John Ratz, MD, MBA,
Staff Dermatologist, Mohs Surgeon, Center for
Dermatology and Skin Surgery, Inc
Nothing to disclose.
Coauthor(s)
Daniel B Ward Jr, MD,
Clinical Assistant Professor, Department of
Dermatology and Dermatologic Surgery, Medical University of
South Carolina
Nothing to disclose.
Specialty Editor(s)
Eleftherios Mylonakis, MD,
Clinical and Research Fellow, Department of
Internal Medicine, Division of Infectious Diseases,
Massachusetts General Hospital
Nothing to disclose.
Francisco Talavera, PharmD, PhD,
Senior Pharmacy Editor,
eMedicine
eMedicine Salary Employment
Gordon L Woods, MD,
Consulting Staff, Department of Internal
Medicine, University Medical Center
Nothing to disclose.
Gregory William Rutecki, MD,
Associate Professor, Program Director,
Department of Internal Medicine, Feinberg School of Medicine,
Northwestern University
Nothing to disclose.
Chief Editor
Burke A Cunha, MD,
Professor of Medicine, State University of
New York School of Medicine at Stony Brook; Chief, Infectious
Disease Division, Winthrop-University
Hospital
Nothing to disclose.
Background
Impetigo is an acute, contagious, superficial pyogenic skin infection that occurs most commonly in children, especially those who live in hot humid climates. Clinically, physicians recognize two separate forms of impetigo—bullous and nonbullous. Bullous impetigo is caused almost exclusively by Staphylococcus aureus, whereas nonbullous impetigo is caused by S aureus, group A Streptococcus (Streptococcus pyogenes), or a combination of both.
Impetigo most often develops at a site of minor trauma or insult in which the integrity of the skin is disrupted. Causative organisms enter the epidermis. Alternatively, scratching may directly inoculate bacteria beneath the skin surface, causing impetiginization.
The sequence of spread of the two causative organisms differs. S pyogenes is spread from a person who is infected or colonized with the bacteria onto the skin of another individual, where it may cause impetigo. The organism then colonizes the nose and throat. S aureus, in contrast, spreads first to the nose. It then spreads to the skin, where it may cause impetigo.
Nonbullous impetigo can affect all ages, but it most commonly affects children aged 2-5 years.
Bullous impetigo affects all ages, but, historically, it occurs more often in newborns and older infants. Some authors disagree, stating that adult cases often go underreported.
Patients with impetigo may report a history of minor trauma, insect bites, scabies, herpes simplex, varicella, or eczema at the site of infection, and any history of preexisting skin disease should raise the clinician's index of suspicion.
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A nummular eczema lesion on the knee, impetiginized with Staphylococcus aureus.
Lesions have usually been present for days or weeks rather than months. The lesions are usually painless, although patients may report burning and pruritus.
Constitutional symptoms are usually absent.
Obtain a history of contacts and living conditions; crowding and poor hygiene can be contributing factors to the spread of impetigo.
Clusters in families and outbreaks in institutions are occasionally reported.
One report described an outbreak among rugby players, which demonstrates an opportunity for impetigo to be spread during contact sports.[1]
Lesions first begin as thin-walled vesicles or pustules on an erythematous base. The lesions promptly rupture, releasing their serum, which dries and forms a light brown, honey-colored crust.
Multiple lesions generally occur at the same site, often coalescing. The affected area of skin may enlarge as the infection spreads peripherally.
Skin on any part of the body can be involved, but the face and extremities are affected most commonly.
Pruritus of infected areas may result in excoriations due to scratching.
As the lesions resolve, either spontaneously or after antibiotic treatment, the crusts slough from the affected areas and heal without scarring.
If the course of disease is prolonged and patients do not seek treatment, as many as 90% will develop regional lymphadenopathy.
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Following dermabrasion, this patient developed nonbullous impetigo in the same area as several herpes simplex lesions.
Bullous impetigo
Lesions may form on grossly normal or previously traumatized skin.
The vesicles do not rupture as easily or quickly as in nonbullous lesions, but they do enlarge into bullae that are usually 1-2 cm in diameter. The bullae initially contain a clear yellow fluid that subsequently turns cloudy and dark yellow.
After 1-3 days, the lesions rupture and leave a thin, light brown, varnishlike crust.
Central healing results in circinate lesions.
In contrast to nonbullous impetigo, bullous impetigo may involve the buccal mucous membranes, but regional lymphadenopathy is rare.
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Bullous impetigo on the buttocks. Courtesy of Medical University of South Carolina, Department of Dermatology.
S aureus, group A streptococcus (S pyogenes), or both may be the causative agent(s) in nonbullous impetigo, but researchers disagree about which organism more often plays the primary role in infection.
Early studies pointed to streptococci, but recent investigations suggest that S aureus is increasingly the primary infectious organism, especially in industrialized nations.
Evidence indicates that the primary organism varies with geography and climate; streptococcal impetigo is more common in developing nations and warm climates.
Streptococci are the most common primary cause when both organisms are present.
Bullous impetigo
S aureus phage group II type 71 is the predominant causative organism. This strain of bacteria produces an exfoliatin toxin that causes subcorneal epidermal cleavage.
In immunodeficient or immunocompromised patients, the toxin may disseminate hematogenously and lead to generalized staphylococcal scalded skin syndrome.
Impetigo can usually be diagnosed based on the clinical picture.
Culture of the involved skin confirms the diagnosis and identifies the causative organism, thereby helping the physician choose appropriate antibiotic therapy.
The presence of gram-positive cocci in chains indicates S pyogenes.
Gram-positive cocci in clusters indicate S aureus.
A culture obtained from intact bullae of bullous impetigo reveals S aureus phage group II.
If acute glomerulonephritis presents in a patient with a recent history of impetigo, use a titer of antibodies to streptococcal components (eg, antideoxyribonuclease [DNAse] B, antihyaluronidase, and antistreptolysin O [ASO] titers) to identify a possible etiology for the renal findings.
The epidermal cleavage plane is subcorneal in both bullous and nonbullous impetigo. Obtaining biopsies, which is rarely necessary to establish the diagnosis, reveals neutrophils migrating within the epidermis, an inflammatory infiltrate of neutrophils and lymphocytes in the upper dermis, and subcorneal blisters containing occasional acantholytic cells. The blisters of nonbullous impetigo, which are slight and transient, may also contain occasional gram-positive cocci and numerous neutrophils.
Medical management may involve topical therapy alone or a combination of systemic and topical therapies.
Topical therapy
First, remove the infected crusts and debris with soap and water. If the infection is mild and localized, topical mupirocin alone may be the only necessary therapy. Studies indicate this topical antibiotic, although expensive, is as effective as oral erythromycin for treating impetigo. Furthermore, the cost difference between these two treatments may be offset by the increased incidence of adverse effects associated with erythromycin.
Disadvantages of topical treatment are that it cannot eradicate organisms from the respiratory tract and applying topical medications to extensive lesions is difficult.
No studies indicate that other topical antibiotics are as effective as systemic therapy.
Systemic therapy
When infection is moderate to severe or accompanied by lymphadenopathy, systemic therapy is indicated.
The drug preferred for impetigo caused by S pyogenes is penicillin. Substitute clindamycin in patients who are allergic to penicillin.
In cases caused by S aureus, clindamycin or cephalexin may be used.
Treat erythromycin-resistant S aureus impetigo with a cephalosporin (eg, cephalexin, clindamycin).
Clinical Context:
Interferes with cell wall mucopeptide synthesis during active multiplication, resulting in bactericidal activity against susceptible microorganisms. Not recommended for staphylococcal impetigo.
Clinical Context:
Recommended for impetigo caused by S aureus resistant to erythromycin. First-generation cephalosporin arrests bacterial growth by inhibiting bacterial cell wall synthesis. Bactericidal activity against rapidly growing organisms. Primary activity against skin flora. Used for skin infections or prophylaxis in minor procedures.
Clinical Context:
Indicated for skin and skin structure infections caused by beta-lactamase–producing strains of S aureus that are resistant to erythromycin.
Administration with food may decrease GI adverse effects.
Clinical Context:
Alternative therapy for S aureus resistant to erythromycin. Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Clinical Context:
Topical antibiotic available as a 1% ointment. First of new antibiotic class called pleuromutilins. Inhibits protein synthesis by binding to 50S subunit on ribosome. Indicated for impetigo caused by S aureus or S pyogenes.
Follow-up is important to ensure complete clearing of lesions. Request that patients schedule follow-up visits if lesions worsen or do not improve after beginning therapy.
Acute poststreptococcal glomerulonephritis (AGN) is a rare but potential complication of nonbullous impetigo.
It occurs in less than 1% of cases, depending on the nephritogenic potential of the S pyogenes strain involved. Many strains have no nephritogenic potential, but types M-60 and M-49 cause AGN in 70% and 25% (respectively) of patients with impetigo caused by these strains.
Interestingly, in certain tropical and subtropical climates, skin infection is the most common infection preceding nephritis. Rheumatic fever, however, is not a risk following streptococcal impetigo because it develops after streptococcal pharyngitis. Use anti-DNAse B, antihyaluronidase, and ASO titers to provide evidence of a recent streptococcal infection.
With appropriate treatment, lesions usually heal in 2-3 weeks or less; however, patients with eczema or an underlying parasitic infection may have a prolonged course.
Patients typically do not have scars, but postinflammatory pigment alterations may occur.
Hay RJ, Adriaans BM. Bacterial Infections. In: Champion RH, Breathnach SM, Burns AD, et al, eds. Textbook of Dermatology. 6th ed. Oxford, England: Blackwell Science; 1998:1097-1179.
Hirschmann JV. Bacterial infections of the skin. In: Sams WM Jr, Lynch PJ, eds. Principles and Practice of Dermatology. 2nd ed. New York, NY: Churchill Livingstone; 1993:79-88.
Lee PK, Weinberg AN, Swartz MN, et al. Pyodermas: Staphylococcus aureus, Streptococcus, and Other Gram-Positive Bacteria. In: Fitzpatrick TB, Eisen AZ, Wolff K, et al, eds. Dermatology in General Medicine. 4th ed. New York, NY: McGraw-Hill; 1999:2182-2207.
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