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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.

1,2

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

employed.

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

tolerated.

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

puberty.

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

infection.

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.

1,7

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

further.

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

percent.18

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

itraconazole.3032

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

labeling.35

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

recommended.31,32

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

sedation.38,39

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

recommended.

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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