http://emedicine.medscape.

com/article/1052709-overview

Impetigo
Author: Sadegh Amini, MD, Senior Clinical Research Fellow, Skin Research Group,
Department of Dermatology and Cutaneous Surgery, Miller School of Medicine, University of
Miami
Coauthor(s): 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
Contributor Information and Disclosures

Updated: Sep 8, 2009

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Introduction
Background

Impetigo is a highly contagious gram-positive bacterial infection of the superficial layers of the
epidermis. The 2 forms of impetigo 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. An increasing number of gentamicin-resistant S aureus
strains have also been reported as a cause of impetigo.1

Evidence from 2005 indicates that S aureus is the most prevalent pathogen of both bullous
impetigo and nonbullous impetigo in the United States and Europe,2 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.

Other eMedicine articles on impetigo include Impetigo (Emergency Medicine),

Impetigo (Infectious Diseases), and Impetigo (Pediatrics).

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 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 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. Common mechanisms for secondarily
acquiring the bacterial infection include scratching, which can produce excoriations and rupture
of blisters. Associated conditions may include atopic dermatitis, dermatophytosis, varicella,
herpes simplex, scabies, pediculosis,3 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.

Patients with atopic dermatitis, particularly with history of eczema herpeticum, are at higher risk
of developing an infection caused by MRSA. A current pilot study is being conducted to
determine the underlying mechanisms for S aureus skin infections in patients with atopic
dermatitis with and without history of eczema herpeticum. Results are expected by December
2009.4

Once infection is present, new lesions may develop despite a lack of 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, exfoliative toxin D (ETD) was identified in 10% of S aureus isolates.5 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.

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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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.

Nonbullous impetigo

Nonbullous impetigo is the most frequent form of impetigo and occurs in

approximately 70% of children younger than 15 years with the infection.6 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.

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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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.

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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.

[ CLOSE WINDOW ]
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.

Frequency

United States

Impetigo is a common skin disease, accounting for 10% of skin diseases treated in pediatric
clinics. Impetigo is the most common bacterial skin infection and the third most common skin
disease among children.6 Peak incidence occurs during summer and fall.7

International

British statistics published in 1995 show an annual incidence of impetigo of 2.8% in children age
4 years and younger and 1.69% in children aged 5-15 years. 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 2001.3

Mortality/Morbidity

Most affected individuals recover without complications. One to 5% of individuals with

nonbullous impetigo from streptococcal infections can develop acute poststreptococcal
glomerulonephritis as a very severe complication.8,9 Oral antibiotics may not prevent the
development of renal complications of cutaneous streptococcal infections.

Impetigo can be a complication in patients with chronic renal failure, particularly patients on
dialysis and post renal transplantation.

Less common complications include sepsis, arthritis, osteomyelitis, pneumonia, lymphadenitis,

guttate psoriasis, toxic shock syndrome, and staphylococcal scalded skin syndrome.6,10

Sex

The male-to-female ratio for impetigo 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.

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
autoinoculation.
• 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, scabies, pediculosis, insect bites), 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.
• Primary selective immunoglobulin M (IgM) deficiency has been reported as a
cause of recurrent impetigo in patients with negative S aureus carrier status
and no predisposing factors, such as a preexisting dermatosis.11 Frequent
associations of immunoglobulin A (IgA), IgM, and immunoglobulin G (IgG)
deficiencies have also been reported.
• Impetigo lesions typically heal without scarring.
• If left untreated, impetigo lesions resolve spontaneously after several weeks.
• Adults tend to have a higher risk of complications than children.10,12

Physical

• Bullous impetigo
o Bullous impetigo affects neonates most frequently, but it also occurs in
older children and adults.6
o 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.
o 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.
o Intact bullae are not usually present because they are very fragile.
o When present, intact bullae do not demonstrate a positive Nikolsky
sign.
o Lesions of a primary skin disease, such as atopic dermatitis or
varicella, may be present.
o Lesions may be localized or widely scattered.
o Lesions are often found on intertriginous areas such as neck, axillary
and crural folds, as well as in the diaper area, but they may appear on
the face or anywhere on the body.
o No regional lymphadenopathy is present.
o 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.
o Bullous impetigo is considered to be less contagious than nonbullous
impetigo.13

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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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.

[ CLOSE WINDOW ]

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

o The first noticeable abnormality is a red macule or papule, from 2-5

mm in size.
o 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.
o 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.
o Lesions are located around the nose, mouth, and exposed parts of the
body (eg, arms, legs), sparing the palms and soles.
o Localized lymphadenopathy is usually present, and nodes may be
tender.
o If left untreated, lesions spread by autoinoculation then spontaneously
resolve after a few weeks without scarring.
o 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.
o Patients do not have signs of pharyngitis.

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.

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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 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.

[ CLOSE WINDOW ]

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.

Causes

Impetigo is caused by bacterial infection.

• Bullous impetigo
o Coagulase-positive group II S aureus, most often phage type 71, is the
causative agent.
o Strains are usually resistant to penicillin and may be resistant to
erythromycin.
 o 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
o 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.
o GABHS remains the predominant pathogen in developing populations.
o Groups B, C, and G streptococci are rare causes of nonbullous
impetigo.
o Group B streptococci are associated with impetigo in the newborn.