Young Wrestler With Scaly Purulent Scalp Plaque

Medscape

15-05-2025

Editor's Note:
The Case Challenge series includes difficult-to-diagnose conditions, some of which are not frequently encountered by most clinicians, but are nonetheless important to accurately recognize. Test your diagnostic and treatment skills using the following patient scenario and corresponding questions. If you have a case that you would like to suggest for a future Case Challenge, please email us at [e-mail] with the subject line "Case Challenge Suggestion." We look forward to hearing from you.
Background and Presentation
A previously healthy 11-year-old boy presented with a 1-month history of multiple scaly plaques over the scalp. He is an avid wrestler and recalls that these symptoms appeared shortly after he wrestled with one of his friends. He stopped wrestling as soon as the symptoms appeared. He was prescribed topical corticosteroids (betamethasone valerate 0.1% cream) and topical antifungals (1% clotrimazole and 1% terbinafine) by his primary care physician, with no improvement of his symptoms.
One day prior to presentation, the plaque over his left occiput became more raised and painful, with purulent discharge, prompting a visit to the emergency department.
His medical history is significant only for celiac disease. He has no food or drug allergies and avoids gluten. He is healthy, and his immunizations are up to date. He does not take any other medications, and his family history is unremarkable.
On presentation, the patient had a scaly plaque over his occipital scalp with purulent discharge (Figure 1).
Figure 1. Well-demarcated scaly plaque over the patient's left occiput with purulent discharge.
Physical Examination and Workup
On general inspection, the patient was well-appearing and in no apparent distress. His vital signs were normal, with a blood pressure of 118/79 mm Hg, heart rate of 86 beats/min, respiratory rate of 24 breaths/min, oxygen saturation of 99% without respiratory support, temperature of 97.8 °F (36.6 °C), and weight of 79 lb (36 kg).
On cutaneous examination, the patient had several scaly plaques over his scalp with a raised, boggy exophytic nodule with purulent drainage to his posterior scalp. Wood lamp examination revealed blue and green fluorescence (Figure 2). There was no sign of lymphadenopathy around the occipital region.
Figure 2. Wood lamp examination revealing blue and green fluorescence within a well-demarcated plaque over the left occiput.
Discussion
Tinea capitis is a fungal infection affecting the scalp and hair follicles.[1-4] It typically presents as an itchy, scaly scalp with inflammation, which is the primary clinical presentation observed in this patient.[1,2] However, noninflammatory variants can manifest as gray patches, black dots, or diffuse scaling. In contrast, inflammatory forms, often resulting from untreated infections, can present as diffuse pustules, kerions, favus, and dermatophytid reactions.[2] This patient exhibited a kerion (ie, boggy exophytic nodule with purulent drainage) upon physical examination. The clinical findings are most consistent with tinea capitis with a kerion.
Although irritant or allergic contact dermatitis can present with localized dermatitis and occasionally vesicles and bullae localized to areas of allergen exposure,[5] in this case the patient's symptoms have progressively worsened over the past month even after stopping wrestling, making contact dermatitis less likely.
A drug-induced allergic reaction is unlikely because symptoms of immunoglobulin (Ig)E-mediated drug-induced allergic reactions, such as urticaria, generally present with erythematous wheals featuring pale centers.[6] The absence of these hallmark dermatologic findings reduces the likelihood of an IgE-mediated drug-induced allergic reaction in this patient. Macular and papular drug eruptions are not solitary, but are disseminated and usually involve the trunk rather than the scalp.
Pityriasis rosea is a noncontagious dermatologic condition that presents with a distinctive scaly oval herald patch on the trunk, followed by multiple smaller lesions arranged in a "Christmas tree" distribution.[7] The lack of these distinctive clinical features makes pityriasis rosea an unlikely diagnosis.
Although a bacterial abscess can present with purulence, the patient's history of wrestling and positive Wood lamp examination suggest something more than a bacterial abscess.[8]
Condition Overview
Tinea capitis is a contagious dermatophyte infection primarily affecting preadolescent boys aged 6-10 years, similar to the patient in this case.[1,2] Although the predominant causative species vary by geographic region, the most common dermatophyte species responsible for tinea capitis belong to the Microsporum and Trichophyton genera. The prevalence of specific species typically is influenced by socioeconomic and environmental factors.[1]
Rapid diagnostic modalities include Wood lamp examination, trichoscopy, reflectance confocal microscopy, and direct microscopy with potassium hydroxide staining.[1-3] However, these tests are not definitive and do not provide species differentiation.[1] Histopathologic analysis is another diagnostic tool, although it requires a biopsy and may take up to 5 days to yield results; it also lacks the ability to differentiate fungal species. Alternatively, fungal culture and polymerase chain reaction (PCR) testing provide definitive species identification, but fungal cultures require several weeks and PCR analysis can be costly.[1] In this case, Wood lamp examination was used for rapid screening and helped support the diagnosis of tinea capitis. Of note, a negative Wood lamp result does not rule out a dermatophyte infection, because fungi that invade the hair shaft (an endothrix infection) may not fluoresce on Wood lamp examination.
Preventive measures primarily focus on personal hygiene. Regular scalp washing and hair cleansing can reduce the risk of contracting tinea capitis. Routine scalp inspection is also recommended. Avoiding the sharing of personal items is critical because fungal spores can be transmitted via fomites. Infected individuals should ideally refrain from attending populated environments, such as schools, to reduce the rate of transmission.[1,2]
The treatment of tinea capitis typically involves antifungal therapy. Topical antifungal monotherapy is not recommended because it does not adequately penetrate the hair shaft where the infection resides; however, it may help reduce fungal spore load and transmission. Oral antifungal agents are considered the first-line treatment, and combination therapy with both oral and topical antifungals is generally advised.[1-3] Further treatment options are discussed later in the case.
First-line oral antifungal therapies that have been approved by the US Food and Drug Administration (FDA) for tinea capitis include terbinafine and griseofulvin.[1]
Treatment
Terbinafine has been demonstrated to be particularly effective against Trichophyton species.[2,3] A 2024 network meta-analysis by Gupta and colleagues indicated that terbinafine is generally more effective than griseofulvin in treating tinea capitis.[1] The FDA-approved formulation of terbinafine for tinea capitis treatment consists of granules for individuals aged 4 years and older.[1] The recommended dosage is 125 mg/d in persons weighing < 25 kg, 187.5 mg/d in those weighing 25-35 kg, and 250 mg/d in those weighing > 35 kg, administered over 6 weeks.[1,9,10] It is critical to note that terbinafine is also available in tablet form, which follows a different dosing regimen: 62.5 mg/d in persons weighing 10-20 kg, 125 mg/d in those weighing 20-40 kg, and 250 mg/d in those weighing > 40 kg.[1-3,11,12] Failure to consider formulation differences may result in underdosing.
A randomized controlled trial by Koumantaki and colleagues demonstrated that doubling the standard dosage (125 mg/d in persons weighing 10-25 kg and 250 mg/d in those weighing > 25 kg) led to improved clinical outcomes in children without increasing adverse effects.[13] This study underscores the necessity of appropriate dosing.
In this case, given the patient's weight of 36 kg, the recommended medication with the correct dose is terbinafine granules, 250 mg/d.
Griseofulvin is particularly effective against Microsporum species.[2,3] The recommended dosage is 10-20 mg/kg/d for microsize griseofulvin tablets and 20-25 mg/kg/d for microsize griseofulvin oral suspension, administered for at least 6 weeks. Both formulations are FDA-approved for individuals aged 2 years or older.[1]
Second-line treatment options include itraconazole tablets, administered at 50 mg for individuals weighing < 20 kg or 100 mg for those weighing > 20 kg for 4-6 weeks, depending on the dermatophyte species.[2,3] An oral solution formulation with lower dosing requirements is also available.[1] Fluconazole may be considered in exceptional cases; however, it has demonstrated the lowest efficacy among the four discussed antifungal agents.[1,2]
Monitoring Management
Many antifungal medications have the potential to be hepatotoxic, and liver function tests are warranted in patients with a history of liver impairment. While specific recommendations vary by medication, liver function testing is generally advised after 4-6 weeks of antifungal therapy. For terbinafine, absolute lymphocyte counts can be assessed alongside a liver panel in immunocompromised patients.[1]
Routine liver function tests may not be necessary in healthy patients without a personal or family history of hepatic impairment. A retrospective review of approximately 5000 adult and pediatric patients by Stolmeier and colleagues suggested that abnormal laboratory findings were rarely seen.[11] The few detected abnormalities were primarily low-grade and did not necessitate further investigation. Similar findings have been reported in another retrospective analysis.[12] Thus, current evidence supports a shared decision-making approach regarding bloodwork for patients on oral terbinafine, allowing them to make informed choices on the basis of risk likelihood.
Systemic antifungal medications have been associated with renal, cardiovascular, and thyroid-related adverse effects. A systematic review and meta-analysis conducted by the Cochrane Library on various systemic antifungal therapies for tinea capitis identified nausea, abdominal discomfort, and headache as among the most frequently reported adverse effects.[14] Beyond hepatotoxicity and potential drug interactions, no other rare but serious adverse effects were documented.
After 3 days of taking the systemic antifungal medication, the patient developed disseminated monomorphic erythematous papules on his torso, arms, and legs (Figures 3 and 4). There were also pustules on his forehead and ears bilaterally (Figure 5). Otherwise, the patient is stable with normal vital signs.
Figure 3. Monomorphic erythematous papules on the torso.
Figure 4. Monomorphic erythematous papules on the left anterior thigh.
Figure 5. Multiple monomorphic pustules on the left external auditory canal and inner aspect of the pinna, extending to the posterior left cheek.
Potential Treatment Reactions
A dermatophytid (or "id") reaction is a secondary immune response mediated by activated T lymphocytes or antibodies that typically targets antigens derived from nonliving organisms. Id reactions can arise from various infectious or inflammatory dermatologic conditions, including fungal, bacterial, viral, or parasitic infections. However, fungal infections — particularly tinea capitis — are the most common causative agents. When an id reaction originates from a dermatophyte infection, it is specifically termed a dermatophytid reaction.[15]
Dermatophytid reactions secondary to tinea capitis commonly present as generalized papular or vesicular lesions affecting the scalp, neck, ears, and extremities distant from the original site of infection.[2,16] In some cases, they manifest as small, pale-red follicular papules, which may appear either scattered or clustered. These papules can occasionally develop fine, spiny projections or pustules. In other instances, dermatophytid reactions present as plaquelike lesions resembling seborrheic dermatitis. In rare cases, the rash may exhibit a morbilliform or scarlatinoid pattern.[15]
Studies suggest that dermatophytid reactions may be more prevalent than currently reported.[17,18] They may develop at the peak of fungal infection or at any time before or during systemic antifungal treatment. This temporal association frequently results in misdiagnosis as an allergic reaction. Unlike an id reaction, an allergic reaction typically involves urticaria (itchy wheals or hives); angioedema; swelling of the lips, throat, and tongue; and, in severe cases, anaphylaxis.[6,19,20] Accurate diagnosis is essential because dermatophytid reactions do not warrant discontinuation of antifungal therapy; rather, adherence to the prescribed regimen is safe and necessary to treat the dermatophyte infection.[1,15,17,18]
Although a dermatophytid reaction typically is not life-threatening and does not usually require hospital admission, patient follow-up is essential to prevent long-term complications. If left untreated or unrecognized, tinea capitis may result in scarring, alopecia, chronic infection, and alterations in skin texture. Particularly in pediatric patients, the condition may have substantial psychosocial consequences, affecting self-esteem, peer interactions, and academic performance.[1]
Beyond terbinafine allergy and urticaria, the differential diagnosis includes drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome, a severe drug-induced reaction. DRESS syndrome typically presents with erythroderma, a morbilliform rash, facial edema, and diffuse lymphadenopathy. Systemic manifestations, including fever, pruritus, malaise, and organ involvement, are also common.[21] However, in this case, the patient's stable vital signs, absence of systemic symptoms, and presence of a papular eruption (as opposed to a morbilliform eruption) decrease the likelihood of DRESS syndrome.
Acute generalized exanthematous pustulosis is also unlikely. It is frequently associated with fever and edematous erythema, neither of which are present in this patient.[22]