SUPERFICIAL INFECTIONS

Superficial infections are limited anatomically to the epidermis and the dermis. These infections can occur spontaneously or secondary to minor trauma. Impetigo usually presents with vesicles that leak, producing a thick yellow crust. These lesions are typically located on the face, neck, and extremities. Staphylococcus aureus and Streptococcus pyogenes are the most common causative agents. Bullous impetigo, like impetigo, is most commonly caused by S. aureus. It is characterized by small vesicles that coalesce to form large bullae.

Folliculitis develops as an infection of the hair follicle. The lesions appear as pustules or papules, commonly on the extremities, scalp, or beard. Whirlpool folliculitis is associated with immersion in inadequately chlorinated pools, whirlpools, or hot tubs. Diffuse pustules are seen. Pseudomonas aeruginosa is the classic causative agent. Swimmer’s itch is a folliculitis that develops after freshwater exposure.

Furuncles, deeper inflammatory nodules, can develop from folliculitis. S. aureus is often the causative agent. Carbuncles are coalescing furuncles formed by connecting sinuses. The nape of the neck is the most common anatomic location. S. aureus is most often isolated. Patients often have comorbidities such as diabetes mellitus, alcoholism, immunosuppression, or malnutrition. Systemic infection may result from these lesions.

Cellulitis is an inflammation of the subcutaneous tissue. There is erythema, pain, and edema of varying severity. A portal of entry for the bacteria is usually present. It may be as mundane as a crack in the skin from dryness or athlete’s foot. More substantial trauma may be involved, such as shotgun or shrapnel penetrations. Systemic symptoms may manifest and include fever, chills, malaise, and (infrequently) organ failure. Streptococcus (Groups A, B, C, and G) as well as staphylococcus are frequent culprits. Areas of compromised venous or lymphatic drainage are prone to this infection, and recurrence is common. Pelvic radiation or having had lymphadenectomy, mastectomy, or venectomy makes the development of cellulitis more likely.

DEEP INFECTION

Deeper infections are more frequently life- and limb-threatening. The literature concerning the potentially life-threatening infections is confusing. Multiple terms are used to describe the same disease, depending on the clinical setting in which it arises. The treatment is the same regardless of the term used to describe it. It therefore seems that anatomic classification is more logical and easily remembered. This review uses anatomic characterizations and relate them to older terminology as necessary.

In the medical literature, deep structure infection has masqueraded under a variety of pseudonyms. The term “necrotizing soft tissue infection” (NSTI)is used here. Table 1 lists a variety of terms that may appear in the medical literature to describe this infective process.

Table 1 Terms Used to Describe NSTI

Meleney’s synergistic gangrene	Hospital gangrene
Streptococcal gangrene	Fournier’s gangrene
Gas gangrene	Acute dermal gangrene
Suppurativa fasciitis	Necrotizing erysipelas
Phagedena	Phagedena gangrenosum
“Flesh-eating disease”	Necrotizing fasciitis
Clostridial cellulitis	Necrotizing fasciitis

All the terms describe an infection involving the subcutaneous fat and fascia, with variable skin involvement. The incidence of this infection is not known. A recent report quotes World Health Organization statistics of 500–1500 cases of necrotizing fasciitis annually. Though uncommon, it is not rare. The Centers for Disease Control has monitored Group A streptococcal infections and estimated 10–20 cases per 100,000 population. In Ontario, Canada, a population study estimated an incidence of 0.6 per 100,000.

CLINICAL PRESENTATION

Signs and symptoms of NSTI can be quite nonspecific (Table 2). Pain, erythema, and swelling of the affected area are most frequently present. This same constellation of symptoms may be seen in pathologic processes that have a much more benign course and respond effectively to antibiotic therapy alone. “Hard signs” of necrotizing infection include tense erythema, bullae, skin discoloration, and crepitus, pain out of proportion to examination, or anesthesia of the affected area. Unfortunately, many of these are late signs and indicate that the infective process is well established or they occur only in a small percentage of patients.

Table 2 Frequency of Clinical Signs