ETIOLOGY

Impetigo is a common childhood superficial skin infection seen in preschool and school-aged children that is classically caused by Staphylococcus aureus bacteria but can also be caused by Group A streptococcus species (Streptococcus pyogenes). It usually peaks in incidence during the summer and fall seasons.¹ Given the steady increase in the prevalence of community-acquired methicillin-resistant S. aureus (CA-MRSA) over the past two decades, up to 70% prevalence in some areas, antibiotic selection must take into account this prevailing resistance pattern within the community.^2–4

PATHOPHYSIOLOGY

Impetigo infections occur when bacteria that is usually present on the surface of the skin enters into the epidermal layer through areas of skin breaks, microabrasions, or at sites of skin trauma. The bacteria then replicate beneath the skin, causing the characteristic crusted “honey-colored” gold lesions. Transmission of infection occurs through direct contact or fomites.¹

RECOGNITION

The classic impetigo rash begins with erythematous macular or papular lesions that then progress to superficial vesicles or bullae, which then rupture leaving crusted “honey-colored” gold lesions. Lesions can be solitary, arranged in clusters, or confluent. Typical distribution includes the face, extremities, and/or distal fingers or toes for nonbullous impetigo, and intertriginous areas of the neck, diaper area, or axillae for bullous impetigo (Fig. 91-1).^1,4

MANAGEMENT

Impetigo is often a benign self-limited disease lasting 2 to 3 weeks. However, it is easily transmitted to others and some studies report a 5% chance of Group A strep impetigo leading to acute glomerulonephritis.^1,4 Maintaining good skin hygiene, using antibacterial soaps, and/or dilute bleach baths have shown varying degrees of success in eradicating colonization. Over-the-counter topical agents such as bacitracin or neomycin tend to be ineffective due to the emergence of MRSA. Mupirocin or fusidic acid (not approved in the United States) ointments have been the mainstay of topical treatment for impetigo, and in a recent Cochrane review, shows evidence of being the most effective treatment.⁵ Due to reported resistance to mupirocin, a newer agent that has shown promise for the treatment of resistant impetigo is retapamulin (apply ointment topically to the site BID for 5 days).⁴ Oral antibiotics should be reserved for treatment of moderate/severe cases or refractory cases of impetigo. Oral agents that are effective include cephalosporins and beta lactamase–resistant penicillins such as amoxicillin/clavulanic acid. In communities with a high incidence of MRSA, treatment with clindamycin or trimethoprim/sulfamethoxazole (TMP/SMX) should be initiated to target this specific bacterial etiology.^4,6 Please refer to Table 91-1 for specific dosing and duration of therapy.

ANCILLARY STUDIES

A wound culture from crusted lesions or from the nasopharynx may grow Group A streptococcus or staphylococcus, which can sometimes help guide treatment choices for recurrent or refractory cases of impetigo.

ETIOLOGY

Cellulitis is an infection of the subcutaneous tissue caused by bacteria that results in warm, tender, and erythematous skin at the site of bacterial inoculation. Typical bacterial etiologic agents include Haemophilus influenza, Group A streptococci, and S. aureus.

PATHOPHYSIOLOGY

Bacteria enter the dermal and subcutaneous tissues through small breaks in the patient’s skin. Increased redness, warmth, swelling, and tenderness ensue 1 to 3 days after inoculation.¹ The resultant infection can progress into deeper tissues, leading to bacteremia and the onset of systemic symptoms such as fever, chills, and malaise.

Erysipelas is a superficial cellulitis of the skin with marked lymphatic involvement. It is typically caused by Group A streptococci. The bacteria enters the dermis through breaks in the skin or from the pharynx, leading to a well-demarcated, erythematous, hot, and tender plaque. The face, scalp, and hands are the most common sites of involvement.¹

RECOGNITION

Cellulitis and erysipelas are characterized by an area of skin with marked erythema, warmth, and sometimes tenderness and swelling. There may also be an associated lymphangitis streaking from the cellulitic area to the nearest lymph gland. Regional lymph nodes may be enlarged and in the case of severe or deep tissue infections, there can also be associated fever and malaise. Typical locations for cellulitis are the extremities, face, neck, or other sites of trauma or injury (Fig. 91-2). Erysipelas is classically located on the face.

MANAGEMENT

An outpatient course of oral antibiotics remains the mainstay of treating mild or moderate cellulitis infections. Choice of antibiotics should include agents with good gram-positive coverage such as cephalosporins or amoxicillin/clavulanic. If there is a concern for MRSA, clindamycin or TMP/SMX may be considered.⁶ Erysipelas can be treated with penicillin or amoxicillin, or if penicillin allergic, a macrolide such as azithromycin. Refer to Table 91-1 for specific dosing and duration of therapy. For patients exhibiting systemic symptoms, refractory cases, or for infections involving the eye, inpatient hospitalization with initiation of intravenous (IV) antibiotics (cephalosporins, including ceftaroline,⁶ and clindamycin or vancomycin if MRSA is suspected) is indicated.^6,8

ANCILLARY STUDIES

For mild cases, no ancillary studies are necessary. For moderate or severe cases, particularly if the patient is exhibiting systemic symptoms, a CBC, sedimentation rate, and/or C-reactive protein could help in assessing the severity of the illness as well as trending to see if there is resolution of these inflammatory markers with treatment. Blood cultures in patients with systemic symptoms can help guide appropriate antimicrobial therapy. Skin cultures by needle aspiration or skin biopsy at the leading edge may also recover the inciting organism to further help guide treatment.¹

ETIOLOGY

Folliculitis is an infection of the tissues surrounding the hair follicles. This infection occurs on wet, occluded, or macerated skin. The common offending bacterial agents are usually Staphylococcus or Pseudomonas.

Furuncles are deep red, hot, and tender perifollicular purulent inflammatory nodules that usually result from a worsening folliculitis. Carbuncles are larger lesions of coalesced furuncles.¹ Furuncles/carbuncles are commonly caused by staphylococcus except in the anogenital region where the anaerobic bacteria are the predominant etiologic agent.

PATHOPHYSIOLOGY

Folliculitis and furuncles are commonly found in areas of the skin that are moist, hot, or humid, or areas of the skin where there is poor hygiene or constant friction. These areas include the axilla, groin, buttocks, neck, waist/beltline, and face. Lesions start out as inflammation around the base of the follicle (folliculitis), but with constant friction or trauma (shaving, waxing, etc.) in the setting of warm, moist conditions progress to tender, pus-filled subcutaneous nodules.

RECOGNITION

Folliculitis lesions are pink or red papular lesions in the above distribution that are usually nontender but sometimes pruritic. Furuncles and carbuncles are larger, nodular, erythematous, and tender lesions that sometimes have associated purulent discharge.

MANAGEMENT