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The treatment choice is oral terbinafine for tinea capitis with kerion, a scalp dermatophyte infection with a concurrent inflammatory process. Tinea capitis is a very common infection with the peak occurrence at age 3-7 years. Tinea capitis is caused by a variety of dermatophyte species, most commonly by Trichophyton tonsurans or Microsporum canis. T. tonsurans is an endothrix infection, invading the hair shaft and superficial hair while M. canis is an ectothrix infection. T. tonsurans has a person to person transmission; in contrast, M. canis is a zoonotic infection most commonly acquired from infected pets.1 The epidemiology of tinea capitis is affected by multiple factors, including immigration patterns. For example, in Montreal, a study showed a sixfold increase of African dermatophyte species, M. audouinii and T. soudanense.2 Similarly, global variation has increased prevalence of T. violaceum, more commonly found in Europe and Africa, which has been seen in immigrant populations in the United States.1 Kerion is thought to be a hypersensitivity reaction to dermatophytes. Often, misdiagnosis of kerion can result in unnecessary antibiotic prescription and delays in initiation of antifungal therapy.3,4
Tinea capitis can present with focal, “patchy,” well-demarcated hair loss and overlying scale, broken-off hairs at the scalp, and often with pustules. It may be associated with occipital or posterior cervical lymphadenopathy. which presents as a painful boggy scalp mass with or without purulent drainage. Kerions can have associated fever. It is important to differentiate tinea capitis with kerion from processes requiring a different treatment course.3,5 Bacterial folliculitis may have erythema and pustules but only rarely causes hair loss. Similarly, alopecia areata can present with focal alopecia but lacks the scalp inflammation and pustules. Scalp psoriasis is quite scaly, but is more thickened, and usually does not have pustules, nor would purulent drainage be evident. There is a broader differential for other inflammatory focal alopecias including discoid lupus, lichen planopilaris, and dissecting cellulitis of the scalp, which can have similar pus-filled lumps, and cause permanent hair loss, but may be differentiated by associated conditions such as acne conglobata, hidradenitis suppurativa, and pilonidal sinus.
While some clinicians advocate clinical diagnosis of tinea capitis, we advocate confirmation of infection by fungal culture, which can identify the causative organism and influence therapy selection.1 The presence of a fungal infection can be confirmed on potassium hydroxide wet mount prep if hyphae and small spores are seen.6,7 Wood lamp examination will fluoresce if there are ectothrix species, however a negative fluorescence does not differentiate between an endothrix species or lack of infection.
It is important that tinea capitis with kerion is treated with systemic antifungal treatments to allow resolution of the infection, recovery of hair growth, and to prevent or minimize scarring. Systemic antifungal options include terbinafine, griseofulvin, and azoles. Terbinafine is becoming the treatment of choice given shorter duration of treatment with similar efficacy.1T. tonsurans also is thought to respond better to terbinafine than to griseofulvin.8 Griseofulvin is the historical treatment of choice because of its history of clinical safety and no need for laboratory testing. It is important to note that higher doses of griseofulvin (20-25 mg/kg) are recommended, as older lower dose regimens have high rates of failure. Griseofulvin may be more effective for treatment of Microsporum spp than is terbinafine.8 Fluconazole is the only oral antifungal agent that is approved for patients younger than 2 years of age, however it has lower cure rates, compared with terbinafine and griseofulvin.1 Tinea capitis with kerion does not generally require antibiotics unless there is superimposed bacterial infection. Kerion also do not require incision or drainage, which may increase scarring and complicate the clinical course.
Management of tinea capitis should include evaluation of any other household members for coinfection. Depending on the dermatophyte involved there can be risk of person-to-person transmission.5 Families should be educated about fomite transmission via shared combs or hats. Additionally, if a zoophilic dermatophyte is suspected, pets also should be appropriately examined and treated. Topical antifungals are insufficient to eradicate tinea capitis but can be used as adjunctive therapy. Kerion can be treated with oral prednisone in addition to oral antifungals if the lesions are very painful, however there is limited data on this treatment option.9
Ms. Kaushik is a research fellow and Dr. Eichenfield is professor of dermatology and pediatrics in the division of pediatric and adolescent dermatology at Rady Children’s Hospital and the University of California, both in San Diego. They have no conflicts of interest or relevant financial disclosures.
References
1. “Red Book: Report of the Committee on Infectious Diseases,” 31st Edition, (Elk Grove Village, Ill.: American Academy of Pediatrics, 2018, p. 1264).
2. Pediatr Dermatol. 2018 May;35(3):323-8
3. Arch Dis Child. 2016 May;101(5):503.
4. IDCases. 2018 Jun 28;14:e00418.
5. Int J Dermatol. 2018 Jan;57(1):3-9.
6. Pediatr Rev. 2007 May;28(5):164-74.
7. Clin Cosmet Investig Dermatol. 2010;3:89-98.
8. Cochrane Database Syst Rev. 2016 May 12;(5):CD004685.
9. Med Mycol. 1999 Apr;37(2):97-9.
The treatment choice is oral terbinafine for tinea capitis with kerion, a scalp dermatophyte infection with a concurrent inflammatory process. Tinea capitis is a very common infection with the peak occurrence at age 3-7 years. Tinea capitis is caused by a variety of dermatophyte species, most commonly by Trichophyton tonsurans or Microsporum canis. T. tonsurans is an endothrix infection, invading the hair shaft and superficial hair while M. canis is an ectothrix infection. T. tonsurans has a person to person transmission; in contrast, M. canis is a zoonotic infection most commonly acquired from infected pets.1 The epidemiology of tinea capitis is affected by multiple factors, including immigration patterns. For example, in Montreal, a study showed a sixfold increase of African dermatophyte species, M. audouinii and T. soudanense.2 Similarly, global variation has increased prevalence of T. violaceum, more commonly found in Europe and Africa, which has been seen in immigrant populations in the United States.1 Kerion is thought to be a hypersensitivity reaction to dermatophytes. Often, misdiagnosis of kerion can result in unnecessary antibiotic prescription and delays in initiation of antifungal therapy.3,4
Tinea capitis can present with focal, “patchy,” well-demarcated hair loss and overlying scale, broken-off hairs at the scalp, and often with pustules. It may be associated with occipital or posterior cervical lymphadenopathy. which presents as a painful boggy scalp mass with or without purulent drainage. Kerions can have associated fever. It is important to differentiate tinea capitis with kerion from processes requiring a different treatment course.3,5 Bacterial folliculitis may have erythema and pustules but only rarely causes hair loss. Similarly, alopecia areata can present with focal alopecia but lacks the scalp inflammation and pustules. Scalp psoriasis is quite scaly, but is more thickened, and usually does not have pustules, nor would purulent drainage be evident. There is a broader differential for other inflammatory focal alopecias including discoid lupus, lichen planopilaris, and dissecting cellulitis of the scalp, which can have similar pus-filled lumps, and cause permanent hair loss, but may be differentiated by associated conditions such as acne conglobata, hidradenitis suppurativa, and pilonidal sinus.
While some clinicians advocate clinical diagnosis of tinea capitis, we advocate confirmation of infection by fungal culture, which can identify the causative organism and influence therapy selection.1 The presence of a fungal infection can be confirmed on potassium hydroxide wet mount prep if hyphae and small spores are seen.6,7 Wood lamp examination will fluoresce if there are ectothrix species, however a negative fluorescence does not differentiate between an endothrix species or lack of infection.
It is important that tinea capitis with kerion is treated with systemic antifungal treatments to allow resolution of the infection, recovery of hair growth, and to prevent or minimize scarring. Systemic antifungal options include terbinafine, griseofulvin, and azoles. Terbinafine is becoming the treatment of choice given shorter duration of treatment with similar efficacy.1T. tonsurans also is thought to respond better to terbinafine than to griseofulvin.8 Griseofulvin is the historical treatment of choice because of its history of clinical safety and no need for laboratory testing. It is important to note that higher doses of griseofulvin (20-25 mg/kg) are recommended, as older lower dose regimens have high rates of failure. Griseofulvin may be more effective for treatment of Microsporum spp than is terbinafine.8 Fluconazole is the only oral antifungal agent that is approved for patients younger than 2 years of age, however it has lower cure rates, compared with terbinafine and griseofulvin.1 Tinea capitis with kerion does not generally require antibiotics unless there is superimposed bacterial infection. Kerion also do not require incision or drainage, which may increase scarring and complicate the clinical course.
Management of tinea capitis should include evaluation of any other household members for coinfection. Depending on the dermatophyte involved there can be risk of person-to-person transmission.5 Families should be educated about fomite transmission via shared combs or hats. Additionally, if a zoophilic dermatophyte is suspected, pets also should be appropriately examined and treated. Topical antifungals are insufficient to eradicate tinea capitis but can be used as adjunctive therapy. Kerion can be treated with oral prednisone in addition to oral antifungals if the lesions are very painful, however there is limited data on this treatment option.9
Ms. Kaushik is a research fellow and Dr. Eichenfield is professor of dermatology and pediatrics in the division of pediatric and adolescent dermatology at Rady Children’s Hospital and the University of California, both in San Diego. They have no conflicts of interest or relevant financial disclosures.
References
1. “Red Book: Report of the Committee on Infectious Diseases,” 31st Edition, (Elk Grove Village, Ill.: American Academy of Pediatrics, 2018, p. 1264).
2. Pediatr Dermatol. 2018 May;35(3):323-8
3. Arch Dis Child. 2016 May;101(5):503.
4. IDCases. 2018 Jun 28;14:e00418.
5. Int J Dermatol. 2018 Jan;57(1):3-9.
6. Pediatr Rev. 2007 May;28(5):164-74.
7. Clin Cosmet Investig Dermatol. 2010;3:89-98.
8. Cochrane Database Syst Rev. 2016 May 12;(5):CD004685.
9. Med Mycol. 1999 Apr;37(2):97-9.
The treatment choice is oral terbinafine for tinea capitis with kerion, a scalp dermatophyte infection with a concurrent inflammatory process. Tinea capitis is a very common infection with the peak occurrence at age 3-7 years. Tinea capitis is caused by a variety of dermatophyte species, most commonly by Trichophyton tonsurans or Microsporum canis. T. tonsurans is an endothrix infection, invading the hair shaft and superficial hair while M. canis is an ectothrix infection. T. tonsurans has a person to person transmission; in contrast, M. canis is a zoonotic infection most commonly acquired from infected pets.1 The epidemiology of tinea capitis is affected by multiple factors, including immigration patterns. For example, in Montreal, a study showed a sixfold increase of African dermatophyte species, M. audouinii and T. soudanense.2 Similarly, global variation has increased prevalence of T. violaceum, more commonly found in Europe and Africa, which has been seen in immigrant populations in the United States.1 Kerion is thought to be a hypersensitivity reaction to dermatophytes. Often, misdiagnosis of kerion can result in unnecessary antibiotic prescription and delays in initiation of antifungal therapy.3,4
Tinea capitis can present with focal, “patchy,” well-demarcated hair loss and overlying scale, broken-off hairs at the scalp, and often with pustules. It may be associated with occipital or posterior cervical lymphadenopathy. which presents as a painful boggy scalp mass with or without purulent drainage. Kerions can have associated fever. It is important to differentiate tinea capitis with kerion from processes requiring a different treatment course.3,5 Bacterial folliculitis may have erythema and pustules but only rarely causes hair loss. Similarly, alopecia areata can present with focal alopecia but lacks the scalp inflammation and pustules. Scalp psoriasis is quite scaly, but is more thickened, and usually does not have pustules, nor would purulent drainage be evident. There is a broader differential for other inflammatory focal alopecias including discoid lupus, lichen planopilaris, and dissecting cellulitis of the scalp, which can have similar pus-filled lumps, and cause permanent hair loss, but may be differentiated by associated conditions such as acne conglobata, hidradenitis suppurativa, and pilonidal sinus.
While some clinicians advocate clinical diagnosis of tinea capitis, we advocate confirmation of infection by fungal culture, which can identify the causative organism and influence therapy selection.1 The presence of a fungal infection can be confirmed on potassium hydroxide wet mount prep if hyphae and small spores are seen.6,7 Wood lamp examination will fluoresce if there are ectothrix species, however a negative fluorescence does not differentiate between an endothrix species or lack of infection.
It is important that tinea capitis with kerion is treated with systemic antifungal treatments to allow resolution of the infection, recovery of hair growth, and to prevent or minimize scarring. Systemic antifungal options include terbinafine, griseofulvin, and azoles. Terbinafine is becoming the treatment of choice given shorter duration of treatment with similar efficacy.1T. tonsurans also is thought to respond better to terbinafine than to griseofulvin.8 Griseofulvin is the historical treatment of choice because of its history of clinical safety and no need for laboratory testing. It is important to note that higher doses of griseofulvin (20-25 mg/kg) are recommended, as older lower dose regimens have high rates of failure. Griseofulvin may be more effective for treatment of Microsporum spp than is terbinafine.8 Fluconazole is the only oral antifungal agent that is approved for patients younger than 2 years of age, however it has lower cure rates, compared with terbinafine and griseofulvin.1 Tinea capitis with kerion does not generally require antibiotics unless there is superimposed bacterial infection. Kerion also do not require incision or drainage, which may increase scarring and complicate the clinical course.
Management of tinea capitis should include evaluation of any other household members for coinfection. Depending on the dermatophyte involved there can be risk of person-to-person transmission.5 Families should be educated about fomite transmission via shared combs or hats. Additionally, if a zoophilic dermatophyte is suspected, pets also should be appropriately examined and treated. Topical antifungals are insufficient to eradicate tinea capitis but can be used as adjunctive therapy. Kerion can be treated with oral prednisone in addition to oral antifungals if the lesions are very painful, however there is limited data on this treatment option.9
Ms. Kaushik is a research fellow and Dr. Eichenfield is professor of dermatology and pediatrics in the division of pediatric and adolescent dermatology at Rady Children’s Hospital and the University of California, both in San Diego. They have no conflicts of interest or relevant financial disclosures.
References
1. “Red Book: Report of the Committee on Infectious Diseases,” 31st Edition, (Elk Grove Village, Ill.: American Academy of Pediatrics, 2018, p. 1264).
2. Pediatr Dermatol. 2018 May;35(3):323-8
3. Arch Dis Child. 2016 May;101(5):503.
4. IDCases. 2018 Jun 28;14:e00418.
5. Int J Dermatol. 2018 Jan;57(1):3-9.
6. Pediatr Rev. 2007 May;28(5):164-74.
7. Clin Cosmet Investig Dermatol. 2010;3:89-98.
8. Cochrane Database Syst Rev. 2016 May 12;(5):CD004685.
9. Med Mycol. 1999 Apr;37(2):97-9.
A 10-year-old otherwise-healthy male presents for a progressing lesion on his scalp. One month prior to coming in, he developed some peeling and itch followed by loss of hair. This had worsened, becoming a painful and boggy mass on the back of his head with focal alopecia. He went to the local ED, where he had plain films of his skull, which were normal and was prescribed cephalexin. He has not shown any improvement after starting the antibiotics. He has had no fevers in this time, but the pain persists.
On physical exam, he is noted to have a hairless patch on a boggy left occipital mass, which is tender to palpation. There is a small amount of overlying honey-colored crusting. He has associated posterior occipital nontender lymphadenopathy.
The patient's older sister has a small area of scalp hair loss.