eMedicine Specialties > Dermatology > Bacterial Infections

Impetigo

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

Updated: Sep 8, 2009

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 (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.

Differential Diagnoses

Other Problems to Be Considered

Differentials
 
Bullous impetigo

• Erythema multiforme (bullous)
• Fixed drug reaction (bullous)
• Bullous lupus erythematosus
• Bullous pemphigoid
• Herpes simplex
• Herpes zoster
• Insect bites
• Pemphigus vulgaris
• Staphylococcal scalded skin syndrome
• Stevens-Johnson syndrome
• Thermal burns
• Toxic epidermal necrolysis
• Varicella
• Vesicular stage of incontinentia pigmenti

Nonbullous impetigo

• Atopic dermatitis
• Cutaneous candidiasis
• Ecthyma
• Scabies
• Kerion
• Inflammatory dermatophytosis
• Pediculosis
• Allergic contact dermatitis
• Irritant contact dermatitis
• Dermatophytic Infections
• Insect bites
• Varicella
• Herpes simplex
• Discoid lupus erythematosus
• Pemphigus foliaceus
• Sweet syndrome

Workup

Laboratory Studies

• Impetigo is usually diagnosed on the basis of clinical findings.
• Bacterial culture and sensitivity are recommended (1) in cases to identify methicillin-resistant Staphylococcus aureus (MRSA), (2) if an outbreak of impetigo has occurred, or (3) if poststreptococcal glomerulonephritis is present. Exudate from underneath the crust is sent for culture.
• Leukocytosis is present in approximately 50% of impetigo cases.
• Antideoxyribonuclease (anti-DNAase) B antibody levels are often elevated in persons with streptococcal impetigo.
• Urinalysis is necessary to evaluate for acute poststreptococcal glomerulonephritis if the patient develops new-onset edema or hypertension. Hematuria, proteinuria, and cylindruria are indicators of renal involvement.
• A potassium hydroxide wet mount may be performed to exclude bullous dermatophyte infection.
• A Tzanck preparation or viral culture may be performed to exclude herpes simplex infection.
• A bacterial culture of the nares may be obtained to determine whether a patient is an S aureus carrier.
• If the nares culture is negative and the patient has persistent recurrent episodes of impetigo, bacterial cultures should be obtained from the axillae, pharynx, and perineum.
• Obtain serum IgM levels in cases of recurrent impetigo in patients with negative S aureus carrier status and no predisposing factors such as a preexisting dermatosis.¹¹ Serum level determination of IgA, IgM, and IgG, including IgG subclasses, is necessary to rule out other immunodeficiencies.

Histologic Findings

In bullous impetigo, few or no inflammatory cells are present within the bulla. A polymorphous infiltrate is present in the upper dermis. Acantholysis is noted in the granular layer.

In nonbullous impetigo, a serum crust is present above the epidermis. Neutrophils are common within the crust. In addition, gram-positive cocci are seen. Epidermal spongiosis and a severe dermal infiltrate of neutrophils and lymphoid cells are seen.

Treatment

Medical Care

Antibiotics are the mainstay of therapy, and the chosen agent must provide coverage against both Staphylococcus aureus and Streptococcus pyogenes. Community-acquired methicillin-resistant S aureus (MRSA) infection most commonly manifests as folliculitis or abscess, rather than impetigo; thus, beta-lactam drugs remain an appropriate initial empiric choice in the treatment of impetigo.
 
Topical antibiotics are used in patients with small or few lesions, applied to affected areas twice or thrice daily for 7-10 days.

Mupirocin ointment has been used for both the lesions and to clear chronic nasal carriers. It has been shown to be superior to topical polymyxin B and neomycin^14,15 and equally effective compared with oral cephalexin. Both mupirocin and oral cephalexin are superior to bacitracin.¹⁶ Unfortunately, S aureus and MRSA resistance to mupirocin has emerged at estimated rates ranging from 5-10%.¹⁴ An experimental drug (TD1414 2% cream) is currently being evaluated in a phase 2, randomized, single-blind (investigator), active control (mupirocin 2% cream), safety/efficacy study in patients with impetigo and secondarily infected traumatic lesions. Results are expected by June 2009.¹⁷

Retapamulin was approved by the US Food and Drug Administration (FDA) in 2007 for the topical treatment of impetigo in adults and children older than 9 months caused by S pyogenes and methicillin-susceptible S aureus.¹⁸ Retapamulin has an excellent spectrum of activity, surpassing the bacterial spectrum of mupirocin.^14,19 It has been shown to preserve its activity against bacteria that were resistant to multiple antibiotic drugs, such as methicillin, erythromycin, fusidic acid, mupirocin, azithromycin, and levofloxacin.²⁰ In more than 1900 patients evaluated in several comparative studies, retapamulin has demonstrated to be as effective as topical fusidic acid and oral cephalexin, with a low rate of adverse events.¹⁴ In another study, retapamulin 1% ointment showed more efficacy than fusidic acid 2% ointment for the treatment of impetigo.²¹

Further, a randomized, double-blind, multicenter study to evaluate the safety and efficacy of topical retapamulin 1% ointment, compared with oral linezolid in the treatment of secondarily-infected traumatic lesions and impetigo caused by MRSA in subjects of aged 2 months and older, is currently being conducted Results are expected by August 2010.²²

Topical sodium fusidate (fusidic acid), currently not available in the United States, has been recognized as first-line of therapy in Europe and other parts of the world.^3,23 High resistance rates have been reported with the use of fusidic acid, ranging from 32.5-50%.^{3,21,24,25,26}

Other topical antibiotics that have reported some benefit for the treatment of impetigo include the following:

• Clindamycin (cream, lotion, and foam) is useful in several MRSA infections.^27,28
• Gentamicin ointment or cream has been used in many countries for some gram-positive infections by Staphylococcus species, including impetigo and pyoderma. Its use is precluded by the potential development of ear and kidney toxicity.^14,27
• Hydrogen peroxide 1% cream, available in many countries, has demonstrated comparable bactericidal activity but longer duration of action than hydrogen peroxide 1% aqueous solution in vitro. It is applied 2-3 times a day on the affected area for a maximum of 3 weeks. Although the potential for sensitization is low, hypersensitivity reactions have been reported to other ingredients in the commercially available product.^27,29
• Tetracycline has been used for localized impetigo, although it is not widely prescribed because of the potential risk of skin photosensitivity reactions.^1,27

Drugs such as sulfanilamide, nitrofurazone, and silver sulfadiazine, widely used for the treatment of burns, are not used by dermatologists for the treatment of impetigo. Because of their antibacterial spectrum and proven efficacy and tolerability, these drugs may need to be considered in the future for the treatment of impetigo and other community-acquired skin infections.^14,27

Oral antibiotics remain appropriate for many patients with impetigo. For empiric antibiotic therapy, a cephalosporin, semisynthetic penicillin, or beta-lactam/beta-lactamase inhibitor is recommended. If bacterial cultures reveal MRSA and the patient is not improving, tetracyclines, trimethoprim/sulfamethoxazole (Bactrim), clindamycin, or linezolid are effective oral antibiotics.

Gentle debridement of lesional crusts using antibacterial soap and a washcloth is also recommended. Good hygiene with antibacterial washes, such as chlorhexidine, may prevent the spread of impetigo and prevent recurrences, but the efficacy of this has not been proven.

A clinical guideline summary from the Infectious Diseases Society of America, Practice guidelines for the diagnosis and management of skin and soft-tissue infections, may be helpful.³⁰

Consultations

Consult a nephrologist if signs and symptoms of acute glomerulonephritis develop.

Medication

The goals of pharmacotherapy for impetigo are to reduce morbidity, to prevent complications, and to prevent spread to other individuals.

Antibiotics

Mupirocin applied topically has been shown to be effective for localized impetigo, but resistance has emerged. Retapamulin is a new option.^23,31 Bacitracin is no longer the preferred topical antibiotic because it causes frequent allergic skin reactions and occasional/rare anaphylaxis.²⁷

The advantages of topical antibiotics include 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, and low cost, while the disadvantages include the potential production of irritant and allergic contact dermatitis, decreased penetration in the affected area, potential rapid appearance of bacterial resistance, potential alteration of cutaneous florae, and potential systemic absorption and consequent toxic effects.²⁷

Systemic antibiotic treatment is indicated for most cutaneous infections, although abscesses may respond to drainage alone. A cephalosporin, semisynthetic penicillin, or beta-lactam/beta-lactamase inhibitor combination is generally suitable for first-line therapy. 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.

Mupirocin (Bactroban)

DOC for localized disease; inhibits bacterial growth by inhibiting RNA and protein synthesis.

Dosing

Adult

Apply thin film to affected area 3-5 times/d for 7-14 d; cleanse lesions prior to application
Recurrent disease: Apply to nostrils twice/d for 5 d monthly

Pediatric

Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Prolonged use may result in growth of nonsusceptible organisms; use with caution over large surface areas, especially in the setting of moderate-to-severe renal disease, due to polyethylene glycol absorption, which is excreted by the kidneys

Retapamulin (Altabax)

Topical antibiotic available as a 1% ointment. First of new antibiotic class called pleuromutilins. Inhibits protein synthesis by binding to 50S subunit on ribosome. Indicated for impetigo caused by S aureus or S pyogenes.

Dosing

Adult

Apply thin layer to affected area bid for 5 d to a total area of <100 cm²; affected area should be covered with sterile dressing after application

Pediatric

Approved for patients 9 mo or older; apply as in adults; total area of treatment should be <2% of total BSA in patients aged 9 mo to 18 y

Interactions

None known

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May cause irritation at application site (1.4%); avoid application to eye area; keep out of reach of children

Dicloxacillin (Dycill, Dynapen)

Binds to one or more penicillin-binding proteins, which, in turn, inhibits synthesis of bacterial cell walls. For treatment of infections caused by penicillinase-producing staphylococci. May use to initiate therapy when S aureus infection is suspected.

Dosing

Adult

125-500 mg PO q6h; not to exceed 2 g/d

Pediatric

Neonates: 4-8 mg/kg PO q6h
<40 kg: 12.5-50 mg/kg/d PO divided q6h
>40 kg: 125-500 mg PO q6h

Interactions

May decrease effects of anticoagulants and oral contraceptives; probenecid and disulfiram may increase penicillin levels; concomitant penicillin and aminoglycoside therapy reported to result in inactivation of aminoglycoside both in vivo and in vitro; penicillins may alter intestinal florae, which, in turn, alters enterohepatic circulation of combination contraceptives, possibly resulting in unintended pregnancies

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Monitor PT in patients taking anticoagulant medications; toxicity may increase in patients with renal impairment

Cephalexin (Keflex)

First-generation cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall synthesis. Bactericidal activity against rapidly growing organisms. Primary activity against skin florae; used for skin infections or prophylaxis in minor procedures.

Dosing

Adult

250 mg PO q6h or 500 mg PO bid for 7-14 d; not to exceed 4 g/d

Pediatric

25-50 mg/kg/d PO divided q12h for 7-14 d; not to exceed 3 g/d

Interactions

Probenecid may increase effect of cephalosporins; tetracyclines may decrease effect of cephalosporins with concurrent use; coadministration with aminoglycosides increases nephrotoxic potential

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy

Clindamycin (Cleocin)

Effective for skin infections; binds to the 50S ribosomal subunit, interfering with protein synthesis. Can also be used for impetigo prophylaxis.

Dosing

Adult

Prophylaxis: 150 mg/d PO for 3 mo
Treatment: 150-300 mg PO q6h for 7-10 d

Pediatric

10-30 mg/kg/d PO divided q6-8h or 25-40 mg/kg/d IV/IM divided q6-8h

Interactions

May potentiate effects of botulinum toxins and other neuromuscular blockers

Contraindications

Documented hypersensitivity, history of antibiotic-associated colitis, caution in liver or renal disease

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in setting of hepatic or renal disease; associated with Clostridium difficile colitis

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

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections. Resistance is prevalent. In children, age, weight, and severity of infection determine proper dosage. When twice-daily dosing is desired, half the total daily dose may be taken q12h.

Dosing

Adult

250 mg erythromycin stearate/base PO q6h or 500 mg q12h for 10 d; increase to 4 g/d depending on severity of infection; 250 mg of erythromycin stearate/base is equivalent to 400 mg of E.E.S.

Pediatric

30-50 mg/kg/d PO divided q6-8h for 7-14 d; double dose for severe infection

Interactions

Coadministration may increase toxicity of carbamazepine, cyclosporine, digoxin, HMG-CoA reductase inhibitors (statins), and theophylline; may potentiate anticoagulant effects of warfarin; drugs metabolized by cytochrome P450 may demonstrate increased toxicity when administered with erythromycin

Contraindications

Documented hypersensitivity; hepatic impairment

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in liver disease; common adverse GI effects include nausea, vomiting, abdominal pain, diarrhea, and anorexia

Rifampin (Rifadin, Rimactane)

Inhibits DNA-dependent RNA polymerase. Used in combination with other antibiotics so that resistance to rifampin does not occur; can also be used to treat nasal carriers of S aureus.

Dosing

Adult

300–600 mg PO bid for 10 d; take 1 h ac or 2 h pc
Nasal carriers: 600 mg/d PO for 5-10 d

Pediatric

15 mg/kg/d divided q12h for 5-10 d

Interactions

Induces hepatic enzymes and may decrease levels of benzodiazepines, cyclosporine, oral contraceptives, HMG-CoA reductase inhibitors, and other drugs metabolized in the liver
May increase acetaminophen toxicity; induces microsomal enzymes, which may decrease effects of acetaminophen, oral anticoagulants, barbiturates, benzodiazepines, beta-blockers, chloramphenicol, oral contraceptives, corticosteroids, mexiletine, cyclosporine, digitoxin, disopyramide, estrogens, hydantoins, methadone, clofibrate, quinidine, dapsone, tazobactam, sulfonylureas, theophyllines, tocainide, and digoxin
Blood pressure may increase with coadministration of enalapril; coadministration with isoniazid or pyrazinamide may result in higher rate of hepatotoxicity than with either agent alone (discontinue one or both agents if alterations in LFTs occur)

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use with caution in hepatic dysfunction; obtain CBC counts and baseline clinical chemistries prior to and throughout therapy; in liver disease, weigh benefits against risk of further liver damage; interruption of therapy and high-dose intermittent therapy are associated with thrombocytopenia that is reversible if therapy is discontinued as soon as purpura occurs; if treatment is continued or resumed after appearance of purpura, cerebral hemorrhage or death may occur

Trimethoprim-sulfamethoxazole (Bactrim, Septra)

Selectively inhibits bacterial dihydrofolate reductase. Has good susceptibility against community-acquired MRSA but is not effective against S pyogenes.

Dosing

Adult

1 DS tab PO tid for 10 d

Pediatric

8-10 mg/kg/d PO q12h (based on trimethoprim)

Interactions

Inhibits hepatic metabolism of other drugs (use with caution with warfarin and other drugs metabolized by the liver); may increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly persons; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine

Contraindications

Documented hypersensitivity to this or any sulfa drug

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Decrease dose in patients with liver or kidney dysfunction; do not use during last trimester of pregnancy due to potential toxicity to newborn (eg, jaundice, hemolytic anemia, kernicterus)
Dosage adjustments (adult adjustments)
CrCl 80-50 mL/min: Recommended IV dose q18h
CrCl 50-10 mL/min: Recommended IV dose q24h
CrCl <10 mL/min: Not recommended
HD: 4-5 mg/kg after HD
During peritoneal dialysis: 0.16-0.8 g q48h
Discontinue at first appearance of rash or sign of adverse reaction; obtain CBC counts frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholism, elderly persons, anticonvulsant therapy, or malabsorption syndrome); hemolysis may occur in G-6-PD deficiency; AIDS patients may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); give fluids to prevent crystalluria and stone formation

Levofloxacin (Levaquin)

Inhibits DNA gyrase and topoisomerase IV for bactericidal activity. Use as an alternative for MRSA infection.

Dosing

Adult

500 mg/d PO for 7-14 d; take 1 h ac or 2 h pc

Pediatric

Not recommended

Interactions

May prolong QT interval if used with antiarrhythmic drugs or TCAs; antacids may reduce serum levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Decrease dose in patients with renal dysfunction; rapid infusions may cause hypotension; fluoroquinolones cause arthropathy and osteochondrosis in juvenile animal laboratory studies (not routinely recommended or used in children <18 y without extreme caution); photosensitivity and seizures (latter especially if also taking NSAIDs) have occurred with this class of medication
Interacts with oral hypoglycemic agents; avoid coadministration with QT-prolonging agents (including class Ia and III antiarrhythmics, erythromycin, cisapride, antipsychotics, and cyclic antidepressants); avoid taking with antacids, zinc, iron, didanosine, or sucralfate; adverse neurologic effects reported (eg, dizziness); musculoskeletal problems (eg, tendinitis, tendon rupture); patient should stay well hydrated

Ciprofloxacin (Cipro)

Inhibits DNA gyrase and topoisomerase IV for bactericidal activity. Use as an alternative for MRSA infection.

Dosing

Adult

500 mg PO bid for 10 d; take 1 h ac or 2 h pc

Pediatric

20-30 mg/kg/d PO divided q12h

Interactions

Inhibits hepatic metabolism (monitor levels of clozapine, warfarin, and theophylline); can lead to increased caffeine levels; probenecid decreases excretion

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Decrease dose in patients with renal dysfunction; rapid infusions may cause hypotension; fluoroquinolones cause arthropathy and osteochondrosis in juvenile animal laboratory studies (not routinely recommended or used in children <18 y without extreme caution); photosensitivity and seizures (latter especially if also taking NSAIDs) have occurred with this class of medication
Interacts with oral hypoglycemic agents; avoid coadministration with QT-prolonging agents (including class Ia and III antiarrhythmics, erythromycin, cisapride, antipsychotics, and cyclic antidepressants); avoid taking with antacids, zinc, iron, didanosine, or sucralfate; adverse neurologic effects reported (eg, dizziness); musculoskeletal problems (eg, tendinitis, tendon rupture); patient should stay well hydrated

Linezolid (Zyvox)

Binds to the 50S ribosomal subunit, interfering with protein synthesis; used for MRSA or complicated skin infections

Dosing

Adult

Uncomplicated infection: 400 mg PO bid for 10-14 d
Complicated infections: 600 mg PO bid for 10-28 d

Pediatric

20-30 mg/kg/d PO divided q8-12h for 10-14 d

Interactions

Has mild MAOI properties (use with caution in patients taking MAOIs or TCAs and in patients with liver or renal dysfunction

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid large quantities of tyramine-containing foods; monitor CBC count qwk because of risk of myelosuppression

Antihistamines

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.

Loratadine (Claritin)

Nonsedating and selectively inhibits peripheral histamine H1 receptors.

Dosing

Adult

10 mg/d PO

Pediatric

<2 years: Not established
2-6 years: 5 mg/d PO
>6 years: Administer as in adults

Interactions

Cimetidine, erythromycin, and ketoconazole may increase levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Starting dose of 10 mg q48h in patients with liver impairment or renal insufficiency (CrCl <30 mL/min)

Desloratadine (Clarinex)

Long-acting tricyclic histamine antagonist selective for H1 receptor. Relieves nasal congestion and systemic effects of seasonal allergy. Major metabolite of loratadine, which, after ingestion, is metabolized extensively to active metabolite 3-hydroxydesloratadine.

Dosing

Adult

5 mg/d PO

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

Data limited; erythromycin and ketoconazole increase desloratadine and 3-hydroxydesloratadine plasma concentrations, but no increase in clinically relevant adverse effects, including QTc, was observed

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Decrease dose in hepatic impairment; rarely causes pharyngitis or dry mouth

Cetirizine (Zyrtec)

Long-acting selective histamine H1 receptor antagonist.

Dosing

Adult

5-10 mg/d PO

Pediatric

6 months to 2 years: 2.5 mg/d PO
2-5 years: 2.5-5 mg/d PO
6-11 years: 5-10 mg/d PO

Interactions

May increase risk of CNS depression when used with other CNS depressants

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May cause somnolence

Hydroxyzine (Atarax, Vistaril)

Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS. Often administered before sleep because of sedating properties.

Dosing

Adult

25-100 mg PO q6-8h prn for pruritus

Pediatric

<6 years: 2 mg/kg/d PO divided q6-8h prn
6-12 years: 12.5-25 mg PO q6-8h prn

Interactions

CNS depression may increase with alcohol or other CNS depressants

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause drowsiness

Follow-up

Further Inpatient Care

• Impetigo typically resolves with topical or oral antibiotics; only rarely do serious complications occur. Vancomycin may be required for complicated methicillin-resistant Staphylococcus aureus (MRSA) infections that do not improve with standard oral antibiotics.

Further Outpatient Care

• Schedule a follow-up visit within 1 week.
• If the lesions have not improved, check the bacterial culture and sensitivity results, look for MRSA, and prescribe alternative antibiotics accordingly.
• If the patient was treated with oral antibiotics, prescribe alternative antibiotics depending on bacterial culture and sensitivity results.

Deterrence/Prevention

• Treat traumatized skin with mupirocin because this has been shown to decrease the rates of impetigo spread.
• Evaluate hospital nursery staff and household members for pyodermas or asymptomatic bacterial carrier states.
• Treat preexisting underlying skin diseases, such as atopic dermatitis. Antihistamines and topical steroids help decrease scratching. Treating the underlying disease has also been shown to decrease the pathogen count on the skin.
• Teach good personal hygiene. For example, keep nails short and clean and wash hands frequently with antibacterial soap and water or waterless antibacterial cleansers.
• For patients with recurrent impetigo, asymptomatic family members, and S aureus nasal carriers, prescribe 2% mupirocin cream or ointment (Bactroban) for application inside nostrils 3 times per day for 5 days each month to reduce colonization in the nose. Retapamulin may replace mupirocin for this indication, although data are needed to support its use in this setting.
• Patients who are chronic nasal carriers can also be treated with clindamycin or rifampin plus dicloxacillin.
• Advise patients about improving environmental conditions through the addition of air conditioning and by keeping surroundings clean.

Complications

Rarely, lesions resolve with scarring and postinflammatory hyperpigmentation or hypopigmentation.

• Bullous impetigo
  • Cellulitis, lymphangitis, bacteremia with subsequent pneumonitis, septic arthritis, and septicemia may develop. This would require hospitalization with intravenous antibiotic therapy.
  • If the exfoliative toxins are absorbed into the bloodstream, staphylococcal scalded skin syndrome can result. This occurs more commonly in younger children, who have not developed antibodies against this toxin.
• Nonbullous impetigo
  • Acute glomerulonephritis develops in 2-5% of individuals with impetigo due to S aureus and group A beta-hemolytic streptococci (GABHS), most often in 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. 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.
  • Ecthyma, a deep dermal infection, can result, after which subsequent scarring can occur. Scarlet fever, erysipelas, cellulitis, lymphangitis, and, rarely, bacterial endocarditis may also develop.
  • Impetigo can complicate patients with chronic renal failure, particularly patients on dialysis and post–renal transplantation patients.
  • Less common complications include sepsis, arthritis, osteomyelitis, pneumonia, lymphadenitis, guttate psoriasis, toxic shock syndrome, and staphylococcal scalded skin syndrome.^6,10

Prognosis

• Spontaneous healing rarely occurs. If left untreated, some lesions may resolve spontaneously, while new lesions appear elsewhere on the body.
• Resolution of lesions usually occurs after 7-10 days of treatment. If lesions have not resolved within 7-10 days of antibiotic therapy, cultures should be performed to look for resistant organisms.

Patient Education

• Children can return to daycare or school once lesions are resolved. Caretakers should be instructed about hygienic issues and prevention.
• For excellent patient education resources, visit eMedicine's Bacterial and Viral Infections Center and Skin, Hair, and Nails Center. Also, see eMedicine's patient education articles Impetigo, Skin Rashes in Children, and Antibiotics.

Miscellaneous

Medicolegal Pitfalls

• Failure to evaluate hospital nursery staff for active impetigo lesions or carrier states if indicated
• Failure to check patient blood pressure for hypertension and urine for hematuria or proteinuria as a screen for poststreptococcal glomerulonephritis

Multimedia

Media file 1: 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.

Media file 2: 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.

Media file 3: 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.

Media file 4: 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.

Media file 5: 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.

Media file 6: 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.

Media file 7: 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.

Media file 8: 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.

Media file 9: 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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Keywords

impetigo, impetigo contagiosa, Fox impetigo, impetigo bullosa, impetigo contagiosa bullosa, impetigo neonatorum

Contributor Information and Disclosures

Author

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.

Coauthor(s)

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: Washington State Medical Association
Disclosure: Nothing to disclose.

Medical Editor

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.

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
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.

Managing Editor

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

CME Editor

Catherine M Quirk, MD, Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania
Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Ivan D. Camacho, MD, in the development and writing of this chapter.

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