Impetigo Medication

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

Medication Summary

Topical antibiotics, systemic antibiotics, or a combination of both is effective therapy for impetigo. Empiric bacterial coverage is aimed at eradicating Staphylococcus aureus and group A beta-hemolytic streptococci (GABHS; also known as Streptococcus pyogenes). Antihistamines may be prescribed for symptomatic relief in patients with pruritus.

Mupirocin applied topically has been shown to be effective for localized impetigo, but resistance has emerged. Retapamulin is a new option.[42, 52] Bacitracin is no longer recommended as it is not as efficacious and causes frequent allergic skin reactions and occasional-to-rare anaphylaxis.[47]

The advantages of topical antibiotics include the following[47] :

  • Low risk of systemic adverse events
  • Higher concentration of the antibiotic when applied to the affected area
  • Smaller amount of drug is used
  • Lack of effect on intestinal florae
  • Low cost
  • Ease of administration to a young child

The disadvantages of topical antibiotics include the following[47] :

  • Potential production of irritant and allergic contact dermatitis
  • Decreased penetration in the affected area
  • Potential rapid appearance of bacterial resistance
  • Potential alteration of cutaneous flora
  • Potential systemic absorption and consequent toxic effects

Systemic antibiotic treatment is indicated for widespread infections, complicated infections, or those associated with systemic manifestations. A cephalosporin, semisynthetic penicillin, or beta-lactam/beta-lactamase inhibitor combination is generally suitable for first-line therapy.

Methicillin-resistant Staphylococcus aureus (MRSA) should be suspected in cases of spontaneous abscess or cellulitis and in lesions that do not resolve with traditional antimicrobial therapy, in which case alternative antibiotics should be considered. These include trimethoprim-sulfamethoxazole, tetracycline, clindamycin, fluoroquinolones, and linezolid.

In areas with a high percentage of community-acquired MRSA, the empiric antibiotic choice should provide coverage for this possibility.

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Topical Antimicrobials

Class Summary

Topical antibiotic treatment with mupirocin is the treatment of choice for uncomplicated localized pyoderma, although S aureus resistance to mupirocin has been increasing.[53]

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Mupirocin (Bactroban, Centany)

 

Mupirocin is a naturally occurring antibiotic produced by fermentation of Pseudomonas fluorescens. The mechanism of action of mupirocin is via inhibition of bacterial protein synthesis.

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Retapamulin (Altabax)

 

Retapamulin is a topical antibiotic available as a 1% ointment. It is the first of a new antibiotic class called pleuromutilins. This agent inhibits protein synthesis by binding to the 50S subunit on the ribosome. It is indicated for impetigo caused by S aureus or Streptococcus pyogenes.

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Antibiotics, Other

Class Summary

Systemic antibiotic treatment is indicated for widespread or complicated pyoderma.

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Amoxicillin and clavulanate (Augmentin)

 

This oral antibiotic combines the broad-spectrum antibiotic amoxicillin with the beta-lactamase inhibitor clavulanate. Amoxicillin inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins, while clavulanate inhibits beta-lactamase producing bacteria.

For children older than 3 months, dosing is based on the amoxicillin content. Because of different amoxicillin-clavulanate ratios in the 250-mg tab (250mg/125mg) versus the 250-mg chewable tab (250mg/62.5mg), do not use the 250-mg tab until the child weighs more than 40 kg.

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Dicloxacillin

 

Dicloxacillin binds to one or more penicillin-binding proteins, which, in turn, inhibits synthesis of bacterial cell walls. It is indicated for treatment of infections caused by penicillinase-producing staphylococci. This agent may be used to initiate therapy when staphylococcal infection is suspected.

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Erythromycin (E.E.S., Ery-Tab, Erythrocin)

 

Erythromycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. It is used for the treatment of staphylococcal and streptococcal infections. However, macrolide resistance in the United States has been increasing. Erythromycin is used only when other options are unavailable or contraindicated.

In children, the patient's age and weight and the severity of the infection determine the proper dosage. When twice-daily dosing is desired, a half-total daily dose may be taken every 12 hours. For more severe infections, double the dose.

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Clindamycin (Cleocin)

 

Clindamycin is a lincosamide used for the treatment of serious skin and soft tissue staphylococcal infections. It is also effective against aerobic and anaerobic streptococci (except enterococci). It inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

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Cloxacillin

 

Cloxacillin is used for the treatment of infections caused by penicillinase-producing staphylococci.

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Trimethoprim-sulfamethoxazole (Bactrim DS, Septra DS)

 

Trimethoprim-sulfamethoxazole selectively inhibits bacterial dihydrofolate reductase. It has good susceptibility against community-acquired MRSA but is not effective against S pyogenes.

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Levofloxacin (Levaquin)

 

This agent inhibits DNA gyrase and topoisomerase IV, resulting in bactericidal activity. It is used as an alternative agent for MRSA infection.

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Ciprofloxacin (Cipro)

 

Ciprofloxacin inhibits DNA gyrase and topoisomerase IV, resulting in bactericidal activity. Use this agent as an alternative for MRSA infection.

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Linezolid (Zyvox)

 

Linezolid binds to the 50S ribosomal subunit, interfering with protein synthesis. This agent is used for MRSA or complicated skin infections.

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Antihistamines, 2nd Generation

Class Summary

If pruritus is significant, antihistamines can be prescribed to possibly help minimize scratching. Avoidance of trauma to the skin may prevent or limit the spread of impetigo by autoinoculation. These agents selectively inhibit peripheral histamine H1 receptors to histamine.

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Desloratadine (Clarinex)

 

Desloratadine is a long-acting tricyclic histamine antagonist that is selective for the H1 receptor. It relieves nasal congestion and systemic effects of seasonal allergy. It is the major metabolite of loratadine, which, after ingestion, is metabolized extensively to the active metabolite 3-hydroxydesloratadine.

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Cetirizine (Zyrtec)

 

Cetirizine selectively inhibits histamine H1 receptor sites in blood vessels, the GI tract, and the respiratory tract, which, in turn, inhibits physiologic effects that histamine normally induces at H1 receptor sites. Once-daily dosing is convenient. Bedtime dosing may be useful if sedation is a problem.

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Loratadine (Claritin, Alavert, Loradamed, Tavist ND)

 

Loratadine is nonsedating and selectively inhibits peripheral histamine H1 receptors.

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Antihistamines, 1st Generation

Class Summary

These agents selectively inhibit peripheral histamine H1 receptors to histamine.

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Hydroxyzine (Vistaril)

 

Hydroxyzine antagonizes H1 receptors in the periphery. It may suppress histamine activity in the subcortical region of the CNS. It is often administered before sleep because of its sedating properties.

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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.

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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.
 
 
 
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