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Impetigo: Diagnosis and Treatment HOLLY HARTMAN-ADAMS, MD; CHRISTINE BANVARD, MD; and GREGORY JUCKETT, MD, MPH West Virginia University Robert C

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Impetigo: Diagnosis and Treatment HOLLY HARTMAN-ADAMS, MD; CHRISTINE BANVARD, MD; and GREGORY JUCKETT, MD, MPH West Virginia University Robert C Impetigo: Diagnosis and Treatment HOLLY HARTMAN-ADAMS, MD; CHRISTINE BANVARD, MD; and GREGORY JUCKETT, MD, MPH West Virginia University Robert C. Byrd Health Sciences Center, Morgantown, West Virginia Impetigo is the most common bacterial skin infection in children two to five years of age. There are two principal types: nonbullous (70% of cases) and bullous (30% of cases). Nonbullous impetigo, or impetigo contagiosa, is caused by Staphylococcus aureus or Streptococcus pyogenes, and is characterized by honey-colored crusts on the face and extremities. Impetigo primarily affects the skin or secondarily infects insect bites, eczema, or herpetic lesions. Bul- lous impetigo, which is caused exclusively by S. aureus, results in large, flaccid bullae and is more likely to affect intertriginous areas. Both types usually resolve within two to three weeks without scarring, and complications are rare, with the most serious being poststreptococcal glomerulonephritis. Treatment includes topical antibiotics such as mupirocin, retapamulin, and fusidic acid. Oral antibiotic therapy can be used for impetigo with large bullae or when topical therapy is impractical. Amoxicillin/clavulanate, dicloxacillin, cephalexin, clindamycin, doxycycline, minocycline, trimethoprim/sulfamethoxazole, and macrolides are options, but penicillin is not. Natural therapies such as tea tree oil; olive, garlic, and coconut oils; and Manuka honey have been anecdotally successful, but lack suf- ficient evidence to recommend or dismiss them as treatment options. Treatments under development include mino- cycline foam and Ozenoxacin, a topical quinolone. Topical disinfectants are inferior to antibiotics and should not be used. Empiric treatment considerations have changed with the increasing prevalence of antibiotic-resistant bacte- ria, with methicillin-resistant S. aureus, macrolide-resistant streptococcus, and mupirocin-resistant streptococcus all documented. Fusidic acid, mupirocin, and retapamulin cover methicillin-susceptible S. aureus and streptococcal infections. Clindamycin proves helpful in suspected methicillin-resistant S. aureus infections. Trimethoprim/sulfa- methoxazole covers methicillin-resistant S. aureus infection, but is inadequate for streptococcal infection. (Am Fam Physician. 2014;90(4):229-235. Copyright © 2014 American Academy of Family Physicians.) CME This clinical content mpetigo is a common bacterial skin to the formation of satellite lesions in adja- conforms to AAFP criteria infection caused by Staphylococcus cent areas.6 The highly contagious nature of for continuing medical education (CME). See aureus, group A beta-hemolytic Strep- impetigo also allows spread from patients to CME Quiz Questions on tococcus pyogenes, a combination of the close contacts. Although impetigo is con- page 226. Itwo, or less commonly, anaerobic bacteria.1,2 sidered a self-limited infection, antibiotic Author disclosure: No rel- In the United States, more than 11 million treatment is often initiated for a quicker cure evant financial affiliations. skin and soft tissue infections are caused and to prevent the spread to others.2 This ▲ 3 Patient information: by S. aureus annually. Impetigo is the most can help decrease the number of school and A handout on this topic, common skin infection in children two work days lost.6 Hygienic practices such as written by the authors of to five years of age, but persons of any age cleaning minor injuries with soap and water, this article, is available can be affected.4 One-third of skin and soft handwashing, regular bathing, and avoiding at http://www.aafp.org/ afp/2014/0815/p229-s1. tissue infections in returning travelers are contact with infected children can help pre- html. attributable to impetigo, usually secondary vent infection.7 to infected mosquito bites.5 Many bacteria inhabit healthy skin; some Clinical Presentation types, such as S. pyogenes and S. aureus, There are two presentations of impetigo: intermittently colonize the nasal, axillary, nonbullous (also known as impetigo conta- pharyngeal, or perineal areas.2,6 These bacte- giosa) and bullous. ria can lead to infection of susceptible skin.6 Other factors that predispose to impetigo NONBULLOUS are skin trauma; hot, humid climates; poor Nonbullous impetigo is the most common hygiene; day care settings; crowding; mal- presentation, comprising 70% of cases. Non- nutrition; and diabetes mellitus or other bullous impetigo can be further classified medical comorbidities.2,6 Autoinoculation as primary or the more prevalent second- via fingers, towels, or clothing often leads ary (common) form.4,8 Primary impetigo is AugustDownloaded 15, 2014 from the◆ Volume American 90, Family Number Physician 4 website at www.aafp.org/afp.www.aafp.org/afp Copyright © 2014 American Academy of FamilyAmerican Physicians. Family For the Physician private, noncom 229- mercial use of one individual user of the website. All other rights reserved. Contact [email protected] for copyright questions and/or permission requests. Impetigo a direct bacterial invasion of intact healthy skin.4,8 Secondary (common) impetigo is a bacterial infection of disrupted skin caused by trauma, eczema, insect bites, scabies, or herpetic outbreaks and other diseases.6 Dia- betes or other underlying systemic condi- tions also increase susceptibility.6 Impetigo starts as maculopapular lesions that transi- Figure 1. Honey-colored crust of nonbullous tion into thin-walled vesicles that rapidly impetigo. rupture, leaving superficial, sometimes pru- Copyright © Logical Images, Inc. ritic or painful erosions covered by the classic honey-colored crusts4,8 (Figure 1). The course of infection can last two to three weeks if untreated.8 Once the crust dries, the remain- ing area heals without scarring. The exposed skin of the face (e.g., nares, perioral region) and the extremities are the most commonly affected sites.1 Regional lymphadenitis may occur, but systemic symptoms are unlikely.1,8 Nonbullous impetigo is usually caused by S. aureus, but S. pyogenes can also be involved, especially in warmer, more humid climates. BULLOUS Bullous impetigo is caused only by S. Figure 2. Flaccid bullae that ooze yellow fluid aureus 1,4,9 and is characterized by large, frag- in a patient with impetigo. ile, flaccid bullae that can rupture and ooze 4 Reprinted with permission from Cole C, Gazewood J. yellow fluid (Figure 2 ). It usually resolves Diagnosis and treatment of impetigo. Am Fam Physician. within two to three weeks without scarring.8 2007;75(6):862. The pathognomonic collarette of scales on its periphery develops after the bullae rupture, leaving a thin, brown crust on the remain- ing erosions1 (Figure 3). These larger bullae form because of exfoliative toxins produced by S. aureus strains that cause loss of cell adhesion in the superficial epidermis.9 Bul- lous impetigo is typically found on the trunk, axilla, and extremities, and in intertriginous (diaper) areas.2 It is the most common cause of ulcerative rash on the buttocks of infants.1 Systemic symptoms are uncommon but can include fever, diarrhea, and weakness.4 Diagnosis The diagnosis of nonbullous and bullous impetigo is nearly always clinical. Differen- tial diagnosis includes many other blistering and rash disorders (Table 1).1,4,10 Skin swabs Figure 3. Brown crust appearing after bullae rupture in a patient with cannot differentiate between bacterial infec- impetigo. tion and colonization.11 In patients in whom Copyright © Logical Images, Inc. first-line therapy fails, culture of the pus or 230 American Family Physician www.aafp.org/afp Volume 90, Number 4 ◆ August 15, 2014 Impetigo bullous fluid, not the intact skin, may be is not practical. Clinicians sometimes may helpful for pathogen identification and anti- choose both topical and systemic therapy.8 microbial susceptibilities.12 Although sero- The ideal treatment should be effective, be logic testing for streptococcal antibodies is inexpensive, have limited adverse effects, and helpful in the diagnosis of acute poststrepto- should not promote bacterial resistance.2,4,8 coccal glomerulonephritis, it does not aid in the diagnosis of impetigo.13 TOPICAL ANTIBIOTICS Topical antibiotics (Table 2 6,8,11,14,17-19) have Complications the advantage of being applied only where Impetigo is usually a self-limited condition, needed, minimizing antibiotic resistance and although rare, complications can occur. and avoiding gastrointestinal and other sys- These include cellulitis (nonbullous form), temic adverse effects.4,8 The length of time of septicemia, osteomyelitis, septic arthritis, topical treatment varies based on product, lymphangitis, lymphadenitis, guttate pso- but in clinical trials, a seven-day course was riasis, staphylococcal scalded skin syndrome, more effective than placebo for resolution and acute poststreptococcal glomerulone- of impetigo.8,11 Local allergic reactions, skin phritis, with poststreptococcal glomerulone- sensitization, and difficulty with application phritis being the most serious.14 The number to areas such as eyelids, mouth, and back of possible causes, incidence, and clinical are potential disadvantages of topical treat- severity of acute poststreptococcal glomer- ments. Three topical antibiotic preparations ulonephritis have decreased, because the recommended for impetigo are mupirocin causative organism of impetigo has shifted 2% cream or ointment (Bactroban), reta- from S. pyogenes to S. aureus.13 Most cases of pamulin 1% ointment (Altabax), and fusidic poststreptococcal glomerulonephritis
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