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September 2016

You have been called for
a long awaited interview.
You dress smartly and
comb your hair.
Unbeknown to you this is
what you take to the

Superficial mycoses
These are superficial cosmetic fungal infections of
the skin or hair shaft
No living tissue is invaded and there is no cellular
response from the host
Essentially no pathological changes are elicited
Patients are often unaware of their condition

Superficial mycoses

Causative organisms


Pityriasis versicolor
including Dandruff
Follicular pityriasis

Malassezia spp.
(a lipophilic yeast)


Tinea nigra

Exophiala werneckii Rare

White piedra

Trichosporon spp.


Black piedra

Piedraia hortae


Malassezia infections
Malassezia species are basidiomycetous yeasts and form
part of the normal skin flora of humans and animals.
Malassezia species may cause various skin
Fungaemia due to lipid-dependent Malassezia species
usually occurs in patients with central line catheters
receiving lipid replacement therapy, especially in infants
Primary isolation and culture of Malassezia species is

Clinical manifestations
(Pityriasis versicolor)

A chronic, superficial fungal disease of the skin characterised by well-demarcated white, pink,
fawn, or brownish lesions, often coalescing, and covered with thin furfuraceous scales

Pityriasis folliculitis:
Characterised by follicular
papules and pustules
localised to the back,
chest and upper arms,
sometimes the neck, and
more seldom the face.
These are itchy and often
appear after sun

Seborrhoeic dermatitis and


Current evidence suggests Malassezia, combined with

multifactorial host factors is also the direct cause of
seborrhoeic dermatitis, with dandruff being the mildest
Host factors include genetic predisposition, an emotional
component (possible endocrine or neurologically mediated
factors), changes in quantity and composition of sebum
Clinical manifestations are characterised by erythema and
scaling in areas with a rich supply of sebaceous glands ie
the scalp, face, eyebrows, ears and upper trunk

Laboratory diagnosis:
1. Clinical material: Skin scrapings from patients with
superficial lesions, blood and indwelling catheter tips from
patients with suspected fungaemia.
2. Direct Microscopy: Skin scrapings taken from
patients with Pityriasis versicolor stain rapidly when
mounted in 10% KOH, glycerol and Parker ink solution and
show characteristic clusters of thick-walled round, budding
yeast-like cells and short angular hyphal forms

Culture: Culture is only necessary in cases of

suspected fumgaemia. M. furfur is a lipophilic
yeast, therefore in vitro growth must be
stimulated by natural oils or other fatty

The most appropriate antifungal treatment for
pityriasis versicolor is to use a topical imidazole in
a solution or lathering preparation.
Ketoconazole shampoo has proven to be very
Alternative treatments include zinc pyrithione
shampoo or selenium sulfide lotion applied daily
for 10-14 days or the use of propylene glycol 50%
in water twice daily for 14 days.

White piedra
White piedra is a superficial cosmetic fungal
infection of the hair shaft caused by Trichosporon.
Infected hairs develop soft greyish-white nodules
along the shaft.
Essentially no pathological changes are elicited.
White piedra is found worldwide, but is most
common in tropical or subtropical regions.

Trichosporon species are a minor component of

normal skin flora, and are widely distributed in
They are regularly associated with the soft
nodules of white piedra, and have been involved
in a variety of opportunistic infections in the
immunosuppressed patient.
Infections are usually localised to the axilla or
scalp but may also be seen on facial hairs and
sometimes pubic hair.

Laboratory diagnosis:

1. Clinical Material: Epilated

hairs with white soft nodules
present on the shaft.
2. Direct Microscopy: Hairs
should be examined using 10%
KOH and Parker ink or calcofluor
white mounts. Look for irregular,
soft, white or light brown
nodules, 1.0-1.5 mm in length,
firmly adhering to the hairs.

Shaving the hairs is the simplest method of
treatment. Topical application of an imidazole
agent may be used to prevent reinfection.

Cutaneous Mycoses
These are superficial fungal infections of the skin,
hair or nails.
No living tissue is invaded, however a variety of
pathological changes occur in the host because of
the presence of the infectious agent and its
metabolic products.

Dermatophytosis (tinea or ringworm) of the scalp,
glabrous skin, and nails is caused by a closely
related group of fungi known as dermatophytes
which have the ability to utilise keratin as a
nutrient source, i.e. they have a unique enzymatic
capacity [keratinase].
The disease process in dermatophytosis is unique
for two reasons:
o Firstly, no living tissue is invaded; the
keratinised stratum corneum is simply
o However, the presence of the fungus and its

Clinical manifestations:
The common anthropophilic species are primarily
parasitic on man
They are unable to colonise other animals and
they have no other environmental sources.
On the other hand, geophilic species normally
inhabit the soil where they are believed to
decompose keratinaceous debris.

Some species may cause infections in animals and man

following contact with soil.
Zoophilic species are primarily parasitic on animals and
infections may be transmitted to humans following
contact with the animal host
Zoophilic infections usually elicit a strong host response
and on the skin where contact with the infective animal
has occurred ie arms, legs, body or face.

Ecology of Common Human Dermatophyte Species


Natural habitat


Epidermophyton floccosum



Trichophyton rubrum


Very Common

Trichophyton interdigitale


Very Common

Trichophyton tonsurans



Trichophyton violaceum


Less Common

Trichophyton concentricum



Trichophyton schoenleinii



Trichophyton soudanense



Microsporum audouinii


Less Common*

Microsporum ferrugineum


Less Common*

Trichophyton mentagrophytes

Mice, rodents


Trichophyton equinum



Trichophyton eriotrephon



Trichophyton verrucosum



Microsporum canis



Nannizzia gypsea



Nannizzia nana



Lophophyton cookei




Trichophyton rubrum...

Microsporum gypseum...

Microsporum canis: cats and dogs

Microsporum nanum: swine Trichophyton
verrucosum: horse and swine

Tinea pedis
Infections by anthropophilic dermatophytes are
usually caused by the shedding of skin scales
containing viable infectious hyphal elements
[arthroconidia] of the fungus.
Desquamated skin scales may remain infectious in
the environment for months or years.
Substrates like carpet and matting that hold skin
scales make excellent vectors.
Thus, transmission of dermatophytes like
Trichophyton rubrum, T. interdigitale and
Epidermophyton floccosum is usually via the feet.

Tinea pedis caused by

T. rubrum. Sub-clinical
infection (left) showing
mild maceration under
the little toe and more
severe infection
showing extensive
maceration of all toe
web spaces

"Moccasin-type" tinea
pedis caused by E.
floccosum (left) and
vesicular type tinea
pedis caused by T.
interdigitale (right).

Tinea cruris
Tinea cruris refers to dermatophytosis of the proximal
medial thighs, preum and buttocks.
It occurs more commonly in males and is usually due to
spread of the fungus from the feet.
Thus the usual causative
agents are T. rubrum,
T. interdigitale and
E. floccosum.

Tinea unguium
Trichophyton rubrum and T.
interdigitale are the
dominant dermatophyte
species involved
Only 50% of dystrophic nails
have a fungal aetiology,
Essential to establish a
correct laboratory diagnosis
by either microscopy and/or
culture, before treating a
patient with a systemic
antifungal agent.

Dermatophyte onychomycosis may be classified

into two main types;
(1) superficial white onychomycosis in which
invasion is restricted to patches or pits on the
surface of the nail; and
(2) invasive, subungual dermatophytosis in which
the lateral, distal or proximal edges of the nail are
first involved, followed by establishment of the
infection beneath the nail plate.

Distal subungual onychomycosis is the most

common form of dermatophyte onychomycosis.
The fungus invades the distal nail bed causing
hyperkeratosis of the nail bed with eventual
onycholysis, and thickening of the nail plate.

Tinea corporis refers to
dermatophytosis of the
glabrous skin and may
be caused by
anthrophophilic species
such as T. rubrum (left)
usually by spread from
another body site or by
geophilic and zoophilic
species such as M.
gypseum and M. canis
(right) following contact
with either
contaminated soil or an

Tinea capitis
Tinea capitis refers to
dermatophytosis of the
scalp. Three types of in vivo
hair invasion are
1. Ectothrix invasion is
characterised by the
development of
arthroconidia on the
outside of the hair shaft.
infected hairs usually
fluoresce a bright
greenish yellow colour
under Wood's ultraviolet
light. Common agents
include Microsporum
canis, Nannizzia.gypsea,
richophyton. equinum

Endothrix hair invasion

is characterised by the
development of
arthroconidia within the
hair shaft only. The cuticle
of the hair remains intact
and infected hairs do not
fluoresce under Wood's
ultraviolet light. All
endothrix producing
agents are anthropophilic
eg Trichophyton tonsurans
and T. violaceum.

3. Favus usually caused by Trichophyton schoenleinii, produces favuslike crusts or scutula and corresponding hair loss.

Laboratory diagnosis
Clinical Material
Skin Scrapings, nail scrapings and epilated hairs.
Laboratory needs enough specimen to perform both
microscopy and culture.
Any ointments or other local applications present should
first be removed with an alcowipe.
Using a blunt scalpel, tweezers, or a bone curette, firmly
scrape the lesion, particularly at the advancing border.

In cases of vesicular tinea pedis, the tops of any fresh

vesicles should be removed as the fungus is often plentiful
in the roof of the vesicle
Onychomycosis - the nail should be pared and scraped
using a blunt scalpel until the crumbling white
degenerating portion is reached.

Up to 30% of suspicious material collected from

nail specimens may be negative by either direct
microscopy or culture.
A positive microscopy result showing fungal
hyphae and/or arthroconidia is generally sufficient
for the diagnosis of dermatophytosis
Culture is often more reliable and permits the
species of fungus involved to be accurately

Direct Microscopy
Skin Scrapings, nail
scrapings and epilated
hairs should be examined
using 10% KOH and Parker
ink or calcofluor white

KOH mount of infected skin

scales (left) and nail
material (right) showing
typical dermatophyte
hyphae breaking up into

KOH mount of infected
hairs showing "small
spored" ectothrix
invasion by M. canis
(left) and "large
spored" ectothrix
invasion by M.
gypseum (right).


KOH mount of an
infected hair
showing an
endothrix invasion
caused by T.


Specimens should be inoculated onto primary isolation

media, like Sabouraud's dextrose agar containing
cycloheximide (actidione) and incubated at 26-28C for 4
The growth of any
dermatophyte is significant.

Treatment of dermatophytosis is often dependant on the
clinical setting.
uncomplicated single cutaneous lesions can be adequately
treated with a topical antifungal agent,
topical treatment of scalp and nail infections is often
ineffective and systemic therapy is usually needed to cure
these conditions.
Chronic or widespread dermatophyte infections, acute
inflammatory tinea and "Moccasin" or dry type T. rubrum
infection involving the sole and dorsum of the foot usually
also require systemic therapy.



Terbinafine 250 mg/day
6 weeks for finger nails,
12 weeks for toe nails.

Tinea capitis

Griseofulvin 500mg/day
[not less than 10 mg/kg/day]
until cure [6-8 weeks].

Griseofulvin 500 mg/day until

cure [4-6 weeks], often
Tinea corporis
combined with a topical
imidazole agent.

Tinea cruris

Tinea pedis

Itraconazole 200 mg/day/3-5 months or 400 mg/day for one
week per month for 3-4 consecutive months.
Fluconazole 150-300 mg/ wk until cure [6-12 months].
Griseofulvin 500-1000 mg/day until cure [12-18 months].
Terbinafine 250 mg/day/4 wks.
Itraconazole 100 mg/day/4wks.
Fluconazole 100 mg/day/4 wks
Terbinafine 250 mg/day for 2-4 weeks.
Itraconazole 100 mg/day for 15 days or 200 mg/day for 1week.
Fluconazole 150-300 mg/week for 4 weeks.

Griseofulvin 500 mg/day

until cure [4-6 weeks].

Terbinafine 250 mg/day for 2-4 weeks.

Itraconazole 100 mg/day for 15 days or 200 mg/day for 1week.
Fluconazole 150-300 mg/week for 4 weeks.

Griseofulvin 500mg/day
until cure [4-6 weeks].

Terbinafine 250 mg/day for 2-4 weeks.

Itraconazole 100 mg/day for 15 days or 200 mg/day for 1week.
Fluconazole 150-300 mg/week for 4 weeks.

Chronic and/or
Terbinafine 250 mg/day
nonfor 4-6 weeks.

Itraconazole 200 mg/day for 4-6 weeks.

Griseofulvin 500-1000 mg/day until cure [3-6 months].