Impetigo


Article Author:
Naomi Nardi


Article Editor:
Timothy Schaefer


Editors In Chief:
Laurie Graham
Andrew Wilt
Mary Cataletto


Managing Editors:
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Frank Smeeks
Kristina Soman-Faulkner
Benjamin Eovaldi
Radia Jamil
Sobhan Daneshfar
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Hajira Basit
Phillip Hynes


Updated:
2/17/2019 9:06:04 AM

Introduction

 Impetigo is a common infection of the superficial layers of the epidermis that is highly contagious and most commonly caused by gram-positive bacteria. It most commonly presents as erythematous plaques with a yellow crust and may be itchy or painful.  The lesions are highly contagious and spread easily. Diagnosis is typically based on the symptoms and clinical manifestations alone. Treatment involves topical and oral antibiotics and symptomatic care.[1][2][3]

Etiology

Impetigo accounts for approximately 10% of skin complaints in the pediatric population. When considering all age ranges, the incidence is the same in males and females.  In adults, men are more commonly affected.  It is most prevalent in children aged 2-5 years old but can occur at any age. The peak incidence is during summer and fall. Bullous impetigo is more common in infants.  Children younger than two account for 90% of cases of bullous impetigo.[4][5][6][7]

Epidemiology

Nonbullous impetigo is most commonly caused by S aureus which is responsible for 80% of cases. Group A beta-hemolytic Strep (GABHS) accounts for 10% of cases and the causative agent is a combination of S. aureus and GABHS 10% of the time. Methicillin-resistant S aureus (MRSA) has become more prevalent, especially in hospitalized patients.

Bullous impetigo is caused almost exclusively by S aureus.

Pathophysiology

Impetigo can be classified as either primary or secondary.  Primary impetigo involves previously normal skin affected by direct bacterial invasion.  Secondary impetigo involves infection forming at a previous skin wound site.

Any disturbance of the skin barrier leads to access to fibronectin receptors by GABHS and S aureus which require fibronectin for colonization. Trauma, cuts, insect bites, surgery, atopic dermatitis, burns, and varicella are common mechanisms of skin breakdown. Once a lesion is present, self-inoculation to other sites is very common. Malnutrition, immunosuppression, daycare attendance, overcrowding, diabetes, and poor hygiene make one more susceptible to impetigo.

Toxicokinetics

History and Physical

Nonbullous impetigo often starts as a vesicle or a pustule. Multiple vesicles often coalesce and rupture after which the purulent exudate forms the characteristic honey-colored crust. An erythematous base is also present.  There are often multiple lesions on the face and extremities, especially in areas in which disruption of the skin barrier has occurred.  The rapid spread and satellite lesion formation follow self-inoculation, often in areas with no apparent break in the skin barrier. Mild regional lymphadenopathy is a common associated finding. Systemic symptoms such as fever are typically absent in nonbullous impetigo.

Bullous impetigo begins with small vesicles that become flaccid bullae. The exfoliative toxin A produced by S. aureus causes loss of cell adhesion in the superficial epidermis. The bullae contain a clear or yellow fluid which eventually progresses to become purulent or dark. Surrounding erythema and edema are typically absent.  Once the bullae rupture, an erythematous base with a rim of scale remains. Bullous impetigo does not form a honey-colored crust. Lesions most commonly form in the intertriginous regions and on the trunk and, unlike nonbullous impetigo, may occur in the buccal membranes.  There are typically fewer lesions present than in non-bullous impetigo.  Regional lymphadenopathy is absent. Systemic symptoms, such as fever, are more common than in nonbullous impetigo.

Ecthyma is a deep tissue form of impetigo. Ulcerative lesions penetrate through the epidermis and deep into the dermis.  These ulcers appear as “punched out” lesions with violaceous margins. The crusts can be honey colored or brown-black. The lesions may be purulent.

Evaluation

History and physical exam are essential to the diagnosis of impetigo.  Bacterial cultures can be used for confirmation of diagnosis and should be obtained if methicillin-resistant staph aureus (MRSA) is suspected or if an impetigo outbreak is present.  A skin biopsy may be considered if the case is refractory.

The anti-streptolysin O (ASO) response is weak from impetigo alone. Therefore, serologic testing for streptococcal antibodies is not indicated for the diagnosis of impetigo. However, it may be useful if poststreptococcal glomerulonephritis is suspected in a patient with a recent impetigo outbreak.

Human immunodeficiency virus (HIV) testing should be considered when a previously healthy adult develops bullous impetigo.

Treatment / Management

Topical antibiotics alone or in conjunction with systemic antibiotics are used to treat impetigo. Antibiotic coverage should cover both S aureus and S pyogenes (i.e. GABHS). While untreated impetigo is often self-limiting, antibiotics decrease the duration of illness and spread of lesions. In addition, antibiotic treatment decreases the chances of complications involving kidneys, joints, bones, and lungs, as well as acute rheumatic fever.[8][9][10]

For localized, uncomplicated, non-bullous impetigo, topical therapy alone is the treatment of choice.  The crust should be removed with soap and water before application of topical antibiotic therapy. Mupirocin, retapamulin, and fusidic acid are the treatments of choice.

Systemic antibiotics should be prescribed for all cases of bullous impetigo and cases of non-bullous impetigo with more than five lesions, deep tissue involvement, systemic signs of infection, lymphadenopathy or lesions in the oral cavity. Beta-lactamase-resistant antibiotics such as cephalosporins, amoxicillin-clavulanate, dicloxacillin are the treatment of choice. Cephalexin is commonly used. If culture confirms an infection solely caused by streptococci, oral penicillin is the preferred therapy.

In areas of high prevalence of MRSA  or if cultures are positive for MRSA, clindamycin or doxycycline are the preferred treatments. Trimethoprim-sulfamethoxazole is effective against MRSA, but should only be used if group A streptococci are not the causative agent, or in addition to an anti-streptococcal antibiotic.

Children with impetigo should maintain good personal hygiene and avoid other children during the active outbreak. It is important to wash hands, linens, clothes and affected areas that may have come into contact with infected fluids. Sores can be covered with a bandage to help prevent spread by contact. If impetigo is recurrent, evaluation for carriage of the causative bacteria should be performed.  The nose is a common reservoir and carriers can be treated with mupirocin (Bactroban Nasal) applied in the nostrils.

Pearls and Other Issues

Approximately 5% of patients with impetigo will develop an associated glomerulonephritis.  There is inconclusive evidence about whether or not antibiotics help reduce the incidence of poststreptococcal glomerulonephritis.  Poststreptococcal glomerulonephritis typically occurs one to two weeks after a streptococcal infection. Patients may experience fever, hypertension, edema and hematuria.

Enhancing Healthcare Team Outcomes

Impetigo is usually managed by a multidisciplinary team that consists of a nurse practitioner, primary care provider, pediatrician, and a dermatologist. Topical antibiotics alone or in conjunction with systemic antibiotics are used to treat impetigo. Antibiotic coverage should cover both S aureus and S pyogenes (i.e. GABHS). While untreated impetigo is often self-limiting, antibiotics decrease the duration of illness and spread of lesions. In addition, antibiotic treatment decreases the chances of complications involving kidneys, joints, bones, and lungs, as well as acute rheumatic fever.

In areas of high prevalence of MRSA  or if cultures are positive for MRSA, clindamycin or doxycycline are the preferred treatments. Trimethoprim-sulfamethoxazole is effective against MRSA, but should only be used if group A streptococci are not the causative agent, or in addition to an anti-streptococcal antibiotic.

Children with impetigo should maintain good personal hygiene and avoid other children during the active outbreak. It is important to wash hands, linens, clothes and affected areas that may have come into contact with infected fluids. Sores can be covered with a bandage to help prevent spread by contact. If impetigo is recurrent, evaluation for carriage of the causative bacteria should be performed.  The nose is a common reservoir and carriers can be treated with mupirocin (Bactroban Nasal) applied in the nostrils. Children with severe impetigo should be followed because a small number may develop glomerulonephritis. The outcomes in most other cases are excellent. [11][12](Level V)

 


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Impetigo - Questions

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A toddler has impetigo contagiosa and will receive mupirocin applications three times a day for one to two weeks. When should the parents be told to return if there is no improvement?



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A 4-year-old has a 2 cm left knee lesion that has a honey-colored crust. The diagnosis is impetigo and antibiotics are started. What is the most likely complication?



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Which of the following antibiotics is indicated for the treatment of impetigo?



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What is the most likely infectious cause of an erythematous, crusty lesion over the angle of an individual's mouth?

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What is the best method for preventing the spread of impetigo?



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Which of the following medications may be used for the initial treatment of widespread impetigo?



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Which of the following is the most appropriate treatment of impetigo?



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Which of the following diseases typically presents with honey-crusted vesicles around the mouth and nostrils?

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Which of the following is the treatment of choice for vesicular lesions around the mouth and nostrils with an overlying honey-colored crust?



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Impetigo is associated with which of the following?



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What is the most common skin infection in children?



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Which of the following is true of impetigo?



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Which of the following statements about impetigo is false?



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Which of the following is the most likely diagnosis in a child with a tender crusting honey-colored rash associated with erythema around the nares?



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Which group A streptococcal disease is highly communicable in infants?



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A 12-month-old is brought in for a rash on the face. There is a plaque that is erythematous with several small vesicles. The surface is moist with a honey yellow crust. What is the best diagnostic test?



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What is the best initial treatment for impetigo?



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After tending her children, a woman develops red facial macules. These lesions subsequently become vesicles that rupture and form yellow "stuck-on" crusts. What is the most likely diagnosis?



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A 4-year-old girl is brought in for assessment of multiple sores on her face. Her mother states that it started as one small lesion that appeared to burst and subsequently formed a yellow scab. She then developed several other similar lesions on her face. Which two organisms would most likely be most likely?



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A 6-month-old girl is brought for assessment of multiple sores in her diaper region. Her mother states that the lesions started as blisters that were filled with a yellow fluid. They ruptured easily the night before. The patient has also had a temperature of 101.4 F for two days. On exam, the patient has five small lesions with a collarette of scale surrounding an erythematous base in the patient’s upper thigh folds. There is no crusting present. The patient is non-toxic appearing and has no lymphadenopathy. What is the appropriate treatment and management?



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A 6-month-old girl is brought to the clinic for assessment of multiple sores in her diaper region. Her mother states that the lesions started as blisters that were filled with a yellow fluid. They ruptured easily the night before. The patient has also had a temperature of 101.4 F for 2 days. On exam, the patient has five small lesions with a collarette of scale surrounding an erythematous base in the patient’s upper thigh folds. There is no crusting present. The patient is non-toxic appearing and has no lymphadenopathy. What should be expected on microscopic evaluation?



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A young child is seen because of a skin rash on her face. The mother reports that 12 days ago the child developed a single lesion on her face, and over the past few days, similar lesions have spread as seen in the image below. The child has no other symptoms except for moderate pruritus. This is the second time the child has had this type of rash. A few months ago the rash disappeared on its own. The child's vital signs are within normal limits and she is afebrile. There is no history of travel, allergies, or use of medications. The child does, however, attend school. How can this rash be differentiated from tinea infection?

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A mother brings her 7-year-old son to the emergency department because of a recent skin rash on his face (see image). Which of the following is true regarding this condition? Select all that apply.

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Impetigo - References

References

May PJ,Tong SYC,Steer AC,Currie BJ,Andrews RM,Carapetis JR,Bowen AC, Treatment, prevention and public health management of impetigo, scabies, crusted scabies and fungal skin infections in endemic populations: a systematic review. Tropical medicine     [PubMed]
Leung TN,Hon KL,Leung AK, Group A Streptococcus disease in Hong Kong children: an overview. Hong Kong medical journal = Xianggang yi xue za zhi. 2018 Dec;     [PubMed]
Clebak KT,Malone MA, Skin Infections. Primary care. 2018 Sep;     [PubMed]
Breyre A,Frazee BW, Skin and Soft Tissue Infections in the Emergency Department. Emergency medicine clinics of North America. 2018 Nov;     [PubMed]
Sahu JK,Mishra AK, Ozenoxacin: a novel drug discovery for the treatment of impetigo. Current drug discovery technologies. 2018 May 2;     [PubMed]
Castro MCR,Ramos-E-Silva M, Cutaneous infections in the mature patient. Clinics in dermatology. 2018 Mar - Apr;     [PubMed]
Dayrit JF,Bintanjoyo L,Andersen LK,Davis MDP, Impact of climate change on dermatological conditions related to flooding: update from the International Society of Dermatology Climate Change Committee. International journal of dermatology. 2018 Aug;     [PubMed]
Loadsman MEN,Verheij TJM,van der Velden AW, Impetigo incidence and treatment: a retrospective study of Dutch routine primary care data. Family practice. 2018 Oct 19;     [PubMed]
Smith DRM,Dolk FCK,Pouwels KB,Christie M,Robotham JV,Smieszek T, Defining the appropriateness and inappropriateness of antibiotic prescribing in primary care. The Journal of antimicrobial chemotherapy. 2018 Feb 1;     [PubMed]
Rush J,Dinulos JG, Childhood skin and soft tissue infections: new discoveries and guidelines regarding the management of bacterial soft tissue infections, molluscum contagiosum, and warts. Current opinion in pediatrics. 2016 Apr;     [PubMed]
Rosen T,Albareda N,Rosenberg N,Alonso FG,Roth S,Zsolt I,Hebert AA, Efficacy and Safety of Ozenoxacin Cream for Treatment of Adult and Pediatric Patients With Impetigo: A Randomized Clinical Trial. JAMA dermatology. 2018 Jul 1;     [PubMed]
Nasr SH,Fidler ME,Valeri AM,Cornell LD,Sethi S,Zoller A,Stokes MB,Markowitz GS,D'Agati VD, Postinfectious glomerulonephritis in the elderly. Journal of the American Society of Nephrology : JASN. 2011 Jan;     [PubMed]

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