AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Impetigo is a highly contagious gram-positive bacterial infection of the superficial layers of the epidermis. The 2 forms of the disease are bullous impetigo and nonbullous impetigo. Impetigo is caused by Staphylococcus aureus and group A beta-hemolytic streptococci (GABHS). GABHS is also known as Streptococcus pyogenes. Both organisms may be present at the same time in the affected site. Infection by S aureus may be preceded by a primary infection by GABHS. Methicillin-resistant S aureus (MRSA), which can be hospital or community acquired, has been noted as a cause of impetigo; this infection is observed more commonly with the nonbullous form of impetigo than the bullous form.

Evidence from 2005 indicates that S aureus is now the most prevalent pathogen in both bullous and nonbullous impetigo in the United States and Europe,²² while S pyogenes is prevalent in developing countries. Most infections begin as a streptococcal infection, but then staphylococci replace the streptococci over time.

While impetigo can manifest as a primary pyoderma of intact skin, it may occur as a secondary infection of preexisting skin disease or traumatized skin, which has been referred to as impetiginous dermatitis. Impetigo rarely progresses to systemic infection, although poststreptococcal glomerulonephritis is a rare complication with GABHS infection only.

The following additional eMedicine articles on impetigo may be helpful:

• Impetigo (Emergency Medicine)
• Impetigo (Infectious Diseases)
• Impetigo (Pediatrics)

Additionally, the following Medscape CME courses might be of interest:

• Managing the Complicated Skin and Soft Tissue Infection
• Strategies for Diagnosis and Treatment of Impetigo

Pathophysiology

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 normal 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 florae. 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.

The organism often passes from one individual to another through direct hand contact, entering through broken skin created by cutaneous diseases (eg, atopic dermatitis, dermatophytosis, varicella, herpes simplex), thermal burns, surgery, trauma, radiation therapy, or insect bites. Immunosuppression by medications (eg, systemic corticosteroids, oral retinoids, chemotherapy), systemic diseases (eg, HIV infection, diabetes mellitus), intravenous drug abuse, and dialysis encourages bacterial growth.

Once infection is present, new lesions may develop despite no apparent skin breakage.

Bullous impetigo

The bullous form of impetigo is less common than the nonbullous form. The causative agent of bullous impetigo is gram-positive, coagulase-positive, group II S aureus, most often phage type 71. S aureus produces the extracellular exfoliative exotoxins termed exfoliatins A and B. In 2006, the exfoliative toxin D (ETD) was identified in 10% of S aureus isolates.³⁰ 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.

Nonbullous impetigo

While in the past GABHS and S aureus occurred with equal frequency as the causative agents for nonbullous impetigo, currently S aureus is the prominent pathogen responsible for nonbullous impetigo, accounting for 50-60% of the cases. In addition, approximately 20-45% of the cases are due to a combination of S aureus and S pyogenes. In developing nations, GABHS is still the more common cause. 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.

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.

Frequency

United States

Impetigo is a common skin disease, accounting for 10% of skin diseases treated in pediatric clinics. Peak incidence occurs during summer and fall.

Mortality/Morbidity

Most affected individuals recover without complications. Individuals with impetigo from streptococcal infections can develop glomerulonephritis as a rare complication. Oral antibiotics may not prevent the development of renal complications of cutaneous streptococcal infections.

Sex

The male-to-female ratio is equal.

Age

Impetigo occurs in individuals of all ages. Children younger than 6 years have a higher incidence of impetigo than adults. Bullous impetigo is most common in neonates and infants. If premature rupture of membranes occurs during labor, lesions of impetigo may be present at birth. Ninety percent of bullous impetigo occurs in children younger than 2 years. Nonbullous impetigo is most common in children aged 2-5 years. Group B streptococcal infection is associated with newborn impetigo.

The Medscape Pediatric Dermatology Resource Center may be helpful.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

• Nonbullous impetigo begins with a single erythematous macule that rapidly evolves into a vesicle or pustule, and ruptures leaving a crusted yellow exudate over the erosion.
• Bullous impetigo begins as a rapid onset of blisters that enlarge and rupture.
• Lesions are usually asymptomatic. Occasionally, patients report pain or itching.
• Infection spreads to contiguous and distal areas through direct inoculation.
• Individuals with impetigo frequently recall exposure to a person who is a known carrier of S aureus or streptococcal organisms or who has a pyoderma.
• Hot humid weather, participation in contact sports, crowded living conditions, poor personal hygiene, or an unhygienic work environment encourages contamination of the skin by pathogenic bacteria that can cause impetigo.
• A compromised immune system resulting from disease or disease treatment (eg, HIV, AIDS, posttransplantation, type 1 diabetes, hemodialysis, chemotherapy, radiation therapy, systemic corticosteroids), intravenous drug abuse, cutaneous conditions (eg, atopic dermatitis, dermatophytosis, varicella, herpes simplex), recent surgical wounds, insect bites, thermal burns, or abrasions creates an environment conducive to bacterial infection.
• Symptoms of a sore throat or fever are not usually present.

Physical

• Bullous impetigo
• • The characteristic lesion is a vesicle that develops into a superficial flaccid bulla less than 1 cm in diameter on intact skin, with minimal or no surrounding redness. Initially, the vesicle contains clear fluid that becomes turbid.
  • The roof of the bulla ruptures, often leaving a peripheral collarette of scale or a tubelike rim at the periphery. A varnishlike crust develops centrally, which, if removed, reveals a moist red base.
  • Intact bullae are not usually present because they are very fragile.
  • When present, intact bullae do not demonstrate a positive Nikolsky sign.
  • Lesions of a primary skin disease, such as atopic dermatitis or varicella, may be present.
  • Lesions may be localized or widely scattered.
  • Lesions are often found on the face but may appear anywhere on the body.
  • No regional lymphadenopathy is present.
  • In infants, extensive lesions may be associated with fever, malaise, generalized weakness, and diarrhea. Rarely, infants may present with signs of pneumonia, septic arthritis, or osteomyelitis.
• Nonbullous impetigo
• • The first noticeable abnormality is a red macule or papule, from 2-5 mm in size.
  • The characteristic lesion is a fragile vesicle or pustule that readily ruptures and becomes a honey-yellow, adherent, crusted papule or plaque smaller than 2 cm and with minimal or no surrounding redness.
  • Lesions develop on either normal or traumatized skin or are superimposed on a preexisting skin condition (eg, scabies, varicella, atopic dermatitis) and can spread rapidly.
  • Lesions are located around the nose, mouth, and exposed parts of the body (eg, arms, legs), sparing the palms and soles.
  • Localized lymphadenopathy is usually present, and nodes may be tender.
  • If left untreated, lesions spread by autoinoculation then spontaneously resolve after a few weeks.
  • Rarely, pedal edema and hypertension may be noted in an individual with nonbullous impetigo. Both are signs of renal dysfunction most likely resulting from glomerulonephritis.
  • No signs of pharyngitis are present.

Causes

Impetigo is caused by bacterial infection.

• Bullous impetigo
• • Coagulase-positive group II S aureus, most often phage type 71, is the causative agent.
  • Strains are usually resistant to penicillin and may be resistant to erythromycin.
  • MRSA is also seen in cases of impetigo and has been isolated in as many as 20% of bullous impetigo cases. 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. MRSA is a commonly encountered nosocomial infection, but, over the past several years, it has emerged in the community. A patient is determined to have community-acquired MRSA if the patient does not have any risk factors for nosocomial MRSA (eg, working in a health care center, hospitalization within the past year, residence in a long-term facility, having a chronic indwelling catheter or medical device). 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 as high as 50%.
• Nonbullous impetigo
• • GABHS (types 49, 52, 53, 55-57, 59, 61), S aureus, or a mixture of both organisms can cause nonbullous impetigo, although S aureus is the most common cause.
  • GABHS remains the predominant pathogen in developing populations.
  • Groups B, C, and G streptococci are rare causes of nonbullous impetigo.
  • Group B streptococci are associated with impetigo in the newborn.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Varicella
Herpes Zoster
Insect bites
Inflammatory dermatophytosis
Kerion
Pediculosis
Bullous erythema multiforme
Bullous fixed drug reaction
Stevens-Johnson syndrome
Vesicular stage of incontinentia pigmenti

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Impetigo is usually diagnosed clinically.
• Bacterial culture and sensitivity are recommended (1) in cases to identify MRSA, (2) if an outbreak of impetigo has occurred, or (3) if poststreptococcal glomerulonephritis is present. Exudate from underneath the crust is sent for culture.
• Leukocytosis is present in approximately 50% of impetigo cases.
• Antideoxyribonuclease (anti-DNAase) B antibody levels are often elevated in persons with streptococcal impetigo.
• Urinalysis is necessary to evaluate for acute poststreptococcal glomerulonephritis 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.

Histologic Findings

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, vesicopustules are present in the upper epidermis, usually within the stratum corneum. Neutrophils are common within the vesicopustule. In addition, gram-positive cocci are seen. Epidermal spongiosis and a severe dermal infiltrate of neutrophils and lymphoid cells are seen.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

Antibiotics are the mainstay of therapy and the chosen agent must provide coverage against both S aureus and S pyogenes. Community-acquired MRSA infection most commonly manifests as folliculitis or abscess, rather than impetigo; thus, beta-lactam drugs remain an appropriate initial empiric choice in the treatment of impetigo.

Topical antibiotics are used in patients with small or few lesions, applied to affected areas twice or thrice daily for 7-10 days. Mupirocin ointment has been used for both the lesions and to clear chronic nasal carriers. Unfortunately, resistance to mupirocin has emerged. Retapamulin has an excellent spectrum of activity, and resistance to this newer agent will take time to emerge. Oral antibiotics remain appropriate for many patients with impetigo.

For empiric antibiotic therapy, a cephalosporin, semisynthetic penicillin, or beta-lactam/beta-lactamase inhibitor is recommended. If bacterial cultures reveal MRSA and the patient is not improving, tetracyclines, trimethoprim/sulfamethoxazole (Bactrim), clindamycin, or linezolid are effective oral antibiotics.

Gentle debridement of lesional crusts using antibacterial soap and a washcloth is also recommended. Good hygiene with antibacterial washes, such as chlorhexidine, may prevent the spread of impetigo and prevent recurrences, but the efficacy of this has not been proven.

Consultations

Consult a nephrologist if signs and symptoms of acute glomerulonephritis develop.

MEDICATION

Section 7 of 11  

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• Follow-up
• Miscellaneous
• Multimedia
• References

The goals of pharmacotherapy are to reduce morbidity, to prevent complications, and to prevent spread to other individuals.

Drug Category: Antibiotics

Mupirocin applied topically has been shown to be effective for localized impetigo, but resistance has emerged. Retapamulin is a new option. Bacitracin is no longer the preferred topical antibiotic because it causes frequent allergic skin reactions.

Systemic antibiotic treatment is indicated for most cutaneous infections, although abscesses may respond to drainage alone. A cephalosporin, semisynthetic penicillin, or beta-lactam/beta-lactamase inhibitor combination is generally suitable for first-line therapy. 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.

Drug Category: Antihistamines

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.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• Impetigo typically resolves with topical or oral antibiotics; only rarely do serious complications occur. Vancomycin may be required for complicated MRSA infections that do not improve with standard oral antibiotics.

Further Outpatient Care

• 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.

Deterrence/Prevention

• Treat traumatized skin with mupirocin because this has been shown to decrease the rates of impetigo spread.
• Evaluate hospital nursery staff and household members for pyodermas or asymptomatic bacterial carrier states.
• 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.
• 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.
• Advise patients about improving environmental conditions through the addition of air conditioning and by keeping surroundings clean.

Complications

• Rarely, lesions resolve with scarring and postinflammatory hyperpigmentation or hypopigmentation.
• Bullous impetigo
• • Cellulitis, lymphangitis, bacteremia with subsequent pneumonitis, septic arthritis, and septicemia may develop. This would require hospitalization with intravenous antibiotic therapy.
  • 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.
• Nonbullous impetigo
• • Acute glomerulonephritis develops in 2-5% of individuals with impetigo due to GABHS, most often in 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. Transient proteinuria and hematuria may occur during impetigo and resolve before renal involvement develops. Antibiotic treatment will not prevent the development of glomerulonephritis, but will limit the spread of the disease to other individuals.
  • Ecthyma, a deep dermal infection, can result, after which subsequent scarring can occur. Scarlet fever, erysipelas, cellulitis, lymphangitis, and, rarely, bacterial endocarditis may also develop.

Prognosis

• Spontaneous healing rarely occurs. If left untreated, some lesions may resolve spontaneously, while new lesions appear elsewhere on the body.
• Resolution of lesions usually occurs after 7-10 days of treatment. If lesions have not resolved within 7-10 days of antibiotic therapy, cultures should be performed to look for resistant organisms.

Patient Education

• Children can return to daycare or school once lesions are resolved. Caretakers should be instructed about hygienic issues and prevention.
• For excellent patient education resources, visit eMedicine's Bacterial and Viral Infections Center and Skin, Hair, and Nails Center. Also, see eMedicine's patient education articles Impetigo, Skin Rashes in Children, and Antibiotics.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Failure to evaluate hospital nursery staff for active impetigo lesions or carrier states if indicated
• Failure to check patient blood pressure for hypertension and urine for hematuria or proteinuria as a screen for poststreptococcal glomerulonephritis

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  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.
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Media file 2:  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.
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Media file 3:  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.
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Media file 4:  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.
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Media file 5:  Nonbullous impetigo resulting from an infected insect bite. See Image 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.
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Media file 6:  Group A beta-hemolytic streptococci pure culture from a lesion of nonbullous impetigo resulting from an infected insect bite. See Image 5. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.
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Media file 7:  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.
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Media file 8:  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.
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Media file 9:  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.
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REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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Article Last Updated: Jan 24, 2007