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    [ C A S E R E P O R T A N D L I T E R A T U R E R E V I E W ]

    ABSTRACTTinea capitis is a reasonably common infection among the pediatric population; however, it is still a relatively rare entity

    among infants less than one year of age. As such, a high index of suspicion is necessary for diagnosis among infants and an

    appropriate diagnostic work up should be employed in any case where a dermatophyte infection is suspected. Several methods

    are available for diagnosis. In addition, proper identification of the specific dermatophyte genera involved should be considered

    as treatment options may be altered based on the causative pathogen identified. (J Clin Aesthet Dermatol. 2012;5(2):4959.)

    DISCLOSURE: Dr. Michaels reports no relevant conflicts of interest. Dr. Del Rosso is a consultant, speaker, and/or researcher for Coria/Valeant,

    Allergan, Galderma, Graceway, Intendis, Medicis, Onset Dermatologics, Obagi Medical Products, Ortho Dermatologics, PharmaDerm/Nycomed,

    Promius, Ranbaxy, Stiefel/GSK, TriaBeauty, Triax, Unilever, and Warner-Chilcott.

    ADDRESS CORRESPONDENCE TO:J ames Q. Del Rosso, DO; E-mail: [email protected]

    Tinea Capitis in InfantsRecognition, Evaluation, and Management Suggestions

    aBRENT D. MICHAELS, DO; bJAMES Q. DEL ROSSO, DO, FAOCDaChief Resident (Dermatology, PGY-4), Valley Hospital Medical Center, Las Vegas, Nevada; bDermatology Residency Program Director,

    Valley Hospital Medical Center, Las Vegas, Nevada; Clinical Professor (Dermatology), Touro University College of Osteopathic Medicine,Henderson, Nevada; Las Vegas Skin & Cancer Clinics/J DRx Dermatology, Las Vegas and Henderson, Nevada

    Tinea capitis infection is on the rise in North America and

    continues to be a significant public health concern.


    Infact, tinea capitis infection has been described as a

    modern-day epidemic.3 It is the most commonly diagnosed

    dermatophytosis of childhood and is more frequently seen

    among prepubescent children.4 In fact, it has been stated by

    Boni Elewski, MD, an international expert on cutaneous

    mycotic infections, that when scalp scaling is noted in children,

    the fungus is guilty until proven innocent (personal

    communication with Boni Elewski, MD, May 1999). However,

    among infants, while the infection still occurs, it is relatively

    rare. Further complicating the diagnosis in infants is the

    variability in clinical presentation. For these reasons, a highindex of suspicion is needed for diagnosis, as one must first

    consider the possible presence of a disorder before the

    diagnosis can be made. The practitioner should approach each

    case of a potential dermatophyte infection with a similar

    diagnostic approach regardless of age, which includes direct

    microscopy and fungal culture.

    The two more common genera of dermatophytes

    responsible for tinea capitis infection are Trichophyton

    tonsurans and Microsporum canis, with T. tonsurans the

    most common cause of tinea capitis in the United States. 5

    However,M. canis is increasing in incidence in parts of Europe

    and the United States.6 Diagnostically, there are several

    methods available for identifying a tinea capitis infection. In

    terms of treatment, the standard therapy for tinea capitis

    remains oral griseofulvin; however, depending on the specific

    pathogen identified, different treatment regimens may be


    CASE REPORTAn eight-month-old Caucasian girl presented to the authors

    office with a seven-month history of a rash on the scalp. Prior

    treatments included an unknown topical corticosteroid cream

    and most recently, topical nystatin cream. The patients mother

    reported some minimal improvement with the nystatin cream,

    but upon discontinuation of the cream, the rash returned to

    pretreatment intensity. Clinical examination and review of past

    medical history revealed an otherwise healthy female infant

    with no prior significant past medical or surgical history andnormal progression of childhood development. The mother

    noted no change in her infants behavior since the development

    of the scalp eruption. A recent history of ringworm infection

    of the family cat was elicited with subsequent treatment and

    resolution by a veterinarian. The family cat completed

    treatment approximately two months prior to the mother

    noting the rash on her childs scalp. No one else in the home

    was affected with any skin or scalp problems.

    On physical examination, the patient presented with diffuse,

    erythematous, ill-defined patches with focal areas of scaling

    and hyperkeratosis on the scalp, predominantly involving the

    vertex region (Figure 1). The child had diffusely thin hair,

    which was unchanged by history according to the mother, with

    no appreciable alopecia noted clinically. The remainder of the

    physical examination revealed an active healthy-appearing, and

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    playful infant with no cutaneous abnormalities noted other than

    the scalp eruption who was accompanied by a very anxious

    mother. There were no areas of pustulation, erosion, induration,

    or boggy inflammation noted on the scalp, with absence of

    cervical and occipital adenopathy on palpation.

    Based on the history and physical examination, scrapings of

    the scale from the involved areas of the scalp were obtained as

    well as samples of plucked hairs from the affected scalp regions,

    with all of the obtained specimens placed on glass microscope

    slides. This was followed by application of potassium hydroxide(KOH) 10% with dimethyl sulfoxide (DMSO) for examination

    by light microscopy (KOH prep). Scale and hair samples from

    the scalp were also placed in dermatophyte test medium (DTM)

    for preliminary fungal culture. Examination of the KOH prep

    revealed an ectothrix pattern of hair shaft invasion by fungal

    elements with numerous spores located outside the surface of

    the hair shaft and with multiple long branched hyphae also

    noted (Figures 2A, 2B). The results of the DTM assessed at Day

    7 revealed positive growth with white fluffy colonies and turning

    of the medium color from yellow to red, indicating growth of a

    dermatophyte. The positive DTM culture containing the

    dermatophyte growth was subsequently sent intact to

    microbiology for specific identification of genera and species.

    Fungal sequencing completed on the already grown

    dermatophyte specimen in the positive DTM was determined to

    be genetically consistent withM. canis. Interestingly, there was

    a prior history of the family cat being treated for a ringworm

    infection, which if this was dermatophytosis affecting the cat,

    would be a very likely explanation for the M. canis infection

    affecting the infant, as the cat often sleeps next to the infant

    during naps according to the mother.

    Treatment was initiated on the first visit after the positive

    KOH results. The risk-benefit ratio of various options was

    discussed, including the explanation that tinea capitis is poorly

    responsive to topical therapy alone, and necessitates treatment

    with oral antifungal therapy. The infant was treated with

    griseofulvin suspension 125mg/5cc and directed to take one

    teaspoon twice a day to achieve a daily dose closely

    approximating 25mg/kg/day of oral griseofulvin. The patient

    was also prescribed ciclopirox 1% shampoo for use every other

    day with instructions to avoid sharing combs, brushes, andtowels used to dry the scalp of the child. The patient was

    treated for eight weeks in total with both medications. After just

    two weeks of treatment, improvement was noted, and complete

    clinical clearance was obtained after eight weeks (Figures 3A,

    3B). An additional KOH prep obtained from the previously

    affected scalp, including some hairs in the region, was

    performed with microscopic examination completed at the end

    of treatment (8 weeks) and was negative for any fungal

    elements. No adverse effects from either medication were

    reported by the mother, with the treatment regimen very well


    Additionally, the family cat was rechecked by the

    veterinarian immediately after the diagnosis of tinea capitis in

    the infant was made, and was retreated for possible

    dermatophyte infection prophylactically, although there was no

    evidence of feline infection.

    DISCUSSIONTinea capitis is a dermatophyte infection involving the scalp,

    which is characterized predominantly by involvement of the

    hair shaft as well as contiguous skin. Overall, there are more

    Figure 1. Infant girl (8 months of age)presenting with erythematous, ill-definedpatches and thin plaques with scaling andfocal hyperkeratosis diffusely involving thescalp

    Figure 2A. Microscopic examination ofplucked hairs and skin scrapings from thesame patient using KOH 10% with DMSOdemonstrating ectrothrix pattern of hairinvasion. Note the round spores lined up onthe outer surface of the hair shaft on theupper right portion of the field. Multiple longhyphae are also noted externally around thehair shaft and within scale from skin scrap-ings along the horizontal diameter at thecentral aspect of the field. This latter findingis less consistently observed in tinea capitis.

    Figure 2B. Close up of KOH examinationfrom Figure 2A demonstrating primarily themultiple long branched hyphae

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    than 40 different known species of dermatophytes; however, a

    much more limited number of species commonly cause

    cutaneous infection, with between 6 to 8 of these species

    associated with causing tinea capitis worldwide.7,8

    The predominant genus and species of dermatophytes

    causing tinea capitis often varies based on geographic location;

    however, children remain the predominant age group affected.Dermatophytes causing tinea capitis in the United

    States. At present, the two main dermatophytes that cause

    tinea capitis in the United States in order of frequency are T.

    tonsurans and M. canis. T. tonsurans is by far the most

    common causative species, accounting for more than 95

    percent of positive cultures in the United States.9 In other parts

    of the world, the specific species of dermatophyte responsible

    for tinea capitis will vary from each country. The overall

    incidence of tinea capitis in the United States has been

    estimated to be 3 to 8 percent; however, the incidence is

    reported to be on the rise.5 Although tinea capitis can affectindividuals of any age, with cases reported as early as six days

    of life and as late as 70 years of age, the vast majority of cases

    of tinea capitis affect prepubescent children, with the average

    age reported between 3 and 7 years.10 One study cites the point

    prevalence in school-age children to be as high as 13 percent.11

    Tinea capitis, however, still remains a relatively rare entity

    among infants. One reference cites only 50 known reported

    cases of tinea capitis in infants less than one year of age at the

    time of their evaluation.12

    Dermatophytes causing tinea capitis arise from one of three

    main reservoirs and can be classified by this host preference:

    anthropophilic (humans) fungi, which include T. tonsurans;

    zoophilic (animals) fungi, which includeM. canis; and geophilic

    (soil) fungi, which includeM. gypseum.4 The source for most

    tinea capitis infections in children are usually either

    anthropophilic or zoophilic dermatophytes. However, even if

    the infection is zoophilic, the main source of transmission in

    infants is from a visibly infected family member who transfers

    the organism directly, or in the case of anthropophilic fungus,

    may transfer from active infection sites or through

    asymptomatic carriage of the organism, as not all humans

    become clinically infected when exposed to anthropophilic

    fungi.12 Variability in host response to anthropophilic fungi is

    common, including with T. tonsurans, with affected individuals

    ranging from asymptomatic carriage, to non-inflamed or

    minimally inflamed patches of involvement, to affected regions

    of brisk inflammation that is likely related to a greater intensity

    of a cell-mediated host response to the specific organism bysome individuals. On the other hand, asymptomatic carriage

    may occur in those individuals who are otherwise

    immunocompetent, but are typified by an immunologic blind

    spot against that specific dermatophyte. Therefore, these

    carriers can pass the dermatophyte (i.e., T. tonsurans) to

    others who eventually exhibit a clinical infection. However, the

    silent carrier does not develop clinically evident infection.

    Asymptomatic dermatophyte carriage can occur on the scalp of

    children and/or adults.

    Modes of transmission in tinea capitis. A variety of

    different modes of transmission from these reservoirs arepossible, making tinea capitis a contagious and communicable

    fungal infection.2,4 Spore transmission has been described from

    person-to-person, such as among family members, classmates,

    and in infant day care centers. Animal contact and fomite

    contact spread are additional potential sources of infection.

    Fomite/inanimate objects responsible for transmission have

    included hats, brushes, towels, couches, pillows, fallen hair,

    sheets, rugs, telephone receivers, desquamated epithelial cells,

    soil, and toys.2,4 Dermatophytes are hardy organisms, with the

    longevity of viable dermatophytes contributing to the

    communicable spread of tinea capitis. Dermatophytes, which

    are potentially contagious, can be present in fomites for

    months, with viable dermatophytes observed in stubs of hair for

    up to two years.2,4

    The reason why prepubescent children are more prone to

    tinea capitis is at least partially explained by the fact that

    sebum, which is rich in lipids (i.e., fatty acids, certain precursor

    lipids) and fungistatic, is minimally present before the onset of


    Modes of hair shaft invasion. In addition to designation

    by mode of transmission, tinea capitis can also be categorized

    Figure 3A. Complete clinical clearance of tinea capitis after

    eight weeks of oral griseofulvin therapy in the same patient(8-month-old infant girl)

    Figure 3B. Closer view of complete clinical clearance of tinea

    capitis after eight weeks of oral griseofulvin therapy in thesame patient (8-month-old infant girl)

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    b y

    mode of hair invasion.7 The types of hair invasion include

    endothrix, ectothrix, and favus. In ectothrix infection, the

    fungus grows within the hair follicle and covers the hair surface,

    so fungal spores (and sometimes hyphae) are seen on the

    outside of the hair shaft (Figures 2A, 2B). In endothrix

    infection, the dermatophyte progresses down the hair follicle,

    invades the hair shaft, and grows within the hair shaft.

    Therefore, the fungal spores are retained within the hair shaft,

    often appearing like a bag of marbles (Figure 4).7 In general,

    common endothrix dermatophytes include several species of

    the Trichophyton genera (i.e., T. tonsurans), and common

    ectothrix dermatophytes include several species of the

    Microsporum genera, with exceptions.7 In favus, the maincausative organism is T. schoenleinii, with microscopic

    examination revealing hyphae arranged parallel to the hair

    shaft, along with bubbles of air in the hair shaft. 13 Clinically,

    favus is typified around the hair shaft by a yellow cup-shaped

    crusting (scutula) as well as matted hair on the scalp. 13 On

    Woods lamp examination, favus fluoresces a gray-green color.11

    Importantly, T. tonsurans infected hair does not fluoresce on

    Woods lamp exposure due to the endothrix growth pattern.

    Tinea capitis caused by M. canis does exhibit blue-green

    fluorescence of affected hair shafts on Woods lamp exposure as

    the pattern of hair invasion is ectothrix.

    Clinical presentations of tinea capitis. There are also

    numerous recognized clinical patterns of tinea capitis, including

    seborrheic dermatitis-like, black dot type, alopecia areata type,

    kerion, and favus (described above).7 Additional terms have

    also been used to describe the clinical patterns of tinea capitis,

    including gray-type, moth-eaten, and pustular type.1 The

    clinical pattern of tinea capitis present in a given patient is

    dependent upon several factors, including the genus and

    species of dermatophyte, and the host response of the patient.

    As with dermatophyte infection involving other cutaneous

    locations, the degree of visible inflammation in tinea capitis also

    reflects the intensity of host response, and also the specific

    causative dermatophyte, with zoophilic organisms often

    producing visible inflammation.1,4,7,10,11 In many cases of tinea

    capitis in children, cervical and/or occipital lymphadenopathy is

    often present, and id reactions may also occur especially after

    initiating treatment with an oral antifungal agent.

    The most common pattern seen in the United States is the

    seborrheic dermatitis-like pattern that presents as diffuse

    scaling, is usually associated with erythema, without localized

    alopecia.11 This clinical presentation of tinea capitis is easily

    misdiagnosed as seborrheic dermatitis resulting in erroneous

    treatment, often with a topical corticosteroid. As withessentially all cases of tinea capitis, this clinical pattern requires

    use of oral antifungal agent for clearance, so use of an antifungal

    shampoo prescribed for the misdiagnosis of seborrheic

    dermatitis is not adequate for clearance of the fungal infection.

    Other clinical patterns of tinea capitis in children are also

    commonly encountered in the United States, including patterns

    often seen with T. tonsurans, such as round-oval scaly patches

    with or without localized hair loss and little-to-no visible

    inflammation, round-oval patches of hair loss with the

    appearance of black dots that are intrafollicular hair shafts that

    have fractured and broken off as the shaft protrudes above the

    skin surface (black dot fungus), round-oval patches of silver-

    gray scaling devoid of inflammation (gray-type) as shown in

    Figure 5 with the KOH exam from this patient shown in Figure

    4 (endothrix pattern), round-oval patches of shiny skin

    completely devoid of hair and without inflammation (alopecia

    areata-type), and round-oval inflammatory patches or plaques

    with hair loss, the latter also commonly seen with M. canis


    Differential diagnosis and simulant disorders. The

    wide variation in clinical patterns as well as the similar

    Figure 4. Microscopic examination of plucked hairs and skinscrapings from a three-year-old African boy presenting withmultiple scaly patches on the scalp (from same patient asshown in Figure 5). Slide was prepared using KOH 10% withDMSO. Note the endothrix pattern of hair invasion with multi-ple round spores present within the hair shaft (bag of mar-bles). There is absence of long branched hyphae, which isusually the case on KOH exam with both endothrix andectothrix hair invasion.

    Figure 5. A three-year-old African boy presenting with

    multiple round-oval patches of silver-gray scaling devoid ofinflammation with little-to-no hair loss. KOH examination fromthis patient is shown in Figure 4 (endothrix). A fungal cultureconfirmed dermatophyte growth. This clinical presentation isreferred to as gray-type tinea capitis.

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    appearance to other clinical disease states in some cases (i.e.,

    seborrheic dermatitis, alopecia areata) can confound the

    accurate diagnosis of tinea capitis. This is especially true in the

    infant population where tinea capitis is a rare entity and may be

    dismissed easily as seborrheic dermatitis (cradle cap), a muchmore common diagnosis in this age group. In fact, the most

    common presenting sign of tinea capitis in infants is scaling,

    although alopecia has also been reported as a common clinical

    finding.12 It is important that the clinician keep in mind several

    other dermatological conditions that can present with scalp

    scaling in children, including common diagnoses, such as

    seborrheic dermatitis and psoriasis, and rare disorders, such as

    Langerhans cell histiocytosis, dermatomyositis, pityriasis rubra

    pilaris, leukemia cutis, and pemphigus foliaceous.14 Therefore,

    given the infrequent nature of tinea capitis in infancy, a high

    index of suspicion is warranted anytime an infant presents witha seborrheic dermatitis-like scalp eruption in addition to other

    clinical signs such as alopecia or hair thinning.

    Dermatophytes associated with tinea capitis in

    infants. T. tonsurans is still the most common causative

    dermatophyte for tinea capitis in the United States. However, in

    terms of the specific causative species among infants,M. canis

    also appears to be one of the predominate dermatophytes

    causing infection worldwide, including the United States. This

    is due to common contact with house pets that are perceived as

    safe around children, including infants. The main sources of

    infection for tinea capitis caused byM. canis infection are cats

    and dogs. In a specific catch area in Spain, 90 percent of infant

    tinea capitis cases between 1991 and 1995 were caused byM.

    canis.12Additionally, reported cases of tinea capitis in infants in

    the Spanish and English literature showed the predominate

    causative dermatophyte to beM. canis.12 This observation was

    further supported by a report from Italy where 9 of the 15 cases

    of tinea capitis in infants were caused by M. canis.15 Thus,

    based at least on these European reports, although T.

    tonsurans may cause tinea capitis in infants, M. canis is

    commonly the culprit pathogen in this age group, and a housepet, usually a cat, is often the reservoir source ofM. canis.12,15

    Diagnosis of tinea capitis. Given the rarity of tinea capitis

    in infants, a high index of suspicion is necessary in any infant

    presenting with scaling and/or alopecia. Diagnosis based only

    on presenting clinical symptoms is often difficult, and fraught

    with potential for misdiagnosis. If tinea capitis infection is

    suspected, both a KOH prep and fungal culture are important

    for diagnosis. For light microscopy examination, a scraping of

    the scale and samples of affected hair should be placed on a

    microscope slide and 10- to 20-percent KOH should be added.

    KOH with DMSO is preferred by the authors as this

    circumvents the need to heat-fix the slide. For culture, the hair

    and scalp samples should be placed on either Sabouraud

    dextrose agar with chloramphenicol and cycloheximide,

    dermatophyte identification medium or DTM.4 Growth on DTM

    typically occurs within 1 to 2 weeks; however, fungal growth by

    cultures may take 3 to 4 weeks with some media or at some

    laboratories.11 Before obtaining a sample for culture, the area

    should be cleaned with alcohol to avoid cross contamination

    with bacteria.4 There are several methods for obtaining

    samples for culture, including using a surgical blade, brushing

    hair, plucking hair with forceps, or using adhesive tape.1 Less

    traumatic methods for obtaining culture samples include

    running a toothbrush over the hair or, as an alternative,

    rubbing a moistened, but sterile cotton swab or gauze pad over

    the affected area.


    It must be emphasized that attempts to beless traumatic than with hair plucking when obtaining

    specimen for KOH and culture are only of value if they do not

    significantly reduce the potential for a positive yield when tinea

    capitis is present.

    With regard to diagnostic aids that serve to support clinical

    diagnosis, there are important nuances to diagnostic testing

    methods.1,4,7,10,11 Unfortunately, some clinicians, especially non-

    dermatologists, rely on Woods light examination as a

    distinguishing method for diagnosis or exclusion of tinea capitis.

    Woods lamp may be helpful in ectothrix infection (i.e., M.

    canis) with a blue-green fluorescence noted, althoughsensitivity is poor.4 Therefore, a positive Woods lamp

    examination supports the diagnosis of tinea capitis. However, a

    negative examination does not exclude tinea capitis.

    Microscopic identification with KOH prep of long-branched

    hyphae, often with septation, confirms the diagnosis; however,

    the genus and species of dermatophyte remain unknown. DTM

    is a very effective screening medium for culturing

    dermatophytes, provided the site from where the specimen is

    obtained is properly prepped to reduce potential contamination

    by nonpathogenic bacteria or fungi, a proper specimen is

    obtained, the cap on the bottle is kept loose, and the medium is

    checked after one week and after two weeks of incubation.

    Positive growth of a dermatophyte on DTM occurs almost

    always within two weeks. Although growth of contaminant

    bacteria and/or fungi can appear on DTM at any time point, the

    potential for contaminant growth increases after two weeks.

    Also, overgrowth of the causative dermatophyte by

    contaminant organisms may occur and can preclude an

    accurate recognition of dermatophyte colonies on DTM. Given

    the differences in susceptibility of some genera and species to

    individual antifungal agents, identification of the specificdermatophyte that is causing tinea capitis may be clinically

    relevant in some cases. Therefore, if a dermatophyte is grown

    on DTM, and the clinician is not capable of further defining the

    actual dermatophyte that is present, the DTM bottle containing

    the fungal growth can be forwarded to a microbiology/mycology

    laboratory that is capable of determining the genus and species

    of dermatophyte, such as through fungal deoxyribonucleic acid

    (DNA) sequencing.

    Fungal culture may be obtained using media other than

    DTM, with the inoculated medium sent to the reference

    mycology laboratory. The mycology laboratory is then

    responsible for proper incubation, organism identification, and

    reporting of results. It is best that the clinician work directly

    with the mycology laboratory to be certain that the laboratory

    provides the appropriate media for identification of

    dermatophytes along with information on proper storage of the

    culture media before use, and transport instructions.

    Misdiagnosis of tinea capitis. It is common for the

    treatment of tinea capitis in an infant to be delayed, usually due

    to misdiagnosis. As tinea capitis is uncommon in infancy, the

    diagnosis is often not considered, especially when the eruption

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    simulates seborrheic dermatitis of the scalp, or exhibits

    pustulation that is clinically diagnosed incorrectly as a bacterial

    infection. It has been reported that only seven percent of

    children with tinea capitis received appropriate antifungal

    treatment from their primary care provider before referral to adermatologist.1,16 In one study of children with misdiagnosed

    tinea capitis, three were diagnosed as seborrheic dermatitis and

    were treated with topical corticosteroids, three were diagnosed

    as bacterial folliculitis and treated with topical antibiotics, and

    one was treated with oral antibiotics for a suspected bacterial

    infection when the correct diagnosis was kerion.15 The high

    potential for clinical misdiagnosis of tinea capitis, especially by

    a non-dermatologist, makes it all the more incumbent upon the

    dermatologist to ensure that tinea capitis is readily identified

    and properly treated on the presenting visit. Delay in diagnosis

    and/or improper treatment may lead to more extensive scalpinvolvement, spread to non-scalp locations such as the face, and

    if significant inflammation is present (i.e., kerion), to scarring

    alopecia. Moreover, tinea capitis is contagious and spread to

    other family members or other close contacts may occur.

    Management of tinea capitis. Management of tinea

    capitis involves more than simply selecting the right

    medication. As this infection is common in children, dissuading

    parental fears and concerns regarding the disease and/or its

    treatment with oral antifungal therapy is a major responsibility

    for the clinician. Also, consideration of the specific causative

    organism with regard to selection of therapy, daily dose, and

    anticipated duration of treatment, incorporation of adjunctive

    topical antifungal therapy, and handling of fomites, which may

    promote transmission to others are significant aspects to

    address with parents of affected children. When tinea capitis is

    present in an infant, as the age of the child is very young,

    parental fears and concerns are likely to be heightened even


    The importance of oral antifungal therapy in the

    treatment of tinea capitis. With very rare to no exception,

    oral antifungal therapy is needed to eradicate tineacaptis.14,7,8,10,11,19,22 Griseofulvin remains a very effective treatment

    for many cases of tinea capitis caused by both Trichophyton

    spp andMicrosporum spp, provided an adequate daily dose is

    administered and an appropriate duration of therapy is

    completed commensurate with what is needed in each

    individual case. Unlike the newer oral antifungal agents,

    which include the allylamine agent, terbinafine, and the

    triazoles, fluconazole and itraconazole, griseofulvin does not

    persist in cutaneous tissue for a prolonged time period after

    discontinuation, often necessitating a longer duration of

    therapy in many cases in order to achieve complete cure

    (clinical cure + mycological cure).4,7,8,10,22 Importantly, although

    use of oral griseofulvin in children was initially plagued by

    exaggerated fears of major side effects, such as hepatotoxicity

    and hematological disturbances, such side effects have proven

    to be very rare in both adults and children. 4,7,8,10,11,22

    Some reference sources, including approved product

    labeling with certain oral antifungal agents, suggest specific

    durations or duration ranges of treatment for tinea capitis.

    These general recommendations are made as they are effective

    overall based on available data, but their existence should not

    be interpreted to imply complete clearance in all cases. Almost

    without exception, outlier cases exist with all disease states

    and therapies for a variety of reasons, necessitating the clinician

    to adjust therapy based on clinical assessment and index of

    suspicion. It is clear to the authors from available literature thatnot all cases of tinea capitis respond to a specified fixed

    course of oral antifungal therapy. Depending on disease

    severity, the specific fungal pathogen, variations in

    pharmacokinetic and pharmacological properties of the oral

    antifungal agent, and/or characteristics of the individual

    patient, longer courses of therapy may be needed.

    In this case of tinea capitis in an infant, the authors elected

    to repeat a microscopic examination by KOH exam at the end

    of eight weeks of oral griseofulvin treatment, as the eruption

    had cleared visibly. The purpose of this test was to further

    confirm the clinical assessment that the infection had resolved.The repeat KOH exam was negative and oral griseofulvin was

    discontinued at that time. In addition to the KOH exam, it is

    reasonable to also repeat a fungal culture (such as with DTM

    media) at the end of treatment if the clinician feels this

    additional test is warranted. However, a KOH exam allows for

    immediate determination of the possible need for a longer

    course of oral antifungal therapy, as if test results are positive

    for fungal elements, therapy can be continued at that time

    without the delay of waiting for culture results. This principle is

    especially true with oral griseofulvin as this agent exhibits little

    tendency to persist in tissue after discontinuation.22 However,

    with the newer antifungal agents (i.e., terbinafine, fluconazole,

    itraconazole), mycological clearance may not be noted until

    weeks after discontinuation of therapy (e.g., 48 weeks), as

    these agents tend to persist within cutaneous structures (e.g.,

    epidermis, hair, nails) for several weeks after oral

    administration.1,4,7,10,1822 Therefore, clinical judgment is a major

    factor in the determination of when to discontinue oral

    antifungal therapy for tinea capitis.

    Individual oral antifungal agents used to treat tinea

    capitis. Griseofulvin. Overall, griseofulvin remains the goldstandard of oral antifungal treatment for tinea capitis in the

    United States and is approved for this indication by the

    FDA.14,7,8,10,11,19,22 In use for about five decades, griseofulvin

    exhibits an excellent long-term safety profile and proven

    efficacy, provided it is dosed properly based on the weight of

    the patient, and administered over an adequate duration of

    treatment.17 Safety is an obviously important consideration,

    especially when dealing with infants. The most common side

    effects associated with oral griseofulvin are headache,

    gastrointestinal upset (GI), and rash, with the latter reported

    to occur in up to 15 percent of patients, with some cases

    representing id reaction.1,7 The GI side effects are lessened

    when the medication is taken with meals. Rarely reported

    adverse events include various genitourinary, musculoskeletal,

    nervous system, and hematological effects.7

    Two main oral forms of griseofulvin are available, microsized

    and ultramicrosized, relating to the particle size of active

    ingredient incorporated into the formulation. These

    formulations were designed to reduce GI upset and to optimize

    GI absorption of griseofulvin. The microsized form has the

    advantage of a liquid formulation, which is highly acceptable

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    and convenient for infants and young children. Optimal dosing

    in children is based on body weight. Recommendations

    regarding the daily dose of microsized griseofulvin have ranged

    from 10 to 25mg/kg/day. However, the current recommendation

    in the United States is 20 to 25mg/kg/day, which differs from the

    older approved product labeling. Commonly, a treatment

    duration of 6 to 8 weeks is generally recommended, with longer

    durations often needed due to reported treatment failures.4,7

    One report suggests a duration of treatment of 6 to 12 weeks.18

    Others suggest continuation of oral griseofulvin therapy for two

    weeks beyond resolution of clinical signs and symptoms of tinea

    capitis.1 The oral microsized suspension contains 125mg/5mL.

    For the ultramicrosized formulation, a dosing of 10 to

    15mg/kg/day is suggested; however, it may be prudent to favor

    the higher end of the dose range, especially with M. canis

    infection.18 With oral griseofulvin, mycological cure rates havebeen reported between 80 and 95 percent and effective therapy

    (mycological and clinical cure) rates between 88 and 100


    Interestingly, The American Academy of Pediatrics (AAP)

    suggests dosing of 10 to 20mg/kg/day for microsized

    griseofulvin and 5 to 10mg/kg/day for ultramicrosized in a single

    daily dosing for 4 to 6 weeks with possible continuation of

    treatment for two weeks beyond the resolution of clinical

    symptoms of tinea capitis.9 These AAP recommendations

    appear low, with the authors recommending a starting dose of

    20mg/kg/day in children with tinea capitis, with an increase to

    25mg/kg/day in some cases caused byM. canis.

    For infants, different dosage regimens of griseofulvin have

    been reported to be efficacious. In one study involving tinea

    capitis in infants, micronized griseofulvin was the antifungal

    used most often at a dose of 15mg/kg/day for 45 to 60 days, and

    most patients using griseofulvin experienced full recovery.12 In

    another study, most infants received topical imidazole and oral

    griseofulvin (either ultramicronized formulation at 10mg/kg/day

    or 15mg/kg/day for micronized formulation) for 30 to 60 days

    and complete clinical and mycological recovery was noted inpatients, regardless of whether the infection was caused by

    Trichophyton orMicrosporum species.15

    However, effective treatment can often depend on the genus

    and species of dermatophyte causing tinea capitis. For

    Microsporum species, griseofulvin is still the preferred oral

    antifungal agent. In guidelines on the management of tinea

    capitis from the European Society of Pediatric Dermatology, it

    was concluded that griseofulvin is the treatment of choice for

    Microsporum species, with griseofulvin determined to be more

    efficacious than oral terbinafine.19Although there was similarity

    in efficacy and oral treatment duration with griseofulvin,

    itraconazole, and fluconazole, griseofulvin was found to be less

    expensive.19 In the Cochrane Review, griseofulvin was also

    found to be the treatment of choice for tinea capitis caused by

    Microsporum species.20 Given the need for a high daily dose

    and a relatively long treatment duration with griseofulvin, other

    non-FDA approved oral antifungal agents are proposed as an

    alternative treatment forM. canis-induced tinea capitis where

    applicable. In general, the duration of oral griseofulvin therapy

    that is needed to clear tinea capitis caused byM. canis is likely

    to be longer than what is needed for effective treatment of T.

    tonsurans. With oral griseofulvin therapy, a good general rule

    is to treat for two weeks beyond the clearance of visible signs

    and symptoms of tinea capitis.

    Itraconazole. Oral itraconazole has been studied in infants

    with tinea capitis caused by M. canis. In one study, infants

    between 3 and 46 weeks of age were treated with itraconazole

    for 3 to 6 weeks at a dose of 5mg/kg/day using the oral capsules. 6

    Not only was complete clinical and mycological cure achieved,

    no side effects were reported.6 Pulse dosing of itraconazole has

    also been shown to be effective, administered using oral

    capsules at 5mg/kg/day for one week per month (1 week on and

    3 weeks off) for 2 to 4 months.22As the oral capsules are filled

    with active drug encapsulated in small beads, the capsules can

    be opened and the beads placed in custard, peanut butter, or

    apple sauce, for administration to children. As the oral solution

    of itraconazole is better absorbed, a dose of 3mg/kg/day isrecommended for children; however, due to use of cyclodextrin

    to better solubilize itraconazole into solution, diarrhea is more

    likely to occur with the solution formulation.22

    In one report, pulse dosing of oral itraconazole was used in

    treating an eight-month old patient.21 Itraconazole at a dose of

    6.5mg/kg/day was employed for two pulse doses, each lasting

    one week (a total of two weeks treatment). As far out as eight

    weeks post-treatment, there were no clinical signs of infection

    on KOH and fungal cultures were negative. Thus, oral

    itraconazole appears to be an effective alternative therapy in

    infants with tinea capitis caused byM. canis, especially given

    its shorter treatment duration as compared to griseofulvin. Oral

    itraconazole is not FDA-approved for the treatment of tinea

    capitis in the United States.

    Terbinafine. Oral terbinafine, available as oral granules, is

    FDA approved for treatment of tinea capitis in children four

    years of age or older. This agent has also been suggested as an

    alternative treatment for tinea capitis in children, including

    cases caused by M. canis. While the effectiveness of oral

    terbinafine in infants withM. canis-induced tinea capitis has

    not been extensively studied, there are reports of its use in suchcases.12 Oral terbinafine was used in one infant patient with

    tinea capitis caused byM. canis and clinical and mycological

    recovery were achieved when used daily for 3 to 4 weeks. 15

    However, assessment of available data and case reports

    suggests that tinea capitis caused by M. canis is more

    refractory to oral terbinafine as compared to griseofulvin, with

    the former considered less effective than griseofulvin for this

    pathogen.19 The lower efficacy of oral terbinafine for ectothrix

    scalp infections (i.e.,M. canis) in children may be related to

    the pharmacokinetic properties of the drug.3 After oral

    administration, terbinafine accumulates in high concentrations

    in sebum due to its marked lipophilicity, and thus would be

    expected to be effective for a dermatophyte infection involving

    scalp hair follicles. However, as sebaceous glands remain

    immature and do not develop fully in terms of size and

    functionality until puberty, access of terbinafine into the follicle

    is believed to be markedly reduced.3 Additionally, terbinafine

    does not penetrate into eccrine sweat after oral administration,

    which could serve as a potential secondary mode of passive

    access. Thus, the lack of penetration into eccrine sweat and the

    low levels of sebum before puberty are viable explanations for


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    the lesser efficacy of oral terbinafine for tinea capitis caused by

    organisms that produce ectothrix hair invasion (i.e.,M. canis).3

    Based on product labeling in the United States, the dosing of

    oral terbinafine granules for tinea capitis in children is

    125mg/day (35kg child), administered once daily, with the

    weight-based dosing recommendations differing slightly from

    previous reports in published literature with oral terbinafine.22

    For use in children, oral granules can be sprinkled on nonacidic

    food such as pudding or mashed potatoes. Although US product

    labeling suggests a treatment duration of six weeks for tinea

    capitis, the exact dosing and duration for effective treatment for

    M. canis has been debated in the literature. In one study, oral

    terbinafine was shown to be relatively ineffective in treating

    M. canis tinea capitis for six weeks.23 In contrast, another study

    suggests that a six-week course of oral terbinafine is safe, welltolerated and can result in at least an acceptable level of

    efficacy.24 Moreover, the study suggests that increases in cure

    rates may have more to do with increases in dosing, not

    duration.24 In regard to duration, some believe that while

    terbinafine is effective for M. canis, it still requires a longer

    duration of treatment and suggest the lack of success is linked

    to treatment duration rather than drug dosage.25 Regardless of

    the debate, terbinafine has been shown to be effective in M.

    canis infection and should be considered as a possible

    alternative given the potential for a shorter duration of

    treatment, although griseofulvin still remains the preferred

    treatment over oral terbinafine.

    Fluconazole. Although approved for use in children for

    other types of fungal infections (primarily systemic), oral

    fluconazole is not FDA-approved for treatment of tinea capitis.

    However, oral fluconazole is active against dermatophytes and

    is another option for treatment of tinea capitis in children,

    available for oral administration as a freshly reconstituted oral

    suspension or as a tablet (multiple strengths available).2628

    The safety of systemic fluconazole use, both oral and

    intravenous, in the pediatric population (N=562), wasevaluated based on data from 12 clinical trials.29 These studies,

    in which fluconazole was dosed based on body weight

    (112mg/kg), included predominantly immunocompromised

    children with severe underlying medical disorders, and with

    98.6 percent also receiving a variety of concomitant

    medications. This assessment concluded that oral fluconazole in

    the pediatric population was very well tolerated, with the

    authors stating that the safety profile of fluconazole in children

    mirrors the excellent safety profile seen in adults.30Additional

    studies have demonstrated that oral fluconazole is well

    tolerated in children treated for tinea capitis.27,28

    Oral fluconazole 8mg/kg once weekly for 8 weeks was

    evaluated in an open study of children with tinea capitis.27

    Longer durations of therapy were administered if clinically

    indicated based on clinical assessment. All cases of T.

    tonsurans (n=11) responded with clinical and mycological

    cure (complete cure) to eight weeks of once-weekly oral

    fluconazole. M. canis was cleared clinically in 12 of 17 cases

    after eight weeks of once-weekly oral fluconazole, with one case

    requiring 12 weeks, and three cases requiring 16 weeks to

    achieve complete cure. Overall, 16 of 17 cases of tinea capitis

    treated with once-weekly fluconazole were completely cured at

    eight weeks after completion of oral antifungal treatment.27

    In a multicenter, triple-blind study, fluconazole 6mg/kg/day

    for three weeks or fluconazole 6mg/kg/day for six weeks were

    shown to be comparable in efficacy to oral griseofulvin

    11mg/kg/day for six weeks in children with tinea capitis.

    However, mycological cure rates were only approximately 50

    percent in all three treatment groups at the end of treatment.28

    Regardless of the genus and species of causative dermatophyte,

    the daily dose of oral griseofulvin suggested in this study was

    too low when using the microsize formulation based on the

    more common fungal pathogens currently encountered.22 In

    addition, a duration of treatment of six weeks or less (in one

    fluconazole arm) with both agents was also likely to be

    inadequate in many of the patients, with longer durations of

    therapy needed in some cases. Oral griseofulvin (microsize) isrecommended at a dose of 20 to 25mg/kg/day for a usual

    duration of 6 to 2 weeks.22

    Ketoconazole. Oral ketoconazole has been suggested for

    treatment of dermatophyte infections in cases where

    griseofulvin is not tolerated. However, due to the higher

    apparent risk of hepatotoxicity with oral ketoconazole as

    compared to other oral antifungal agents, reported overall as

    serum transaminase elevation in 5 to 10 percent of cases and

    estimation of symptomatic hepatitis in up to 1 in 10,000

    patients, the authors do not consider oral ketoconazole to be as

    prudent an alternative as oral terbinafine, fluconazole, or


    Use in tinea capitis caused by Trichophytonspecies

    including T. tonsurans. When Trichophyton species are

    implicated, other agents have been shown to be as efficacious

    as griseofulvin, but with the additional advantage of requiring

    shorter dosing periods. This advantage is helpful, especially

    when considering treatment for infants. Again, however, no

    agent has been specifically approved for treatment in infants

    by the FDA. In tinea capitis caused by Trichophyton spp in

    children, the guidelines for European Society of PediatricDermatologists note that itraconazole, fluconazole, and

    terbinafine have efficacy rates and potential adverse effects

    similar to those of griseofulvin and although more expensive,

    they require shorter dose durations.19 One report further

    suggests that several small studies have shown that short-

    term terbinafine, itraconazole, and fluconazole therapy were

    comparable in efficacy and safety to griseofulvin.17 The

    Cochrane report also establishes that there is evidence that

    terbinafine, dosed based on body weight, for 2 to 4 weeks is

    effective in the treatment of tinea capitis caused by

    Trichophyton spp.20 Terbinafine has been shown to be at least

    as effective as griseofulvin in Trichophyton-induced tinea

    capitis in other reports.5,33,34 In fact, one study noted that

    terbinafine oral granules achieved a higher complete cure and

    mycological cure rate than terbinafine oral suspension for

    T. tonsurans-induced tinea capitis.5 Thus, in situations in

    which griseofulvin fails, an adverse reaction results in

    discontinuation of griseofulvin, or griseofulvin is not an

    available option, terbinafine, fluconazole, or itraconazole can

    be considered as viable alternatives in tinea capitis caused by

    T. tonsurans.

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    Monitoring considerations when using oral antifungal

    agents in children with tinea capitis. Overall, oral antifungal

    therapy has been safe and well tolerated in children with a

    variety of superficial and systemic fungal infections, including

    infants with tinea capitis and other mycotic infections in some

    analyses and case reports.39,1114,16,2029As with any other therapy,

    especially with a systemic agent, patient monitoring to assess

    both efficacy and safety is vital to the success of treatment and

    allows for adjustments in therapy if needed based on clinical

    response and/or suspicion of adverse reactions.

    Clinical monitoring. Clinical monitoring of oral antifungal

    therapy necessitates obtaining a complete medical history.

    Suggestions for use or avoidance of some oral agents and

    monitoring recommendations during treatment relate to the

    presence of underlying medical disorders, especially pre-

    existing hepatic or hematological disorders. For example, use ofterbinafine oral granules is not recommended for patients with

    chronic or active liver disease, according to approved product


    As a general recommendation, when treating tinea capitis in

    children, including infants, the authors suggest monthly follow-

    up appointments to assess tolerability, safety, and clinical

    response. With regard to education of the parents or legal

    guardian of the child undergoing treatment, or with patients

    mature enough to understand, it is important to explain that

    although most patients experience little to no difficulty with

    oral antifungal treatment, side effects may occur and are best

    detected early. Therefore, if the patient complains of any

    potential side effects, such as frequent, severe, or intractable

    cephalgia, gastrointestinal upset, an inexplicable feeling of

    weakness or fatigue without resolution after an adequate rest,

    or flu-like symptoms, such complaints may reflect an adverse

    drug reaction and the clinician should be contacted. The same

    would be true if the patient experienced abdominal discomfort,

    nausea, vomiting, diarrhea, dizziness, or other symptoms that

    are out of step with the individuals normal course of behavior.

    In children and infants too young to express symptoms verbally,changes in behavior, especially poor eating, excessive tiredness,

    or listless behavior may reflect an adverse drug reaction, as can

    other gastrointestinal signs such as vomiting or diarrhea.

    Laboratory monitoring. There are several publications,

    including those reviewed and referenced in this article that

    discuss the use of oral antifungal agents in children with tinea

    capitis and other superficial fungal infections, with some

    including use in infants. General recommendations regarding

    laboratory monitoring guidelines with the use of oral antifungal

    therapy, including griseofulvin, terbinafine, fluconazole, and

    itraconazole, appear in the literature, including in approved

    product labeling, and may serve as a guide to the clinician. 31,32,3537

    Importantly, FDA approval status in pediatric patients for tinea

    capitis with available oral antifungal agents does not necessarily

    encompass all clinical situations that the clinician may

    encounter in clinical practice. Although general monitoring

    guidelines exist in the literature with the use of oral griseofulvin,

    terbinafine, fluconazole, and itraconazole, the authors feel that

    clinical monitoring is of primary importance. The risk of

    hepatocellular injury or hematological reactions with these

    agents is low in both adults and children.31,32,35,36

    With oral griseofulvin, although there was some suggestion

    of periodic laboratory monitoring in the past, clinical monitoring

    appears to be sufficient, especially in children with tinea capitis

    who are without underlying major medical disorders.31,32,37 The

    long track record of extensive experience with oral griseofulvin

    in children with dermatophyte infections (e.g., tinea capitis) for

    more than four decades supports a very favorable safety profile,

    with a conspicuous absence in the literature of any new or

    major side effects that appear to be common.31,32,37 Overall, it

    does not appear necessary to routinely perform laboratory

    monitoring, such as complete blood cell counts (CBC) or serum

    transaminase testing in children treated with oral griseofulvin

    for tinea capitis including infants, although in the latter subset

    experience is more limited. Ultimately, the clinician may elect in

    individual cases to perform baseline and/or follow-up

    monitoring if he or she feels that details of the patient historywarrant this approach (e.g., major underlying medical

    disorders, strong parental concern).

    General laboratory monitoring guidelines with the use of oral

    terbinafine (e.g., >46 weeks) suggest baseline testing of serum

    transaminases (e.g., alanine transaminase [ALT]; aspartate

    transaminase [AST]) and CBC in cases where hematological

    side effects may be of specific concern or with duration of

    therapy greater than six weeks. Repeat testing periodically

    (e.g., after 1 month and after 3 months) during active treatment

    has also been suggested.31,32 Specifically, with the use of

    terbinafine oral granules, which are FDA-approved for

    treatment of tinea capitis in patients four years of age or older,

    pretreatment serum transaminase (ALT and AST) tests are

    advised for all patients, according to approved product

    labeling.35 Notably, aganulocytosis has been reported rarely with

    oral terbinafine after 4 to 6 weeks of therapy, with an overall

    estimated incidence of 1 in 400,000.31

    Monitoring of serum transaminases may also be prudent

    with itraconazole and fluconazole and are suggested in patients

    with baseline liver function abnormalities.32,36 In fact, the risk of

    clinically relevant hepatic reactions with these agents are low,general guidelines with these agents have not been consistently

    emphatic, and the available guidelines are not definitive

    mandates with these agents in otherwise healthy patients.31,32,36

    If the clinician elects to perform laboratory monitoring, a

    reasonable general recommendation is serum transaminase

    testing at baseline, after one month, after three months, and at

    three-month intervals thereafter, although such prolonged

    therapy (e.g., >1216 weeks) with these agents is not likely to

    be needed for tinea capitis in children.31 The decision to perform

    baseline and repeat serum transaminase testing during

    treatment of tinea capitis with fluconazole or itraconazole in

    children and infants is ultimately left to the decision of the

    clinician along with the patient (or parent/legal guardian when

    applicable) on a case-by-case basis after discussion of the

    benefits versus risks of oral antifungal therapy. Additionally, in

    the presence of underlying major medical disorders of concern,

    the clinician may elect to monitor more closely, both clinically

    and through laboratory testing, when treating tinea capitis in

    children and infants with oral antifungal therapy.

    Importantly, as oral ketoconazole does not offer any

    advantage over the other available oral antifungal agents for

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    treatment of dermatophyte infections (including tinea capitis)

    and is associated with a higher risk of both symptomatic and

    asymptomatic hepatotoxicity than other agents, its use is not


    With regard to tinea capitis specifically in infants, the relative

    infrequency of this clinical scenario warrants clinical judgment

    regarding both clinical and laboratory monitoring with oral

    antifungal therapy. As stated above, clinical monitoring to

    assess therapeutic response and tolerability of treatment is of

    primary importance, with baseline and periodic laboratory

    monitoring incorporated to support clinical assessment and

    follow up.

    Drug interactions with oral antifungal agents. An

    extensive review of drug interactions with oral antifungal agents

    is beyond the scope of this article and is provided in detail

    elsewhere.38,39 The vast majority of drugs that are associatedwith potentially significant interactions with any of the available

    oral antifungal agents are not commonly used in children,

    although they may be clinically relevant in selected cases.

    These include certain antihypertensive or cardiac medications

    (nifedipine, quinidine, digoxin, metoprolol), some cholesterol-

    lowering agents (atorvastatin, simvastatin, lovastatin), certain

    antidepressants (nortrypityline, some selective serotonin

    reuptake inhibitors [SSRIs]), certain sedative-hypnotic drugs

    (triazolam), and warfarin. In any event, it is prudent in all

    patients to cross check against their medication list, and to

    update their medication list at each visit. In children with

    underlying medical disorders who are likely to be using

    systemic medications, it is also prudent to exclude potentially

    significant drug interactions, which vary depending on the oral

    antifungal agent prescribed.38,39

    The following two scenarios are examples of notable drug

    interactions that the clinician may be more likely to encounter

    when treating children for tinea capitis with certain oral

    antifungal agents. In these situations, the affected children have

    specific medical disorders necessitating systemic immuno-

    suppressive therapy or the child may be undergoing sedationfor a procedure. Oral cyclosporine is sometimes used in

    children with severe atopic dermatitis, severe psoriasis, some

    autoimmune disorders, and in organ transplant recipients.

    Serum levels of cyclosporin may be increased by concurrent use

    of fluconazole or itraconazole.38,39 Also, in children who are

    undergoing sedation for a surgical procedure, serum levels of

    the hypnotic agent midazolam may be markedly increased by

    oral itraconazole, leading to excessive and prolonged


    Adjunctive topical therapies. Adjunctive topical

    antifungal therapies are also an important consideration in

    management of tinea capitis, but they are not to be used as

    monotherapy, as their cure rate is very low for tinea

    capitis.14,7,8,10,11,26 Adjunctive topical antifungal agents (i.e.,

    selenium sulfide 1% or ketoconazole 2%), usually utilized as a

    shampoo formulation for ease of use especially in children, have

    been shown to decrease dermatophyte colony counts and

    shorten the duration of oral antifungal therapy in some cases of

    tinea capitis.17,19,26,4042 Shampoos are applied for 5 to 10 minutes

    before rinsing, with an application frequency of at least three

    times a week, although daily use is likely to be optimal.17,19,26,40

    Lotion, solution, cream, or gel formulations of antifungal agents

    (i.e., ketoconazole, selenium sulfide, ciclopirox, sulconazole)

    may also be utilized on the scalp as adjunctive treatment for

    tinea capitis, but may be harder or messier to use and will likely

    require more time for application, which may be difficult with

    children who are less cooperative.

    Ketoconazole 2% shampoo used daily for eight weeks has

    exhibited clinical improvement of tinea capitis caused by T.

    tonsurans in 15 children 3 to 6 years of age, with culture

    negativity in 6 of 15 (40%) at Week 8, although use of shampoo

    therapy alone is not recommended for tinea capitis.26,40

    Careful hair hygiene should also be practiced. Patients

    should not share such items as hats, combs, or pillows. Also,

    in the event a family pet is the source of infection,

    appropriate treatment of the cat or dog by a veterinarian is


    CONCLUSIONTinea capitis is the most common fungal infection seen in

    children, but is rare in infants. As tinea capitis can look identical

    to seborrheic dermatitis of the scalp, with the latter very

    common in infants, and as tinea capitis in infants is rare, is it not

    surprising that tinea capitis in infancy is often misdiagnosed and

    improperly treated. The importance of appropriate treatment is

    essential, especially given the potential long-term sequelae.

    While the only FDA-approved oral antifungals in children are

    griseofulvin and terbinafine, no agent has been specifically

    approved for the treatment of tinea capitis in infants. However,

    data are available on the use of other oral anitfungal agents, in

    addition to griseofulvin and terbinafine, for tinea capitis in

    children, including some cases in infants. Some differences

    appear to exist in efficacy, suggested daily dose, and duration of

    therapy among the different oral antifungal agents for tinea

    capitis depending on the genera and species of dermatophyte

    and disease severity. Proper diagnosis and identification of the

    causative fungal pathogen are both important components of

    optimal management. Ultimately, as tinea capitis may affectboth sides of the age spectrum, practitioners are encouraged to

    employ a heightened awareness of the multiple clinical

    presentations of tinea capitis and remain cognizant of the fact

    that tinea capitis can affect any patient at any age. Oral

    antifungal therapy is needed to eradicate tinea capitis. In

    addition, adjunctive topical antifungal therapy (e.g., shampoo)

    may be beneficial in expediting clinical and mycological

    response, in decreasing the fungal organism load, reducing

    transmission to others, and mitigating the asymptomatic carrier

    state on the scalp.

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