Robert T. Brodell, MD

A 35-year-old woman sought care at our dermatology clinic with the self-diagnosis of “recurrent shingles,” noting that she’d had a rash over her sacrum on and off for the past 10 years. She said that the tender blisters typically appeared in this area 3 to 4 times per year (FIGURE) and that their onset was occasionally associated with stress. The rash tended to resolve—without treatment—within 5 to 7 days. The patient had no other medical problems or symptoms. Physical examination revealed 3 groups of vesicular lesions, each on an erythematous base, located bilaterally over the gluteal cleft.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Recurrent herpes simplex virus-2

While the presentation of herpes zoster (shingles) and herpes simplex virus (HSV) is similar—grouped vesicles on an erythematous base—recurrent shingles is rare in immunocompetent patients. Also, the herpes zoster rash is generally unilateral and is not common on the buttocks.^1,2

Herpes simplex virus-1 (HSV-1) generally occurs around the mouth. Herpes simplex virus-2 (HSV-2) is generally a genital rash. (Our patient was not aware that she’d had a genital primary HSV-2 infection.) That said, non-genital recurrences in the sacral region and lower extremities occur in up to 60% of patients whose primary genital HSV-2 infection also involved non-genital sites.³

Following a genital primary infection, HSV-2 lies dormant in the sacral nerve root ganglia, which innervate both the genitals and sacrum.

HSV-2 infects an estimated 5% to 25% of adults in western nations.⁴ In 2012, approximately 417 million people ages 15 to 49 were living with HSV-2 worldwide, including 19 million who were newly infected.⁵

A dormant infection that is reactivated. Following a genital primary infection, HSV-2 lies dormant in the sacral nerve root ganglia, which innervate both the genitals and sacrum. Reactivation can thus result in recurrences anywhere over the sacral dermatome.⁶ The sacral area is the most common non-genital site for recurrent HSV-2.³ Reactivation of HSV-2 is more common and more severe in patients with human immunodeficiency virus infection.⁷

Neurologic complications in some patients with genital herpes (eg, sacral radiculopathy, hyperesthesia) reinforce the hypothesis that genital herpes can infect ganglia that are also associated with sacral nerves.⁸ Contrary to popular belief, sacral HSV-2 is not commonly contracted from toilet seats.

How to differentiate herpes simplex from herpes zoster

As noted earlier, the location of the vesicles and unilateral nature of herpes zoster are useful in differentiating HSV from herpes zoster.

Tzanck preparation can’t be used to differentiate HSV and herpes zoster because it will demonstrate multinucleated giant cells in both cases. When necessary, viral culture can be used to distinguish the 2 conditions, although HSV often takes 24 to 72 hours to grow and herpes zoster may take up to 2 weeks.^9,10 Increasingly, polymerase chain reaction is being used for this purpose.

Antivirals are used for both genital and non-genital recurrences

The mainstay of treatment for HSV is antiviral therapy with acyclovir. Famciclovir and valacyclovir can be used as well (TABLE).¹¹ These antivirals inhibit viral DNA replication, shorten duration of symptoms, increase lesion healing, and decrease viral shedding time.¹² They are generally safe; the main adverse effects of oral therapy are nausea, vomiting, and diarrhea.

In general, non-genital recurrences of HSV are treated the same as genital recurrences.¹³ Dosing during prodromal symptoms, or at the first sign of a recurrence is recommended for maximum efficacy.¹³ Suppressive therapy can be effective in patients who experience frequent recurrences and is generally recommended for 6 months to a year or longer.

Patients should also be warned that because of increased genital viral shedding during sacral recurrences, they should avoid sexual contact during outbreaks.¹⁴

Our patient began taking oral valacyclovir 1 g daily and had no recurrences over the next year.

CORRESPONDENCE
Robert T. Brodell, MD, Department of Dermatology, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216; rbrodell@umc.edu

A 35-year-old woman sought care at our dermatology clinic with the self-diagnosis of “recurrent shingles,” noting that she’d had a rash over her sacrum on and off for the past 10 years. She said that the tender blisters typically appeared in this area 3 to 4 times per year (FIGURE) and that their onset was occasionally associated with stress. The rash tended to resolve—without treatment—within 5 to 7 days. The patient had no other medical problems or symptoms. Physical examination revealed 3 groups of vesicular lesions, each on an erythematous base, located bilaterally over the gluteal cleft.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Recurrent herpes simplex virus-2

While the presentation of herpes zoster (shingles) and herpes simplex virus (HSV) is similar—grouped vesicles on an erythematous base—recurrent shingles is rare in immunocompetent patients. Also, the herpes zoster rash is generally unilateral and is not common on the buttocks.^1,2

Herpes simplex virus-1 (HSV-1) generally occurs around the mouth. Herpes simplex virus-2 (HSV-2) is generally a genital rash. (Our patient was not aware that she’d had a genital primary HSV-2 infection.) That said, non-genital recurrences in the sacral region and lower extremities occur in up to 60% of patients whose primary genital HSV-2 infection also involved non-genital sites.³

Following a genital primary infection, HSV-2 lies dormant in the sacral nerve root ganglia, which innervate both the genitals and sacrum.

HSV-2 infects an estimated 5% to 25% of adults in western nations.⁴ In 2012, approximately 417 million people ages 15 to 49 were living with HSV-2 worldwide, including 19 million who were newly infected.⁵

A dormant infection that is reactivated. Following a genital primary infection, HSV-2 lies dormant in the sacral nerve root ganglia, which innervate both the genitals and sacrum. Reactivation can thus result in recurrences anywhere over the sacral dermatome.⁶ The sacral area is the most common non-genital site for recurrent HSV-2.³ Reactivation of HSV-2 is more common and more severe in patients with human immunodeficiency virus infection.⁷

Neurologic complications in some patients with genital herpes (eg, sacral radiculopathy, hyperesthesia) reinforce the hypothesis that genital herpes can infect ganglia that are also associated with sacral nerves.⁸ Contrary to popular belief, sacral HSV-2 is not commonly contracted from toilet seats.

How to differentiate herpes simplex from herpes zoster

As noted earlier, the location of the vesicles and unilateral nature of herpes zoster are useful in differentiating HSV from herpes zoster.

Tzanck preparation can’t be used to differentiate HSV and herpes zoster because it will demonstrate multinucleated giant cells in both cases. When necessary, viral culture can be used to distinguish the 2 conditions, although HSV often takes 24 to 72 hours to grow and herpes zoster may take up to 2 weeks.^9,10 Increasingly, polymerase chain reaction is being used for this purpose.

Antivirals are used for both genital and non-genital recurrences

The mainstay of treatment for HSV is antiviral therapy with acyclovir. Famciclovir and valacyclovir can be used as well (TABLE).¹¹ These antivirals inhibit viral DNA replication, shorten duration of symptoms, increase lesion healing, and decrease viral shedding time.¹² They are generally safe; the main adverse effects of oral therapy are nausea, vomiting, and diarrhea.

In general, non-genital recurrences of HSV are treated the same as genital recurrences.¹³ Dosing during prodromal symptoms, or at the first sign of a recurrence is recommended for maximum efficacy.¹³ Suppressive therapy can be effective in patients who experience frequent recurrences and is generally recommended for 6 months to a year or longer.

Patients should also be warned that because of increased genital viral shedding during sacral recurrences, they should avoid sexual contact during outbreaks.¹⁴

Our patient began taking oral valacyclovir 1 g daily and had no recurrences over the next year.

CORRESPONDENCE
Robert T. Brodell, MD, Department of Dermatology, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216; rbrodell@umc.edu

A 35-year-old woman sought care at our dermatology clinic with the self-diagnosis of “recurrent shingles,” noting that she’d had a rash over her sacrum on and off for the past 10 years. She said that the tender blisters typically appeared in this area 3 to 4 times per year (FIGURE) and that their onset was occasionally associated with stress. The rash tended to resolve—without treatment—within 5 to 7 days. The patient had no other medical problems or symptoms. Physical examination revealed 3 groups of vesicular lesions, each on an erythematous base, located bilaterally over the gluteal cleft.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Recurrent herpes simplex virus-2

While the presentation of herpes zoster (shingles) and herpes simplex virus (HSV) is similar—grouped vesicles on an erythematous base—recurrent shingles is rare in immunocompetent patients. Also, the herpes zoster rash is generally unilateral and is not common on the buttocks.^1,2

Herpes simplex virus-1 (HSV-1) generally occurs around the mouth. Herpes simplex virus-2 (HSV-2) is generally a genital rash. (Our patient was not aware that she’d had a genital primary HSV-2 infection.) That said, non-genital recurrences in the sacral region and lower extremities occur in up to 60% of patients whose primary genital HSV-2 infection also involved non-genital sites.³

Following a genital primary infection, HSV-2 lies dormant in the sacral nerve root ganglia, which innervate both the genitals and sacrum.

HSV-2 infects an estimated 5% to 25% of adults in western nations.⁴ In 2012, approximately 417 million people ages 15 to 49 were living with HSV-2 worldwide, including 19 million who were newly infected.⁵

A dormant infection that is reactivated. Following a genital primary infection, HSV-2 lies dormant in the sacral nerve root ganglia, which innervate both the genitals and sacrum. Reactivation can thus result in recurrences anywhere over the sacral dermatome.⁶ The sacral area is the most common non-genital site for recurrent HSV-2.³ Reactivation of HSV-2 is more common and more severe in patients with human immunodeficiency virus infection.⁷

Neurologic complications in some patients with genital herpes (eg, sacral radiculopathy, hyperesthesia) reinforce the hypothesis that genital herpes can infect ganglia that are also associated with sacral nerves.⁸ Contrary to popular belief, sacral HSV-2 is not commonly contracted from toilet seats.

How to differentiate herpes simplex from herpes zoster

As noted earlier, the location of the vesicles and unilateral nature of herpes zoster are useful in differentiating HSV from herpes zoster.

Tzanck preparation can’t be used to differentiate HSV and herpes zoster because it will demonstrate multinucleated giant cells in both cases. When necessary, viral culture can be used to distinguish the 2 conditions, although HSV often takes 24 to 72 hours to grow and herpes zoster may take up to 2 weeks.^9,10 Increasingly, polymerase chain reaction is being used for this purpose.

Antivirals are used for both genital and non-genital recurrences

The mainstay of treatment for HSV is antiviral therapy with acyclovir. Famciclovir and valacyclovir can be used as well (TABLE).¹¹ These antivirals inhibit viral DNA replication, shorten duration of symptoms, increase lesion healing, and decrease viral shedding time.¹² They are generally safe; the main adverse effects of oral therapy are nausea, vomiting, and diarrhea.

In general, non-genital recurrences of HSV are treated the same as genital recurrences.¹³ Dosing during prodromal symptoms, or at the first sign of a recurrence is recommended for maximum efficacy.¹³ Suppressive therapy can be effective in patients who experience frequent recurrences and is generally recommended for 6 months to a year or longer.

Patients should also be warned that because of increased genital viral shedding during sacral recurrences, they should avoid sexual contact during outbreaks.¹⁴

Our patient began taking oral valacyclovir 1 g daily and had no recurrences over the next year.

CORRESPONDENCE
Robert T. Brodell, MD, Department of Dermatology, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216; rbrodell@umc.edu

CASE 1: A 13-year-old Caucasian girl sought treatment for a pruritic, scaling patch on her right cheek. The patient had a 10-year history of atopic eczema, with rashes primarily in flexural areas, and a history of skin reactions to earrings and rivets in her blue jeans. She had gone 3 years without a rash on her earlobes and periumbilical areas by scrupulously avoiding contact with metal.

The 2 x 2-cm patch of pruritic, scaling, lichenified skin with focal excoriation that brought her in on this day had been on her right cheek for the past 3 months ( FIGURE 1 ). It had not responded to hydrocortisone 2.5% cream and desonide 0.05% cream when she applied it twice daily, nor had it responded to an intralesional injection of 2 cc of 2.5 mg/cc triamcinolone acetonide.

CASE 2: A 13-year-old African American girl with a history of atopic dermatitis went to her doctor for a rash beneath the umbilicus. She’d had the rash, which she said was extremely itchy, for 6 weeks; over the previous 10 days, it had become more widespread. A 6 x 5-cm scaling, lichenified, hyperpigmented plaque was present in the infra-umbilical region. She also had a papular rash on the dorsal hands and axillae.

CASE 3: A 15-year-old Caucasian girl sought care for a pruritic, erythematous rash circumscribing her left wrist in an 8-mm diameter band. She’d had the rash for 6 weeks.

CASE 4: A 58-year-old Caucasian woman presented with a pruritic, erythematous, scaling rash on both upper cheeks just below her lower eyelids. She told the physician that she had a similar pruritic rash on her earlobes when she wore costume jewelry.

CASE 5: A 50-year-old woman went to her doctor for a pruritic, erythematous patch on the anterior and posterior sides of her ear-lobes, bilaterally. She told the physician that her ears had been pierced 2 weeks earlier.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU MANAGE THIS CONDITION?

Diagnosis: Nickel dermatitis

Each of these 5 patients had allergic contact dermatitis caused by nickel. The cheek dermatitis was produced by contact with the circular “menu” button on the patient’s cell phone (Case 1/ FIGURE 1 ), the periumbilical rash by the rivet behind a blue jeans button (Case 2/ FIGURE 2 ), the wrist dermatitis by a bracelet (Case 3/ FIGURE 3 ), the rash on the upper cheeks by eyeglass frames (Case 4/ FIGURE 4 ), and the earlobe dermatitis by earrings (Case 5/ FIGURE 5 ). The presence of nickel in each object was confirmed with a positive dimethylglyoxime (DMG) test.

What you’ll see. Besides an erythematous, pruritic, scaling rash, other findings can include vesicles and bullae that break and form crusts at sites of contact. Extreme pruritus is also commonly seen and prompts chronic rubbing and scratching, resulting in the development of lichenification and hyper-pigmentation.

FIGURE 1
Scaling patch on cheek

FIGURE 2
Rash beneath umbilicus

FIGURE 3
… around the wrist

FIGURE 4
… on the cheeks

FIGURE 5
… on the earlobes

Nickel dermatitis is increasingly common

Nickel is a leading cause of allergic contact dermatitis and is responsible for more cases than all other metals combined.^1,2 The incidence of nickel dermatitis has been increasing in the United States for the last 15 years, annually affecting an estimated 14% to 20% of women and 2% to 4% of men.^3,4 The higher percentage in women is related to nickel exposure associated with ear piercing and nickel-plated jewelry. In fact, the highest risk for nickel allergy is in young females with pierced ears.^2,5,6 The number of affected males, however, is increasing, as earrings and body piercing gain popularity in this group.³

Certain occupations with high exposure to nickel, such as cashiers, hairdressers, metal workers, domestic cleaners, food handlers, bar workers, and painters, are also at risk for acquiring nickel dermatitis.⁷ Patients with atopic eczema are also at increased risk.^8,9

Sweating may increase the severity of the dermatitis. Sodium chloride in the sweat causes corrosion of the metal and increases nickel exposure.¹⁰ Nickel release is therefore common in areas of the body that tend to be sweaty—for example, the hands, especially around the fingers, where inexpensive rings containing nickel are worn, or on the hands of individuals who carry metal key rings.

Consider oral intake of nickel, too. Another far less common, but important, nickel allergy presentation is systemic contact dermatitis from oral intake of nickel. Nuts, legumes, and chocolate can cause a flare-up reaction in a previously positive patch test site or previous site of nickel dermatitis.¹¹ Patients can also develop a dyshidrotic eczema on the hands. Itching and general symptoms, such as headache, nausea, and malaise, have also been reported after the oral nickel exposure of nickel-sensitive individuals.¹² Dietary intervention studies indicate that it is possible to reduce the activity of dermatitis in these patients by maintaining a diet low in nickel.^13-16

Finally, severe local reactions to nickel and other contact allergens can lead to auto-eczematization, in which a papular or papulosquamous eruption and pruritus appear distant from the site of exposure.

Is it atopic eczema or contact dermatitis?

It can be difficult to distinguish a flare in atopic eczema from chronic allergic contact dermatitis in individuals who may display both processes concurrently. The primary clue to the diagnosis is the peculiar localization of the rash, as evidenced by the cases we have described.

Patch testing is not required for diagnosis

Nickel contact dermatitis is often suspected when patients present with an acute or sub-acute eruption characterized by erythema, vesicles, and scaling in a distribution corresponding to a metal contact allergen. Nickel allergy is one of the few types of allergic contact dermatitis where the history of exposure along with the signs and symptoms are so distinctive that patch testing is often not required.

Amelioration of the rash associated with the withdrawal of the contactant serves as adequate confirmation of the diagnosis in many cases. A DMG test is a simple, inexpensive way to determine whether the object in question contains nickel. It can be used in the physician’s office or by the patient at home. Therefore, in some clinical situations, as in the presented cases, it is appropriate to make a presumptive diagnosis of nickel dermatitis, confirm the presence of nickel with a DMG test, remove the off ending metal item, treat with topical anti-inflammatory medications, and confirm the diagnosis by monitoring the patient’s response.

When patients do not respond to withdrawal of the suspected allergen and anti-inflammatory treatment, when multiple allergens are suspected, or when a definitive diagnosis is required for legal purposes, patch testing with nickel can confirm the diagnosis. In some cases, when the distribution of the rash is not distinctive, patch test screening may elicit a positive test to nickel that prompts the physician to investigate the source of the exposure.

Tx: Remove the item, apply topical steroids

Acute episodes of nickel dermatitis are treated with topical steroid creams to break the scratch-itch cycle (which potentiates the reaction) and to reduce the inflammation. This tactic is futile, however, if the allergen remains in contact with the skin. The source of the nickel must be identified and eliminated by the patient, as was done by the 5 patients we cared for.

Clothing accessories containing nickel, such as buckles, zippers, buttons, and metal clips, must be eliminated, as well as other sources of nickel: jewelry, watches, eyeglasses, and cell phones. The situation is complicated by the fact that many patients have underlying atopic eczema/irritant dermatitis, and patients may have more than 1 form of allergic contact dermatitis. For instance, self-treatment with neomycin-containing topical antibiotics may lead to superimposed allergic contact dermatitis from this agent.

Easy preventive steps. Routine prophylactic measures should focus on eliminating exposure to nickel from all identifiable sources. You can suggest that your patient with nickel dermatitis:

• Use a clear plastic cover over the nickel-containing parts of a cell phone.
• Apply a clear coat of nail polish to the buttons and rivets on pants; this can prevent nickel release and will last through at least 2 wash and dry cycles.¹⁷ (Tucking shirts in to prevent buttons and belt buckles from touching the skin is generally ineffective; not only is the shirt unlikely to stay in place all day, but perspiration and friction can also cause problems.)
• Use other barrier coatings, such as Nickel Guard and Beauty Secrets Hardener, which may be effective in preventing contact dermatitis.¹⁸
• Replace rivets on pants with a plastic button, or cover the rivet with a sew-on denim patch. This offers a more permanent approach to eliminating nickel exposure.
• Use plastic covers for earring studs.
• Replace metal eyeglass frames with ones made out of plastic.
• Choose “hypoallergenic” or nickel-free jewelry. Of note, though: Nickel may be present in jewelry labeled hypoallergenic. The patient can perform a DMG test to verify its nickel content.

In patients who continue to react in the absence of nickel jewelry, co-sensitization to gold must be considered, as many patients do react to multiple metals. Gold is a more common allergen than previously reported and is statistically linked to allergic reactions to nickel and cobalt metals.¹⁹ Unlike nickel dermatitis, the clinical relevance of a positive gold patch test is harder to ascertain because rashing distant from areas in direct contact with gold jewelry often occurs. In fact, in some cases of eyelid dermatitis induced by contact allergy to gold, titanium dioxide particles on the skin from cosmetics and sunscreen are thought to adsorb gold particles and carry them to the eyelids.

Disclosure

Dr. Brodell reports that he receives grants/research support from Amgen Inc., Doak Dermatologics, Galderma, and OrthoNeutrogena. He serves as a consultant for, or is on the speakers bureau of, 3M/Graceway Pharmaceuticals, Allergan, CollagGenex Pharmaceuticals, Connetics Corp., Dermik/BenzaClin, Galderma, Genentech, Inc., Genentech/ Raptiva, GlaxoSmithKline, Janssen, MDsConnect.net, Medicis, Novartis Pharmaceuticals Corp., Pedinol Pharmacal, Inc., Roerig-Pfizer, Sandoz/Novartis, sanofi-aventis, Sirius Laboratories, Stiefel, Westwood-Squibb, and Upjohn. Ms. Uhlenhake and Dr. Nedorost reported no potential conflict of interest relevant to this article.

CORRESPONDENCE
Robert Brodell, MD, 2660 East Market Street, Warren, OH 44483; rtb@neoucom.edu

CASE 1: A 13-year-old Caucasian girl sought treatment for a pruritic, scaling patch on her right cheek. The patient had a 10-year history of atopic eczema, with rashes primarily in flexural areas, and a history of skin reactions to earrings and rivets in her blue jeans. She had gone 3 years without a rash on her earlobes and periumbilical areas by scrupulously avoiding contact with metal.

The 2 x 2-cm patch of pruritic, scaling, lichenified skin with focal excoriation that brought her in on this day had been on her right cheek for the past 3 months ( FIGURE 1 ). It had not responded to hydrocortisone 2.5% cream and desonide 0.05% cream when she applied it twice daily, nor had it responded to an intralesional injection of 2 cc of 2.5 mg/cc triamcinolone acetonide.

CASE 2: A 13-year-old African American girl with a history of atopic dermatitis went to her doctor for a rash beneath the umbilicus. She’d had the rash, which she said was extremely itchy, for 6 weeks; over the previous 10 days, it had become more widespread. A 6 x 5-cm scaling, lichenified, hyperpigmented plaque was present in the infra-umbilical region. She also had a papular rash on the dorsal hands and axillae.

CASE 3: A 15-year-old Caucasian girl sought care for a pruritic, erythematous rash circumscribing her left wrist in an 8-mm diameter band. She’d had the rash for 6 weeks.

CASE 4: A 58-year-old Caucasian woman presented with a pruritic, erythematous, scaling rash on both upper cheeks just below her lower eyelids. She told the physician that she had a similar pruritic rash on her earlobes when she wore costume jewelry.

CASE 5: A 50-year-old woman went to her doctor for a pruritic, erythematous patch on the anterior and posterior sides of her ear-lobes, bilaterally. She told the physician that her ears had been pierced 2 weeks earlier.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU MANAGE THIS CONDITION?

Diagnosis: Nickel dermatitis

Each of these 5 patients had allergic contact dermatitis caused by nickel. The cheek dermatitis was produced by contact with the circular “menu” button on the patient’s cell phone (Case 1/ FIGURE 1 ), the periumbilical rash by the rivet behind a blue jeans button (Case 2/ FIGURE 2 ), the wrist dermatitis by a bracelet (Case 3/ FIGURE 3 ), the rash on the upper cheeks by eyeglass frames (Case 4/ FIGURE 4 ), and the earlobe dermatitis by earrings (Case 5/ FIGURE 5 ). The presence of nickel in each object was confirmed with a positive dimethylglyoxime (DMG) test.

What you’ll see. Besides an erythematous, pruritic, scaling rash, other findings can include vesicles and bullae that break and form crusts at sites of contact. Extreme pruritus is also commonly seen and prompts chronic rubbing and scratching, resulting in the development of lichenification and hyper-pigmentation.

FIGURE 1
Scaling patch on cheek

FIGURE 2
Rash beneath umbilicus

FIGURE 3
… around the wrist

FIGURE 4
… on the cheeks

FIGURE 5
… on the earlobes

Nickel dermatitis is increasingly common

Nickel is a leading cause of allergic contact dermatitis and is responsible for more cases than all other metals combined.^1,2 The incidence of nickel dermatitis has been increasing in the United States for the last 15 years, annually affecting an estimated 14% to 20% of women and 2% to 4% of men.^3,4 The higher percentage in women is related to nickel exposure associated with ear piercing and nickel-plated jewelry. In fact, the highest risk for nickel allergy is in young females with pierced ears.^2,5,6 The number of affected males, however, is increasing, as earrings and body piercing gain popularity in this group.³

Certain occupations with high exposure to nickel, such as cashiers, hairdressers, metal workers, domestic cleaners, food handlers, bar workers, and painters, are also at risk for acquiring nickel dermatitis.⁷ Patients with atopic eczema are also at increased risk.^8,9

Sweating may increase the severity of the dermatitis. Sodium chloride in the sweat causes corrosion of the metal and increases nickel exposure.¹⁰ Nickel release is therefore common in areas of the body that tend to be sweaty—for example, the hands, especially around the fingers, where inexpensive rings containing nickel are worn, or on the hands of individuals who carry metal key rings.

Consider oral intake of nickel, too. Another far less common, but important, nickel allergy presentation is systemic contact dermatitis from oral intake of nickel. Nuts, legumes, and chocolate can cause a flare-up reaction in a previously positive patch test site or previous site of nickel dermatitis.¹¹ Patients can also develop a dyshidrotic eczema on the hands. Itching and general symptoms, such as headache, nausea, and malaise, have also been reported after the oral nickel exposure of nickel-sensitive individuals.¹² Dietary intervention studies indicate that it is possible to reduce the activity of dermatitis in these patients by maintaining a diet low in nickel.^13-16

Finally, severe local reactions to nickel and other contact allergens can lead to auto-eczematization, in which a papular or papulosquamous eruption and pruritus appear distant from the site of exposure.

Is it atopic eczema or contact dermatitis?

It can be difficult to distinguish a flare in atopic eczema from chronic allergic contact dermatitis in individuals who may display both processes concurrently. The primary clue to the diagnosis is the peculiar localization of the rash, as evidenced by the cases we have described.

Patch testing is not required for diagnosis

Nickel contact dermatitis is often suspected when patients present with an acute or sub-acute eruption characterized by erythema, vesicles, and scaling in a distribution corresponding to a metal contact allergen. Nickel allergy is one of the few types of allergic contact dermatitis where the history of exposure along with the signs and symptoms are so distinctive that patch testing is often not required.

Amelioration of the rash associated with the withdrawal of the contactant serves as adequate confirmation of the diagnosis in many cases. A DMG test is a simple, inexpensive way to determine whether the object in question contains nickel. It can be used in the physician’s office or by the patient at home. Therefore, in some clinical situations, as in the presented cases, it is appropriate to make a presumptive diagnosis of nickel dermatitis, confirm the presence of nickel with a DMG test, remove the off ending metal item, treat with topical anti-inflammatory medications, and confirm the diagnosis by monitoring the patient’s response.

When patients do not respond to withdrawal of the suspected allergen and anti-inflammatory treatment, when multiple allergens are suspected, or when a definitive diagnosis is required for legal purposes, patch testing with nickel can confirm the diagnosis. In some cases, when the distribution of the rash is not distinctive, patch test screening may elicit a positive test to nickel that prompts the physician to investigate the source of the exposure.

Tx: Remove the item, apply topical steroids

Acute episodes of nickel dermatitis are treated with topical steroid creams to break the scratch-itch cycle (which potentiates the reaction) and to reduce the inflammation. This tactic is futile, however, if the allergen remains in contact with the skin. The source of the nickel must be identified and eliminated by the patient, as was done by the 5 patients we cared for.

Clothing accessories containing nickel, such as buckles, zippers, buttons, and metal clips, must be eliminated, as well as other sources of nickel: jewelry, watches, eyeglasses, and cell phones. The situation is complicated by the fact that many patients have underlying atopic eczema/irritant dermatitis, and patients may have more than 1 form of allergic contact dermatitis. For instance, self-treatment with neomycin-containing topical antibiotics may lead to superimposed allergic contact dermatitis from this agent.

Easy preventive steps. Routine prophylactic measures should focus on eliminating exposure to nickel from all identifiable sources. You can suggest that your patient with nickel dermatitis:

• Use a clear plastic cover over the nickel-containing parts of a cell phone.
• Apply a clear coat of nail polish to the buttons and rivets on pants; this can prevent nickel release and will last through at least 2 wash and dry cycles.¹⁷ (Tucking shirts in to prevent buttons and belt buckles from touching the skin is generally ineffective; not only is the shirt unlikely to stay in place all day, but perspiration and friction can also cause problems.)
• Use other barrier coatings, such as Nickel Guard and Beauty Secrets Hardener, which may be effective in preventing contact dermatitis.¹⁸
• Replace rivets on pants with a plastic button, or cover the rivet with a sew-on denim patch. This offers a more permanent approach to eliminating nickel exposure.
• Use plastic covers for earring studs.
• Replace metal eyeglass frames with ones made out of plastic.
• Choose “hypoallergenic” or nickel-free jewelry. Of note, though: Nickel may be present in jewelry labeled hypoallergenic. The patient can perform a DMG test to verify its nickel content.

In patients who continue to react in the absence of nickel jewelry, co-sensitization to gold must be considered, as many patients do react to multiple metals. Gold is a more common allergen than previously reported and is statistically linked to allergic reactions to nickel and cobalt metals.¹⁹ Unlike nickel dermatitis, the clinical relevance of a positive gold patch test is harder to ascertain because rashing distant from areas in direct contact with gold jewelry often occurs. In fact, in some cases of eyelid dermatitis induced by contact allergy to gold, titanium dioxide particles on the skin from cosmetics and sunscreen are thought to adsorb gold particles and carry them to the eyelids.

Disclosure

Dr. Brodell reports that he receives grants/research support from Amgen Inc., Doak Dermatologics, Galderma, and OrthoNeutrogena. He serves as a consultant for, or is on the speakers bureau of, 3M/Graceway Pharmaceuticals, Allergan, CollagGenex Pharmaceuticals, Connetics Corp., Dermik/BenzaClin, Galderma, Genentech, Inc., Genentech/ Raptiva, GlaxoSmithKline, Janssen, MDsConnect.net, Medicis, Novartis Pharmaceuticals Corp., Pedinol Pharmacal, Inc., Roerig-Pfizer, Sandoz/Novartis, sanofi-aventis, Sirius Laboratories, Stiefel, Westwood-Squibb, and Upjohn. Ms. Uhlenhake and Dr. Nedorost reported no potential conflict of interest relevant to this article.

CORRESPONDENCE
Robert Brodell, MD, 2660 East Market Street, Warren, OH 44483; rtb@neoucom.edu

CASE 1: A 13-year-old Caucasian girl sought treatment for a pruritic, scaling patch on her right cheek. The patient had a 10-year history of atopic eczema, with rashes primarily in flexural areas, and a history of skin reactions to earrings and rivets in her blue jeans. She had gone 3 years without a rash on her earlobes and periumbilical areas by scrupulously avoiding contact with metal.

The 2 x 2-cm patch of pruritic, scaling, lichenified skin with focal excoriation that brought her in on this day had been on her right cheek for the past 3 months ( FIGURE 1 ). It had not responded to hydrocortisone 2.5% cream and desonide 0.05% cream when she applied it twice daily, nor had it responded to an intralesional injection of 2 cc of 2.5 mg/cc triamcinolone acetonide.

CASE 2: A 13-year-old African American girl with a history of atopic dermatitis went to her doctor for a rash beneath the umbilicus. She’d had the rash, which she said was extremely itchy, for 6 weeks; over the previous 10 days, it had become more widespread. A 6 x 5-cm scaling, lichenified, hyperpigmented plaque was present in the infra-umbilical region. She also had a papular rash on the dorsal hands and axillae.

CASE 3: A 15-year-old Caucasian girl sought care for a pruritic, erythematous rash circumscribing her left wrist in an 8-mm diameter band. She’d had the rash for 6 weeks.

CASE 4: A 58-year-old Caucasian woman presented with a pruritic, erythematous, scaling rash on both upper cheeks just below her lower eyelids. She told the physician that she had a similar pruritic rash on her earlobes when she wore costume jewelry.

CASE 5: A 50-year-old woman went to her doctor for a pruritic, erythematous patch on the anterior and posterior sides of her ear-lobes, bilaterally. She told the physician that her ears had been pierced 2 weeks earlier.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU MANAGE THIS CONDITION?

Diagnosis: Nickel dermatitis

Each of these 5 patients had allergic contact dermatitis caused by nickel. The cheek dermatitis was produced by contact with the circular “menu” button on the patient’s cell phone (Case 1/ FIGURE 1 ), the periumbilical rash by the rivet behind a blue jeans button (Case 2/ FIGURE 2 ), the wrist dermatitis by a bracelet (Case 3/ FIGURE 3 ), the rash on the upper cheeks by eyeglass frames (Case 4/ FIGURE 4 ), and the earlobe dermatitis by earrings (Case 5/ FIGURE 5 ). The presence of nickel in each object was confirmed with a positive dimethylglyoxime (DMG) test.

What you’ll see. Besides an erythematous, pruritic, scaling rash, other findings can include vesicles and bullae that break and form crusts at sites of contact. Extreme pruritus is also commonly seen and prompts chronic rubbing and scratching, resulting in the development of lichenification and hyper-pigmentation.

FIGURE 1
Scaling patch on cheek

FIGURE 2
Rash beneath umbilicus

FIGURE 3
… around the wrist

FIGURE 4
… on the cheeks

FIGURE 5
… on the earlobes

Nickel dermatitis is increasingly common

Nickel is a leading cause of allergic contact dermatitis and is responsible for more cases than all other metals combined.^1,2 The incidence of nickel dermatitis has been increasing in the United States for the last 15 years, annually affecting an estimated 14% to 20% of women and 2% to 4% of men.^3,4 The higher percentage in women is related to nickel exposure associated with ear piercing and nickel-plated jewelry. In fact, the highest risk for nickel allergy is in young females with pierced ears.^2,5,6 The number of affected males, however, is increasing, as earrings and body piercing gain popularity in this group.³

Certain occupations with high exposure to nickel, such as cashiers, hairdressers, metal workers, domestic cleaners, food handlers, bar workers, and painters, are also at risk for acquiring nickel dermatitis.⁷ Patients with atopic eczema are also at increased risk.^8,9

Sweating may increase the severity of the dermatitis. Sodium chloride in the sweat causes corrosion of the metal and increases nickel exposure.¹⁰ Nickel release is therefore common in areas of the body that tend to be sweaty—for example, the hands, especially around the fingers, where inexpensive rings containing nickel are worn, or on the hands of individuals who carry metal key rings.

Consider oral intake of nickel, too. Another far less common, but important, nickel allergy presentation is systemic contact dermatitis from oral intake of nickel. Nuts, legumes, and chocolate can cause a flare-up reaction in a previously positive patch test site or previous site of nickel dermatitis.¹¹ Patients can also develop a dyshidrotic eczema on the hands. Itching and general symptoms, such as headache, nausea, and malaise, have also been reported after the oral nickel exposure of nickel-sensitive individuals.¹² Dietary intervention studies indicate that it is possible to reduce the activity of dermatitis in these patients by maintaining a diet low in nickel.^13-16

Finally, severe local reactions to nickel and other contact allergens can lead to auto-eczematization, in which a papular or papulosquamous eruption and pruritus appear distant from the site of exposure.

Is it atopic eczema or contact dermatitis?

It can be difficult to distinguish a flare in atopic eczema from chronic allergic contact dermatitis in individuals who may display both processes concurrently. The primary clue to the diagnosis is the peculiar localization of the rash, as evidenced by the cases we have described.

Patch testing is not required for diagnosis

Nickel contact dermatitis is often suspected when patients present with an acute or sub-acute eruption characterized by erythema, vesicles, and scaling in a distribution corresponding to a metal contact allergen. Nickel allergy is one of the few types of allergic contact dermatitis where the history of exposure along with the signs and symptoms are so distinctive that patch testing is often not required.

Amelioration of the rash associated with the withdrawal of the contactant serves as adequate confirmation of the diagnosis in many cases. A DMG test is a simple, inexpensive way to determine whether the object in question contains nickel. It can be used in the physician’s office or by the patient at home. Therefore, in some clinical situations, as in the presented cases, it is appropriate to make a presumptive diagnosis of nickel dermatitis, confirm the presence of nickel with a DMG test, remove the off ending metal item, treat with topical anti-inflammatory medications, and confirm the diagnosis by monitoring the patient’s response.

When patients do not respond to withdrawal of the suspected allergen and anti-inflammatory treatment, when multiple allergens are suspected, or when a definitive diagnosis is required for legal purposes, patch testing with nickel can confirm the diagnosis. In some cases, when the distribution of the rash is not distinctive, patch test screening may elicit a positive test to nickel that prompts the physician to investigate the source of the exposure.

Tx: Remove the item, apply topical steroids

Acute episodes of nickel dermatitis are treated with topical steroid creams to break the scratch-itch cycle (which potentiates the reaction) and to reduce the inflammation. This tactic is futile, however, if the allergen remains in contact with the skin. The source of the nickel must be identified and eliminated by the patient, as was done by the 5 patients we cared for.

Clothing accessories containing nickel, such as buckles, zippers, buttons, and metal clips, must be eliminated, as well as other sources of nickel: jewelry, watches, eyeglasses, and cell phones. The situation is complicated by the fact that many patients have underlying atopic eczema/irritant dermatitis, and patients may have more than 1 form of allergic contact dermatitis. For instance, self-treatment with neomycin-containing topical antibiotics may lead to superimposed allergic contact dermatitis from this agent.

Easy preventive steps. Routine prophylactic measures should focus on eliminating exposure to nickel from all identifiable sources. You can suggest that your patient with nickel dermatitis:

• Use a clear plastic cover over the nickel-containing parts of a cell phone.
• Apply a clear coat of nail polish to the buttons and rivets on pants; this can prevent nickel release and will last through at least 2 wash and dry cycles.¹⁷ (Tucking shirts in to prevent buttons and belt buckles from touching the skin is generally ineffective; not only is the shirt unlikely to stay in place all day, but perspiration and friction can also cause problems.)
• Use other barrier coatings, such as Nickel Guard and Beauty Secrets Hardener, which may be effective in preventing contact dermatitis.¹⁸
• Replace rivets on pants with a plastic button, or cover the rivet with a sew-on denim patch. This offers a more permanent approach to eliminating nickel exposure.
• Use plastic covers for earring studs.
• Replace metal eyeglass frames with ones made out of plastic.
• Choose “hypoallergenic” or nickel-free jewelry. Of note, though: Nickel may be present in jewelry labeled hypoallergenic. The patient can perform a DMG test to verify its nickel content.

In patients who continue to react in the absence of nickel jewelry, co-sensitization to gold must be considered, as many patients do react to multiple metals. Gold is a more common allergen than previously reported and is statistically linked to allergic reactions to nickel and cobalt metals.¹⁹ Unlike nickel dermatitis, the clinical relevance of a positive gold patch test is harder to ascertain because rashing distant from areas in direct contact with gold jewelry often occurs. In fact, in some cases of eyelid dermatitis induced by contact allergy to gold, titanium dioxide particles on the skin from cosmetics and sunscreen are thought to adsorb gold particles and carry them to the eyelids.

Disclosure

Dr. Brodell reports that he receives grants/research support from Amgen Inc., Doak Dermatologics, Galderma, and OrthoNeutrogena. He serves as a consultant for, or is on the speakers bureau of, 3M/Graceway Pharmaceuticals, Allergan, CollagGenex Pharmaceuticals, Connetics Corp., Dermik/BenzaClin, Galderma, Genentech, Inc., Genentech/ Raptiva, GlaxoSmithKline, Janssen, MDsConnect.net, Medicis, Novartis Pharmaceuticals Corp., Pedinol Pharmacal, Inc., Roerig-Pfizer, Sandoz/Novartis, sanofi-aventis, Sirius Laboratories, Stiefel, Westwood-Squibb, and Upjohn. Ms. Uhlenhake and Dr. Nedorost reported no potential conflict of interest relevant to this article.

CORRESPONDENCE
Robert Brodell, MD, 2660 East Market Street, Warren, OH 44483; rtb@neoucom.edu

A healthy 29-year-old woman presented to the clinic with pustules and boil-like lesions in the axillary areas, on the left forearm, and on the right thigh (FIGURE). She indicated that she’d had the lesions for 4 weeks. She said that she had not had any recent infections, and there was no evidence of immune compromise in her history.

We incised a pustule in the right axilla and expressed the pus. We sent the sample out for bacterial culture and sensitivity testing.

We immediately considered bacterial folliculitis and hidradenitis suppurativa as part of the differential. The acute nature of the process led us to favor a diagnosis of bacterial folliculitis.

FIGURE
Papules and papulopustules on right axilla

Would you favor this diagnosis?
What would you choose for initial empiric antibiotic treatment?

Diagnosis: MRSA folliculitis

We began empiric systemic antibiotic therapy with doxycycline 100 mg daily and topical treatment with clindamycin 1% lotion twice a day. The bacterial culture came back positive for methicillin-resistant Staphylococcus aureus (MRSA) and the organism proved to be tetracycline sensitive.

Staphylococci species have long been the most common causes of skin and soft tissue infections.¹ A recent study in 11 major US cities identified MRSA as the most common cause of acute purulent skin and soft tissue infections in patients presenting to the emergency department.² This rate, however, varied from 15% to 74% in various cities.² Today, clinicians must consider MRSA as a potential causative agent whenever they treat a patient with a skin and soft tissue infection.

Community-acquired MRSA: Don’t expect typical risk factors

Community-acquired MRSA (CA-MRSA) cases differ from hospital-acquired MRSA (HA-MRSA) cases demographically, microbiologically, and clinically. CA-MRSA infections typically occur in young, healthy individuals without traditional MRSA risk factors such as recent hospitalization, residence in a long-term care facility, or prior antibiotic use.^3,4

CA-MRSA outbreaks have been associated with participation in team sports, living in prison, dormitory, or group home settings, IV drug use, sharing personal items, and men who have sex with men.^4,5 However, the prevalence of MRSA infections in patients without any recognized risk factors, like our patient, is increasing.⁶

CA-MRSA is genetically distinct from HA-MRSA in that it contains the Panton-Valentine leukocidin, an important virulence factor, and carries the type IV or type V SCCmec cassette, which resides at a different methicillin-resistant locus.^7,8 CA-MRSA also does not demonstrate the multi-drug resistance typical of HA-MRSA, and these infections tend to be susceptible to most non-beta-lactam antibiotics.⁶

Is it MRSA or another pathogen?

When considering the differential diagnosis of MRSA folliculitis, consider methicillin-susceptible staphylococci species as equally likely pathogens. Gram-negative bacteria, including Pseudomonas aeruginosa, Malassezia furfur, and Candida species are less common, but notable causes of folliculitis. Other causes include eosinophilic folliculitis, non-bacterial/irritant folliculitis, pseudofolliculitis (chronic in-grown hairs), hidradenitis suppurativa, and acne vulgaris.

Use a low threshold for obtaining cultures CA-MRSA sometimes presents as an edematous, tender abscess, an expanding cellulitis, or both.^9,10 These presentations, however, are neither sensitive nor specific. Cutaneous infection may also present as erythematous papules, nodules, pustules, crusted plaques, and infrequently suppurative folliculitis.^3,10 Therefore, the clinician should have a low threshold to perform bacterial culture and sensitivity studies whenever a skin and soft tissue infection is suspected.

The potential complications of CA-MRSA infection, including pneumonia, sepsis, and endocarditis, can be avoided or minimized with early diagnosis and initiation of appropriate treatment.^4,11,12

Consider community factors

In the past, folliculitis and other localized skin infections were traditionally caused by methicillin-susceptible Staphylococcus aureus and treated with beta-lactam antibiotics. In communities with high prevalence of CA-MRSA skin and soft tissue infections, beta-lactam antibiotics like cephalexin or dicloxacillin may no longer be appropriate.^2,5 Therefore, let the prevalence of CA-MRSA in your community help guide your initial antibiotic choice while recognizing that empiric antibiotic therapy may be adjusted after cultures are available.

Good initial choices for CA-MRSA skin and soft tissue infections are trim-ethoprim/sulfamethoxazole with or without rifampin, clindamycin, gentamicin, and tetracycline,^2,4,5,7 but inducible clindamycin resistance has been reported.¹³ if your community has a high prevalence of CA-MRSA, you may decide to begin empiric therapy that provides MRSA coverage.² In addition, incision and drainage is necessary for adequate treatment of furuncles, carbuncles, and abscesses.⁵ Healthy, afebrile, immunocompetent patients without cellulitis may not require systemic antibiotics to clear local infections.^2,4

Take steps to prevent spread of the disease

Early diagnosis of CA-MRSA infection is important to prevent the spread of this highly virulent disease in the community. It’s important to cover the infected area with sterile gauze and instruct the patient to avoid direct skin-to-skin contact with others, not share sports equipment or personal items, and decontaminate linens and surfaces.^4,6

Stress the importance of frequent hand washing and using alcohol-based hand rubs to reduce transmission. Adjuvant topical therapy may be useful: intra-nasal mupirocin 2% ointment to prevent colonization and a persistent carrier state is prudent. Bathing with antimicrobial povidone-iodine or chlorhexidine gluconate is often recommended as an adjunctive treatment for skin and soft tissue infections, colonization, or both.¹⁴

Mupirocin 2% for our patient

We instructed our patient to continue the initial medications and to apply mupirocin 2% ointment to the nares twice a day for 1 week to eliminate the possibility of a staphylococcal carrier state.

At follow-up 2 weeks later, only a few excoriated papules and some post-inflammatory erythema remained. The topical clindamycin lotion and the doxycycline were continued for an additional 30 days, at which time the patient was clear and treatment was discontinued.

A healthy 29-year-old woman presented to the clinic with pustules and boil-like lesions in the axillary areas, on the left forearm, and on the right thigh (FIGURE). She indicated that she’d had the lesions for 4 weeks. She said that she had not had any recent infections, and there was no evidence of immune compromise in her history.

We incised a pustule in the right axilla and expressed the pus. We sent the sample out for bacterial culture and sensitivity testing.

We immediately considered bacterial folliculitis and hidradenitis suppurativa as part of the differential. The acute nature of the process led us to favor a diagnosis of bacterial folliculitis.

FIGURE
Papules and papulopustules on right axilla

Would you favor this diagnosis?
What would you choose for initial empiric antibiotic treatment?

Diagnosis: MRSA folliculitis

We began empiric systemic antibiotic therapy with doxycycline 100 mg daily and topical treatment with clindamycin 1% lotion twice a day. The bacterial culture came back positive for methicillin-resistant Staphylococcus aureus (MRSA) and the organism proved to be tetracycline sensitive.

Staphylococci species have long been the most common causes of skin and soft tissue infections.¹ A recent study in 11 major US cities identified MRSA as the most common cause of acute purulent skin and soft tissue infections in patients presenting to the emergency department.² This rate, however, varied from 15% to 74% in various cities.² Today, clinicians must consider MRSA as a potential causative agent whenever they treat a patient with a skin and soft tissue infection.

Community-acquired MRSA: Don’t expect typical risk factors

Community-acquired MRSA (CA-MRSA) cases differ from hospital-acquired MRSA (HA-MRSA) cases demographically, microbiologically, and clinically. CA-MRSA infections typically occur in young, healthy individuals without traditional MRSA risk factors such as recent hospitalization, residence in a long-term care facility, or prior antibiotic use.^3,4

CA-MRSA outbreaks have been associated with participation in team sports, living in prison, dormitory, or group home settings, IV drug use, sharing personal items, and men who have sex with men.^4,5 However, the prevalence of MRSA infections in patients without any recognized risk factors, like our patient, is increasing.⁶

CA-MRSA is genetically distinct from HA-MRSA in that it contains the Panton-Valentine leukocidin, an important virulence factor, and carries the type IV or type V SCCmec cassette, which resides at a different methicillin-resistant locus.^7,8 CA-MRSA also does not demonstrate the multi-drug resistance typical of HA-MRSA, and these infections tend to be susceptible to most non-beta-lactam antibiotics.⁶

Is it MRSA or another pathogen?

When considering the differential diagnosis of MRSA folliculitis, consider methicillin-susceptible staphylococci species as equally likely pathogens. Gram-negative bacteria, including Pseudomonas aeruginosa, Malassezia furfur, and Candida species are less common, but notable causes of folliculitis. Other causes include eosinophilic folliculitis, non-bacterial/irritant folliculitis, pseudofolliculitis (chronic in-grown hairs), hidradenitis suppurativa, and acne vulgaris.

Use a low threshold for obtaining cultures CA-MRSA sometimes presents as an edematous, tender abscess, an expanding cellulitis, or both.^9,10 These presentations, however, are neither sensitive nor specific. Cutaneous infection may also present as erythematous papules, nodules, pustules, crusted plaques, and infrequently suppurative folliculitis.^3,10 Therefore, the clinician should have a low threshold to perform bacterial culture and sensitivity studies whenever a skin and soft tissue infection is suspected.

The potential complications of CA-MRSA infection, including pneumonia, sepsis, and endocarditis, can be avoided or minimized with early diagnosis and initiation of appropriate treatment.^4,11,12

Consider community factors

In the past, folliculitis and other localized skin infections were traditionally caused by methicillin-susceptible Staphylococcus aureus and treated with beta-lactam antibiotics. In communities with high prevalence of CA-MRSA skin and soft tissue infections, beta-lactam antibiotics like cephalexin or dicloxacillin may no longer be appropriate.^2,5 Therefore, let the prevalence of CA-MRSA in your community help guide your initial antibiotic choice while recognizing that empiric antibiotic therapy may be adjusted after cultures are available.

Good initial choices for CA-MRSA skin and soft tissue infections are trim-ethoprim/sulfamethoxazole with or without rifampin, clindamycin, gentamicin, and tetracycline,^2,4,5,7 but inducible clindamycin resistance has been reported.¹³ if your community has a high prevalence of CA-MRSA, you may decide to begin empiric therapy that provides MRSA coverage.² In addition, incision and drainage is necessary for adequate treatment of furuncles, carbuncles, and abscesses.⁵ Healthy, afebrile, immunocompetent patients without cellulitis may not require systemic antibiotics to clear local infections.^2,4

Take steps to prevent spread of the disease

Early diagnosis of CA-MRSA infection is important to prevent the spread of this highly virulent disease in the community. It’s important to cover the infected area with sterile gauze and instruct the patient to avoid direct skin-to-skin contact with others, not share sports equipment or personal items, and decontaminate linens and surfaces.^4,6

Stress the importance of frequent hand washing and using alcohol-based hand rubs to reduce transmission. Adjuvant topical therapy may be useful: intra-nasal mupirocin 2% ointment to prevent colonization and a persistent carrier state is prudent. Bathing with antimicrobial povidone-iodine or chlorhexidine gluconate is often recommended as an adjunctive treatment for skin and soft tissue infections, colonization, or both.¹⁴

Mupirocin 2% for our patient

We instructed our patient to continue the initial medications and to apply mupirocin 2% ointment to the nares twice a day for 1 week to eliminate the possibility of a staphylococcal carrier state.

At follow-up 2 weeks later, only a few excoriated papules and some post-inflammatory erythema remained. The topical clindamycin lotion and the doxycycline were continued for an additional 30 days, at which time the patient was clear and treatment was discontinued.

A healthy 29-year-old woman presented to the clinic with pustules and boil-like lesions in the axillary areas, on the left forearm, and on the right thigh (FIGURE). She indicated that she’d had the lesions for 4 weeks. She said that she had not had any recent infections, and there was no evidence of immune compromise in her history.

We incised a pustule in the right axilla and expressed the pus. We sent the sample out for bacterial culture and sensitivity testing.

We immediately considered bacterial folliculitis and hidradenitis suppurativa as part of the differential. The acute nature of the process led us to favor a diagnosis of bacterial folliculitis.

FIGURE
Papules and papulopustules on right axilla

Would you favor this diagnosis?
What would you choose for initial empiric antibiotic treatment?

Diagnosis: MRSA folliculitis

We began empiric systemic antibiotic therapy with doxycycline 100 mg daily and topical treatment with clindamycin 1% lotion twice a day. The bacterial culture came back positive for methicillin-resistant Staphylococcus aureus (MRSA) and the organism proved to be tetracycline sensitive.

Staphylococci species have long been the most common causes of skin and soft tissue infections.¹ A recent study in 11 major US cities identified MRSA as the most common cause of acute purulent skin and soft tissue infections in patients presenting to the emergency department.² This rate, however, varied from 15% to 74% in various cities.² Today, clinicians must consider MRSA as a potential causative agent whenever they treat a patient with a skin and soft tissue infection.

Community-acquired MRSA: Don’t expect typical risk factors

Community-acquired MRSA (CA-MRSA) cases differ from hospital-acquired MRSA (HA-MRSA) cases demographically, microbiologically, and clinically. CA-MRSA infections typically occur in young, healthy individuals without traditional MRSA risk factors such as recent hospitalization, residence in a long-term care facility, or prior antibiotic use.^3,4

CA-MRSA outbreaks have been associated with participation in team sports, living in prison, dormitory, or group home settings, IV drug use, sharing personal items, and men who have sex with men.^4,5 However, the prevalence of MRSA infections in patients without any recognized risk factors, like our patient, is increasing.⁶

CA-MRSA is genetically distinct from HA-MRSA in that it contains the Panton-Valentine leukocidin, an important virulence factor, and carries the type IV or type V SCCmec cassette, which resides at a different methicillin-resistant locus.^7,8 CA-MRSA also does not demonstrate the multi-drug resistance typical of HA-MRSA, and these infections tend to be susceptible to most non-beta-lactam antibiotics.⁶

Is it MRSA or another pathogen?

When considering the differential diagnosis of MRSA folliculitis, consider methicillin-susceptible staphylococci species as equally likely pathogens. Gram-negative bacteria, including Pseudomonas aeruginosa, Malassezia furfur, and Candida species are less common, but notable causes of folliculitis. Other causes include eosinophilic folliculitis, non-bacterial/irritant folliculitis, pseudofolliculitis (chronic in-grown hairs), hidradenitis suppurativa, and acne vulgaris.

Use a low threshold for obtaining cultures CA-MRSA sometimes presents as an edematous, tender abscess, an expanding cellulitis, or both.^9,10 These presentations, however, are neither sensitive nor specific. Cutaneous infection may also present as erythematous papules, nodules, pustules, crusted plaques, and infrequently suppurative folliculitis.^3,10 Therefore, the clinician should have a low threshold to perform bacterial culture and sensitivity studies whenever a skin and soft tissue infection is suspected.

The potential complications of CA-MRSA infection, including pneumonia, sepsis, and endocarditis, can be avoided or minimized with early diagnosis and initiation of appropriate treatment.^4,11,12

Consider community factors

In the past, folliculitis and other localized skin infections were traditionally caused by methicillin-susceptible Staphylococcus aureus and treated with beta-lactam antibiotics. In communities with high prevalence of CA-MRSA skin and soft tissue infections, beta-lactam antibiotics like cephalexin or dicloxacillin may no longer be appropriate.^2,5 Therefore, let the prevalence of CA-MRSA in your community help guide your initial antibiotic choice while recognizing that empiric antibiotic therapy may be adjusted after cultures are available.

Good initial choices for CA-MRSA skin and soft tissue infections are trim-ethoprim/sulfamethoxazole with or without rifampin, clindamycin, gentamicin, and tetracycline,^2,4,5,7 but inducible clindamycin resistance has been reported.¹³ if your community has a high prevalence of CA-MRSA, you may decide to begin empiric therapy that provides MRSA coverage.² In addition, incision and drainage is necessary for adequate treatment of furuncles, carbuncles, and abscesses.⁵ Healthy, afebrile, immunocompetent patients without cellulitis may not require systemic antibiotics to clear local infections.^2,4

Take steps to prevent spread of the disease

Early diagnosis of CA-MRSA infection is important to prevent the spread of this highly virulent disease in the community. It’s important to cover the infected area with sterile gauze and instruct the patient to avoid direct skin-to-skin contact with others, not share sports equipment or personal items, and decontaminate linens and surfaces.^4,6

Stress the importance of frequent hand washing and using alcohol-based hand rubs to reduce transmission. Adjuvant topical therapy may be useful: intra-nasal mupirocin 2% ointment to prevent colonization and a persistent carrier state is prudent. Bathing with antimicrobial povidone-iodine or chlorhexidine gluconate is often recommended as an adjunctive treatment for skin and soft tissue infections, colonization, or both.¹⁴

Mupirocin 2% for our patient

We instructed our patient to continue the initial medications and to apply mupirocin 2% ointment to the nares twice a day for 1 week to eliminate the possibility of a staphylococcal carrier state.

At follow-up 2 weeks later, only a few excoriated papules and some post-inflammatory erythema remained. The topical clindamycin lotion and the doxycycline were continued for an additional 30 days, at which time the patient was clear and treatment was discontinued.