Chapter 77: Infections of the Skin & Skin Structures

Infections of the skin and skin structures are some of the most common infectious diagnoses and result in hundreds of thousands of medical office and emergency room visits each year. These infections often occur following a break in normal skin integrity from either trauma or skin disease (e.g., atopic dermatitis). The vast majority of these infections are caused by Staphylococcus aureus and Streptococcus pyogenes (Table 77–1). Rarely, infections in patients with burns, diabetes mellitus, or decubitus ulcers may involve gram-negative rods such as Pseudomonas or anaerobes. Hematogenous seeding of organisms into the skin can occur but is uncommon. Normal histology of the skin can be seen in Figure 77–1.

Definition

Impetigo is an infection of the epidermal layer of skin.

Pathophysiology

There are two modes of acquisition of impetigo, primary infection, which occurs in otherwise normal skin, or secondary impetigo, which occurs following a break in normal skin integrity. Bacteria invade into the epidermal layer and cause local damage. Bullous impetigo occurs when strains of S. aureus secrete exfoliative toxin, a protease that degrades desmoglein, resulting in loss of adhesion of the superficial epidermis. This is the same toxin that causes staphylococcal scalded skin syndrome.

Clinical Manifestations

There are three clinical variants of impetigo: (1) classic impetigo, (2) bullous impetigo, and (3) ecthyma. Classic impetigo begins as papules that progress to vesicles surrounded by erythema. Subsequently, the fluid-filled lesions enlarge and break down to form thick, adherent crusts with a characteristic golden “honey-colored” appearance (Figure 77–2 A and B). Bullous impetigo is similar to classic impetigo, but bullae form (Figure 77–3) via the mechanism described earlier. Ecthyma is an ulcerating form of impetigo where the lesion penetrates through the epidermis into the dermis (Figure 77–4). Some strains of S. pyogenes that cause impetigo have been associated with poststreptococcal glomerulonephritis, and providers should be aware of this potential complication. Rheumatic fever is a less common sequel to streptococcal skin infections.

Pathogens

S. aureus and S. pyogenes are the two main pathogens that cause impetigo. In neutropenic patients, a clinical syndrome termed ecthyma gangrenosum is due to disseminated Pseudomonas aeruginosa infection. Its cutaneous findings are a result of hematogenous seeding of dermal vessels with bacteria, resulting in thrombosis, ischemia, and focal skin necrosis. This is not a superficial skin infection.

Diagnosis

The diagnosis of impetigo is made clinically in most cases. Culture of bullous fluid or pus can be considered when patients do not respond to standard treatment.

Treatment

Antibacterial therapy should be directed against both S. aureus and S. pyogenes. Topical therapy with mupirocin or retapamulin is preferred when only a few lesions are present. Ozenoxacin cream can also be used. In patients with widespread disease, a systemic antimicrobial is preferred. If concern for methicillin-resistant S. aureus (MRSA) exists, clindamycin is recommended; otherwise, cephalexin or dicloxacillin would be appropriate.

Prevention

Handwashing and covering draining lesions should be used to prevent spread of bacteria.

Definition

Cellulitis and erysipelas are infections of the dermis.

Pathophysiology

These infections occur following a break in normal skin integrity. Cellulitis and erysipelas both involve the dermis, but erysipelas involves the upper dermis and superficial lymphatics, whereas cellulitis involves the deeper dermis and subcutaneous fat.

Clinical Manifestations

Cellulitis and erysipelas both manifest with erythema, swelling, and pain in the affected region plus or minus fever. However, erysipelas lesions are raised above the level of surrounding skin, and there is a clear line of demarcation between involved and uninvolved tissue (Figure 77–5). In contrast, the lesions of cellulitis are not significantly raised and have an irregular line of demarcation (Figure 77–6 A and B).

Pathogens

Beta-hemolytic streptococci are the most common pathogens to cause these infections, with S. pyogenes and Streptococcus agalactiae being the most common species. S. aureus is not a common cause of these types of infections. Other less common pathogens are listed in Table 77–2 by exposure risk.

Diagnosis

Diagnosis is made clinically because it is difficult to obtain cultures from the skin in the absence of pus. Sometimes patients will have bacteremia.

Treatment

Empiric therapy should be focused on beta-hemolytic streptococci. A systemic oral agent can be used for mild infection (cephalexin, dicloxacillin, or clindamycin), but for severe infection, hospitalization and the administration of intravenous antibiotics (cefazolin or vancomycin) are recommended.

Prevention

In patients with recurrent cellulitis, a strategy of chronic suppressive antibiotics may effectively prevent subsequent infections.

Definition

Folliculitis is a superficial infection of the hair follicles.

Pathophysiology

Bacteria and purulent material accumulate in hair follicles in the epidermal layer of the skin.

Clinical Manifestations

Folliculitis presents with pinpoint erythema around individual hair follicles. A small amount of purulence may be seen (Figure 77–7). This can be seen in an isolated body area or throughout the skin.

Pathogens

S. aureus is the most common cause of folliculitis. P. aeruginosa is associated with folliculitis following the use of unchlorinated hot tubs. Rarely, Candida and certain dermatophytes can cause folliculitis.

Diagnosis

Diagnosis is made clinically, but if purulent material is present, it can be cultured.

Treatment

Folliculitis often resolves on its own, and treatment is not needed. Warm compresses or topical antibiotics can be considered in select cases.

Prevention

Handwashing and covering draining lesions should be used to prevent spread of bacteria. Avoiding unchlorinated hot tubs is recommended.

Definition

A skin abscess is an infection of the dermis and deeper layers of skin that contains purulent material.

Pathophysiology

Abscesses occur when pathogens enter a break in the skin following trauma or when they spread from infected hair follicles (Figure 77–8). When a single follicle is infected and tracks down into the dermis, it is termed a furuncle (“boil”), and when multiple infected hair follicles coalesce, it is termed a carbuncle. Occasionally, an abscess may develop following hematogenous dissemination of an infection.

Clinical Manifestations

A furuncle consists of a central pustule usually surrounded by an area of erythema, warmth, and tenderness with underlying fluctuance. Patients may have multiple furuncles. A carbuncle is a larger, more serious lesion than a furuncle. It is composed of several adjacent furuncles that have coalesced into an inflamed, indurated lesion that typically extends deep into subcutaneous tissue. Carbuncles are often found on the nape of the neck, where a shirt collar rubs in people with poor hygiene (Figure 77–9). Patients may have signs and symptoms of systemic infection, and this should alert the provider that more severe disease exists.

Pathogens

S. aureus is, by far, the most common cause of skin abscesses (more than 75% of cases). Beta-hemolytic streptococci are also capable of causing these types of infections. Rarely Mycobacterium tuberculosis, nontuberculous mycobacteria, and fungi such as Coccidioides, Candida, and Cryptococcus can cause abscesses.

Diagnosis

Gram stain and culture of purulent material obtained from the abscess allow for diagnosis. Radiographic imaging such as ultrasound or computed tomography (CT) may help further define the size and extent of an abscess.

Treatment

The primary treatment for abscesses is incision and drainage and is highly effective alone. However, a short course (≤7 days) of active antibiotics increased cure rates and can help reduce the risk of recurrent disease. Antibiotics should also be added when the patient has signs and symptoms of systemic infection, a rapidly progressive or severe infection, infection in a hard-to-drain area of the body, extremes of age, immunocompromised state, or failure to resolve with previous incision and drainage.

When antibiotics are indicated, the patient should be treated with an empiric antibiotic regimen that has activity against MRSA. Such oral antibiotic regimens include clindamycin, trimethoprim-sulfamethoxazole, delafloxacin, or doxycycline (Table 77–3). Empiric intravenous regimens include vancomycin or daptomycin. If antibiotic susceptibility testing demonstrates that MSSA is the pathogen, oral regimens can include cephalexin or dicloxacillin, whereas intravenous antibiotics would include nafcillin or cefazolin.

Prevention

Handwashing and covering draining lesions should be used to prevent the spread of bacteria.

Definition

Necrotizing fasciitis is a necrotizing infection of the deep structures of the skin including the underlying fascia. In myonecrosis, the underlying muscle becomes necrotic.

Pathophysiology

A break in the skin caused by trauma or surgery allows for passage of organisms to deeper structures. Infection in the fascial layer results in thrombosis of the vascular supply and adjacent nerve tissue. Destruction of these vital structures manifests as necrosis and anesthesia of the more superficial layers of skin.

Clinical Manifestations

Early symptoms of necrotizing fasciitis are skin erythema, warmth, and tenderness. Patients may have pain out of proportion of the examination findings. These skin changes often spread and progress very quickly and are followed by evidence of skin hypoperfusion, blue-gray coloring, bullae, and anesthesia (Figure 77–10). Crepitus may be felt. Patients often demonstrate signs and symptoms of systemic infection progressing to severe sepsis.

Pathogens

There are two classifications of necrotizing fasciitis—type I, which is polymicrobial, and type II, which is monomicrobial. Type I infection is often due to both aerobic and anaerobic bacteria and is more common following intra-abdominal surgery, in diabetics, and in intravenous drug users. It can be seen also in the male perineum, a disease called Fournier’s gangrene (Figure 77–11). Ludwig’s angina, an infection of the sub-mandibular facial space, is another example.

Type II infection is most often due to S. pyogenes but can also be caused by Vibrio vulnificus following trauma in brackish (salt) water, Aeromonas species following trauma in fresh water, Clostridium perfringens from soil-contaminated wounds caused by motor vehicle/motorcycle accidents or shrapnel (gas gangrene), and community-acquired MRSA.

Diagnosis

Gram stain and culture from debrided tissue can assist in making a microbiologic diagnosis. Radiographic imaging may be useful. Plain films may demonstrate presence of gas in tissues, and a CT scan may reveal enhancement in the fascial plane. Magnetic resonance imaging is the most sensitive approach but is limited in specificity.

Treatment

Necrotizing soft tissue infections are a medical emergency, and treatment requires a combination of surgical debridement of infected tissue and antibiotic therapy. Antibiotic therapy should be directed at S. pyogenes, MRSA, and anaerobic and aerobic gram-negative rods. A common empiric regimen would include clindamycin plus vancomycin plus piperacillin-tazobactam.

Prevention

Handwashing and covering draining lesions should be used to prevent the spread of bacteria.