DelRosso_Michaels.

qxp

[CASE

2/9/12

2:51 PM

REPORT

Page 49

AND

LITERATURE

REVIEW]

Tinea Capitis in Infants

Recognition, Evaluation, and Management Suggestions
a

BRENT D. MICHAELS, DO; bJAMES Q. DEL ROSSO, DO, FAOCD

Chief 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/JDRx Dermatology, Las Vegas and Henderson, Nevada

ABSTRACT
Tinea 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.)

inea capitis infection is on the rise in North America and

continues to be a significant public health concern.1,2 In
fact, 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 high
index 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 REPORT
An 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 and
normal 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

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: James Q. Del Rosso, DO; E-mail: jqdelrosso@yahoo.com

[ February 2012 Volume 5 Number 2]

49

DelRosso_Michaels.qxp

2/9/12

2:51 PM

Figure 1. Infant girl (8 months of age)

presenting with erythematous, ill-defined
patches and thin plaques with scaling and
focal hyperkeratosis diffusely involving the
scalp

Page 50

Figure 2A. Microscopic examination of

plucked hairs and skin scrapings from the
same patient using KOH 10% with DMSO
demonstrating ectrothrix pattern of hair
invasion. Note the round spores lined up on
the outer surface of the hair shaft on the
upper right portion of the field. Multiple long
hyphae are also noted externally around the
hair shaft and within scale from skin scrapings along the horizontal diameter at the
central aspect of the field. This latter finding
is less consistently observed in tinea capitis.

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 with M. 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.
50

Figure 2B. Close up of KOH examination

from Figure 2A demonstrating primarily the
multiple long branched hyphae

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, and
towels 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.

DISCUSSION
Tinea 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

[February 2012 Volume 5 Number 2]

50

DelRosso_Michaels.qxp

2/9/12

2:51 PM

Page 51

Figure 3A. Complete clinical clearance of tinea capitis after

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

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 affect
individuals 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 include M. canis; and geophilic
(soil) fungi, which include M. 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

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

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

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 by
some 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 are
possible, 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

[ February 2012 Volume 5 Number 2]

51

DelRosso_Michaels.qxp

2/9/12

2:51 PM

Page 52

b y

Figure 4. Microscopic examination of plucked hairs and skin

scrapings from a three-year-old African boy presenting with
multiple scaly patches on the scalp (from same patient as
shown in Figure 5). Slide was prepared using KOH 10% with
DMSO. Note the endothrix pattern of hair invasion with multiple round spores present within the hair shaft (bag of marbles). There is absence of long branched hyphae, which is
usually the case on KOH exam with both endothrix and
ectothrix hair invasion.

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

multiple round-oval patches of silver-gray scaling devoid of
inflammation with little-to-no hair loss. KOH examination from
this patient is shown in Figure 4 (endothrix). A fungal culture
confirmed dermatophyte growth. This clinical presentation is
referred to as gray-type tinea capitis.

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 main
causative 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 with
essentially 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 silvergray 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

52

[February 2012 Volume 5 Number 2]

52

DelRosso_Michaels.qxp

2/9/12

2:51 PM

Page 53

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 much
more 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 with
a 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 by M. 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 by M.
canis.12 Additionally, reported cases of tinea capitis in infants in
the Spanish and English literature showed the predominate
causative dermatophyte to be M. 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 house
pet, usually a cat, is often the reservoir source of M. 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 be
less 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 nondermatologists, 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, although
sensitivity 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 specific
dermatophyte 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

[ February 2012 Volume 5 Number 2]

53

DelRosso_Michaels.qxp

2/9/12

2:51 PM

Page 54

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 a
dermatologist.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 scalp
involvement, 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 tinea
captis.14,7,8,10,11,19,22 Griseofulvin remains a very effective treatment
for many cases of tinea capitis caused by both Trichophyton
spp and Microsporum 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
54

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 that
not 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 gold
standard 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

[February 2012 Volume 5 Number 2]

54

DelRosso_Michaels.qxp

2/9/12

2:51 PM

Page 55

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 have
been 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 by M. 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 in
patients, regardless of whether the infection was caused by
Trichophyton or Microsporum 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.19 Although 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 for M. canis-induced tinea capitis where
applicable. In general, the duration of oral griseofulvin therapy
that is needed to clear tinea capitis caused by M. 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.22 As 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 is
recommended 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 by M. 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 with M. canis-induced tinea capitis has
not been extensively studied, there are reports of its use in such
cases.12 Oral terbinafine was used in one infant patient with
tinea capitis caused by M. 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

[ February 2012 Volume 5 Number 2]

55

DelRosso_Michaels.qxp

2/9/12

2:51 PM

Page 56

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 (<25kg child), 187.5mg/day (2535kg child), and
250mg/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, well
tolerated 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), was
evaluated 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.30 Additional
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
56

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) is
recommended 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 Trichophyton species
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 Pediatric
Dermatologists 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 shortterm 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.

[February 2012 Volume 5 Number 2]

DelRosso_Michaels.qxp

2/9/12

2:51 PM

Page 57

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.39,1114,16,2029 As 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 preexisting hepatic or hematological disorders. For example, use of
terbinafine 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 followup 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 history
warrant 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

[ February 2012 Volume 5 Number 2]

57

DelRosso_Michaels.qxp

2/9/12

2:51 PM

Page 58

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 associated
with 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 cholesterollowering 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 immunosuppressive therapy or the child may be undergoing sedation
for 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
58

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.

CONCLUSION
Tinea 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 affect
both 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.

REFERENCES
1.

2.

3.

Ali S, Graham TAD, Forgie SED. The assessment and

management of tinea capitis in children. Pediatr Emerg
Care. 2007;23(9):662668.
Silverman RA. Pediatric mycoses. In: Elewski BE, ed. Topics
in Clinical Dermatology: Cutaneous Fungal Infections.
New York, NY: Igaku-Shoin; 1992.
Ginter-Hanselmayer G, Seebacher C. Treatment of tinea
capitisa critical appraisal. J Dtsch Dermatol Ges.
2011;9:109114.

[February 2012 Volume 5 Number 2]

DelRosso_Michaels.qxp

4.

5.

6.

7.
8.
9.

10.
11.
12.
13.
14.

15.
16.

17.
18.
19.
20.

21.

22.
23.

24.
25.

2/9/12

2:51 PM

Page 59

Mohrenschlager M, Seidl HP, Ring J, et al. Pediatric tinea

capitis: recognition and management. Am J Clin Dermatol.
2005;6(4):203213.
Elewski BE, Caceres HW, DeLeon L, et al. Terbinafine
hydrochloride oral granules versus oral griseofulvin
suspension in children with tinea capitis: results of two
randomized, investigator-blinded, multicenter, international,
controlled studies. J Am Acad Dermatol. 2008;59:4154.
Binder B, Richtig E, Weger W, et al. Tinea capitis in early
infancy treated with itraconazole: a pilot study. JEADV.
2009;23:11611163.
Elewski BE. Tinea capitis: a current perspective. J Am Acad
Dermatol. 2000;42:120.
Gonzalez U. Tinea capitis. In: Williams H, ed. Evidence-based
Dermatology. Malden, Mass: Blackwell Publishing; 2008.
Lorch Dauk KC, Comrov E, Blumer JL, et al. Tinea capitis:
predictive value of symptoms and time to cure with
griseofulvin treatment. Clin Pediatr. 2010;49(3):280286.
Smith ML. Tinea capitis. Pediatr Ann. 1996;25(2):101105.
Alvarez MS, Silverberg NB. Tinea capitis. Cutis.
2006;78:189196.
Gilaberte Y, Rezusta A, Gil J, et al. Tinea capitis in infants in
their first year of life. Br J Dermatol. 2004;151:886890.
Elewski BE. Treatment of tinea capitis: beyond griseofulvin. J
Am Acad Dermatol. 1999;40:S27S30.
Williams JV, Eichenfield LF, Burke BL, et al. Prevalence of
scalp scaling in prepubertal children. Pediatrics.
2005;115:e1e6.
Romano C, Gianni C, Papini M. Tinea capitis in infants less
than 1 year of age. Pediatr Dermatol. 2001;18(6):465468.
Fuller LC, Child FC, Midgley G, et al. Scalp ringworm in
south-east London and an analysis of a cohort of patients
from a paediatric dermatology department. Br J Dermatol.
2003;148(5):985988.
Cahn Y-C, Friedlander SF. New treatments for tinea capitis.
Curr Opin Infect Dis. 2004;17:97103.
Gupta AK, Cooper EA. Update in antifungal therapy of
dermatophytosis. Mycopathologia. 2008;166:353367.
Kakourou T, Uksal U. Guidelines for the management of tinea
capitis in children. Pediatr Dermatol. 2010;27(3):226228.
Gonzalez U, Seaton T, Bergus G, et al. Systemic antifungal
therapy for tinea capitis in children. Cochrane Database Syst
Rev. 2007;4:172.
Koumantaki E, Georgala S, Rallis, et al. Microsporum canis
tinea capitis in an 8-month-old infant successfully treated
with 2 weekly pulses of oral itraconazole. Pediatr Dermatol.
2001;18(1):6062.
Roberts BJ, Friedlander SF. Tinea capitis: a treatment update.
Pediatric Annals. 2005;34(3):191200.
Dragos V, Lunder M. Lack of efficacy of 6-week treatment
with oral terbinafine for tinea capitis due to Microsporum
canis in children. Pediatr Dermatol. 1997;14:4648.
Aste N, Pau M. Tinea capitis caused by Microsporum canis
treated with terbinafine. Mycoses. 2004;47:428430.
Lipozencic J, Skerlev M, Orofino-Costa R, et al. A randomized,
double-blind, parallel-group, duration-finding study of oral
terbinafine and open-label, high-dose griseofulvin in children
with tinea capitis due to Microsporum species. Br J

26.

27.

28.

29.

30.

31.

32.

33.

34.

35.
36.

37.
38.

39.

40.
41.

42.

Dermatol. 2002;146:816823.
Higgins EM. Tinea captitis. In: Lebwohl MG, Heymann WR,
Berth-Jones J, Coulson I, eds. Treatment of Skin Disease:
Comprehensive Treatment Strategies. 3rd ed. Philadelphia:
Saunders-Elsevier; 2010:736739.
Gupta AK, Dlova N, Taborda P, et al. Once weekly fluconazole
is effective in children in the treatment of tinea capitis: a
prospective multicenter study. Br J Dermatol. 2000;142:
965968.
Foster KW, Friedlander SF, Panzer H, at al. A randomized
controlled trial assessing the efficacy of fluconazole in the
treatment of pediatric tinea capitis. J Am Acad Dermatol.
2005;53(5):798809.
Novelli V, Holzel H. Safety and tolerability of fluconazole in
children. Antimicrob Agents Chemother. 1999;43(8):
19551960.
Lewis JH, Zimmerman HJ, Benson GD, et al. Hepatic injury
associated with ketoconazole therapy: analysis of 33 cases.
Gastroenterology. 1984;86:503513.
Wolverton SE, Remlinger K. Suggested guidelines for patient
monitoring: hepatic and hematologic toxicity attributable to
systemic dermatologic drugs. Dermatol Clin. 2007;25:
195205.
Gupta AK. Systemic antifungal agents. In Wolverton SE, ed.
Comprehensive Dermatologic Drug Therapy, 2nd Edition.
Philadelphia: Saunders-Elsevier; 2007:7599.
Fleece D, Gaughan JP, Aronoff SC. Griseofulvin versus
terbinafine in the treatment of tinea capitis: a meta-analysis of
randomized, clinical trials. Pediatrics. 2004; 114(5):
13121315.
Fuller LC, Smith CH, Cerio R, et al. A randomized comparison
of 4 weeks of terbinafine vs. 8 weeks of griseofulvin for the
treatment of tinea capitis. Br J Dermatol. 2001;144:321327.
Lamisil Oral Granules. Physicians Desk Reference. 2010:
22642265.
Sporanox (Itraconazole Capsules). Drug Information User
Reviews. www.rxlist.com/sporanox-drug.htm/. Accessed
6/29/2011.
Grifulvin V Oral Suspension (Griseofulvin Oral Suspension).
Physicians Desk Reference; 2006.
Gupta A, Katz I, Shear NH. Drug interactions with
itraconazole, fluconazole, and terbinafine and their
management. J Am Acad Dermatol. 1999;41:237248.
Shapiro LE, Shear NH. Drug interactions. In: Wolverton SE,
ed. Comprehensive Dermatologic Drug Therapy, 2nd
Edition. Philadelphia: Saunders-Elsevier; 2007:949975.
Greer DL. Successful treatment of tinea capitis with 2%
ketoconazole shampoo. Int J Dermatol. 2000;39:302304.
Gibbens TG, Murray MM, Baker RC. Comparison of 1% and
2.5% selenium sulphide in the treatment of tinea capitis. Arch
Pediatr Adolesc Med. 1995;149:808811.
Allen HB, Honig PJ, Leyden JJ, et al. Selenium sulphide:
adjunctive treatment for tinea capitis. Pediatrics. 1992;69:
8183.

[ February 2012 Volume 5 Number 2]

59