Atopic Dermatitis Challenge Center

The history and findings in this case are consistent with atopic dermatitis (AD). 

AD is a chronic inflammatory skin condition that affects more than 200 million people worldwide, including as many as 30% of children and 10% of adults. Although it is more common in children (and may persist into adulthood), approximately 1 in 4 adults with AD have adult-onset disease.

The etiology of AD is complex and includes both genetic and environmental factors, including a weakened skin barrier, immune dysregulation, and abnormalities of the skin microbiome. AD is a member of the atopic triad (ie, AD, allergic rhinoconjunctivitis, and asthma), which may commence concurrently or in succession in what is referred to as the "atopic march."

The presentation of adult-onset AD may differ from that seen in children. For example, the most commonly reported body regions affected in adult-onset AD are the hands, eyelids, neck, and flexural surfaces of the upper limbs. In contrast, childhood-onset AD is less specific to body regions other than flexural areas. Xerosis is a prominent feature, and lichenification may be present. Some patients may have a rippled, brown macular ring around the neck, simulating the pigmentations seen in macular amyloid but due instead to postinflammatory melanin deposition. Pruritus is the most common and bothersome symptom associated with AD; patients may also experience anxiety, depression, and sleep disturbances.

Diminished quality of life, reduced productivity at work and school, and increased healthcare costs (hospitalizations, emergency visits, outpatient visits, and medications) have all been reported in patients with AD. Triggers for flare-ups vary among individuals; commonly reported triggers include physical or emotional stress, changes in temperature or humidity, sweating, allergens, and irritants.

AD is typically diagnosed clinically given the characteristic distribution of lesions in various age groups (infancy, childhood, and adult). Associated findings such as keratosis pilaris may help to facilitate the diagnosis. No biomarker for the diagnosis of AD has been found and laboratory testing is rarely necessary. However, a swab of infected skin may help to isolate a specific involved organism (eg, Staphylococcus or Streptococcus) and antibiotic sensitivity. Allergy and radioallergosorbent testing are not necessary to make the diagnosis. A swab for viral polymerase chain reaction may be beneficial to help identify superinfection with herpes simplex virus and identify a diagnosis of eczema herpeticum. Testing for serum IgE level can also be helpful for supporting the diagnosis of AD.

The management of AD includes trigger avoidance, daily skin care with application of emollients, anti-inflammatory therapy, and other complementary modalities. For mild or moderate AD, first-line treatment consists of topical anti-inflammatory ointments and creams, including topical corticosteroids, which are available in a broad range of potencies. Other topical medications include topical calcineurin inhibitors (tacrolimus and pimecrolimus for patients aged ≥ 2 years), which may be particularly appropriate when there is concern for adverse events secondary to corticosteroid use; topical phosphodiesterase 4 inhibitor (crisaborole ointment for patients aged ≥ 3 months); and topical Janus kinase inhibitor (ruxolitinib cream for patients aged ≥ 12 years).

For patients with moderate to severe AD, or for those who are refractory to topical medications, treatment may include biologic therapy (dupilumab and tralokinumab for patients aged ≥ 6 months and ≥ 18 years, respectively), oral Janus kinase inhibitors (upadacitinib and abrocitinib for patients ages ≥ 12 and ≥ 18 years, respectively), phototherapy (commonly narrow-band ultraviolet light type B treatment), and oral immunomodulators (including methotrexate, mycophenolate, and azathioprine). Combination therapy may be required for the long-term management of more severe AD. 

William D. James, MD, Professor, Department of Dermatology, University of Pennsylvania, Philadelphia.

Disclosure: William D. James, MD, has disclosed the following relevant financial relationships:
Received income in an amount equal to or greater than $250 from: Elsevier.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The history and findings in this case are consistent with atopic dermatitis (AD). 

AD is a chronic inflammatory skin condition that affects more than 200 million people worldwide, including as many as 30% of children and 10% of adults. Although it is more common in children (and may persist into adulthood), approximately 1 in 4 adults with AD have adult-onset disease.

The etiology of AD is complex and includes both genetic and environmental factors, including a weakened skin barrier, immune dysregulation, and abnormalities of the skin microbiome. AD is a member of the atopic triad (ie, AD, allergic rhinoconjunctivitis, and asthma), which may commence concurrently or in succession in what is referred to as the "atopic march."

The presentation of adult-onset AD may differ from that seen in children. For example, the most commonly reported body regions affected in adult-onset AD are the hands, eyelids, neck, and flexural surfaces of the upper limbs. In contrast, childhood-onset AD is less specific to body regions other than flexural areas. Xerosis is a prominent feature, and lichenification may be present. Some patients may have a rippled, brown macular ring around the neck, simulating the pigmentations seen in macular amyloid but due instead to postinflammatory melanin deposition. Pruritus is the most common and bothersome symptom associated with AD; patients may also experience anxiety, depression, and sleep disturbances.

Diminished quality of life, reduced productivity at work and school, and increased healthcare costs (hospitalizations, emergency visits, outpatient visits, and medications) have all been reported in patients with AD. Triggers for flare-ups vary among individuals; commonly reported triggers include physical or emotional stress, changes in temperature or humidity, sweating, allergens, and irritants.

AD is typically diagnosed clinically given the characteristic distribution of lesions in various age groups (infancy, childhood, and adult). Associated findings such as keratosis pilaris may help to facilitate the diagnosis. No biomarker for the diagnosis of AD has been found and laboratory testing is rarely necessary. However, a swab of infected skin may help to isolate a specific involved organism (eg, Staphylococcus or Streptococcus) and antibiotic sensitivity. Allergy and radioallergosorbent testing are not necessary to make the diagnosis. A swab for viral polymerase chain reaction may be beneficial to help identify superinfection with herpes simplex virus and identify a diagnosis of eczema herpeticum. Testing for serum IgE level can also be helpful for supporting the diagnosis of AD.

The management of AD includes trigger avoidance, daily skin care with application of emollients, anti-inflammatory therapy, and other complementary modalities. For mild or moderate AD, first-line treatment consists of topical anti-inflammatory ointments and creams, including topical corticosteroids, which are available in a broad range of potencies. Other topical medications include topical calcineurin inhibitors (tacrolimus and pimecrolimus for patients aged ≥ 2 years), which may be particularly appropriate when there is concern for adverse events secondary to corticosteroid use; topical phosphodiesterase 4 inhibitor (crisaborole ointment for patients aged ≥ 3 months); and topical Janus kinase inhibitor (ruxolitinib cream for patients aged ≥ 12 years).

For patients with moderate to severe AD, or for those who are refractory to topical medications, treatment may include biologic therapy (dupilumab and tralokinumab for patients aged ≥ 6 months and ≥ 18 years, respectively), oral Janus kinase inhibitors (upadacitinib and abrocitinib for patients ages ≥ 12 and ≥ 18 years, respectively), phototherapy (commonly narrow-band ultraviolet light type B treatment), and oral immunomodulators (including methotrexate, mycophenolate, and azathioprine). Combination therapy may be required for the long-term management of more severe AD. 

William D. James, MD, Professor, Department of Dermatology, University of Pennsylvania, Philadelphia.

Disclosure: William D. James, MD, has disclosed the following relevant financial relationships:
Received income in an amount equal to or greater than $250 from: Elsevier.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The history and findings in this case are consistent with atopic dermatitis (AD). 

AD is a chronic inflammatory skin condition that affects more than 200 million people worldwide, including as many as 30% of children and 10% of adults. Although it is more common in children (and may persist into adulthood), approximately 1 in 4 adults with AD have adult-onset disease.

The etiology of AD is complex and includes both genetic and environmental factors, including a weakened skin barrier, immune dysregulation, and abnormalities of the skin microbiome. AD is a member of the atopic triad (ie, AD, allergic rhinoconjunctivitis, and asthma), which may commence concurrently or in succession in what is referred to as the "atopic march."

The presentation of adult-onset AD may differ from that seen in children. For example, the most commonly reported body regions affected in adult-onset AD are the hands, eyelids, neck, and flexural surfaces of the upper limbs. In contrast, childhood-onset AD is less specific to body regions other than flexural areas. Xerosis is a prominent feature, and lichenification may be present. Some patients may have a rippled, brown macular ring around the neck, simulating the pigmentations seen in macular amyloid but due instead to postinflammatory melanin deposition. Pruritus is the most common and bothersome symptom associated with AD; patients may also experience anxiety, depression, and sleep disturbances.

Diminished quality of life, reduced productivity at work and school, and increased healthcare costs (hospitalizations, emergency visits, outpatient visits, and medications) have all been reported in patients with AD. Triggers for flare-ups vary among individuals; commonly reported triggers include physical or emotional stress, changes in temperature or humidity, sweating, allergens, and irritants.

AD is typically diagnosed clinically given the characteristic distribution of lesions in various age groups (infancy, childhood, and adult). Associated findings such as keratosis pilaris may help to facilitate the diagnosis. No biomarker for the diagnosis of AD has been found and laboratory testing is rarely necessary. However, a swab of infected skin may help to isolate a specific involved organism (eg, Staphylococcus or Streptococcus) and antibiotic sensitivity. Allergy and radioallergosorbent testing are not necessary to make the diagnosis. A swab for viral polymerase chain reaction may be beneficial to help identify superinfection with herpes simplex virus and identify a diagnosis of eczema herpeticum. Testing for serum IgE level can also be helpful for supporting the diagnosis of AD.

The management of AD includes trigger avoidance, daily skin care with application of emollients, anti-inflammatory therapy, and other complementary modalities. For mild or moderate AD, first-line treatment consists of topical anti-inflammatory ointments and creams, including topical corticosteroids, which are available in a broad range of potencies. Other topical medications include topical calcineurin inhibitors (tacrolimus and pimecrolimus for patients aged ≥ 2 years), which may be particularly appropriate when there is concern for adverse events secondary to corticosteroid use; topical phosphodiesterase 4 inhibitor (crisaborole ointment for patients aged ≥ 3 months); and topical Janus kinase inhibitor (ruxolitinib cream for patients aged ≥ 12 years).

For patients with moderate to severe AD, or for those who are refractory to topical medications, treatment may include biologic therapy (dupilumab and tralokinumab for patients aged ≥ 6 months and ≥ 18 years, respectively), oral Janus kinase inhibitors (upadacitinib and abrocitinib for patients ages ≥ 12 and ≥ 18 years, respectively), phototherapy (commonly narrow-band ultraviolet light type B treatment), and oral immunomodulators (including methotrexate, mycophenolate, and azathioprine). Combination therapy may be required for the long-term management of more severe AD. 

William D. James, MD, Professor, Department of Dermatology, University of Pennsylvania, Philadelphia.

Disclosure: William D. James, MD, has disclosed the following relevant financial relationships:
Received income in an amount equal to or greater than $250 from: Elsevier.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Atopic dermatitis (AD) is one of the most common chronic, inflammatory skin diseases encountered by dermatologists. AD is characterized by pruritus and a chronic course of exacerbations and remissions. AD is thought to involve the interplay of genetic predisposition, immune dysregulation, and environmental factors. It is also associated with other allergic conditions, including asthma. 

Although AD typically presents with pruritus as the hallmark symptom in all patients, the appearance of skin lesions may vary among different skin types. In individuals with light-colored skin, AD often appears as erythematous patches and plaques. It also more commonly affects the flexor surfaces of the skin. In individuals with darker skin tones, AD may more often result in follicularly centered papules, lichenification, and pigmentary changes. Lesions may also present on extensor surfaces rather than the typical flexure surfaces. Erythema in darker skin types may appear reddish-brown, have a violaceous hue, or be an ashen gray or darker brown color rather than bright red. Because erythema is more difficult to detect in darker skin types, clinicians may mistakenly minimize the severity of AD. 

Clinical severity may also differ between ethnicities. Black patients have an increased tendency toward hyperlinearity of the palms, periorbital dark circles, Dennie-Morgan lines, and diffuse xerosis. Compared with White patients, Black patients with AD are also more likely to develop prurigo nodularis and lichenification. In contrast, Asian patients with AD often experience psoriasiform features, with lesions having more well-defined borders and increased scaling and lichenification.

Beyond differences in clinical appearance, AD may appear molecularly and histologically distinct in ethnic skin. One study suggests that Black patients with AD may have decreased Th1 and Th17 but share similar upregulation of Th2 and Th22 as seen in White patients. Another study showed that Asian patients may have higher Th17 and Th22 and lower Th1/interferon compared with White patients. 

Regardless of skin type, treatment goals remain the same. Treatment goals aim to repair and improve the function of the skin barrier while preventing and managing flares. Clinical studies have shown that skincare regimens incorporating ceramide-containing moisturizers may improve AD by increasing the lipid content in the skin. This may offer clinical benefit in patients with skin of color. However, some treatments often used for AD may lead to other skin issues in skin in color. For example, long-term use of topical steroids may worsen hypopigmentation in darker skin types. Management strategies should take into account the unique clinical and genetic features of AD among different patient demographic groups. 

William D. James, MD, Professor, Department of Dermatology, University of Pennsylvania, Philadelphia.

Disclosure: William D. James, MD, has disclosed the following relevant financial relationships:
Received income in an amount equal to or greater than $250 from: Elsevier.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Atopic dermatitis (AD) is one of the most common chronic, inflammatory skin diseases encountered by dermatologists. AD is characterized by pruritus and a chronic course of exacerbations and remissions. AD is thought to involve the interplay of genetic predisposition, immune dysregulation, and environmental factors. It is also associated with other allergic conditions, including asthma. 

Although AD typically presents with pruritus as the hallmark symptom in all patients, the appearance of skin lesions may vary among different skin types. In individuals with light-colored skin, AD often appears as erythematous patches and plaques. It also more commonly affects the flexor surfaces of the skin. In individuals with darker skin tones, AD may more often result in follicularly centered papules, lichenification, and pigmentary changes. Lesions may also present on extensor surfaces rather than the typical flexure surfaces. Erythema in darker skin types may appear reddish-brown, have a violaceous hue, or be an ashen gray or darker brown color rather than bright red. Because erythema is more difficult to detect in darker skin types, clinicians may mistakenly minimize the severity of AD. 

Clinical severity may also differ between ethnicities. Black patients have an increased tendency toward hyperlinearity of the palms, periorbital dark circles, Dennie-Morgan lines, and diffuse xerosis. Compared with White patients, Black patients with AD are also more likely to develop prurigo nodularis and lichenification. In contrast, Asian patients with AD often experience psoriasiform features, with lesions having more well-defined borders and increased scaling and lichenification.

Beyond differences in clinical appearance, AD may appear molecularly and histologically distinct in ethnic skin. One study suggests that Black patients with AD may have decreased Th1 and Th17 but share similar upregulation of Th2 and Th22 as seen in White patients. Another study showed that Asian patients may have higher Th17 and Th22 and lower Th1/interferon compared with White patients. 

Regardless of skin type, treatment goals remain the same. Treatment goals aim to repair and improve the function of the skin barrier while preventing and managing flares. Clinical studies have shown that skincare regimens incorporating ceramide-containing moisturizers may improve AD by increasing the lipid content in the skin. This may offer clinical benefit in patients with skin of color. However, some treatments often used for AD may lead to other skin issues in skin in color. For example, long-term use of topical steroids may worsen hypopigmentation in darker skin types. Management strategies should take into account the unique clinical and genetic features of AD among different patient demographic groups. 

William D. James, MD, Professor, Department of Dermatology, University of Pennsylvania, Philadelphia.

Disclosure: William D. James, MD, has disclosed the following relevant financial relationships:
Received income in an amount equal to or greater than $250 from: Elsevier.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Atopic dermatitis (AD) is one of the most common chronic, inflammatory skin diseases encountered by dermatologists. AD is characterized by pruritus and a chronic course of exacerbations and remissions. AD is thought to involve the interplay of genetic predisposition, immune dysregulation, and environmental factors. It is also associated with other allergic conditions, including asthma. 

Although AD typically presents with pruritus as the hallmark symptom in all patients, the appearance of skin lesions may vary among different skin types. In individuals with light-colored skin, AD often appears as erythematous patches and plaques. It also more commonly affects the flexor surfaces of the skin. In individuals with darker skin tones, AD may more often result in follicularly centered papules, lichenification, and pigmentary changes. Lesions may also present on extensor surfaces rather than the typical flexure surfaces. Erythema in darker skin types may appear reddish-brown, have a violaceous hue, or be an ashen gray or darker brown color rather than bright red. Because erythema is more difficult to detect in darker skin types, clinicians may mistakenly minimize the severity of AD. 

Clinical severity may also differ between ethnicities. Black patients have an increased tendency toward hyperlinearity of the palms, periorbital dark circles, Dennie-Morgan lines, and diffuse xerosis. Compared with White patients, Black patients with AD are also more likely to develop prurigo nodularis and lichenification. In contrast, Asian patients with AD often experience psoriasiform features, with lesions having more well-defined borders and increased scaling and lichenification.

Beyond differences in clinical appearance, AD may appear molecularly and histologically distinct in ethnic skin. One study suggests that Black patients with AD may have decreased Th1 and Th17 but share similar upregulation of Th2 and Th22 as seen in White patients. Another study showed that Asian patients may have higher Th17 and Th22 and lower Th1/interferon compared with White patients. 

Regardless of skin type, treatment goals remain the same. Treatment goals aim to repair and improve the function of the skin barrier while preventing and managing flares. Clinical studies have shown that skincare regimens incorporating ceramide-containing moisturizers may improve AD by increasing the lipid content in the skin. This may offer clinical benefit in patients with skin of color. However, some treatments often used for AD may lead to other skin issues in skin in color. For example, long-term use of topical steroids may worsen hypopigmentation in darker skin types. Management strategies should take into account the unique clinical and genetic features of AD among different patient demographic groups. 

William D. James, MD, Professor, Department of Dermatology, University of Pennsylvania, Philadelphia.

Disclosure: William D. James, MD, has disclosed the following relevant financial relationships:
Received income in an amount equal to or greater than $250 from: Elsevier.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The patient is diagnosed with atopic dermatitis (AD) complicated by skin infection. 

AD is the most common chronic pruritic inflammatory skin disorder that affects both children and adults. In the United States, up to 18% of children and 7% of adults are affected. Atopic dermatitis is associated with diminished quality of life, including disruption in activities of daily living, sleep disturbance, depression, and anxiety. Moreover, patients with AD have an increased risk for infections. A significantly higher prevalence of cutaneous and systemic infections is seen in patients with AD compared with individuals without AD.

Bacterial infections are common in AD and are usually caused by Staphylococcus aureus. Examples include impetigo, which typically presents with oozing serum that dries, resulting in a honey-crusted appearance surrounded by an erythematous base. Fluid-filled blisters (bullous impetigo) may also be present, which can be mistaken for eczema herpeticum (EH).

Nonpurulent skin and soft tissue infections (SSTIs) include erysipelas and cellulitis. In most cases, these infections begin in a focal skin area but spread rapidly across the affected sites such as the arms, legs, trunk, or face. Signs typically include focal erythema, swelling, warmth, and tenderness; fever and bacteremia may also be present. 

Purulent SSTIs present as skin abscesses, involving fluctuant or nonfluctuant nodules or pustules surrounded by an erythematous swelling; the lesions may also be tender and warm. Methicillin-resistant S aureus (MRSA) is a common cause of purulent SSTIs. 

Systemic complications of SSTI in AD may include bacteremia, osteomyelitis, septic arthritis, or bursitis; less often, endocarditis and staphylococcal scalded skin syndrome may occur. Clinicians should maintain a high index of suspicion for these complications in patients who present with an ill-looking appearance, lethargy, focal point tenderness of the bone, joint swelling, heart murmur, and widespread desquamation. Persistent elevated inflammatory markers (eg, C-reactive protein or erythrocyte sedimentation rate) should increase the level of suspicion.

Nonbacterial infections can occur concurrently with bacterial skin infections and the two can be difficult to distinguish. For example, EH results from the local spread of herpes simplex virus, which has a predilection for AD lesions. Early during EH, skin lesions appear as superficial clusters of dome‐shaped vesicles and/or small, round, punched‐out erosions. With progression, the lesions may become superficially infected with S aureus and may develop the characteristic honey-colored scale of impetigo.

Factors that contribute to the increased prevalence of infections in AD include skin barrier defects, suppression of cutaneous innate immunity by type 2 inflammation, S aureus colonization, allergen sensitivity, filaggrin loss-of-function mutation, and cutaneous dysbiosis. 

Daily skin hydration and moisturization is a fundamental component of treatment for any patient with AD, both to treat the AD and prevent infection. Patients with AD should bathe daily, followed by gentle drying and application of a moisturizer or a prescribed topical medication. Standard topical anti-inflammatory medications, including topical corticosteroids and topical calcineurin inhibitors, improve skin barrier functions and have been reported to decrease S aureus colonization in AD lesions. Similarly, the monoclonal antibody dupilumab has been shown to decrease S aureus colonization and increase microbial diversity.
 
In the presence of an uncomplicated, nonpurulent skin infection, a beta-lactam antibiotic that covers both S aureus and beta-hemolytic streptococci (eg, cefazolin or cephalexin) may be sufficient, depending on clinical response or culture and in consideration of local epidemiology and resistance patterns. For patients with AD who present with a skin abscess, history of MRSA colonization, close contacts with a history of skin infections, or recent hospitalization, coverage for MRSA should be considered. Acceptable oral options for MRSA skin infections include clindamycin, doxycycline, trimethoprim-sulfamethoxazole, and linezolid, assuming that the isolate is susceptible in vitro. Topical mupirocin ointment can be used for patients with minor, localized skin infections (eg, impetigo). 

William D. James, MD, Professor, Department of Dermatology, University of Pennsylvania, Philadelphia.

Disclosure: William D. James, MD, has disclosed the following relevant financial relationships:
Received income in an amount equal to or greater than $250 from: Elsevier.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The patient is diagnosed with atopic dermatitis (AD) complicated by skin infection. 

AD is the most common chronic pruritic inflammatory skin disorder that affects both children and adults. In the United States, up to 18% of children and 7% of adults are affected. Atopic dermatitis is associated with diminished quality of life, including disruption in activities of daily living, sleep disturbance, depression, and anxiety. Moreover, patients with AD have an increased risk for infections. A significantly higher prevalence of cutaneous and systemic infections is seen in patients with AD compared with individuals without AD.

Bacterial infections are common in AD and are usually caused by Staphylococcus aureus. Examples include impetigo, which typically presents with oozing serum that dries, resulting in a honey-crusted appearance surrounded by an erythematous base. Fluid-filled blisters (bullous impetigo) may also be present, which can be mistaken for eczema herpeticum (EH).

Nonpurulent skin and soft tissue infections (SSTIs) include erysipelas and cellulitis. In most cases, these infections begin in a focal skin area but spread rapidly across the affected sites such as the arms, legs, trunk, or face. Signs typically include focal erythema, swelling, warmth, and tenderness; fever and bacteremia may also be present. 

Purulent SSTIs present as skin abscesses, involving fluctuant or nonfluctuant nodules or pustules surrounded by an erythematous swelling; the lesions may also be tender and warm. Methicillin-resistant S aureus (MRSA) is a common cause of purulent SSTIs. 

Systemic complications of SSTI in AD may include bacteremia, osteomyelitis, septic arthritis, or bursitis; less often, endocarditis and staphylococcal scalded skin syndrome may occur. Clinicians should maintain a high index of suspicion for these complications in patients who present with an ill-looking appearance, lethargy, focal point tenderness of the bone, joint swelling, heart murmur, and widespread desquamation. Persistent elevated inflammatory markers (eg, C-reactive protein or erythrocyte sedimentation rate) should increase the level of suspicion.

Nonbacterial infections can occur concurrently with bacterial skin infections and the two can be difficult to distinguish. For example, EH results from the local spread of herpes simplex virus, which has a predilection for AD lesions. Early during EH, skin lesions appear as superficial clusters of dome‐shaped vesicles and/or small, round, punched‐out erosions. With progression, the lesions may become superficially infected with S aureus and may develop the characteristic honey-colored scale of impetigo.

Factors that contribute to the increased prevalence of infections in AD include skin barrier defects, suppression of cutaneous innate immunity by type 2 inflammation, S aureus colonization, allergen sensitivity, filaggrin loss-of-function mutation, and cutaneous dysbiosis. 

Daily skin hydration and moisturization is a fundamental component of treatment for any patient with AD, both to treat the AD and prevent infection. Patients with AD should bathe daily, followed by gentle drying and application of a moisturizer or a prescribed topical medication. Standard topical anti-inflammatory medications, including topical corticosteroids and topical calcineurin inhibitors, improve skin barrier functions and have been reported to decrease S aureus colonization in AD lesions. Similarly, the monoclonal antibody dupilumab has been shown to decrease S aureus colonization and increase microbial diversity.
 
In the presence of an uncomplicated, nonpurulent skin infection, a beta-lactam antibiotic that covers both S aureus and beta-hemolytic streptococci (eg, cefazolin or cephalexin) may be sufficient, depending on clinical response or culture and in consideration of local epidemiology and resistance patterns. For patients with AD who present with a skin abscess, history of MRSA colonization, close contacts with a history of skin infections, or recent hospitalization, coverage for MRSA should be considered. Acceptable oral options for MRSA skin infections include clindamycin, doxycycline, trimethoprim-sulfamethoxazole, and linezolid, assuming that the isolate is susceptible in vitro. Topical mupirocin ointment can be used for patients with minor, localized skin infections (eg, impetigo). 

William D. James, MD, Professor, Department of Dermatology, University of Pennsylvania, Philadelphia.

Disclosure: William D. James, MD, has disclosed the following relevant financial relationships:
Received income in an amount equal to or greater than $250 from: Elsevier.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The patient is diagnosed with atopic dermatitis (AD) complicated by skin infection. 

AD is the most common chronic pruritic inflammatory skin disorder that affects both children and adults. In the United States, up to 18% of children and 7% of adults are affected. Atopic dermatitis is associated with diminished quality of life, including disruption in activities of daily living, sleep disturbance, depression, and anxiety. Moreover, patients with AD have an increased risk for infections. A significantly higher prevalence of cutaneous and systemic infections is seen in patients with AD compared with individuals without AD.

Bacterial infections are common in AD and are usually caused by Staphylococcus aureus. Examples include impetigo, which typically presents with oozing serum that dries, resulting in a honey-crusted appearance surrounded by an erythematous base. Fluid-filled blisters (bullous impetigo) may also be present, which can be mistaken for eczema herpeticum (EH).

Nonpurulent skin and soft tissue infections (SSTIs) include erysipelas and cellulitis. In most cases, these infections begin in a focal skin area but spread rapidly across the affected sites such as the arms, legs, trunk, or face. Signs typically include focal erythema, swelling, warmth, and tenderness; fever and bacteremia may also be present. 

Purulent SSTIs present as skin abscesses, involving fluctuant or nonfluctuant nodules or pustules surrounded by an erythematous swelling; the lesions may also be tender and warm. Methicillin-resistant S aureus (MRSA) is a common cause of purulent SSTIs. 

Systemic complications of SSTI in AD may include bacteremia, osteomyelitis, septic arthritis, or bursitis; less often, endocarditis and staphylococcal scalded skin syndrome may occur. Clinicians should maintain a high index of suspicion for these complications in patients who present with an ill-looking appearance, lethargy, focal point tenderness of the bone, joint swelling, heart murmur, and widespread desquamation. Persistent elevated inflammatory markers (eg, C-reactive protein or erythrocyte sedimentation rate) should increase the level of suspicion.

Nonbacterial infections can occur concurrently with bacterial skin infections and the two can be difficult to distinguish. For example, EH results from the local spread of herpes simplex virus, which has a predilection for AD lesions. Early during EH, skin lesions appear as superficial clusters of dome‐shaped vesicles and/or small, round, punched‐out erosions. With progression, the lesions may become superficially infected with S aureus and may develop the characteristic honey-colored scale of impetigo.

Factors that contribute to the increased prevalence of infections in AD include skin barrier defects, suppression of cutaneous innate immunity by type 2 inflammation, S aureus colonization, allergen sensitivity, filaggrin loss-of-function mutation, and cutaneous dysbiosis. 

Daily skin hydration and moisturization is a fundamental component of treatment for any patient with AD, both to treat the AD and prevent infection. Patients with AD should bathe daily, followed by gentle drying and application of a moisturizer or a prescribed topical medication. Standard topical anti-inflammatory medications, including topical corticosteroids and topical calcineurin inhibitors, improve skin barrier functions and have been reported to decrease S aureus colonization in AD lesions. Similarly, the monoclonal antibody dupilumab has been shown to decrease S aureus colonization and increase microbial diversity.
 
In the presence of an uncomplicated, nonpurulent skin infection, a beta-lactam antibiotic that covers both S aureus and beta-hemolytic streptococci (eg, cefazolin or cephalexin) may be sufficient, depending on clinical response or culture and in consideration of local epidemiology and resistance patterns. For patients with AD who present with a skin abscess, history of MRSA colonization, close contacts with a history of skin infections, or recent hospitalization, coverage for MRSA should be considered. Acceptable oral options for MRSA skin infections include clindamycin, doxycycline, trimethoprim-sulfamethoxazole, and linezolid, assuming that the isolate is susceptible in vitro. Topical mupirocin ointment can be used for patients with minor, localized skin infections (eg, impetigo). 

William D. James, MD, Professor, Department of Dermatology, University of Pennsylvania, Philadelphia.

Disclosure: William D. James, MD, has disclosed the following relevant financial relationships:
Received income in an amount equal to or greater than $250 from: Elsevier.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.