CLINICAL
Tinea capitis (scalp ringworm) is a common paediatric infection usually affecting school-aged children. The
commonest causative organisms are dermatophytes from the genera Trichophyton or Microsporum.
Dermatophytes are keratinophilic and invade the stratum corneum, hair and nails.
The diagnosis and
management of
TINEA CAPITIS
Prof HF Jordaan, Department of Dermatology, University of Stellenbosch
Summary
Dermatophytosis encompasses several distinct
clinical entities, namely tinea capitis (scalp
ringworm), tinea corporis (ringworm of
glabrous skin), tinea cruris (ringworm of the
groin), tinea unguium or onychomycosis
(ringworm of the nail), tinea pedis (ringworm of
the feet), tinea barbae (ringworm of the beard),
and tinea manuum (ringworm of the hand).
Dermatophyte fungi causing tinea capitis can
be divided into anthropophilic and zoophilic
organisms. Anthropophilic fungi grow preferen-
tially on humans, and the most common type
forms large conidia of approximately 3-4 mm in
diameter within the hair shaft (endothrix).
Common causes of endothrix infection include
Trichophyton tonsurans , T schoenleinii and T
violaceum. Zoophilic fungi are acquired
through direct contact with infected animals
(e.g. puppy, kitten). Smaller conidia of
approximately 1-3 mm in diameter extend
around the exterior of the hair shaft (ectothrix).
Ectothrix infection is caused by T verrucosum,
Note:
Contact INFOMED at the T mentagrophytes, and all Microsporum
Tygerberg Campus species.
Library at
mailto:infomed@sun.ac.za
to request one of Tinea capitis is seen most commonly in
the references children younger than 10 years of age Peak
Stellmed
Updates,Faculty of Health age range is in patients aged 3-7 years.
Sciences,Stellenbosch Gender distribution is approximately equal.
University. Tinea capitis is the most common paediatric
All Articles are Peer
Reviewed. dermatophyte infection worldwide. Tinea
8 SA Pharmaceutical Journal October 2006
capitis occurs occasionally in other age groups.
The fungistatic properties of post-pubertal
sebum may repel dermatophytes.
The following morphological presentations
have been described: black dot type, sebor-
rhoeic dermatitis type, gray patch type, yellow
patch type, pustular type, annular type, kerion,
favus and dermatophytic mycetoma (Figures 1-
6). Combinations of these lesions are not
uncommon. The common denominator of all
types is the presence of hair loss. Pruritus is
usually minimal. Infected hairs are brittle, and
by the third week, broken hairs are evident.
Hair loss is subtle in the seborrhoeic type.
Secondary impetigo may complicate any form
of tinea capitis. Regional occipital lympha-
denopathy is not uncommon. Impetigo of the
scalp should always arouse suspicion of under-
lying tinea capitis. Other causes of scalp
impetigo in this age group include pediculosis
capitis, scabies, atopic dermatitis and primary
impetigo.
Dermatophyte infection of the scalp can usually
be diagnosed clinically. Additional diagnostic
methods include a potassium hydroxide (KOH)
preparation and microscopy, culture on
Sabouraud dextrose agar (SDA), Woods lamp
examination and skin biopsy.
Infection may resolve spontaneously at puberty.
Treatment using X-ray epilation was reported in
1904. Griseofulvin became available in the

1950s and is the treatment of choice at
a dosage of 10-25 mg/kg/day for 6-8
weeks. Drug absorption is enhanced
when fatty food is taken simultaneously
(e.g. glass of milk). There are three
reasons for treatment failure with
griseofulvin: dosage too low, treatment
duration too short, and, failure to take
the drug with a meal. The drug accu-
mulates in keratin of the horny layer,
hair, and nails, rendering them resis-
tant to invasion by the fungus. Treat-
ment must continue long enough for
infected keratin to be replaced by
resistant keratin, usually 4-6 weeks.
Resistant strains of dermatophytes are
rare.
Contraindications include documented
hypersensitivity, porphyria and hepato-
cellular failure. Griseofulvin may
decrease the hypoprothrombinoemic
activity of warfarin (adjust dose);
coadministration decreases contra-
ceptive effects, resulting in break-
through bleeding, amenorrhea, or un-
intended pregnancy; may reduce
effects of cyclosporine and salicylates;
barbiturates may decrease griseofulvin
effects. The oral form is embryotoxic
and teratogenic to pregnant rats; there-
fore, do not prescribe for women con-
Figures 1 & 2: Child with one large, irregularly shaped area of scaling and several smaller
scaly areas on the scalp. Note hair loss and crusting.
Figure 4: Gray patch tinea capitis above the
ear involving the parietal area of the scalp.
SA Pharmaceutical Journal October 2006
templating pregnancy. Adverse effects
are reported occasionally, including
headache, nausea, fatigue, abdominal
discomfort, or transient rash; less
common adverse reactions include urti-
caria, diarrhoea, and photosensitivity;
may precipitate acute intermittent
porphyria and systemic lupus ery-
thematosus in predisposed individuals.
Alternative treatment methods include
itraconazole (Sporanox ), terbinafine
(Lamisil) and fluconazole (Diflucan ).
Although oral ketoconazole (Nizoral )
is an acceptable alternative, the risk of
hepatotoxicity is significant. Topical
treatment is usually ineffective. Oral
steroids may help reduce the risk for
and extent of permanent alopecia in
the treatment of kerion. Topical cortico-
steroids should be avoided. Povidone-
iodine (Betadine ) or selenium sul-
phide shampoo may diminish the
spread of spores. The shampoo is
applied twice weekly for 15 minutes for
4 consecutive weeks.
Clinical presentation, diagnosis
and treatment
Black dot tinea capitis refers to an
infection with fractures of the hair
Figure 5: Gray patch tinea capitis of the
postauricular area. Note hair loss caused
by tight braiding
CLINICAL
leaving the infected dark stubs visible
in the follicular orifices. Closely shaven
hair may simulate black dot tinea
capitis (personal observation). Black
dot tinea capitis is caused by T
tonsurans and T schoenleinii.
A kerion is an abscess-like lesion
studded with pustules. Lesions heal
with scarring and permanent alopecia.
Kerion is commonly caused by T
tonsurans.
Favus is caused most commonly by T
schoenleinii and occasionally by T
violaceum or Microsporum gypsum.
Yellow, saucer-shaped crusts termed
scutulae surround infected hair
follicles. Favus heals with scarring.
Dermatophytic mycetoma is uncommon
and is characterised by the presence of
one or more reddish nodules on the
scalp. Histology shows granules com-
posed of masses of dermatophytes,
usually T rubrum, in a background of
inflammation.
Yellow patch tinea capitis is charac-
terised by one, a few or several
patches of hair loss covered fully or
partially by yellowish scale-crust.
Figure 3: Child with a large elevated plaque
devoid of hair. Extensive pustulation and
crusting are evident.
Figure 6: A kerion-like lesion. Note
nodularity of the lesion.
9
CLINICAL
Secondary infection (= impetigo) by
Staphylococcus aureus or beta
haemolytic streptococci causes this
appearance. Regional lymphadeno-
pathy is common.
Gray patch tinea capitis is an ectothrix
infection and by far the commonest
presentation seen at the Dermatology
Clinic at Tygerberg Hospital. This form
is characterised by one, a few or
several patches of hair loss, of variable
shape and size with lack of
inflammation. Fine, grayish scales
cover the surface of these lesions.
Hairs in the involved area are dull,
grayish, discoloured and broken off.
Seborrhoeic dermatitis-like tinea capitis
shows more or less diffuse scaling of
the scalp. Hair loss is often subtle.
Seborrhoeic dermatitis is extremely
uncommon in this age group.
The pustular type of tinea capitis refers
to the presence of one or more areas of
hair loss, of variable shape and size,
peppered with pustules, scaling and
scale-crust.
The annular type is characterised by
papules or pustules forming a ring that
may coalesce with other infected areas.
Combinations of these morphological
presentations are not uncommon.
Ide reactions are manifestations of the
immune response to dermatophytes.
These reactions occur at a distant site
and are devoid of organisms. Ide
reactions may be triggered by anti-
fungal treatment. These patients have a
strong delayed-type hypersensitivity
reaction to intradermal dermatophyte
antigens. These eruptions may be
vesicular, especially of the hands and
feet, dermatitis-like, annular (e.g.
erythema annulare centrifugum) or
nodular (e.g. erythema nodosum).
The causative fungal organisms of
tinea capitis destroy hair and pilo-
sebaceous structures, resulting in
severe hair loss and scarring alopecia.
The disease is detrimental, both
physically and mentally, to children
who are affected. Young patients with
itchy scalp and patchy or total hair loss
frequently are ridiculed, isolated and
bullied by classmates or playmates. In
10
some cases the disease can cause
severe emotional impairment in vul-
nerable children and can destabilise
family relationships.
Four diagnostic methods are
utilised in the diagnosis of tinea
capitis
Potassium hydroxide and micro-
scopy
The belly of a number 15 blade is
applied to the surface of a scaly patch.
Scales are gently scraped off onto a
clean glass slide. A drop of 20% KOH
is placed next to the material and there-
after thoroughly mixed. The preparation
is left for 15-20 minutes. Gentle heat
may be applied. A coverslip is placed
on the glass slide and viewed with a
microscope (x 40 magnification).
Rubbings (with a moist gauze pad or
toothbrush), pluckings or clippings from
lesions may be prepared similarly. The
presence of fungal hyphae and spores
within (endothrix) or around (ectothrix)
hair shafts is diagnostic.
Culture on Sabourauds dextrose
agar
Material is collected as for microscopy.
Scales, crusts and/or hair are placed
between two glass sides, taped at the
ends and despatched to the laboratory.
This material is incubated on SDA +
cycloheximide (suppresses the growth
of environmental contaminant fungi)
and SDA + chloramphenicol (to prevent
bacterial overgrowth). Most dermato-
phytes can be identified within 2
weeks. Identification depends on gross
colony and microscopic morphology.
Woods lamp examination
Woods lamp is a source of long wave
(365 nm) ultraviolet light. Hairs infected
by M canis, M audouinii and M ferru-
gineum fluoresce a bright green to
yellow-green color. Hairs infected by T
schoenleinii may show a dull green or
blue-white color. T verrucosum exhibits
a green fluorescence in cow hairs, but
infested human hairs do not fluoresce.
T violaceum, the causative fungus of
grey patch tinea capitis, is Woods light
negative. Woods light is not used in
the Department of Dermatology.
Scalp biopsy
This procedure is seldom employed in
SA Pharmaceutical Journal October 2006
the diagnosis of tinea capitis. Hair loss,
not responding to treatment, may be an
indication for skin biopsy. Dermato-
phytes may be visualised on routine
staining, but a PAS&D stain facilitates
identification of fungi. In endothrix
infection, spheric-to-box-like spores are
found within the hair shaft. In ectothrix
infection, organisms form a sheath
around the hair shaft. The cuticle is
destroyed. Fungal elements may also
be present in the epidermis and
dermis.
In the differential diagnosis of tinea
capitis one should consider alopecia
areata, primary impetigo, lupus
erythematosus, psoriasis, seborrhoeic
dermatitis, secondary syphilis and
trichotillomania.
Alopecia areata is characterised by
patches of complete hair loss, of
variable number, shape and size.
Inflammatory changes are absent. The
exclamation mark hairs seen in
alopecia areata, in which broken hairs
taper from the fractured end towards
the skin surface, are pathognomonic.
Alopecia areata is an autoimmune
disease. Regrowing hairs are usually
thin and non-pigmented.
Primary impetigo is caused by S
aureus or group A beta haemolytic
streptococci. Lesions show pustulation
and honey-coloured crusts. Hairs tend
to be firmly seated in impetigo.
Regional lymphadenopathy is
common. Skin lesions of lupus erythe-
matosus show atrophy, scaling and
follicular plugging. Hair loss is
permanent.
Psoriasis shows patches of erythema
with silvery scaling. Hair loss is un-
common. Hairs are not broken. Lesions
may be present elsewhere, such as the
elbows, knees and lower back.
Seborrhoeic dermatitis, characterised
by greasy scaling and variable hair
loss, is uncommon in childhood.
Seborrhoeic dermatitis may also
involve the ears, eyebrows, paranasal
area, chin, anterior chest, back and
intertriginous areas. In seborrhoeic
dermatitis hairs are not broken.
Patchy hair loss occurs in secondary
 CLINICAL

syphilis (motheaten alopecia). When
secondary syphilis is suspected, one
should look for generalised lympha-
denopathy, symmetrical skin eruptions
with palmoplantar involvement, snail-
track ulcers of the oral mucosae and
condylomata lata. Serological tests for
syphilis are positive.
Griseofulvin is the treatment of choice
for tinea capitis.
Alternative treatments for tinea capitis
include itraconazole, fluconazole and
terbinafine.
Itraconazole should be administered at
a dosage of 3-5 mg/kg for 2-6 weeks
(usual range, 2-4 weeks). The oral
solution contains cyclodextrin, which
may cause diarrhoea in children.
Contraindications include documented
hypersensitivity; concomitant adminis-
tration with HMG-CoA reductase
inhibitors (e.g. lovastatin, simvastatin),
astemizole (recalled from US Market),
cisapride, midazolam, triazolam, or
terfenadine (recalled from the US
market) are contraindicated. Antacids
may reduce absorption of itraconazole;
oedema may occur with coadministra-
tion of calcium channel blockers (e.g.
amlodipine, nifedipine); hypoglycaemia
occur with coadministration of HMG-
CoA reductase inhibitors (lovastatin or
simvastatin); coadministration with
cisapride can cause cardiac rhythm
abnormalities and death; may increase
digoxin levels; coadministration may
increase plasma levels of midazolam
or triazolam; phenytoin and rifampin
may reduce itraconazole levels. Safety
for use during pregnancy has not been
established.
Terbinafine is given in a dosage of 62.5
mg/day (<20 kg), 125 mg/day (20-40
kg) and 250 mg/day (>40 kg). Treat-
ment should be given for 2-6 weeks
(usual range, 2-4 weeks). Documented
hypersensitivity is the main contra-
indication. May decrease cyclosporine
effects; toxicity of terbinafine may
increase with rifampin and cimetidine.
The drug is safe in pregnancy but
benefits must outweigh the risks.
The dosage of fluconazole is 6 mg/kg
for 20 days. Documented hyper-
sensitivity is the main contraindication.
Levels may increase with hydro-
chlorothiazides; fluconazole levels may
decrease with chronic coadministration
of rifampin; coadministration of flucona-
zole may decrease phenytoin
clearance; may increase concen-
creases in cyclosporine concentrations
may occur when administered con-
currently. Safety for use during
pregnancy has not been established.
Patients should be followed up
clinically, by KOH-preparation and
microscopy, by Woods light examina-
tion, and myocologically (= culture).
Children receiving treatment may
attend school. Haircuts, shaving of the
head, and wearing a cap during
treatment are not necessary.
Deterrence/prevention
Asymptomatic carriers should be
detected and treated, since they are the
continuous source of infection. Sib-
lings and playmates of patients should
avoid close physical contact and
sharing of toys or other personal
objects, such as combs and hair-
brushes, since organisms can spread
from one person to another and infec-
tious agents can be transported to
different classrooms within the same or
different schools. Shared facilities and
objects also may promote spread of
disease, both within the home and
classroom.

REFERENCES

may occur with sulphonylureas; may
increase tacrolimus and cyclosporine
plasma concentrations when high
doses are used; rhabdomyolysis may
trations of theophylline, tolbutamide,
glyburide, and glipizide; effects of
anticoagulants may increase with
fluconazole coadministration; in-
1. Koa GF. Tinea capitis. eMedicine Journal
2002;3(1):1-17.
www.emedicine.com/derm/topic420.htm
2. Frieden IJ and Howard R. Tinea Capitis:
epidemiology, diagnosis, treatment and control. J
Am Acad Dermatol 1994;31:542-546.

THE ROLE OF PHARMACIST COUNSELLING IN PREVENTING

ADVERSE DRUG EVENTS AFTER HOSPITALISATION

I n March 2006, the Archives of Internal Medicine

published a paper reporting on a recent randomised trial
conducted at a large teaching hospital.
Pharmacists observed the following drug-related problems in
the intervention group:

The authors of the paper recognised that hos-pitalisation
and subsequent discharge home often involve discontinuity
of care, multiple changes in medication regimens, and
inadequate patient education, which can lead to adverse
drug events (ADEs) and avoidable health care utilisation.
Their objectives were to identify drug-related problems
during and after hospitalisation and to determine the effect
of patient counselling and follow-up by pharmacists on
preventable ADEs.
Patients in the intervention group received pharmacist
counselling when they were discharged from hospital, as well
as a follow-up telephone call 3 to 5 days later. Inter-ventions
focused on clarifying medication regimens, reviewing
indications, directions and potential side effects of
medications, screening for barriers to adherence and early
side effects, and providing patient counselling and/or
physician feedback when appropriate.
unexplained discrepancies between patients pre-
admission medication regimens and discharge medication
orders in 49% of patients
unexplained discrepancies between discharge medi-
cation lists and postdischarge regimens in 29% of
patients
medication nonadherence in 23%.
Comparing trial outcomes 30 days after discharge,
preventable ADEs were detected in 11% of patients in the
control group and 1% of patients in the intervention group
(P = .01). No differences were found between groups in total
ADEs or total health care utilisation.
The authors concluded that pharmacist medication
review, patient counselling, and telephone follow-up were
associated with a lower rate of preventable ADEs 30 days
after hospital discharge.

SA Pharmaceutical Journal October 2006 11