Tinea Capitis

This is ringworm of the scalp in

which the essential feature is
invasion of the hair shafts by a
dermatophyte fungus.

Causative organism Most species of

dermatophyte are capable of invading hair
e.g. T. tonsurans, T. schoenleiniiand T.
violaceum
Pathophysiology
The spores of ringworm fungi causing
tinea capitis can be demonstrated in the
air in close proximity to patients with
the condition. It is highly likely that
scalp hair acts as a trapping device
The wall contains mannans,
glycoproteins and enzymes, some of
which are secreted into the surrounding
environment and break down complex
organic compounds prior to their
absorption. Fungi have an absorptive
mode of nutrition.
 Invasion of the stratum corneum of the scalp skin must first
Trauma assists inoculation, which is followed, after approximately 3
weeks, by clinical evidence of hair shaft infection. Infection spread to
other follicles, then for a period of variable duration the infection
persists but does not spread further.
Finally, there is a period of regression with or without an
inflammatory phase.
Type of hair invasion
In this type, the hair shaft is invaded midfollicle. The intrapilary hyphae continue
Ectothrix to grow inwards towards the bulb of the hair. Secondary, extrapilary hyphae burst
out and grow in a tortuous manner over the surface of the hair shaft, which is
type growing outwards continuously. Fluorescence (+)

Intrapilary hyphae fragment into arthroconidia up to 8 m in diameter, which are

Endothrix entirely contained within and completely fill the hair shaft. Hair thus affected is
especially fragile, and breaks off close to the scalp surface. This type is
type nonfluorescent.

Broad, regularly septate hyphae and air spaces are seen in the hair shaft, but
Favus disarticulated arthroconidia are absent. The affected hair is less damaged than in
other types, and may continue to grow to considerable lengths. Greenish grey
fluorescence is present
 Clinical variants
The clinical appearance of ringworm of the scalp is variable,
depending on the type of hair invasion, the level of host resistance
and the degree of inflammatory host response.

Tinea capitis gray patch type

A large, round hyperkeratotic plaque of alopecia

due to breaking off of hair shafts close to the
surface, giving the appearance of a mowed wheat
field on the scalp of a child. Remaining hair shafts
and scales exhibit a green fluorescence when
examined with a Woods lamp.
The black dot form of tinea capitis is typically
caused by the anthropophilic endothrix organisms
T.tonsurans and T.violaceum. Hairs broken off at
the level of the scalp leave behind grouped black
dots within patches of polygonal shaped alopecia
with finger-like margins. Normal hairs also remain
with in patches of broken hairs. Diffuse scaling is also
often present.
Zoophilic or geophilic pathogens, such as M. canis, M. gypseum,
and T. verrucosum, are more like to cause an inflammatory type
of tinea capitis. Inflammation, which is the result of a
hypersensitivity reaction to the infection, in this setting ranges
from follicular pustules to furunculosis or kerion. Intense
inflammation may also result in scarring alopecia. The scalp is
usually pruritic or tender. Inflammatory tinea capitis is often
associated with posterior cervical lymphadenopathy.
Kerion of the scalp.
 Favus

The classic picture of tinea capitis caused by this organism is

characterized by the presence of yellowish, cupshaped crusts known as
scutula
Each scutulum develops round a hair, which pierces it centrally. Adjacent
crusts enlarge to become confluent and form a mass of yellow crusting.
Many patients may show less distinctive changes, in early cases perhaps
amounting to no more than perifollicular redness and some matting of
the hair.
Extensive, patchy hair loss with cicatricial alopecia and atrophy among
patches of normal hair may be found in longstanding cases, where much
of the hair loss is irreversible.
Treatment
With scalp kerions, the careful removal of crusts
using wet compresses should not be neglected,
and the possibility of coexisting bacterial
infection should be considered.
In general, the kerions are less painful than
their inflammatory appearance suggests, but
analgesics may be needed.
Ketoconazole shampoo or selenium sulphide
can be used to prevent spread in the early
phases of therapy when used in combination
with an oral treatment.
In severely inflammatory forms, there has been
some argument in favour of using oral steroids
to inhibit the inflammatory response.