Impetigo Clinical Presentation

Updated: May 04, 2016
  • Author: Lisa S Lewis, MD; Chief Editor: Russell W Steele, MD  more...
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Presentation

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, [28] 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. [29] 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:

  • Fever
  • Diarrhea
  • Generalized weakness
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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.

The image below depicts nonbullous impetigo.

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

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. [5]

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.

The image below depicts bullous impetigo.

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

  • Scarlet fever
  • Staphylococcal scalded skin syndrome (SSSS)
  • Osteomyelitis
  • Septic arthritis
  • Septicemia
  • Guttate psoriasis
  • Cellulitis
  • Erysipelas
  • Erythema multiforme
  • Urticaria
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