Definition and Etiology

Impetigo is a superficial skin infection usually caused by S. aureus and occasionally by S. pyogenes.

Prevalence and Risk Factors

Impetigo affects approximately 1% of children.

Pathophysiology and Natural History

S. aureus produces a number of cellular and extracellular products, including exotoxins and coagulase, that contribute to the pathogenicity of impetigo, especially when coupled with preexisting tissue injury. Impetigo commonly occurs on the face (especially around the nares) or extremities after trauma.

Signs and Symptoms

Two clinical types of impetigo exist: nonbullous and bullous. The nonbullous type is more common and typically occurs on the face and extremities, initially with vesicles or pustules on reddened skin. The vesicles or pustules eventually rupture to leave the characteristic honey-colored (yellow-brown) crust (Fig. 1). Bullous impetigo, almost exclusively caused by S. aureus, exhibits flaccid bullae with clear yellow fluid that rupture and leave a golden-yellow crust.

Figure 1 Impetigo.

Diagnosis

Diagnosis is by clinical presentation and confirmation by culture.¹

Treatment

For most patients with impetigo, topical treatment is adequate, either with bacitracin (Polysporin) or mupirocin (Bactroban), applied twice daily for 7 to 10 days. Systemic therapy may be necessary for patients with extensive disease (Table 1).^2,3

Table 1 Treatment of Impetigo

Definition and Etiology

Folliculitis is a superficial infection of the hair follicles characterized by erythematous, follicular-based papules and pustules. Furuncles are deeper infections of the hair follicle characterized by inflammatory nodules with pustular drainage, which can coalesce to form larger draining nodules (carbuncles).

Pathophysiology and Natural History

S. aureus is the usual pathogen, although exposure to Pseudomonas aeruginosa in hot tubs or swimming pools can lead to folliculitis. In general, folliculitis is a self-limited entity. Occasionally, a pustule enlarges to form a tender, red nodule (furuncle) that becomes painful and fluctuant after several days. Rupture often occurs, with discharge of pus and necrotic material. With rupture, the pain subsides and the redness and edema diminish.

Signs and Symptoms

Folliculitis is generally asymptomatic, but it may be pruritic or even painful. Commonly affected areas are the beard, posterior neck, occipital scalp, and axillae (Fig. 2). Often a continuum of folliculitis, furunculosis (furuncles), arises in hair-bearing areas as tender, erythematous, fluctuant nodules that rupture with purulent discharge (Fig. 3). Carbuncles are larger and deeper inflammatory nodules, often with purulent drainage (Fig. 4), and commonly occur on the nape of the neck, back, or thighs. Carbuncles are often tender and painful and occasionally accompanied by fever and malaise.^1–3

Figure 2 Folliculitis.

Figure 3 Furuncles.

Figure 4 Carbuncles.

Diagnosis

Diagnosis is by clinical presentation and confirmation by culture.

Treatment

Topical treatment with clindamycin 1% or erythromycin 2%, applied two or three times a day to affected areas, coupled with an antibacterial wash or soap, is adequate for most patients with folliculitis. Systemic antistaphylococcal antibiotics are usually necessary for furuncles and carbuncles, especially when cellulitis or constitutional symptoms are present.² Small furuncles can be treated with warm compresses three or four times a day for 15 to 20 minutes, but larger furuncles and carbuncles often warrant incision and drainage. If methicillin-resistant S. aureus (MRSA) is implicated or suspected, vancomycin (1-2 g IV daily in divided doses) is indicated coupled with culture confirmation. Antimicrobial therapy should be continued until inflammation has regressed or altered depending on culture results. Treatment is summarized in Table 2.

Table 2 Treatment of Folliculitis, Furunculosis, and Carbunculosis

Definition and Etiology

Ecthyma is a cutaneous infection characterized by thickly crusted erosions or ulcerations. Ecthyma is usually a consequence of neglected impetigo and often follows impetigo occluded by footwear or clothing.

Prevalence and Risk Factors

Ecthyma typically occurs in homeless persons and soldiers based in hot and humid climates.

Pathophysiology and Natural History

S. aureus or S. pyogenes is the usual pathogen of ecthyma. Untreated staphylococcal or streptococcal impetigo can extend more deeply, penetrating the dermis, producing a shallow crusted ulcer. Ecthyma can evolve from a primary pyoderma, in a pre-existing dermatosis, or at the site of trauma.

Signs and Symptoms

Infection begins with vesicles and bullae that progress to punched-out ulcerations with an adherent crust, which heals with scarring. The most common site of infection is the legs.

Diagnosis

Diagnosis is by clinical presentation and confirmation by culture.^3,4

Treatment

Treatment is summarized in Table 3.³

Table 3 Treatment of Ecthyma

Definition and Etiology

Erysipelas is a superficial cutaneous infection of the skin involving dermal lymphatic vessels. Cellulitis is a deeper process that extends to the subcutis.

Prevalence and Risk Factors

Erysipelas has a predilection for young children and the elderly. Lymphedema, venous stasis, web intertrigo, diabetes mellitus, trauma, alcoholism, and obesity are risk factors in the adult patient.^3,4

Pathophysiology and Natural History

Group A β-hemolytic streptococcus is the most common pathogen responsible for erysipelas, and S. aureus is by far the most common pathogen for cellulitis. S. pyogenes produces enzymes that promote infection with systemic manifestations, such as fever and chills, tachycardia, and hypotension. Left untreated, cellulitic skin can become bullous and necrotic, and an abscess or fasciitis, or both, can occur.

Signs and Symptoms

Classically, erysipelas is a tender, well-defined, erythematous, indurated plaque on the face or legs (Fig. 5). Cellulitis is a warm, tender, erythematous, and edematous plaque with ill-defined borders that expands rapidly. Cellulitis is often accompanied by constitutional symptoms, regional lymphadenopathy, and occasionally bacteremia (Fig. 6).^3,4

Figure 5 Erysipelas.

Figure 6 Cellulitis.

Diagnosis

Diagnosis is by clinical presentation and confirmation by culture (if clinically indicated, ie., bullae or abscess formation).

Treatment

Penicillin (250-500 mg, qid × 7-10 days) is the treatment of choice for erysipelas; parenteral therapy may be necessary for extensive or facial disease. An oral antistaphylococcal antibiotic is the treatment of choice for cellulitis; parenteral therapy is warranted for patients with extensive disease or with systemic symptoms as well as for immunocompromised patients. Good hygiene, warm compresses three or four times a day for 15 to 20 minutes, and elevation of the affected limb help to expedite healing. Treatment is summarized in Table 4.³

Table 4 Treatment of Erysipelas and Cellulitis

Definition and Etiology

Necrotizing fasciitis is a rare infection of the subcutaneous tissues and fascia that eventually leads to necrosis. Predisposing factors include injuries to soft tissues, such as abdominal surgery, abrasions, surgical incisions, diabetes, alcoholism, cirrhosis, and intravenous drug abuse.^5,6

Pathophysiology and Natural History

S. pyogenes can be the sole pathogen responsible for necrotizing fasciitis, but most patients have a mixed infection with other aerobes (groups B and C streptococci, MRSA) and anaerobes (Clostridium spp).

Signs and Symptoms

Infection begins with warm, tender, reddened skin and inflammation that rapidly extends horizontally and vertically. Necrotizing fasciitis commonly occurs on the extremities, abdomen, or perineum or at operative wounds (Fig. 7). Within 48 to 72 hours, affected skin becomes dusky, and bullae form, followed by necrosis and gangrene, often with crepitus. Without prompt treatment, fever, systemic toxicity, organ failure, and shock can occur, often followed by death. Computed tomography (CT) or magnetic resonance imaging (MRI) can help to delineate the extent of infection. Biopsy for histology, Gram stain, and tissue culture help to identify the causative organism(s).^5,6

Figure 7 Necrotizing fasciitis.

Diagnosis

Diagnosis is by clinical presentation; CT or MRI; skin biopsy for pathology, Gram stain, and tissue culture; culture of fluid from bullae or fluctuant plaques; and blood cultures.