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.
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.
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.
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, has a pyoderma, or has a skin condition (eg, atopic dermatitis) that predisposes that individual to be an S aureus or streptococcal carrier.
- 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
- Bullous impetigo affects neonates most frequently, but it also occurs in older children and adults.6
- 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 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.
- No regional lymphadenopathy is present.
- 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.
- 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.
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
- 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 without scarring.
- 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.
- 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.
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
- 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 countries.
- Groups B, C, and G streptococci are rare causes of nonbullous impetigo.
- Group B streptococci are associated with impetigo in the newborn.
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References
Kuniyuki S, Nakano K, Maekawa N, Suzuki S. Topical antibiotic treatment of impetigo with tetracycline. J Dermatol. Oct 2005;32(10):788-92. [Medline].
Moran GJ, Amii RN, Abrahamian FM, Talan DA. Methicillin-resistant Staphylococcus aureus in community-acquired skin infections. Emerg Infect Dis. Jun 2005;11(6):928-30. [Medline].
Treating impetigo in primary care. Drug Ther Bull. Jan 2007;45(1):2-4. [Medline].
Leung D. Pilot Study To Determine The Underlying Mechanisms For Infection And Colonization By Staphylococcus Aureus Of The Skin Of Atopic Dermatitis Subjects With And Without A History Of Eczema Herpeticum. ClinicalTrials.gov Identifier: NCT00822276. ClinicalTrials.gov. Available at http://www.clinicaltrials.gov/ct2/show/NCT00822276?term=impetigo&rank=9.. Accessed 06-12-2009.
Yamasaki O, Tristan A, Yamaguchi T, et al. Distribution of the exfoliative toxin D gene in clinical Staphylococcus aureus isolates in France. Clin Microbiol Infect. Jun 2006;12(6):585-8. [Medline].
Cole C, Gazewood J. Diagnosis and treatment of impetigo. Am Fam Physician. Mar 15 2007;75(6):859-64. [Medline].
Loffeld A, Davies P, Lewis A, Moss C. Seasonal occurrence of impetigo: a retrospective 8-year review (1996-2003). Clin Exp Dermatol. Sep 2005;30(5):512-4. [Medline].
Brown J, Shriner DL, Schwartz RA, Janniger CK. Impetigo: an update. Int J Dermatol. Apr 2003;42(4):251-5. [Medline].
George A, Rubin G. A systematic review and meta-analysis of treatments for impetigo. Br J Gen Pract. Jun 2003;53(491):480-7. [Medline].
Mancini AJ. Bacterial skin infections in children: the common and the not so common. Pediatr Ann. Jan 2000;29(1):26-35. [Medline].
Belgemen T, Suskan E, Dogu F, Ikinciogullari A. Selective immunoglobulin M deficiency presenting with recurrent impetigo: a case report and review of the literature. Int Arch Allergy Immunol. 2009;149(3):283-8. [Medline].
Sladden MJ, Johnston GA. Common skin infections in children. BMJ. Jul 10 2004;329(7457):95-9. [Medline].
Hirschmann JV. Impetigo: etiology and therapy. Curr Clin Top Infect Dis. 2002;22:42-51. [Medline].
Scheinfeld N. A Primer In Topical Antibiotics For The Skin And Eyes. J Drugs Dermatol. 2008;7(4):409-415.
Wilkinson RD, Carey WD. Topical mupirocin versus topical neosporin in the treatment of cutaneous infections. Int J Dermatol. Sep 1988;27(7):514-5. [Medline].
Bass JW, Chan DS, Creamer KM, et al. Comparison of oral cephalexin, topical mupirocin and topical bacitracin for treatment of impetigo. Pediatr Infect Dis J. Jul 1997;16(7):708-10. [Medline].
Free AL. Efficacy, Safety and Tolerability of TD1414 2% Cream in Impetigo and Secondarily Infected Traumatic Lesions (SITL). ClinicalTrials.gov Identifier: NCT00626795. ClinicalTrials.gov. Available at http://www.clinicaltrials.gov/ct2/show/NCT00626795?term=impetigo&rank=5.. Accessed 06-12-2009.
Jacobs MR. Retapamulin: a semisynthetic pleuromutilin compound for topical treatment of skin infections in adults and children. Future Microbiol. Dec 2007;2:591-600. [Medline].
Jones RS. Expert advice on erasing the MRSA threat. Pract Dermatol. 2005;34-7.
Boyd B, Castañar J. Retapamulin. Drugs Future. 2006;31:107.
Oranje AP, Chosidow O, Sacchidanand S, et al. Topical retapamulin ointment, 1%, versus sodium fusidate ointment, 2%, for impetigo: a randomized, observer-blinded, noninferiority study. Dermatology. 2007;215(4):331-40. [Medline].
GlaxoSmithKline. A Randomized, Double-Blind, Double Dummy, Comparative, Multicenter Study to Assess the Safety and Efficacy of Topical Retapamulin Ointment, 1%, Versus Oral Linezolid in the Treatment of Secondarily-Infected Traumatic Lesions and Impetigo Due to Methicillin-Resistant Staphylococcus Aureus. ClinicalTrials.gov identifier: NCT00852540. ClinicalTrials.gov. Available at http://www.clinicaltrials.gov/ct2/show/NCT00852540?term=impetigo&rank=3.. Accessed 06-12-2009.
Drug and Therapeutics Bulletin. Retapamulin for impetigo and other infections. Drug Ther Bull. Oct 2008;46(10):76-9. [Medline].
Denton M, O'Connell B, Bernard P, Jarlier V, Williams Z, Henriksen AS. The EPISA study: antimicrobial susceptibility of Staphylococcus aureus causing primary or secondary skin and soft tissue infections in the community in France, the UK and Ireland. J Antimicrob Chemother. Mar 2008;61(3):586-8. [Medline].
O'Neill AJ, Larsen AR, Skov R, Henriksen AS, Chopra I. Characterization of the epidemic European fusidic acid-resistant impetigo clone of Staphylococcus aureus. J Clin Microbiol. May 2007;45(5):1505-10. [Medline].
Laurent F, Tristan A, Croze M, et al. Presence of the epidemic European fusidic acid-resistant impetigo clone (EEFIC) of Staphylococcus aureus in France. J Antimicrob Chemother. Feb 2009;63(2):420-1; author reply 421. [Medline].
Gelmetti C. Local antibiotics in dermatology. Dermatol Ther. May-Jun 2008;21(3):187-95. [Medline].
Langner A, Chu A, Goulden V, Ambroziak M. A randomized, single-blind comparison of topical clindamycin + benzoyl peroxide and adapalene in the treatment of mild to moderate facial acne vulgaris. Br J Dermatol. Jan 2008;158(1):122-9. [Medline].
Capizzi R, Landi F, Milani M, Amerio P. Skin tolerability and efficacy of combination therapy with hydrogen peroxide stabilized cream and adapalene gel in comparison with benzoyl peroxide cream and adapalene gel in common acne. A randomized, investigator-masked, controlled trial. Br J Dermatol. Aug 2004;151(2):481-4. [Medline].
[Guideline] Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. Nov 15 2005;41(10):1373-406. [Medline].
Yang LP, Keam SJ. Retapamulin: a review of its use in the management of impetigo and other uncomplicated superficial skin infections. Drugs. 2008;68(6):855-73. [Medline].
Aly R. The pathogenic staphylococci. Semin Dermatol. Dec 1990;9(4):292-9. [Medline].
Blume JE, Levine EG, Heymann WR. Bacterial diseases. In: Bolognia JL, Jorizzo JL, Rapini RP. Dermatology. Vol 1. London: Mosby; 2003:1117-8.
Burd R. Impetigo. In: Lebwohl MG, Heymann WR , Berth-Jones J, et al. Treatment of Skin Disease: Comprehensive Therapeutic Strategies. London: Mosby; 2006:299-300.
Cohen PR, Kurzrock R. Community-acquired methicillin-resistant Staphylococcus aureus skin infection: an emerging clinical problem. J Am Acad Dermatol. Feb 2004;50(2):277-80. [Medline].
Dagan R. Impetigo in childhood: changing epidemiology and new treatments. Pediatr Ann. Apr 1993;22(4):235-40. [Medline].
Dagan R, Bar-David Y. Double-blind study comparing erythromycin and mupirocin for treatment of impetigo in children: implications of a high prevalence of erythromycin-resistant Staphylococcus aureus strains. Antimicrob Agents Chemother. Feb 1992;36(2):287-90. [Medline].
Darmstadt GL, Lane AT. Impetigo: an overview. Pediatr Dermatol. Dec 1994;11(4):293-303. [Medline].
Dillon HC Jr. Impetigo contagiosa: suppurative and non-suppurative complications. I. Clinical, bacteriologic, and epidemiologic characteristics of impetigo. Am J Dis Child. May 1968;115(5):530-41. [Medline].
Eichenfield LF, Carney PS, Chow MJ, Tal A, Weinberg JM, Yurko M. Unique approaches for the topical treatment and prevention of cutaneous infections: report from a clinical roundtable. Cutis. Aug 2004;74(2 Suppl):2-23. [Medline].
Galin WK, Cohen I, Rogers M, Smith MHD. Bacterial infections. In: Schachner LA, Hansen RC. Pediatric Dermatology. 2nd ed. New York, NY: Churchill Livingstone; 1995:1169-72.
Habif TB. Clinical Dermatology: A Color Guide to Diagnosis and Therapy. 3rd ed. St. Louis, Mo: Mosby-Year Book; 1996:236-41.
Kluytmans-Vandenbergh MF, Kluytmans JA. Community-acquired methicillin-resistant Staphylococcus aureus: current perspectives. Clin Microbiol Infect. Mar 2006;12 Suppl 1:9-15. [Medline].
Koning S, Mohammedamin RS, van der Wouden JC, van Suijlekom-Smit LW, Schellevis FG, Thomas S. Impetigo: incidence and treatment in Dutch general practice in 1987 and 2001--results from two national surveys. Br J Dermatol. Feb 2006;154(2):239-43. [Medline].
Koning S, Verhagen AP, van Suijlekom-Smit LW, Morris A, Butler CC, van der Wouden JC. Interventions for impetigo. Cochrane Database Syst Rev. 2004;CD003261. [Medline].
Lee PK, Weinberg AN, Suritz MN, Johnson RA. Pyodermas: Staphylococcus aureus, Streptococcus, and other gram-positive bacteria. In: Freedberg IM, Goldsmith LA, Eisen AZ, et al. Fitzpatrick's Dermatology in General Medicine. 5th ed. New York, NY: McGraw-Hill; 1999:2182-5; 2194-6.
Lucas S. Bacterial diseases. In: Elder D, Elenitsas R, Jaworsky C, Johnson JB. Lever's Histopathology of the Skin. 8th ed. Philadelphia, Pa: Lippincott-Raven; 1997:457-502.
Sadick NS. Bacterial diseases of the skin. In: Rakel RE. Conn's Current Therapy. Philadelphia, Pa: WB Saunders; 1997:823-8.
Sadick NS. Current aspects of bacterial infections of the skin. Dermatol Clin. Apr 1997;15(2):341-9. [Medline].
Sanfilippo AM, Barrio V, Kulp-Shorten C, Callen JP. Common pediatric and adolescent skin conditions. J Pediatr Adolesc Gynecol. Oct 2003;16(5):269-83. [Medline].
Shriner DL, Schwartz RA, Janniger CK. Impetigo. Cutis. Jul 1995;56(1):30-2. [Medline].
Siberry GK. Fighting a rising tide of MRSA infection in the young. Contemp Pediatr. 2005;22:44-53.
Taylor JS. Interventions for impetigo. Am Fam Physician. Nov 1 2004;70(9):1680-1. [Medline].
Williams RE, MacKie RM. The staphylococci. Importance of their control in the management of skin disease. Dermatol Clin. Jan 1993;11(1):201-6. [Medline].
Further Reading
Keywords
impetigo, impetigo contagiosa, Fox impetigo, impetigo bullosa, impetigo contagiosa bullosa, impetigo neonatorum
