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Judith D. Laval, MD


Impetigo is a common, contagious, superficial skin infection that is produced by streptococci, staphylococci, or a combination of both bacteria. There are two different clinical presentations: bullous impetigo and nonbullous impetigo. Both begin as vesicles with a very thin, fragile roof consisting only of stratum corneum. Bullous impetigo is primarily a staphylococcal disease. Nonbullous impetigo was once thought to be primarily a streptococcal disease, but staphylococci are isolated from the majority of lesions in both bullous and nonbullous impetigo. S. aureus is now known to be the primary pathogen in both bullous and nonbullous impetigo.

Children in close physical contact with each other have a higher rate of infection than do adults. Symptoms of itching and soreness are mild; systemic symptoms are infrequent. Impetigo may occur after a minor skin injury such as an insect bite, but it most frequently develops on apparently unimpaired skin. The disease is self-limiting, but when untreated it may last for weeks or months. Poststreptococcal glomerulonephritis may follow impetigo. Rheumatic fever has not been reported as a complication of impetigo.

Bullous impetigo

Bullous impetigo (staphylococcal impetigo) is caused by an epidermolytic toxin produced at the site of infection, most commonly by staphylococci of phage Group II, and usually is not secondarily contaminated by streptococci. The toxin causes intraepidermal cleavage below or within the stratum granulosum.

Clinical manifestations.

Bullous impetigo is most common in infants and children but may occur in adults. It typically occurs on the face, but it may infect any body surface. There may be a few lesions localized in one area, or the lesions may be so numerous and widely scattered that they resemble poison ivy. One or more vesicles enlarge rapidly to form bullae in which the contents turn from clear to cloudy. The center of the thin-roofed bulla collapses, but the peripheral area may retain fluid for many days in an inner tube-shaped rim. A thin, flat, honey-colored, "varnishlike" crust may appear in the center and, if removed, discloses a bright red, inflamed, moist base that oozes serum. The center may dry without forming a crust, leaving a red base with a rim of scale. In most cases, a tinea-like scaling border replaces the fluid-filled rim as the round lesions enlarge and become contiguous with the others.  The border dries and forms a crust. The lesions have little or no surrounding erythema. In some untreated cases, lesions may extend radially and retain a narrow, bullous, inner tube rim. These individual lesions reach 2 to 8 cm and then cease to enlarge, but they may remain for months. Thick crust accumulates in these longer lasting lesions. Lesions heal with hyperpigmentation in black patients. Regional lymphadenitis is uncommon with pure staphylococcal impetigo. There is some evidence that the responsible staphylococci colonize in the nose and then spread to normal skin prior to infection.

Serious secondary infections (e.g., osteomyelitis, septic arthritis, and pneumonia) may follow seemingly innocuous superficial infections in infants.

Nonbullous impetigo

Nonbullous impetigo originates as a small vesicle or pustule that ruptures to expose a red, moist base. A honey
yellow to white-brown, firmly adherent crust accumulates
as the lesion extends radially. There is little surrounding erythema. Satellite lesions appear beyond the periphery. The lesions are generally asymptomatic. The skin around the nose and mouth and the limbs are the sites most commonly affected. The palms and soles are not affected. Untreated cases last for weeks and may extend in a continuous manner to involve a wide area. Most cases heal without scarring. The sequence of events leading to nonbullous impetigo is exposure to the infectious agent, carriage on exposed normal skin, and finally skin infection after a minor trauma that is aggravated by scratching. The infecting strain has been found on normal skin surfaces 2 or more weeks prior to the appearance of lesions.

Intact skin is resistant to colonization or infection with group A beta-hemolytic streptococci, but skin injury by insect bites, abrasions, lacerations, and burns allows the streptococci to invade. A pure culture of group A beta-hemolytic streptococci may sometimes be isolated from early lesions, but most lesions promptly become contaminated with staphylococci. Regional lymphadenopathy
is common. The reservoirs for streptococcus infection include the unimpaired normal skin or the lesions of other individuals rather than the respiratory tract. Children ages 2 to 5 years commonly have streptococcal impetigo.Warm, moist climates and poor hygiene are predisposing factors. The antistreptolysin O (ASO) titer does not rise to a significant level following impetigo. Anti-DNAase B rises to high levels and is a much more sensitive indicator of streptococcal impetigo.

Acute nephritis

Acute nephritis tends to occur when many individuals in a family have impetigo. Most cases occur in the southern part of the United States. Infants under 1˝years of age are rarely affected by nephritis following impetigo. The highest incidence of nephritis following impetigo is in children between 2 and 4 years of age. After the appearance of the skin lesions, the anterior nares and, possibly later, the pharynx are colonized with streptococci responsible for the skin infection. The streptococci responsible for impetigo are of different strains than those causing pharyngeal infections. The latent period between the acquisition of a nephritogenic streptococcus in skin lesions and the onset of acute nephritis varies between 1 and 5 weeks and averages 10 days. The overall incidence of acute nephritis with impetigo varies between 2% and 5%, but, in the presence of a nephritogenic strain of streptococcus, the rate varies between 10% and 15%. During the initial streptococcal infection, hematuria and proteinuria may be found in approximately one third of the patients. The urinary findings disappear for several days before development of poststreptococcal acute glomerulonephritis.

The overall incidence and clinical features of acute nephritis are as follows. Hematuria occurs in 90% of patients. Gross hematuria occurs in 25% of patients, followed by microscopic hematuria with erythrocyte casts and proteinuria that last for a variable time. Edema occurs in the majority of patients; the degree varies with the amount of dietary sodium. In the early morning, there is periorbital edema and lower extremity swelling. Hypertension occurs in 60% of patients; adults have moderate elevation of 160/100 mm Hg; children are close to normal. The degree varies with dietary sodium. Cerebral symptoms (headache and disturbance of consciousness), congestive heart failure, and acute renal failure are less common.

Laboratory findings

After impetigo, ASO titer elevations are low or absent, but anti-DNAase B and antihyaluronidase increase significantly. Total serum complement activity is low during the initial stages of acute nephritis. The C3 level parallels the total serum complement. The sedimentation rate parallels the activity of the disease. C-reactive protein is usually normal. Cultures of the pharynx and any skin lesion should be made and the serotype of the group A streptococcus that is responsible should be determined by typing with M-group and T-type antisera. M-T serotypes associated with acute nephritis are 2, 49, 55, 57, and 60.

Acute nephritis heals without therapeutic intervention. Symptoms and signs such as hypertension should be managed as they occur.

Prevention of impetigo

Mupirocin (Bactroban) or Triple antibiotic ointment, containing bacitracin, polysporin, and neomycin, applied three times daily to sites of minor skin trauma (e.g., mosquito bites and abrasions) can be efficacious as a preventative treatment.

Recurrent impetigo

Patients with recurrent impetigo should be evaluated for carriage of S. aureus. The nares are the most common sites of carriage, but the perineum, axillae, and toe webs may also be colonized. Mupirocin ointment (Bactroban) applied to the nares twice each day for 5 days significantly reduces S. aureus carriage in the nose and hands at 3 days and in the nasal carriage for as long as 1 year.

Treatment of impetigo

Impetigo may resolve spontaneously or become chronic and widespread. Studies show that 2% mupirocin ointment is as safe and effective as oral erythromycin in the treatment of patients with impetigo. Local treatment does not treat lesions that evolve in other areas. Infected children should be briefly isolated until treatment is under way.

Oral antibiotics.

Because some cases of impetigo have a mixed infection of staphylococci and streptococci, penicillin is inadequate for treatment. A 5- to 10-day course of an oral antibiotic such as cloxacillin, dicloxacillin, or cephalexin induces rapid healing. Erythromycin may not be as effective because strains of resistant staphylococci are appearing in some areas. Azithromycin given over 5 days as a once-a-day regimen (500 mg on day 1, 250 mg on days 2 through 5) is as effective and better tolerated than either erythromycin or cloxacillin. Short-course therapy also may improve patient compliance. 

Mupirocin (Bactroban).

Mupirocin ointment is the first topical antibiotic approved for the treatment of impetigo. It is active against staphylococci (including methicillin-resistant strains) and streptococci. The drug is not active against Enterobacteriaceae, Pseudomonas aeruginosa, or fungi. It is as effective as oral antibiotics and is associated with fewer adverse effects. In superficial skin infections that are not widespread, mupirocin ointment offers several advantages. It is highly active against the most frequent skin pathogens, even those resistant to other antibiotics, and the topical route of administration allows delivery of high drug concentrations to the site of infection. Mupirocin is applied three times a day until all lesions have cleared. If topical treatment is elected, then it might be worthwhile to wash the involved areas once or twice a day with an antibacterial soap such as Hibiclens or Betadine. Washing the entire body with these soaps may prevent recurrence at distant sites. Crusts should be removed because they block the penetration of antibacterial creams. To facilitate removal, crusts are softened by soaking with a wet cloth compress.