Impetigo

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Practice Essentials

Impetigo is the most common bacterial infection in children. This acute, highly contagious infection of the superficial layers of the epidermis is primarily caused by Streptococcus pyogenes or Staphylococcus aureus. Secondary skin infections of existing skin lesions (eg, cuts, abrasions, insect bites, chickenpox) can also occur.[1] Methicillin-resistant S aureus (MRSA)[2] and gentamicin-resistant S aureus strains have also been reported to cause impetigo.[3] Impetigo is classified as either nonbullous (impetigo contagiosa) (about 70% of cases[4] ) or bullous.

Essential update: Short-course PO co-trimoxazole may be noninferior to IM benzathine benzylpenicillin for extensive impetigo

Short-course oral (PO) co-trimoxazole appears to be noninferior to intramuscular (IM) benzathine benzylpenicillin for the treatment of extensive impetigo, according to a randomized, controlled, noninferiority trial in 508 Australian children (age, 3 mo to 13 y) with purulent or crusted nonbullous impetigo in a highly endemic region.[5]

In children randomly assigned to receive benzathine benzylpenicillin IM (n=156 analyzed of 165), twice-daily co-trimoxazole PO for 3 days (n=173 analyzed of 175), or once-daily co-trimoxazole PO for 5 days (n=161 analyzed of 168), successful outcomes occurred in 133 (85%) in the benzathine benzylpenicillin group and 283 (85%) children in the pooled co-trimoxazole group (absolute difference 0.5%; 95% confidence interval -6.2 to 7.3).[5] There were similar outcomes between the co-trimoxazole groups. The majority of reported adverse events were observed in 54 patients, of whom 49 (90%) were treated with benzathine benzylpenicillin.[5]

Signs and symptoms

Children with nonbullous impetigo commonly have multiple coalescing lesions on their face (perioral, perinasal) and extremities or in areas with a break in the natural skin defense barrier. The initial lesions are small vesicles or pustules (< 2 cm) that rupture and become a honey-colored crust with a moist erythematous base. Pharyngitis is absent, but mild regional lymphadenopathy is commonly present. Nonbullous impetigo is usually a self-limited process that resolves within 2 weeks.

Bullous impetigo is considered to be less contagious than the nonbullous form.[6] It tends to affect the face, extremities, axillae, trunk, and perianal region of neonates, but older children and adults can also be infected.[4] The initial lesions are fragile thin-roofed, flaccid, and transparent bullae (< 3 cm) with a clear, yellow fluid that turns cloudy and dark yellow. Once the bullae rupture, they leave behind a rim of scale around an erythematous moist base but no crust, followed by a brown-lacquered or scalded-skin appearance, with a collarette of scale or a peripheral tubelike rim.

Bullous impetigo also differs from nonbullous impetigo in that bullous impetigo may involve the buccal mucous membranes, and regional adenopathy rarely occurs. However, extensive lesions in infants may be associated with systemic symptoms such as fever, malaise, generalized weakness, and diarrhea. Rarely, infants may present with signs of pneumonia, septic arthritis, or osteomyelitis.

See Clinical Presentation for more detail.

Diagnosis

The diagnosis of impetigo is usually made on the basis of the history and physical examination. However, bacterial culture and sensitivity can be used to confirm the diagnosis and are recommended in the following scenarios:

Biopsy may be appropriate in doubtful or refractory cases of impetigo.[7]

See Workup for more detail.

Management

Treatment of impetigo typically involves local wound care in conjunction with either a topical antibiotic or a combination of systemic and topical agents. In general, the antibiotic selection has coverage against both S aureus and S pyogenes. In areas with a high prevalence of community-acquired MRSA with susceptible isolates, children older than 8 years may take clindamycin or doxycycline in cases. Trimethoprim-sulfamethoxazole can be used in situations in which group A streptococci are unlikely.

See Treatment and Medication for more detail.

Image library


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Nonbullous impetigo with vesicles, pustules, and sharply demarcated regions of honey-colored crusts.

Background

Impetigo is an acute, highly contagious gram-positive bacterial infection of the superficial layers of the epidermis. Skin lesions such as cuts, abrasions, and chickenpox can also become secondarily infected (impetiginized) with the same pathogens that produce classic impetigo.

Impetigo occurs most commonly in children, especially those who live in hot, humid climates. The name is believed to be derived from the Latin impetere (to assail).

Impetigo occurs in 2 forms: bullous and nonbullous, as shown in the photographs below. Nonbullous impetigo is the more common form, constituting approximately 70% of impetigo cases.[4] It tends to affect skin on the face or extremities that has been disrupted by bites, cuts, abrasions, other trauma, or diseases such as varicella.[1]


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Nonbullous impetigo with vesicles, pustules, and sharply demarcated regions of honey-colored crusts.


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Bullous impetigo with circumscribed lesions with a thin collarette of scale.

Nonbullous impetigo, also known as impetigo contagiosa, is the most common skin infection in children, accounting for approximately 10% of all cutaneous problems in pediatric clinics. It is more contagious than the bullous type.[6] Common impetigo is the term applied when the infection occurs in preexisting wounds. Impetigo as a secondary infection of preexisting skin disease or traumatized skin has also been referred to as impetiginous dermatitis.

Nonbullous impetigo is caused by Staphylococcus aureus, group A beta hemolytic streptococci (GABHS, also known as Streptococcus pyogenes), or a combination of both. Most infections begin as a streptococcal infection, but staphylococci replace the streptococci over time.

Methicillin-resistant S aureus (MRSA), which can be hospital or community acquired, is an increasingly common cause of impetigo[2] ; this pathogen is observed more often with the nonbullous form of impetigo than the bullous form. Over the last decade, an increasing number of community-acquired MRSA and gentamicin-resistant S aureus strains have been reported as a cause of impetigo.[3]

Bullous impetigo may affect intact skin and is caused almost exclusively by S aureus. Bullous impetigo is a toxin-mediated erythroderma in which the epidermal layer of the skin sloughs, resulting in large areas of skin loss. Ecthyma is a deeper, ulcerated infection, often occurring with lymphadenitis, that may be a complication of impetigo.

Impetigo seldom progresses to systemic infection, although poststreptococcal glomerulonephritis is a rare complication with GABHS infection only. Certain serotypes of GABHS (eg, types 49, 55, 57, 59) are associated with impetigo and acute glomerulonephritis.

Impetigo can also present as folliculitis, which is considered to be impetigo of the hair follicles caused by S aureus. Chronic recalcitrant impetigo/folliculitis can result in sycosis barbae (similar to lupoid sycosis) with scarring and a presentation similar to that of discoid lupus. Tinea may also cause this presentation.

Diagnosis of impetigo is usually based solely on the history and clinical appearance. Treatment typically involves local wound care, along with antibiotic therapy, either topical or systemic plus topical.

Pathophysiology

Intact skin is usually resistant to colonization or infection by S aureus or GABHS. These bacteria can be introduced from the environment and only transiently colonize the cutaneous surface. Experimental studies have shown that inoculation of multiple strains of GABHS on to the surface of subjects did not produce cutaneous disease unless skin disruption had occurred.

The teichoic acid adhesions for GABHS and S aureus require the epithelial cell receptor component, fibronectin, for colonization. These fibronectin receptors are unavailable on intact skin; however, skin disruption may reveal fibronectin receptors and allow for colonization or invasion in these disrupted surfaces. Factors that can modify the usual skin flora and facilitate transient colonization by GABHS and S aureus include high temperature or humidity, preexisting cutaneous disease, young age, or recent antibiotic treatment.

Common mechanisms for disruption of skin that can facilitate bacterial colonization or infection include the following:

Immunosuppression by medications (eg, systemic corticosteroids, oral retinoids, chemotherapy), systemic diseases (eg, HIV infection, diabetes mellitus), intravenous drug abuse, and dialysis encourages bacterial growth.

After initial infection, new lesions may be seen in areas with no apparent break in the skin. Frequently, however, upon close examination, these lesions will demonstrate some underlying physical damage.

GABHS colonization

If an individual is in close contact with others (eg, household members, classmates, teammates) who have GABHS skin infection or who are carriers of the organism, the normal skin of that individual may be colonized. Once the healthy skin is colonized, minor trauma, such as abrasions or insect bites, may result in the development of impetigo lesions within 1-2 weeks.

GABHS can be detected in the nose and throat of some individuals 2-3 weeks after lesions develop, although they do not have symptoms of streptococcal pharyngitis. This is because impetigo and pharyngitis are caused by different strains of the bacteria. Impetigo is usually due to pattern D strains, whereas pharyngitis is due to pattern A, B, and C strains.

Staphylococcus aureus colonization

Approximately 30% of the population is colonized in the anterior nares by S aureus. Some individuals colonized by S aureus experience recurrent episodes of impetigo on the nose and lip. Bacteria can spread from the nose to healthy skin within 7-14 days, with impetigo lesions appearing 7-14 days later.

Approximately 10% of individuals are colonized with S aureus in the perineum and, more uncommonly, in the axillae, pharynx, and hands. Individuals who are permanent carriers serve as reservoirs of the infection for other people. Most healthy persons transiently harbor S aureus as part of their microbial flora. S aureus often passes from one individual to another through direct hand contact, entering through broken skin created by cutaneous diseases.

Patients with atopic dermatitis or other inflammatory skin conditions more commonly have skin colonized by S aureus. Studies have shown a 60-90% S aureus colonization rate in patients with atopic dermatitis. Patients with atopic dermatitis, particularly those with a history of eczema herpeticum, are at higher risk of developing an infection caused by MRSA.

One study found significantly lower expression of proteins related to the skin barrier and generation of natural moisturizing factor in lesional versus nonlesional sites in patients with atopic dermatitis. In addition, epidermal fatty acid–binding protein was expressed at significantly higher levels in patients colonized with MRSA, and this might perpetuate the inflammatory response through eicosanoid signaling.[9]

Bullous impetigo

Bullous impetigo (see the image below) is commonly due to exfoliative toxins of S aureus termed exfoliatins A and B. In 2006, exfoliative toxin D (ETD) was identified in 10% of S aureus isolates.[10] These exotoxins cause a loss of cell adhesion in the superficial dermis, which, in turn, causes blisters and skin sloughing by cleaving of the granular cell layer of the epidermis.

One of the target proteins for exotoxin A is desmoglein I, which maintains cell adhesion. These molecules are also superantigens that act locally and activate T lymphocytes. Coagulase may cause these toxins to remain localized within the upper epidermis by producing fibrin thrombi. Unlike nonbullous impetigo, the lesions of bullous impetigo occur on intact skin.


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Superficial flaccid bullae of bullous impetigo caused by Staphylococcus aureus. Courtesy of Professor David Taplin, Department of Dermatology and Cuta....

While the number of isolates of community- and hospital-acquired MRSA in lesions of impetigo remains low, this incidence has been increasing. Community-acquired MRSA can be differentiated from hospital-acquired MRSA. Most strains of community-acquired MRSA contain Panton-Valentine leucocidin (P-VL), a highly virulent, pore-forming exotoxin that causes dermal necrosis and has cytolytic activity against neutrophils and monocytes. Destruction of leukocytes by P-VL is one of the reasons that MRSA is more likely to produce clinical infection.

P-VL-positive S aureus strains are more frequently associated with cellulitis (38%) and abscesses (75%).[7, 11, 12, 13] In immunodeficient or immunocompromised patients, the toxin may disseminate hematogenously and lead to generalized staphylococcal scalded skin syndrome.

Etiology

Impetigo is caused by bacterial infection. Both S aureus and GABHS cause nonbullous impetigo; S aureus accounts for approximately 80% of cases, GABHS accounts for 10% of cases, and both organisms are recovered in 10% of cases. Bullous impetigo is caused almost exclusively by S aureus.

Nonbullous impetigo

Nonbullous impetigo can be caused by GABHS (types 49, 52, 53, 55-57, 59, 61) or by S aureus; in approximately 20-45% of cases, both agents are present. S aureus produces bacteriotoxins toxic to streptococci. These bacteriotoxins may be the reason that only S aureus is isolated in lesions that are caused predominantly by streptococci.

While in the past, GABHS and S aureus were equally frequent causative agents for nonbullous impetigo, currently S aureus accounts for 50-60% of cases. In developing nations and warm climates, however, GABHS is still the more common cause.[7]

Groups B, C, and G streptococci are rare causes of nonbullous impetigo. Group B streptococci are associated with impetigo in the newborn.

Bullous impetigo

Coagulase-positive group II S aureus, most often phage type 71, is the predominant causative organism. This strain of bacteria produces an exfoliating toxin that causes subcorneal epidermal cleavage and the condition known as Staphylococcal scalded skin syndrome (SSSS).

MRSA has been isolated in as many as 20% of bullous impetigo cases.[7] Methicillin resistance is found on the mecA gene, which has 4 elements, I-IV. Element IV is associated with community-acquired MRSA, and elements I-III are associated with hospital-acquired MRSA.

Among the risk factors for hospital-acquired MRSA are the following:

Community-acquired MRSA is a growing problem. Community-acquired MRSA is seen in greater frequency in closed populations in prisons, day care centers, and athletic teams, as well as in patients with diabetes or an underlying skin condition. The prevalence in these communities has been reported to be as high as 50%.

Epidemiology

United States statistics

Impetigo accounts for approximately 10% of skin problems observed in pediatric clinics. It is the most common bacterial skin infection and the third most common skin disease among children.[4]

Because it occurs more frequently in a warm, humid environment, impetigo is more common in the southeastern United States than in the cooler northern states. The prevalence of impetigo varies seasonally, with peak incidence during summer and fall[14] ; however, in regions that remain warm and humid throughout the year, seasonality may not occur.

International statistics

Impetigo occurs more frequently in tropical climates and at lower altitudes. Warm, humid conditions combined with frequent cutaneous disruption via biting insects favor its development throughout the year in tropical climates. Crowded conditions or poor hygiene also promote impetigo.

British statistics published in 1995 show an annual incidence of impetigo of 2.8% in children aged 4 years and younger and 1.69% in children aged 5-15 years. Impetigo has been reported as the third most frequent skin condition in children seen by general practitioners in the Netherlands, with a mean incidence of 10.8-22.2 cases per 1000 children per year, depending on the geographic region in the country.[15, 16]

A Dutch study reported an increase in the annual incidence in children younger than 18 years from 1.65% in 1987 to 2.06% in 2001.[8] In an observational study from Queensland, Australia, impetigo was diagnosed in 22 of 60 patients (37%) who presented with purulent skin infections; the median age was 19 years (range, 2 months to 91 years), and 38% of patients were male.[17]

Race-, sex-, and age-related demographics

Impetigo can affect people of all races. Overall, the incidence in males and that in females are equal; in adults, however, impetigo is more common in men. Impetigo occurs in individuals of all ages but is most common in children 2-5 years of age. Rapid dissemination can occur through day care centers, nurseries, and grade schools.

Bullous impetigo is most common in neonates and infants; 90% of cases occur in children younger than 2 years. If premature rupture of membranes occurs during labor, lesions of impetigo may be present at birth. However, some authors suggest that statistics on bullous impetigo may be skewed because adult cases often go underreported.

Prognosis

Even without treatment, impetigo usually heals within 2-3 weeks.[18] Randomized placebo arms in prospective clinical trials have noted a 13-52% spontaneous resolution rate.[19] However, treatment produces a higher cure rate and reduces the spread of infection to other parts of the body (via inoculation) or to other people.[20, 21] Scarring is unusual, but postinflammatory hyperpigmentation or hypopigmentation may occur. Untreated lesions of nonbullous impetigo may rarely progress to ecthyma, a deep dermal infection, after which subsequent scarring can occur.

With appropriate treatment, lesions usually resolve after 7-10 days. If lesions persist beyond that point, cultures should be performed to look for resistant organisms. However, patients with eczema or an underlying parasitic infection may have a protracted course.

Beyond the neonatal period, patients who receive early and appropriate therapy have an excellent chance of recovery without complications. Neonates have a much higher incidence of developing a more generalized infection and meningitis.

Cellulitis, lymphangitis, and suppurative lymphadenitis may occur in as many as 10% of patients with impetigo. No correlation between the amount of impetiginous lesions and the involvement of the surrounding soft tissues, lymphatics, or regional lymph nodes has been observed. Cellulitis rarely follows bullous impetigo.

If the exfoliative toxins are absorbed into the bloodstream, staphylococcal scalded skin syndrome can result. This occurs more commonly in younger children, who have not developed antibodies against this toxin.

Acute poststreptococcal glomerulonephritis (APSGN) is a rare complication of nonbullous impetigo from nephritogenic strains of GABHS, with an annual incidence of less than 1 case per 1,000,000 population in developed countries.[21, 22, 23] The frequency of APSGN varies widely, depending on the strain of GABHS. Many GABHS strains have no nephritogenic potential, but types M-60 and M-49 cause APSGN in 70% and 25% of cases, respectively.

APSGN appears 18-21 days after infection. No difference between the clinical appearance of impetigo due to nephritogenic and impetigo due to nonnephritogenic strains has been observed. Children aged 3-7 years are most commonly affected. Treatment of impetigo with systemic antibiotics does not prevent the development of APSGN, most likely because activation of the immune response precedes antibiotic treatment.

Interestingly, in certain tropical and subtropical climates, skin infection is the most common predecessor of APSGN. Recent evidence in Pacific communities where rheumatic fever is endemic demonstrate increasing evidence that skin-associated strains of group A streptococcal organisms being linked to cases of rheumatic fever.[24] Uncommon complications include the following[4, 25] :

Patient Education

Discourage touching the lesions. Inform patients about early and proper care of predisposing factors (eg, insect bites, minor trauma). Recommend that patients properly cleanse and apply a topical antibiotic to minor skin traumas.

Because of the contagious nature, children should not return to daycare or school until 24 hours after the initiation of appropriate antimicrobial therapy.[26] Caretakers should be instructed about hygienic issues and prevention. A history of poor hygiene and crowded living situations are common. This infection is transmitted by direct contact and by fomites, including hygiene items, clothing, and toys.

For patient education information, see the Bacterial and Viral Infections Center and Skin, Hair, and Nails Center, as well as Impetigo, Skin Rashes in Children, and Antibiotics.

History

Nonbullous impetigo begins with a single erythematous macule that rapidly evolves into a vesicle or pustule and ruptures; the released serous contents then dry, leaving a crusted, honey-colored exudate over the erosion. Rapid spread follows by contiguous extension or to distal areas through inoculation of other wounds from scratching.

Skin on any part of the body can be involved, but the face and extremities are affected most commonly. Lesions are usually asymptomatic, with occasional pruritus. Little or no surrounding erythema or edema is present. Regional adenopathy is common.

Patients with impetigo may report a history of minor trauma, insect bites, scabies, herpes simplex, varicella, or eczema at the site of infection. Any history of preexisting skin disease should raise the clinician's index of suspicion.

Bullous impetigo usually consists of small or large, superficial, fragile bullae. Often, these quickly appear, spontaneously rupture, and drain so that only the remnants, or collarettes, are seen at the time of presentation. The lesions usually spread locally in the face, trunk, extremities, buttocks, or perineal regions and may reach distal areas through direct autoinoculation.

Lesions typically appear on intact skin but may secondarily invade preexisting lesions (eg, eczema) to cause generalized lesions. There is minimal or no surrounding erythema and no regional lymphadenopathy.

Individuals with impetigo frequently recall exposure to a person who is a known carrier of S aureus or streptococcal organisms, has a pyoderma, or has a skin condition (eg, atopic dermatitis) that predisposes that individual to be an S aureus or streptococcal carrier. Clusters in families and outbreaks in institutions are occasionally reported.

Hot humid weather, participation in contact sports,[27] crowded living conditions, poor personal hygiene, or an unhygienic work environment encourages contamination of the skin by pathogenic bacteria that can cause impetigo.

Conditions such as HIV infection, posttransplantation, diabetes mellitus, hemodialysis, chemotherapy, radiation therapy, or systemic corticosteroid treatment increase susceptibility.

Primary selective immunoglobulin M (IgM) deficiency has been linked to recurrent impetigo in patients with negative S aureus carrier status and no predisposing factors, such as a preexisting dermatosis.[28] Frequent associations of immunoglobulin A (IgA), IgM, and immunoglobulin G (IgG) deficiencies have also been reported.

The following symptoms usually are absent in impetigo contagiosa but may be present in bullous impetigo:

Physical Examination

Generally, the patient is nontoxic and appears well. The appearance of lesions varies between nonbullous and bullous impetigo. Some authors assert a continuum of disease including nonbullous impetigo, bullous impetigo, and abscess formation caused by S aureus with differing exotoxin characteristics.

Nonbullous impetigo

The lesion begins as a tiny vesicle or pustule that ruptures and is replaced by honey-colored crusting, usually measuring less than 2 cm. Elevation of the crust reveals a moist erythematous base. As the lesions resolve, either spontaneously or after antibiotic treatment, the crusts slough from the affected areas and heal without scarring.

Multiple lesions generally occur at the same site, often coalescing. The affected area of skin may enlarge as the infection spreads peripherally. Pruritus of infected areas may result in excoriations due to scratching.

Lesions are usually located on the face (around the mouth and the nose) and exposed parts of the body (eg, arms, legs) or in areas with a break in the natural skin defense barrier. The palms and soles are spared. Little or no surrounding erythema or edema is present. Regional lymphadenopathy is present in 90% of patients. Patients do not have a sore throat.

Images of nonbullous impetigo are shown below.


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Following dermabrasion, this patient developed nonbullous impetigo in the same area as several herpes simplex lesions.


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Nonbullous (crusted) impetigo resulting from a chigger bite infected by group A beta-hemolytic streptococci. Courtesy of Professor David Taplin, Depar....


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Nonbullous impetigo from an abrasion infected by group A beta-hemolytic streptococci. Courtesy of Professor David Taplin, Department of Dermatology an....


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Nonbullous impetigo secondary to group A beta-hemolytic streptococci. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surg....


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Nonbullous impetigo resulting from an infected insect bite. See Media File 6 for a pure culture of group A beta-hemolytic streptococci from this lesio....


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Group A beta-hemolytic streptococci pure culture from a lesion of nonbullous impetigo resulting from an infected insect bite. See Media File 5. Courte....

Bullous impetigo

Bullous impetigo affects neonates most frequently. However, the infection also occurs in older children and adults.[4] Thin-roofed, flaccid, and transparent bullae usually measure less than 3 cm. Intact bullae are not usually present because they are very fragile.

The bullae initially contain a clear, yellow fluid that subsequently turns cloudy and dark yellow. Bullae rupture easily, within 1-3 days, leaving a rim of scale around an erythematous moist base. After desiccation, the lesion has a brown-lacquered or scalded-skin appearance, with a collarette of scale or a tubelike rim at the periphery. Removal of the crust reveals a moist, red base. Central healing results in circinate lesions.

Bullous lesions occur on intact skin of intertriginous areas such as the neck, the axillary and crural folds, and the diaper area, but they may appear on the face or anywhere on the body. No surrounding erythema or edema is present. Bullous impetigo differs from nonbullous impetigo in that bullous impetigo may involve the buccal mucous membranes and regional adenopathy rarely occurs in bullous impetigo. In addition, bullous impetigo is considered to be less contagious than nonbullous impetigo.[6]

In infants, extensive lesions may be associated with systemic symptoms such as fever, malaise, generalized weakness, and diarrhea. Rarely, infants may present with signs of pneumonia, septic arthritis, or osteomyelitis.

Images of bullous impetigo are shown below.


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Bullous impetigo on the buttocks. Courtesy of Medical University of South Carolina, Department of Dermatology.


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Bullous impetigo caused by Staphylococcus aureus. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of M....


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Peripheral collarettes of scale on the abdomen after rupture of bullae of bullous impetigo caused by Staphylococcus aureus. Courtesy of Professor Davi....

Complications

Rarely, pedal edema and hypertension may be noted in a patient with nonbullous impetigo. These are signs of renal dysfunction most likely resulting from poststreptococcal glomerulonephritis. Most often, these are children aged 2-4 years. The onset is usually 10 days after impetigo lesions first appear, but it can occur from 1-5 weeks later.

The onset of poststreptococcal glomerulonephritis is usually 10 days after impetigo lesions first appear, but it can occur from 1-5 weeks later. Transient proteinuria and hematuria may occur during impetigo and resolve before renal involvement develops. Antibiotic treatment does not prevent the development of glomerulonephritis, but it limits the spread of the disease to other individuals.

Other complications may include the following:

Approach Considerations

Diagnosis of impetigo is usually based solely on history and clinical appearance. Bacterial culture and sensitivity are recommended (1) to identify possible methicillin-resistant Staphylococcus aureus (MRSA), (2) if an outbreak of impetigo has occurred, or (3) if poststreptococcal glomerulonephritis is present. Evidence of previous streptococcal skin infection may be sought in individuals in whom acute poststreptococcal glomerulonephritis (APSGN) is suspected.

In patients with nonbullous lesions, after cleansing the honey-colored crusted lesion and uplifting the scab, a bacterial culture of the fresh exudate underneath the scab may be obtained. In patients with bullous lesions, Gram stain and culture of the blister fluid is performed. On Gram stain, the presence of gram-positive cocci in chains indicates Streptococcus pyogenes; gram-positive cocci in clusters indicate S aureus. Culture and sensitivity results can help the physician choose appropriate antibiotic therapy.

Documentation of a recent streptococcal skin infection in the differential diagnosis of APSGN is accomplished best by obtaining antideoxyribonuclease B (anti-DNase B) and antihyaluronidase (AH) titers. More than 92% of patients with impetigo-associated APSGN have elevated anti-DNase B titers. Patients with impetigo have a poor antistreptolysin O (ASO) serologic response; only 51% of patients with impetigo-associated APSGN develop an increased ASO titer.

Urinalysis is necessary to evaluate for APSGN if the patient develops new-onset edema or hypertension. Hematuria, proteinuria, and cylindruria are indicators of renal involvement.

A potassium hydroxide wet mount may be performed to exclude bullous dermatophyte infection. A Tzanck preparation or viral culture may be performed to exclude herpes simplex infection.

A bacterial culture of the nares may be obtained to determine whether a patient is an S aureus carrier. If the nares culture is negative and the patient has persistent recurrent episodes of impetigo, bacterial cultures should be obtained from the axillae, pharynx, and perineum.

Obtain serum IgM levels in cases of recurrent impetigo in patients with negative S aureus carrier status and no predisposing factors such as a preexisting dermatosis.[28] Serum level determination of IgA, IgM, and IgG, including IgG subclasses, is necessary to rule out other immunodeficiencies.

Histologic Findings

Biopsy may be appropriate in doubtful or refractory cases of impetigo.[7] In bullous impetigo, few or no inflammatory cells are present within the bulla. A polymorphous infiltrate is present in the upper dermis. Acantholysis is noted in the granular layer.

In nonbullous impetigo, a serum crust is present above the epidermis. Neutrophils are common within the crust. In addition, gram-positive cocci are seen. Epidermal spongiosis and a severe dermal infiltrate of neutrophils and lymphoid cells are seen.

Approach Considerations

Treatment of impetigo typically involves local wound care along with antibiotic therapy. Antibiotic therapy for impetigo may be with a topical agent alone or a combination of systemic and topical agents.

Gentle cleansing, removal of the honey-colored crusts of nonbullous impetigo using antibacterial soap and a washcloth, and frequent application of wet dressings to areas affected by lesions are recommended. Good hygiene with antibacterial washes, such as chlorhexidine or sodium hypochlorite baths, may prevent the transmission of impetigo and prevent recurrences, but the efficacy of this has not been proven.

For antibiotic therapy, the chosen agent must provide coverage against both Staphylococcus aureus and Streptococcus pyogenes. The prevalence of methicillin-resistant S aureus (MRSA) and macrolide-resistant Streptococcus has changed empiric treatment options for impetigo. MRSA was responsible for 78% of all community staphylococcal-related skin and soft tissue skin infections in a multicenter US study.[34]

As community-acquired MRSA (CA-MRSA) infection most commonly manifests as folliculitis or abscess, rather than impetigo, beta-lactam drugs remain an appropriate initial empiric choice. However, the continued increased presence of CA-MRSA may limit the utility of these agents. In this situation, clindamycin or doxycycline in children older than 8 years can be used if the isolate is susceptible.[35] Trimethoprim-sulfamethoxazole can be used in situations in which group A streptococci are unlikely.

Topical mupirocin or retapamulin is adequate treatment for single lesions of nonbullous impetigo or small areas of involvement. Systemic antibiotics are indicated for nonbullous impetigo with extensive involvement, in athletic teams, childcare clusters, multiple family members, or for s bullous impetigo.[26]

In patients with bullous impetigo who present to the emergency department with large areas of involvement resulting in denuded skin from ruptured bullae, management also includes intravenous fluid resuscitation. Fluid is given at a volume and rate similar to standard volume replacement for burns.

Inpatient care is required for patients with impetigo who have widespread disease or for infants at risk of sepsis and/or dehydration due to skin loss. If inpatient care is warranted in the child with untreated impetigo, contact isolation is recommended.

A clinical guideline summary from the Infectious Diseases Society of America that includes recommendations on impetigo, Practice guidelines for the diagnosis and management of skin and soft-tissue infections, may be helpful.

Topical Antibiotic Treatment

Topical antibiotic therapy is considered the treatment of choice for individuals with uncomplicated localized impetigo. Topical therapy eradicates isolated disease and limits the individual-to-individual spread. The topical agent is applied after removal of the infected crusts and debris with soap and water. Disadvantages of topical treatment are that it cannot eradicate organisms from the respiratory tract and that applying topical medications to extensive lesions is difficult.

Mupirocin

Mupirocin ointment (Bactroban) has been used for both the lesions and to clear chronic nasal carriers. Although it is expensive, it has been shown to be superior to topical polymyxin B and neomycin[36, 37] and to be equally effective as oral cephalexin. Both mupirocin and oral cephalexin are superior to bacitracin.[38] It is applied to the affected area 2-3 times daily. A 7-day course is usually standard, although few large studies have been performed to verify this as the most effective approach. Unfortunately, S aureus and MRSA resistance to mupirocin has emerged at estimated rates ranging from 5-10%.[36, 39]

Retapamulin

Retapamulin (Altabax) ointment is in a new class of topical antimicrobials. It is approved by the US Food and Drug Administration (FDA) for treatment of localized impetigo caused by S pyogenes and methicillin-susceptible S aureus in children older than 9 months.[40, 41] It is applied twice daily for 5 days. It is not for mucosal use; epistaxis has been reported with nasal mucosa application.

Retapamulin has an excellent spectrum of activity, surpassing the bacterial spectrum of mupirocin.[36, 42, 43] It has been shown to preserve its activity against bacteria that were resistant to multiple antibiotic drugs, such as methicillin, erythromycin, fusidic acid, mupirocin, azithromycin, and levofloxacin.[44, 45] The spectrum of retapamulin also includes erythromycin-resistant S pyogenes, fusidic acid–resistant and mupirocin-resistant S aureus, and MRSA (including P-VL–positive strains).[7]

In more than 1900 patients evaluated in several comparative studies, retapamulin has been demonstrated to be as effective as topical fusidic acid and oral cephalexin, with a low rate of adverse events.[36] In another study, retapamulin 1% ointment showed more efficacy than fusidic acid 2% ointment for the treatment of impetigo.[46]

Fusidic acid

Topical sodium fusidate (fusidic acid), currently not available in the United States, has been recognized as first-line therapy in Europe and other parts of the world.[8, 47] High resistance rates have been reported with the use of fusidic acid, however, ranging from 32.5-50%.[8, 46, 48, 49, 50]

A Swedish study of 38 patients with impetigo showed resistance of S aureus to fusidic acid in 75% of bullous cases and 32% of nonbullous ones. The authors recommended restricted use of fusidic acid in order to limit the rising levels of resistance.[51]

Other topical antibiotics

Other topical antibiotics have been reported to have some benefit for the treatment of impetigo. Clindamycin (cream, lotion, and foam) is useful in several MRSA infections.[52, 53] Gentamicin ointment or cream has been used in many countries for some gram-positive staphylococcal infections, including impetigo and pyoderma. Its use is precluded by the potential development of ear and kidney toxicity.[36, 52]

Hydrogen peroxide 1% cream, available in many countries, has demonstrated comparable bactericidal activity and longer duration of action than hydrogen peroxide 1% aqueous solution in vitro. It is applied 2-3 times a day on the affected area for a maximum of 3 weeks. Although the potential for sensitization is low, hypersensitivity reactions have been reported to other ingredients in the commercially available product.[52, 54]

Tetracycline has been used for localized impetigo. It is not widely prescribed because of the potential risk of skin photosensitivity reactions[3, 52] and because it is contraindicated in children younger than 8 years.

Drugs such as sulfanilamide, nitrofurazone, and silver sulfadiazine, which are widely used for the treatment of burns, are not currently used for the treatment of impetigo. Because of their antibacterial spectrum and proven efficacy and tolerability, these drugs may need to be considered in the future for the treatment of impetigo and other community-acquired skin infections.[36, 52]

Systemic Antibiotic Treatment

Infections that are widespread, complicated, or are associated with systemic manifestations are usually treated with antibiotics that have gram-positive bacterial coverage. Systemic therapy is also recommended if multiple incidents of pyoderma occur within daycare, family, or athletic team settings.

Beta-lactamase resistant antibiotics (eg, cephalosporins, amoxicillin-clavulanate, cloxacillin, dicloxacillin) are recommended. Cephalexin appears to be the drug of choice for oral antimicrobial therapy in children.

Community-acquired MRSA has become widespread.[34, 55] If MRSA is suspected, alternative antibiotics include clindamycin, trimethoprim-sulfamethoxazole, and vancomycin. Empiric treatment depends on the prevalence and sensitivities of MRSA in a particular geographic region.[56] Physicians should be aware of local resistance patterns.

Erythromycin and clindamycin are alternatives in patients with penicillin hypersensitivity. Macrolide resistance has been increasing in the United States. Thus, avoid treatment of impetigo with erythromycin in geographic regions that are known to have a high resistance rate. Group A beta hemolytic streptococci (GABHS) and S aureus resistance to clindamycin has also been reported.

Deterrence and Prevention

Children with impetigo should avoid close contact with other children if possible. Current recommendations call for the exclusion of children with impetigo from school or day care for 24 hours after the initiation of antibiotics. This recommendation primarily assumes that GABHS is the cause. If S aureus is documented to be the etiology, exclusion from school or day care is not necessary.

Inspect household members for impetiginous lesions. With neonatal impetigo, also evaluate hospital nursery staff and household members for pyodermas or asymptomatic bacterial carrier states. Failure to treat other infected persons may result in continued transmission.

Treat traumatized skin with mupirocin because this has been shown to decrease the rates of impetigo spread. Treat preexisting underlying skin diseases, such as atopic dermatitis. Antihistamines and topical steroids help decrease scratching. Treating the underlying disease has also been shown to decrease the pathogen count on the skin.

Teach good personal hygiene. For example, keep nails short and clean and wash hands frequently with antibacterial soap and water or waterless antibacterial cleansers. Advise patients about improving environmental conditions through the addition of air conditioning and by keeping surroundings clean.

For patients with recurrent impetigo, asymptomatic family members, and S aureus nasal carriers, prescribe 2% mupirocin cream or ointment (Bactroban) for application inside nostrils 3 times per day for 5 days each month to reduce colonization in the nose. Retapamulin may replace mupirocin for this indication, although data are needed to support its use in this setting. Patients who are chronic nasal carriers can also be treated with clindamycin or rifampin plus dicloxacillin.

Polymerase chain reaction to detect the mecA gene has become an effective tool for the screening for MRSA colonization upon hospital admission. However, screening has not been shown to significantly reduce transmission of and infection with MRSA.[7]

Consultations and Long-Term Monitoring

The need for consultation is determined by the extent of involvement and the age of the patient. Neonates with bullous impetigo may require a consultation with a neonatologist.

Recurrent disease should trigger a specialist consult. Consult a nephrologist if signs and symptoms of acute glomerulonephritis develop.

Follow-up is important to ensure complete clearing of lesions. Schedule a follow-up visit within 1 week. If the lesions have not improved, check the bacterial culture and sensitivity results, look for MRSA, and prescribe alternative antibiotics accordingly. If the patient was treated with oral antibiotics, prescribe alternative antibiotics depending on bacterial culture and sensitivity results.

Medication Summary

Topical antibiotics, systemic antibiotics, or a combination of both is effective therapy for impetigo. Empiric bacterial coverage is aimed at eradicating Staphylococcus aureus and group A beta-hemolytic streptococci (GABHS; also known as Streptococcus pyogenes). Antihistamines may be prescribed for symptomatic relief in patients with pruritus.

Mupirocin applied topically has been shown to be effective for localized impetigo, but resistance has emerged. Retapamulin is a newer option.[47, 57] Bacitracin is no longer recommended as it is not as efficacious and causes frequent allergic skin reactions and occasional-to-rare anaphylaxis.[52]

The advantages of topical antibiotics include the following[52, 58] :

The disadvantages of topical antibiotics include the following[52] :

Systemic antibiotic treatment is indicated for widespread infections, complicated infections, or those associated with systemic manifestations. A cephalosporin, semisynthetic penicillin, or beta-lactam/beta-lactamase inhibitor combination is generally suitable for first-line therapy.

Methicillin-resistant Staphylococcus aureus (MRSA) should be suspected in cases of spontaneous abscess or cellulitis and in lesions that do not resolve with traditional antimicrobial therapy, in which case alternative antibiotics should be considered. These include trimethoprim-sulfamethoxazole, tetracycline, clindamycin, fluoroquinolones, and linezolid.

In areas with a high percentage of community-acquired MRSA, the empiric antibiotic choice should provide coverage for this possibility.

Mupirocin (Bactroban, Centany)

Clinical Context:  Mupirocin is a naturally occurring antibiotic produced by fermentation of Pseudomonas fluorescens. The mechanism of action of mupirocin is via inhibition of bacterial protein synthesis.

Retapamulin (Altabax)

Clinical Context:  Retapamulin is a topical antibiotic available as a 1% ointment. It is the first of a new antibiotic class called pleuromutilins. This agent inhibits protein synthesis by binding to the 50S subunit on the ribosome. It is indicated for impetigo caused by S aureus or Streptococcus pyogenes.

Class Summary

Topical antibiotic treatment with mupirocin is the treatment of choice for uncomplicated localized pyoderma, although S aureus resistance to mupirocin has been increasing.[59]

Amoxicillin and clavulanate (Augmentin)

Clinical Context:  This oral antibiotic combines the broad-spectrum antibiotic amoxicillin with the beta-lactamase inhibitor clavulanate. Amoxicillin inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins, while clavulanate inhibits beta-lactamase producing bacteria.

For children older than 3 months, dosing is based on the amoxicillin content. Because of different amoxicillin-clavulanate ratios in the 250-mg tab (250mg/125mg) versus the 250-mg chewable tab (250mg/62.5mg), do not use the 250-mg tab until the child weighs more than 40 kg.

Dicloxacillin

Clinical Context:  Dicloxacillin binds to one or more penicillin-binding proteins, which, in turn, inhibits synthesis of bacterial cell walls. It is indicated for treatment of infections caused by penicillinase-producing staphylococci. This agent may be used to initiate therapy when staphylococcal infection is suspected.

Erythromycin (E.E.S., Ery-Tab, Erythrocin)

Clinical Context:  Erythromycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. It is used for the treatment of staphylococcal and streptococcal infections. However, macrolide resistance in the United States has been increasing. Erythromycin is used only when other options are unavailable or contraindicated.

In children, the patient's age and weight and the severity of the infection determine the proper dosage. When twice-daily dosing is desired, a half-total daily dose may be taken every 12 hours. For more severe infections, double the dose.

Clindamycin (Cleocin)

Clinical Context:  Clindamycin is a lincosamide used for the treatment of serious skin and soft tissue staphylococcal infections. It is also effective against aerobic and anaerobic streptococci (except enterococci). It inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Cloxacillin

Clinical Context:  Cloxacillin is used for the treatment of infections caused by penicillinase-producing staphylococci.

Trimethoprim-sulfamethoxazole (Bactrim DS, Septra DS)

Clinical Context:  Trimethoprim-sulfamethoxazole selectively inhibits bacterial dihydrofolate reductase. It has good susceptibility against community-acquired MRSA but is not effective against S pyogenes.

Levofloxacin (Levaquin)

Clinical Context:  This agent inhibits DNA gyrase and topoisomerase IV, resulting in bactericidal activity. It is used as an alternative agent for MRSA infection.

Ciprofloxacin (Cipro)

Clinical Context:  Ciprofloxacin inhibits DNA gyrase and topoisomerase IV, resulting in bactericidal activity. Use this agent as an alternative for MRSA infection.

Linezolid (Zyvox)

Clinical Context:  Linezolid binds to the 50S ribosomal subunit, interfering with protein synthesis. This agent is used for MRSA or complicated skin infections.

Class Summary

Systemic antibiotic treatment is indicated for widespread or complicated pyoderma.

Desloratadine (Clarinex)

Clinical Context:  Desloratadine is a long-acting tricyclic histamine antagonist that is selective for the H1 receptor. It relieves nasal congestion and systemic effects of seasonal allergy. It is the major metabolite of loratadine, which, after ingestion, is metabolized extensively to the active metabolite 3-hydroxydesloratadine.

Cetirizine (Zyrtec)

Clinical Context:  Cetirizine selectively inhibits histamine H1 receptor sites in blood vessels, the GI tract, and the respiratory tract, which, in turn, inhibits physiologic effects that histamine normally induces at H1 receptor sites. Once-daily dosing is convenient. Bedtime dosing may be useful if sedation is a problem.

Loratadine (Claritin, Alavert, Loradamed, Tavist ND)

Clinical Context:  Loratadine is nonsedating and selectively inhibits peripheral histamine H1 receptors.

Class Summary

If pruritus is significant, antihistamines can be prescribed to possibly help minimize scratching. Avoidance of trauma to the skin may prevent or limit the spread of impetigo by autoinoculation. These agents selectively inhibit peripheral histamine H1 receptors to histamine.

Hydroxyzine (Vistaril)

Clinical Context:  Hydroxyzine antagonizes H1 receptors in the periphery. It may suppress histamine activity in the subcortical region of the CNS. It is often administered before sleep because of its sedating properties.

Class Summary

These agents selectively inhibit peripheral histamine H1 receptors to histamine.

Author

Lisa S Lewis, MD, Attending Physician, Division of Emergency Medicine, Cincinnati Children's Hospital Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Allan D Friedman, MD, MPH, Chairman, Division of General Pediatrics, VCUH Health System; Professor of Pediatrics, Virginia Commonwealth University School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD, Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Sadegh Amini, MD Senior Clinical Research Fellow, Skin Research Group, Department of Dermatology and Cutaneous Surgery, Miller School of Medicine, University of Miami

Sadegh Amini, MD is a member of the following medical societies: American Society for Dermatologic Surgery, International Society for Dermatologic Surgery, and International Society of Dermatology

Disclosure: Nothing to disclose.

Anne E Burdick, MD, MPH Professor of Dermatology, Director of Leprosy Program, Associate Dean for TeleHealth and Clinical Outreach, University of Miami Miller School of Medicine

Anne E Burdick, MD, MPH is a member of the following medical societies: Women's Dermatologic Society

Disclosure: Nothing to disclose.

Ivan D Camacho, MD, Assistant Professor of Clinical Dermatology, Department of Dermatology and Cutaneous Surgery, University of Miami, Leonard M Miller School of Medicine; Medical Director of Dermatology Clinic, Jackson Memorial

Ivan D Camacho, MD is a member of American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Florida Medical Association, International Society of Dermatology, and the Women's Dermatologic Society.

Disclosure: Nothing to disclose.

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

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Joseph Domachowske, MD Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York Upstate Medical University

Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Pamela L Dyne, MD Professor of Clinical Medicine/Emergency Medicine, David Geffen School of Medicine at UCLA; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center

Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Dirk M Elston, MD Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Glenn J Fennelly, MD, MPH Director, Division of Pediatric Infectious Diseases, Jacobi Medical Center; Associate Professor, Department of Pediatrics, Albert Einstein College of Medicine

Glenn J Fennelly, MD, MPH is a member of the following medical societies: Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Eric M Kardon, MD, FACEP Attending Emergency Physician, Georgia Emergency Medicine Specialists; Physician, Division of Emergency Medicine, Athens Regional Medical Center

Eric M Kardon, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Paul Krusinski, MD Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Andrew C Miller, MD Fellow, Department of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh Medical Center; Attending Physician, Department of Emergency Medicine, University of Pittsburgh Medical Center

Andrew C Miller, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

James J Nordlund, MD Professor Emeritus, Department of Dermatology, University of Cincinnati College of Medicine

James J Nordlund, MD is a member of the following medical societies: American Academy of Dermatology, Sigma Xi, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Rashid M Rashid, MD, PhD Resident Physician, Department of Dermatology, University of Texas, Houston, MD Anderson Cancer Center, and Morzak Research Initiative

Rashid M Rashid, MD, PhD is a member of the following medical societies: American Academy of Dermatology, Council for Nail Disorders, Houston Dermatological Society, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

John Ratz, MD, MBA Staff Dermatologist, Mohs Surgeon, Center for Dermatology and Skin Surgery, Inc

John Ratz, MD, MBA is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Micrographic Surgery and Cutaneous Oncology, American College of Physicians, American Society for Dermatologic Surgery, American Society for Laser Medicine and Surgery, International Society for Dermatologic Surgery, and Southern Medical Association

Disclosure: Nothing to disclose.

Gregory William Rutecki, MD Associate Professor, Program Director, Department of Internal Medicine, Feinberg School of Medicine, Northwestern University

Gregory William Rutecki, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Nephrology, National Kidney Foundation, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Mark A Silverberg, MD, FACEP, MMB Assistant Professor, Assistant Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate at Brooklyn

Mark A Silverberg, MD, FACEP, MMB is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Daniel B Ward Jr, MD Clinical Assistant Professor, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina

Daniel B Ward Jr, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, and South Carolina Medical Association

Disclosure: Nothing to disclose.

Eric L Weiss, MD, DTM&H Director of Stanford Travel Medicine, Medical Director of Stanford Lifeflight, Assistant Professor, Departments of Emergency Medicine and Infectious Diseases, Stanford University School of Medicine

Eric L Weiss, MD, DTM&H is a member of the following medical societies: American College of Emergency Physicians, American College of Occupational and Environmental Medicine, American Medical Association, American Society of Tropical Medicine and Hygiene, Physicians for Social Responsibility, Southeastern Surgical Congress, Southern Association for Oncology, Southern Clinical Neurological Society, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Michael J Wells, MD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

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Nonbullous impetigo with vesicles, pustules, and sharply demarcated regions of honey-colored crusts.

Nonbullous impetigo with vesicles, pustules, and sharply demarcated regions of honey-colored crusts.

Bullous impetigo with circumscribed lesions with a thin collarette of scale.

Superficial flaccid bullae of bullous impetigo caused by Staphylococcus aureus. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.

Following dermabrasion, this patient developed nonbullous impetigo in the same area as several herpes simplex lesions.

Nonbullous (crusted) impetigo resulting from a chigger bite infected by group A beta-hemolytic streptococci. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.

Nonbullous impetigo from an abrasion infected by group A beta-hemolytic streptococci. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.

Nonbullous impetigo secondary to group A beta-hemolytic streptococci. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.

Nonbullous impetigo resulting from an infected insect bite. See Media File 6 for a pure culture of group A beta-hemolytic streptococci from this lesion. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.

Group A beta-hemolytic streptococci pure culture from a lesion of nonbullous impetigo resulting from an infected insect bite. See Media File 5. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.

Bullous impetigo on the buttocks. Courtesy of Medical University of South Carolina, Department of Dermatology.

Bullous impetigo caused by Staphylococcus aureus. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.

Peripheral collarettes of scale on the abdomen after rupture of bullae of bullous impetigo caused by Staphylococcus aureus. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.

Nonbullous impetigo with vesicles, pustules, and sharply demarcated regions of honey-colored crusts.

Bullous impetigo with circumscribed lesions with a thin collarette of scale.

Bullous impetigo on the buttocks. Courtesy of Medical University of South Carolina, Department of Dermatology.

Following dermabrasion, this patient developed nonbullous impetigo in the same area as several herpes simplex lesions.

A nummular eczema lesion on the knee, impetiginized with Staphylococcus aureus.

Nonbullous (crusted) impetigo resulting from a chigger bite infected by group A beta-hemolytic streptococci. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.

Nonbullous impetigo from an abrasion infected by group A beta-hemolytic streptococci. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.

Nonbullous impetigo secondary to group A beta-hemolytic streptococci. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.

Streptococcal impetigo from an infected insect bite. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.

Nonbullous impetigo resulting from an infected insect bite. See Media File 6 for a pure culture of group A beta-hemolytic streptococci from this lesion. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.

Group A beta-hemolytic streptococci pure culture from a lesion of nonbullous impetigo resulting from an infected insect bite. See Media File 5. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.

Bullous impetigo caused by Staphylococcus aureus. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.

Superficial flaccid bullae of bullous impetigo caused by Staphylococcus aureus. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.

Peripheral collarettes of scale on the abdomen after rupture of bullae of bullous impetigo caused by Staphylococcus aureus. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.