence of lymphedema carries the greatest risk of recurrence.

General Considerations

Cellulitis, a diffuse spreading infection of the dermis and subcutaneous tissue, is usually on the lower leg (Figure 6–27) and most commonly due to gram-positive cocci, especially group A beta-hemolytic streptococci and S aureus. Rarely, gram-negative rods or even fungi can produce a similar picture. In otherwise healthy persons, the most common portal of entry for lower leg cellulitis is toe web intertrigo with fissuring, usually a complication of interdigital tinea pedis. Other diseases that predispose to cellulitis are prior episodes of cellulitis, chronic edema, venous insufficiency with secondary edema, lymphatic obstruction, saphenectomy, and other perturbations of the skin barrier. Bacterial cellulitis is almost never bilateral.

Clinical Findings

A. Symptoms and Signs

Cellulitis begins as a tender small patch. Swelling, erythema, and pain are often present. The lesion expands over hours, so that from onset to presentation is usually 6 to 36 hours. As the lesion grows, the patient becomes more ill with progressive chills, fever, and malaise. Lymphangitis and lymphadenopathy are often present. If septicemia develops, hypotension may develop, followed by shock.

B. Laboratory Findings

Leukocytosis or at least a neutrophilia (left shift) may be present from early in the course. Blood cultures are positive in only 4% of patients. If a central ulceration, pustule, or abscess is present, culture may be of value. Aspiration of the advancing edge has a low yield (less than 20%) and is usually not performed. In immunosuppressed patients, or if an unusual organism is suspected and there is no loculated site to culture, a full-thickness skin biopsy taken before antibiotics are given can be useful. Either two specimens or one divided in half should be sent for routine histologic evaluation and for culture (bacterial, fungal, and mycobacterial). Skin biopsy is particularly important in the immunocompromised patient in whom cellulitis may be due to an uncommon organism. If a primary source for the infection is identified (wound, leg ulcer, toe web intertrigo), cultures from these sites isolate the causative pathogen in half of cases and can be used to guide antibiotic therapy.

Differential Diagnosis

Two potentially life-threatening entities that can mimic cellulitis (ie, present with a painful, red, swollen lower extremity) include deep venous thrombosis and necrotizing fasciitis. The diagnosis of necrotizing fasciitis should be suspected in a patient who has a very toxic appearance, bullae, crepitus or anesthesia of the involved skin, overlying skin necrosis, and laboratory evidence of rhabdomyolysis (elevated creatine kinase) or disseminated intravascular coagulation. While these findings may be present with severe cellulitis and bacteremia, it is essential to rule out necrotizing fasciitis because rapid surgical debridement is essential. Other noninfectious skin lesions that may resemble cellulitis are termed “pseudocellulitis.” Diseases in this differential include sclerosing panniculitis, an acute, exquisitely tender red plaque on the medial lower legs above the malleolus in patients with venous stasis or varicosities, and acute severe contact dermatitis on a limb, which produces erythema, vesiculation, and edema, as seen in cellulitis, but with itching instead of pain. Bilateral lower leg bacterial cellulitis is exceedingly rare, and other diagnoses, especially severe stasis dermatitis (see Figure 12–2), should be considered in this setting. Severe lower extremity stasis dermatitis usually develops over days to weeks rather than the hours of cellulitis. It is also not as tender to palpation as cellulitis. Cryptococcal cellulitis in the organ transplant recipient is often bilateral. The ALT-70 is a predictive model to diagnose cellulitis or a cellulitis mimic and to provide guidance about when a dermatology consultation is needed. The ALT-70 variables are asymmetry (3 points), leukocytosis of 10,000/mcL or more at presentation (2 points), tachycardia above 90 beats per minute (1 point), and age 70 years or older (1 point)). An ALT-70 score above 5 points carries more than an 82% chance of a true cellulitis while a score below 2 points suggests a greater than 83% chance of a cellulitis mimicker.

Treatment

Intravenous or parenteral antibiotics may be required for the first 2–5 days, with adequate coverage for Streptococcus and Staphylococcus. Methicillin-susceptible S aureus (MSSA) can be treated with nafcillin, cefazolin, clindamycin, dicloxacillin, cephalexin, doxycycline, or TMP-SMZ. If MRSA is suspected or proven, treatment options include vancomycin, linezolid, clindamycin, daptomycin, doxycycline, or TMP-SMZ. In mild cases or following the initial parenteral therapy, oral dicloxacillin or cephalexin, 250–500 mg four times daily for 5–10 days, is usually adequate. In patients in whom intravenous treatment is not instituted, the first dose of oral antibiotic can be doubled to achieve high blood levels rapidly. In patients with recurrent lower leg cellulitis (three to four episodes per year), oral penicillin 250 mg twice daily or oral erythromycin 250–500 mg twice daily can decrease the risk of recurrence. Prior episodes of cellulitis, lymphedema, chronic venous insufficiency, peripheral vascular disease, and deep venous thrombosis are associated with an increased risk of recurrent cellulitis. Additional measures to prevent recurrences include compression, treating toe web intertrigo and tinea pedis, and controlling venous insufficiency.

When to Admit

• Severe local symptoms and signs.

• Signs of sepsis.

• Elevated white blood cell count of 10,000/mcL or more with marked left shift. Failure to respond to oral antibiotics.

Some autoimmune skin disorders are characterized by formation of bullae or blisters. The most common of these diseases are pemphigus and its variants and bullous pemphigoid and its variants. Other less common disorders include dermatitis herpetiformis and linear IgA bullous dermatosis.