eMedicine Specialties > Dermatology > Bacterial Infections

Impetigo

Author: Anne E Burdick, MD, MPH, Professor, Department of Dermatology, Director of Telemedicine Program, University of Miami Miller School of Medicine
Coauthor(s): Ivan D Camacho, MD, Fellow, Department of Dermatology and Cutaneous Surgery, University of Miami, Miller School of Medicine
Contributor Information and Disclosures

Updated: Jul 15, 2008

Introduction

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,¹ 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.² 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

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.

• Search for CME/CE on This Topic »

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