Impetigo Clinical Presentation

  • Author: Lisa S Lewis, MD; Chief Editor: Russell W Steele, MD   more...
 
Updated: Oct 27, 2011
 

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,[25] 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.[26] 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
Next

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.

Images of nonbullous impetigo are shown below.

Following dermabrasion, this patient developed nonFollowing dermabrasion, this patient developed nonbullous impetigo in the same area as several herpes simplex lesions. Nonbullous (crusted) impetigo resulting from a chiNonbullous (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 gNonbullous 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-hemoNonbullous 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. Nonbullous impetigo resulting from an infected insNonbullous 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 fGroup 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.

Bullous impetigo

Bullous impetigo affects neonates most frequently. However, the infection also occurs in older children and adults.[1] 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.[3]

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.

Images of bullous impetigo are shown below.

Bullous impetigo on the buttocks. Courtesy of MediBullous impetigo on the buttocks. Courtesy of Medical University of South Carolina, Department of Dermatology. Bullous impetigo caused by Staphylococcus aureus. 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 aftPeripheral 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.
Previous
Next

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
  • Osteomyelitis
  • Septic arthritis
  • Septicemia
  • Guttate psoriasis
  • Cellulitis
  • Erysipelas
  • Erythema multiforme
  • Urticaria
Previous
Proceed to Differential Diagnoses
 
 
Contributor Information and Disclosures
Author

Lisa S Lewis, MD  Consulting Staff, Division of Emergency Medicine, Cincinnati Children's Hospital Medical Center

Lisa S Lewis, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Coauthor(s)

Allan D Friedman, MD, MPH  Chairman, Division of General Pediatrics, VCUH Health System; Professor of Pediatrics, Virginia Commonwealth University School of Medicine

Allan D Friedman, MD, MPH is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD  Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Sadegh Amini, MD Senior Clinical Research Fellow, Skin Research Group, Department of Dermatology and Cutaneous Surgery, Miller School of Medicine, University of Miami

Sadegh Amini, MD is a member of the following medical societies: American Society for Dermatologic Surgery, International Society for Dermatologic Surgery, and International Society of Dermatology

Disclosure: Nothing to disclose.

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

Anne E Burdick, MD, MPH is a member of the following medical societies: Women's Dermatologic Society

Disclosure: Nothing to disclose.

Ivan D Camacho, MD, Assistant Professor of Clinical Dermatology, Department of Dermatology and Cutaneous Surgery, University of Miami, Leonard M Miller School of Medicine; Medical Director of Dermatology Clinic, Jackson Memorial

Ivan D Camacho, MD is amember of American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Florida Medical Association, International Society of Dermatology, and the Women's Dermatologic Society.

Disclosure: Nothing to disclose.

Burke A Cunha, MD Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Joseph Domachowske, MD Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York Upstate Medical University

Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Pamela L Dyne, MD Professor of Clinical Medicine/Emergency Medicine, David Geffen School of Medicine at UCLA; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center

Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Dirk M Elston, MD Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Glenn J Fennelly, MD, MPH Director, Division of Pediatric Infectious Diseases, Jacobi Medical Center; Associate Professor, Department of Pediatrics, Albert Einstein College of Medicine

Glenn J Fennelly, MD, MPH is a member of the following medical societies: Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Eric M Kardon, MD, FACEP Attending Emergency Physician, Georgia Emergency Medicine Specialists; Physician, Division of Emergency Medicine, Athens Regional Medical Center

Eric M Kardon, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Paul Krusinski, MD Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Andrew C Miller, MD Fellow, Department of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh Medical Center; Attending Physician, Department of Emergency Medicine, University of Pittsburgh Medical Center

Andrew C Miller, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

James J Nordlund, MD Professor Emeritus, Department of Dermatology, University of Cincinnati College of Medicine

James J Nordlund, MD is a member of the following medical societies: American Academy of Dermatology, Sigma Xi, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Rashid M Rashid, MD, PhD Resident Physician, Department of Dermatology, University of Texas, Houston, MD Anderson Cancer Center, and Morzak Research Initiative

Rashid M Rashid, MD, PhD is a member of the following medical societies: American Academy of Dermatology, Council for Nail Disorders, Houston Dermatological Society, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

John Ratz, MD, MBA Staff Dermatologist, Mohs Surgeon, Center for Dermatology and Skin Surgery, Inc

John Ratz, MD, MBA is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Micrographic Surgery and Cutaneous Oncology, American College of Physicians, American Society for Dermatologic Surgery, American Society for Laser Medicine and Surgery, International Society for Dermatologic Surgery, and Southern Medical Association

Disclosure: Nothing to disclose.

Gregory William Rutecki, MD Associate Professor, Program Director, Department of Internal Medicine, Feinberg School of Medicine, Northwestern University

Gregory William Rutecki, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Nephrology, National Kidney Foundation, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Mark A Silverberg, MD, FACEP, MMB Assistant Professor, Assistant Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate at Brooklyn

Mark A Silverberg, MD, FACEP, MMB is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Daniel B Ward Jr, MD Clinical Assistant Professor, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina

Daniel B Ward Jr, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, and South Carolina Medical Association

Disclosure: Nothing to disclose.

Eric L Weiss, MD, DTM&H Director of Stanford Travel Medicine, Medical Director of Stanford Lifeflight, Assistant Professor, Departments of Emergency Medicine and Infectious Diseases, Stanford University School of Medicine

Eric L Weiss, MD, DTM&H is a member of the following medical societies: American College of Emergency Physicians, American College of Occupational and Environmental Medicine, American Medical Association, American Society of Tropical Medicine and Hygiene, Physicians for Social Responsibility, Southeastern Surgical Congress, Southern Association for Oncology, Southern Clinical Neurological Society, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Michael J Wells, MD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

References

  1. Cole C, Gazewood J. Diagnosis and treatment of impetigo. Am Fam Physician. Mar 15 2007;75(6):859-64. [Medline].

  2. Moulin F, Quinet B, Raymond J, Gillet Y, Cohen R. [Managing children skin and soft tissue infections]. Arch Pediatr. Oct 2008;15 Suppl 2:S62-7. [Medline].

  3. Hirschmann JV. Impetigo: etiology and therapy. Curr Clin Top Infect Dis. 2002;22:42-51. [Medline].

  4. 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].

  5. Kuniyuki S, Nakano K, Maekawa N, Suzuki S. Topical antibiotic treatment of impetigo with tetracycline. J Dermatol. Oct 2005;32(10):788-92. [Medline].

  6. Treating impetigo in primary care. Drug Ther Bull. Jan 2007;45(1):2-4. [Medline].

  7. Broccardo CJ, Mahaffey S, Schwarz J, et al. Comparative proteomic profiling of patients with atopic dermatitis based on history of eczema herpeticum infection and Staphylococcus aureus colonization. J Allergy Clin Immunol. Jan 2011;127(1):186-93, 193.e1-11. [Medline]. [Full Text].

  8. 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].

  9. Daskalaki M, Rojo P, Marin-Ferrer M, Barrios M, Otero JR, Chaves F. Panton-Valentine leukocidin-positive Staphylococcus aureus skin and soft tissue infections among children in an emergency department in Madrid, Spain. Clin Microbiol Infect. Jan 2010;16(1):74-7. [Medline].

  10. Geria AN, Schuartz RA. Impetigo Update: New Challenges in the Era of Methicillin Resistance. Cutis. 2010;85(2):65-70.

  11. Geng W, Yang Y, Wu D, et al. Molecular characteristics of community-acquired, methicillin-resistant Staphylococcus aureus isolated from Chinese children. FEMS Immunol Med Microbiol. Apr 2010;58(3):356-62. [Medline].

  12. Liu Y, Kong F, Zhang X, Brown M, Ma L, Yang Y. Antimicrobial susceptibility of Staphylococcus aureus isolated from children with impetigo in China from 2003 to 2007 shows community-associated methicillin-resistant Staphylococcus aureus to be uncommon and heterogeneous. Br J Dermatol. Dec 2009;161(6):1347-50. [Medline].

  13. 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].

  14. Koning S, Verhagen AP, van Suijlekom-Smit LW, et al. Interventions for impetigo. Cochrane Database Syst Rev. 2004;CD003261. [Medline].

  15. Razmjou RG, Willemsen SP, Koning S, et al. Determinants of regional differences in the incidence of impetigo. Environ Res. Jul 2009;109(5):590-3. [Medline].

  16. Spurling G, Askew D, King D, Mitchell GK. Bacterial skin infections--an observational study. Aust Fam Physician. Jul 2009;38(7):547-51. [Medline].

  17. Patrizi A, Raone B, Savoia F, Ricci G, Neri I. Recurrent toxin-mediated perineal erythema: eleven pediatric cases. Arch Dermatol. Feb 2008;144(2):239-43. [Medline].

  18. 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]. [Full Text].

  19. 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].

  20. 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].

  21. Brown J, Shriner DL, Schwartz RA, Janniger CK. Impetigo: an update. Int J Dermatol. Apr 2003;42(4):251-5. [Medline].

  22. 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]. [Full Text].

  23. Mancini AJ. Bacterial skin infections in children: the common and the not so common. Pediatr Ann. Jan 2000;29(1):26-35. [Medline].

  24. American Academy of Pediatrics. Group A Streptococcal infections. In: Pickering LK, Baker CJ, Kimberlin DW, Long SS, eds. Red Book: 2009 Report of the Committee on Infectious Diseases. 28th ed. Elk Grove Village, Ill: American Academy of Pediatrics; 2009:616-28.

  25. Ludlam H, Cookson B. Scrum kidney: epidemic pyoderma caused by a nephritogenic Streptococcus pyogenes in a rugby team. Lancet. Aug 9 1986;2(8502):331-3. [Medline].

  26. 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].

  27. Sarabi K, Khachemoune A. Tinea capitis: a review. Dermatol Nurs. Dec 2007;19(6):525-9; quiz 530. [Medline].

  28. Popovich D, McAlhany A. Accurately diagnosing commonly misdiagnosed circular rashes. Dermatol Nurs. Aug 2008;20(4):294-300. [Medline].

  29. Gorani A, Oriani A, Cambiaghi S. Seborrheic dermatitis-like tinea faciei. Pediatr Dermatol. May-Jun 2005;22(3):243-4. [Medline].

  30. Hayakawa K, Hirahara K, Fukuda T, Okazaki M, Shiohara T. Risk factors for severe impetiginized atopic dermatitis in Japan and assessment of its microbiological features. Clin Exp Dermatol. Jul 2009;34(5):e63-5. [Medline].

  31. Rashid R, Hymes S. Folliculitis, follicular mucinosis, and papular mucinosis as a presentation of chronic myelomonocytic leukemia. Dermatol Online J. May 15 2009;15(5):16. [Medline].

  32. Scheinfeld N. A Primer In Topical Antibiotics For The Skin And Eyes. J Drugs Dermatol. 2008;7(4):409-415.

  33. 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].

  34. 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].

  35. Silverberg N, Block S. Uncomplicated skin and skin structure infections in children: diagnosis and current treatment options in the United States. Clin Pediatr (Phila). Apr 2008;47(3):211-9. [Medline].

  36. Koning S, van der Wouden JC, Chosidow O, et al. Efficacy and safety of retapamulin ointment as treatment of impetigo: randomized double-blind multicentre placebo-controlled trial. Br J Dermatol. May 2008;158(5):1077-82. [Medline].

  37. Jacobs MR. Retapamulin: a semisynthetic pleuromutilin compound for topical treatment of skin infections in adults and children. Future Microbiol. Dec 2007;2(6):591-600. [Medline].

  38. Jones RS. Expert advice on erasing the MRSA threat. Pract Dermatol. 2005;34-7.

  39. Woodford N, Afzal-Shah M, Warner M, Livermore DM. In vitro activity of retapamulin against Staphylococcus aureus isolates resistant to fusidic acid and mupirocin. J Antimicrob Chemother. Oct 2008;62(4):766-8. [Medline].

  40. Boyd B, Castañar J. Retapamulin. Drugs Future. 2006;31:107.

  41. 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].

  42. Drug and Therapeutics Bulletin. Retapamulin for impetigo and other infections. Drug Ther Bull. Oct 2008;46(10):76-9. [Medline].

  43. 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].

  44. 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]. [Full Text].

  45. 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].

  46. Alsterholm M, Flytström I, Bergbrant IM, Faergemann J. Fusidic acid-resistant Staphylococcus aureus in impetigo contagiosa and secondarily infected atopic dermatitis. Acta Derm Venereol. 2010;90(1):52-7. [Medline].

  47. Gelmetti C. Local antibiotics in dermatology. Dermatol Ther. May-Jun 2008;21(3):187-95. [Medline].

  48. 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].

  49. 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].

  50. Groner A, Laing-Grayman D, Silverberg NB. Outpatient pediatric community-acquired methicillin-resistant Staphylococcus aureus: a polymorphous clinical disease. Cutis. Feb 2008;81(2):115-22. [Medline].

  51. Bernard P. Management of common bacterial infections of the skin. Curr Opin Infect Dis. Apr 2008;21(2):122-8. [Medline].

  52. 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].

  53. Deshpande LM, Fix AM, Pfaller MA, Jones RN. Emerging elevated mupirocin resistance rates among staphylococcal isolates in the SENTRY Antimicrobial Surveillance Program (2000): correlations of results from disk diffusion, Etest and reference dilution methods. Diagn Microbiol Infect Dis. Apr 2002;42(4):283-90. [Medline].

 
Previous
Next
 
Nonbullous impetigo with vesicles, pustules, and sharply demarcated regions of honey-colored crusts.
Bullous impetigo with circumscribed lesions with a thin collarette of scale.
Bullous impetigo on the buttocks. Courtesy of Medical University of South Carolina, Department of Dermatology.
Following dermabrasion, this patient developed nonbullous impetigo in the same area as several herpes simplex lesions.
A nummular eczema lesion on the knee, impetiginized with Staphylococcus aureus.
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.
Streptococcal impetigo from an infected insect bite. Courtesy of Professor David Taplin, Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, Miami, Fla.
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.
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.
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.
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.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.