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AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: Lisa S Lewis, MD, Consulting Staff, Division of Emergency Medicine, Children's Hospital Medical Center of Cincinnati
Lisa S Lewis is a member of the following medical societies: American Academy of Pediatrics
Coauthor(s):
Allan D Friedman, MD, MPH, Chairman, Division of General Pediatrics, Dept of Pediatrics, Professor of Pediatrics, Virginia Commonwealth University, VCUH Health System
Editors: Glenn J Fennelly, MD, MPH, Director, Division of Pediatric Infectious Diseases, Jacobi Medical Center; Associate Professor, Department of Pediatrics, Albert Einstein College of Medicine; Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc; Joseph Domachowske, MD, Associate Professor, Department of Pediatrics, Division of Infectious Diseases, State University of New York-Upstate Medical University; Robert W Tolan Jr, MD, Chief of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine; 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
Author and Editor Disclosure
Synonyms and related keywords:
impetigo, impetigo contagiosa, impetigo bullosa, streptococcal impetigo, staphylococcal impetigo, nonbullous impetigo, bullous impetigo, crusted tetter, pyoderma, group A beta hemolytic streptococci, GABHS
Background
Impetigo is a superficial pyoderma first described by Dunn and Fox in the 1860s. Impetigo is currently the most common skin infection in children and accounts for approximately one tenth of all cutaneous problems in pediatric clinics. Impetigo can be subdivided into nonbullous and bullous forms. The more common nonbullous form accounts for approximately 70% of individuals with impetigo and affects areas of traumatized skin on the face or extremities. Staphylococcus aureus, group A beta hemolytic streptococci (GABHS), or mixed flora may invade disrupted skin following bites, cuts, abrasions, varicella, or other trauma. Certain serotypes of GABHS (eg, types 49, 55, 57, 59) are associated with impetigo and acute glomerulonephritis. Bullous impetigo may affect intact skin and is usually caused by S aureus infection.
Pathophysiology
Intact skin is usually resistant to colonization or infection by S aureus or GABHS. These bacteria can be introduced from the environment and only transiently colonize the cutaneous surface. High temperature and humidity, underlying dermatologic disease, and young age are associated with colonization. Experimental studies have shown that inoculation of multiple strains of GABHS on to the surface of volunteer subjects did not produce cutaneous disease unless skin disruption had occurred. The teichoic acid adhesions for GABHS and S aureus require the epithelial cell receptor component, fibronectin, for colonization. These fibronectin receptors are unavailable on intact skin; however, skin disruption may reveal fibronectin receptors and allow for colonization or invasion in these disrupted surfaces. Factors that can modify the usual skin flora and facilitate transient colonization by GABHS and S aureus include high temperature or humidity, preexisting cutaneous disease, young age, or recent antibiotic treatment. Bullous impetigo results from invasion by phage group 2 S aureus onto either intact or disrupted skin. This occurs after colonization of the upper respiratory tract, usually involving the nares. Invasion is believed to be a result of an epidermolytic toxin that disrupts epidermal cell attachments.
Frequency
United States
Impetigo accounts for approximately 10% of skin problems observed in pediatric clinics. Because it occurs more frequently in a warm humid environment, impetigo is more common in the southeastern US than in the cooler northern states. The prevalence of impetigo varies seasonally; however, in regions that remain warm and humid throughout the year, seasonality may not occur.
International
Impetigo occurs more frequently in tropical climates and lower altitudes. Warm humid conditions combined with frequent cutaneous disruption via biting insects favor its development throughout the year in tropical climates. Geographic regions that have crowded conditions or poor hygiene also have increased prevalence of impetigo.
Mortality/Morbidity
- Cellulitis, lymphangitis, suppurative lymphadenitis, and staphylococcal scalded skin syndrome occur in as many as 10% of patients with impetigo.
- Acute poststreptococcal glomerulonephritis (APSGN), scarlet fever, osteomyelitis, septic arthritis, pneumonia, septicemia, guttate psoriases, and rheumatic fever have also been observed in patients with impetigo.
Age
- Impetigo is found most commonly in preschool-aged children.
- Rapid dissemination can occur through daycare centers, nurseries, and grade schools.
History
In nonbullous impetigo, a tiny pustule or honey-colored crusted plaque with rapid spread, occasional pruritus, and regional lymphadenopathy may follow a break in the skin. Bullous impetigo usually has a history of thin-roofed bullae that spontaneously rupture without a history of localized lymphadenopathy or cutaneous disruption. - Nonbullous lesions
- Lesions start as tiny pustules that evolve rapidly into honey-colored crusted plaques, which usually measure less than 2 cm in diameter.
- A rash is usually found in exposed areas of the face and extremities where bites, abrasions, lacerations, scratches, burns, or trauma have occurred.
- Rapid spread occurs.
- Lesions are usually asymptomatic, with occasional pruritus.
- Little or no surrounding erythema or edema is present.
- Regional adenopathy is common.
- Bullous lesions
- Thin-roofed bullae that spontaneously rupture are present.
- Bullous lesions usually spread locally in the face, trunk, extremities, buttocks, or perineal regions.
- These lesions may secondarily invade preexisting lesions (eg, eczema) to cause generalized lesions.
- Minimal or no surrounding erythema occurs.
- No regional lymphadenopathy occurs.
Physical
Generally, the patient is nontoxic and well appearing.
- Nonbullous lesions
- A tiny vesicle or pustule that ruptures and is replaced by honey-colored crusting usually measures less than 2 cm.
- Elevation of crust reveals a moist erythematous base.
- Lesions are usually on the face and extremities or in areas with a break in the natural skin defense barrier.
- Little or no surrounding erythema or edema is present.
- Regional lymphadenopathy is present in 90% of individuals with impetigo.
- Bullous lesions
- Thin-roofed, flaccid, and transparent bullae usually measure less than 3 cm.
- Bullae rupture easily, within 1-2 days, leaving a rim of scale around an erythematous moist base. After desiccation, a lacquered or scalded skin appearance with a collarette of scale is noted.
- Bullous lesions occur on intact skin, usually on the face, trunk, extremities, buttocks, and perineum.
- No surrounding erythema or edema is present.
- No regional adenopathy occurs.
Causes
The primary pathogen responsible for impetigo changes from decade to decade. Staphylococci were the causative agents in nonbullous impetigo until the mid 1960s. Subsequently, GABHS became predominant. Since the early 1980s, the predominant pathogen is again S aureus. The etiology of bullous impetigo is almost always S aureus. - Nonbullous impetigo
- Most lesions are caused by S aureus and GABHS.
- Culture results and the relative frequency of each pathogen may vary depending on geographic region, time of year, and age of the host.
- S aureus can be cultured from impetiginous lesions in children of all ages.
- Except for endemic areas, GABHS is uncommon in children younger than 2 years but is found commonly in preschool-aged children.
- Bullous impetigo
- Bullous impetigo is caused almost exclusively by S aureus.
- Phage group 2 S aureus accounts for 80% of these lesions.
- Exfoliative toxins A and B cause a loss of cell adhesion in the superficial epidermis, split the granular cell layer, and form blisters.
Burns, Chemical
Burns, Thermal
Contact Dermatitis
Herpes Simplex Virus Infection
Pediculosis (Lice)
Scabies
Varicella
Other Problems to be Considered
Other bullous disorders
Stevens-Johnson syndrome
Pemphigus vulgaris
Allergic reactions (erythema multiforme, rhus dermatitis)
Tinea corporis, kerion
Nummular eczema
Linear immunoglobulin A bullous dermatosis
Bullous pemphigoid reactions
Ecchymoses
Dermatitis herpetiformis
Lab Studies
- Diagnosis is usually solely based on history and clinical appearance. Occasionally, confirmation by culture and sensitivity testing of the causative organism may be warranted. Similarly, evidence of previous streptococcal skin infection may be sought in individuals in whom acute glomerulonephritis is suspected.
- Leukocytosis is present in approximately 50% of patients with impetigo.
- In patients with nonbullous lesions, after cleansing the honey-colored crusted lesion and uplifting the scab, a bacterial culture of the fresh exudate underneath the scab may be obtained.
- The following studies may be performed in patients with bullous lesions:
- Gram stain and culture of the blister fluid reveal many polymorphonuclear WBCs and gram-positive cocci.
- Bacterial culture yields staphylococci.
- Documentation of a recent streptococcal skin infection in the differential diagnosis of acute glomerulonephritis is accomplished best by obtaining antideoxyribonuclease B (anti-DNase B) and antihyaluronidase (AH) titers.
- More than 92% of patients with impetigo-associated APSGN have elevated anti-DNase B titers.
- Patients with impetigo have a poor antistreptolysin O (ASO) serologic response; only 51% of patients with impetigo-associated poststreptococcal glomerulonephritis develop an increased ASO titer.
Histologic Findings
Typical histologic examination of bullous impetigo reveals a blister in the subcorneal or granular region. Polymorphonuclear cells are generally present within the vesicle. Acantholytic cells in the blister cavity, spongiosis, and papillary dermal edema may be present. Bacteria may be observed on Gram stain. Similar findings are present in nonbullous impetigo; however, vesicle formation is significantly smaller.
Medical Care
Treatment may involve local wound care along with topical or systemic antibiotic therapy. - Local wound care: Cleansing, removal of the honey-colored crusts, and frequent application of wet dressings to areas affected by lesions are recommended.
- Topical antibiotic treatment: Topical mupirocin is considered the treatment of choice for individuals with uncomplicated localized impetigo. Mupirocin has been found to clear 52-68% of patients with methicillin-resistant S aureus (MRSA) colonization. Retapamulin ointment is in a new class of topical antimicrobials and is indicated for treatment of localized impetigo in children older than 9 months.
- Systemic antibiotic treatment
- Persons with infections that are widespread, complicated, or are associated with systemic manifestations are usually treated with antibiotics that have gram-positive bacterial coverage.
- Systemic therapy is also recommended if multiple incidents of pyoderma occur within daycare, family, or athletic team settings.
- Beta-lactamase resistant antibiotics (eg, cephalosporins, amoxicillin-clavulanate, cloxacillin, dicloxacillin) are recommended. Cephalexin appears to be the drug of choice for oral antimicrobial therapy in children.
- In recent years, community-acquired MRSA infections have reached epidemic proportions. If MRSA is suspected, alternative antibiotics include vancomycin, trimethoprim/sulfamethoxazole, and clindamycin.
- Erythromycin and clindamycin are alternatives in patients with penicillin hypersensitivity. Macrolide resistance has been increasing in the United States. Thus, avoid treatment of impetigo with erythromycin in geographic regions that are known to have a high resistance rate. GABHS and S aureus resistance to clindamycin has also been reported.
Topical antibiotics, systemic antibiotics, or a combination are effective therapies for impetigo. Empiric bacterial coverage is aimed at eradicating S aureus and GABHS.
Drug Category: Topical antibiotics
Topical antibiotic treatment with mupirocin is the treatment of choice for uncomplicated localized pyoderma, although S aureus resistance to mupirocin has been reported in vitro.
| Drug Name | Mupirocin (Bactroban) |
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| Description | Naturally occurring antibiotic produced by fermentation of Pseudomonas fluorescens. Mechanism of action of mupirocin is via inhibition of bacterial protein synthesis. |
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| Adult Dose | Apply to affected areas tid for 7-10 d |
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| Pediatric Dose | Administer as in adults |
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| Contraindications | Documented hypersensitivity |
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| Interactions | None reported |
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| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
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| Precautions | Prolonged use may result in growth of nonsusceptible organisms |
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| Drug Name | Retapamulin (Altabax) |
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| Description | 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 Streptococcus pyogenes. |
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| Adult Dose | Apply topically to affected site bid for 5 d |
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| Pediatric Dose | <9 months: Not established
>9 months: Apply as in adults
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| Contraindications | Documented hypersensitivity |
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| Interactions | None known |
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| 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
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| Precautions | May cause irritation at application site (1.4%); avoid application to eye area; keep out of reach of children |
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Drug Category: Systemic antibiotics
Systemic antibiotic treatment is indicated for widespread or complicated pyoderma.
| Drug Name | Cephalexin (Biocef, Keflex, Keftab) |
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| Description | First-generation cephalosporin antibiotic commonly used to treat impetigo and other skin infections. As with other cephalosporins, mechanism of action is through inhibition of cell wall synthesis. |
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| Adult Dose | 500 mg PO q6h |
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| Pediatric Dose | 25-50 mg/kg/d PO divided tid/qid |
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| Contraindications | Documented hypersensitivity |
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| Interactions | Coadministration with aminoglycosides increases nephrotoxic potential |
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| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
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| Precautions | Adjust dosage with renal insufficiency; caution in patients sensitive to penicillin |
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| Drug Name | Amoxicillin and clavulanate (Augmentin) |
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| Description | Oral antibiotic combining broad-spectrum antibiotic amoxicillin with beta-lactamase inhibitor clavulanate. Amoxicillin inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins. Addition of clavulanate inhibits beta-lactamase producing bacteria. For children >3 mo, base dosing protocol on amoxicillin content. Because of different amoxicillin/clavulanic acid ratios in 250-mg tab (250/125) vs 250-mg chewable tab (250/62.5), do not use 250-mg tab until child weighs >40 kg. |
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| Adult Dose | 500 mg PO q12h or 250 mg PO q8h |
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| Pediatric Dose | 20-45 mg/kg/d PO divided bid/tid
<3 months: 125 mg/5 mL PO susp based on amoxicillin; 30 mg/kg/d divided bid for 7 d
>3 months: If using 200 mg/5 mL or 400 mg/5 mL susp, 45 mg/kg/d PO q12h; if using 125 mg/5 mL or 250 mg/5 mL susp, 40 mg/kg/d PO q8h for 7 d
>40 kg: Administer as in adults |
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| Contraindications | Documented hypersensitivity |
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| Interactions | Coadministration with warfarin or heparin increases risk of bleeding; avoid combination with allopurinol, which results in increased incidence of rash |
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| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
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| Precautions | Because chewable tab contain phenylalanine, do not administer to patients with PKU |
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| Drug Name | Dicloxacillin (Dycill, Dynapen) |
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| Description | 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 staphylococcal infection is suspected. |
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| Adult Dose | 125-500 mg PO q6h, administer 1 h ac or 2 h pc |
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| Pediatric Dose | 25 mg/kg/d PO divided q6h, administer 1 h ac or 2 h pc |
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| Contraindications | Documented hypersensitivity |
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| Interactions | Decreases efficacy of oral contraceptives; may decrease effects of anticoagulants; probenecid and disulfiram may increase penicillin levels |
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| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
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| Precautions | Monitor PT in patients taking anticoagulant medications; toxicity may increase in patients who are renally impaired |
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| Drug Name | Erythromycin (E.E.S., E-Mycin, Eryc) |
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| Description | Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections.
In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half-total daily dose may be taken q12h. For more severe infections, double dose. |
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| Adult Dose | 250-500 mg (stearate/base) PO q6h |
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| Pediatric Dose | 30-50 mg/kg/d (stearate/base) PO divided q6-8h |
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| Contraindications | Documented hypersensitivity; hepatic impairment |
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| Interactions | Potent inhibitor of CYP450-3A4; coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis |
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| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
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| Precautions | Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI adverse effects are common (administer doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occurs |
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| Drug Name | Clindamycin (Cleocin) |
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| Description | Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. |
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| Adult Dose | 150-450 mg PO q6h |
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| Pediatric Dose | 10-30 mg/kg/d PO divided q6-8h |
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| Contraindications | Documented hypersensitivity; regional enteritis, ulcerative colitis, hepatic impairment, antibiotic-associated colitis |
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| Interactions | Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin |
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| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
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| Precautions | Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis by allowing overgrowth of Clostridium difficile |
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| Drug Name | Cloxacillin (Cloxapen) |
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| Description | For treatment of infections caused by penicillinase-producing staphylococci. |
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| Adult Dose | 250-500 mg PO q6h |
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| Pediatric Dose | 50-100 mg/kg/d PO divided q6h |
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| Contraindications | Documented hypersensitivity |
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| Interactions | Decreases efficacy of oral contraceptives; may decrease effects of anticoagulants; probenecid and disulfiram may increase penicillin levels |
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| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
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| Precautions | Caution in patients with impaired renal function |
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Further Inpatient Care
- Hospital care is reserved only for impetigo with certain complications.
- If inpatient care is warranted in the child with untreated impetigo, contact isolation is recommended.
Deterrence/Prevention
- Advise the child with impetigo to avoid close contact with other children if possible. Current recommendations call for the exclusion of children with impetigo from school or daycare for 24 hours after the initiation of antibiotics.
- Inspect family members for impetiginous lesions. Failure to treat other infected persons may result in continued transmission.
Complications
- Cellulitis, lymphangitis, suppurative lymphadenitis, and staphylococcal scalded skin syndrome
- These complications may occur in as many as 10% of patients with impetigo.
- No correlation between the amount of impetiginous lesions and the involvement of the surrounding soft tissues, lymphatics, or regional lymph nodes has been observed.
- Cellulitis rarely follows bullous impetigo.
- Acute poststreptococcal glomerulonephritis
- APSGN appears 18-21 days after infection with nephritogenic strains of GABHS. Incidence of APSGN widely varies depending on the strain of GABHS.
- No difference between the clinical appearance of impetigo due to nephritogenic and impetigo due to nonnephritogenic strains has been observed.
- Children aged 3-7 years are most commonly affected.
- Treatment of impetigo with systemic antibiotics does not prevent the development of APSGN in the index case. This is most likely due to the activation of the immune response resulting in APSGN prior to antibiotic treatment.
- Scarlet fever
- Osteomyelitis, septic arthritis
- Pneumonia
- Septicemia
- Guttate psoriases
- Rheumatic fever (not a complication of impetigo)
Patient Education
Medical/Legal Pitfalls
- A practitioner is not likely to be sued because of a diagnosis or failure to make a diagnosis of impetigo. The disease may eventually heal over several weeks. Delay in treatment or incorrect treatment should not result in undue harm; however, the practitioner should be aware and anticipate known complications of impetigo.
| Media file 1:
Nonbullous impetigo with vesicles, pustules, and sharply demarcated regions of honey-colored crusts. |
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Media type: Photo
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| Media file 2:
Bullous impetigo with circumscribed lesions with a thin collarette of scale. |
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Media type: Photo
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Impetigo excerpt Article Last Updated: Aug 24, 2007
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