The document discusses dermatophyte infections, which affect superficial keratinized structures in the skin, hair, and nails, emphasizing three main genera: Trichophyton, Epidermophyton, and Microsporum. It outlines various clinical presentations, such as tinea capitis, tinea corporis, and tinea pedis, along with their causes, symptoms, and treatment considerations. Factors influencing infection include immune status, body location, and the type of dermatophyte, with descriptions of typical patterns of infection and response to treatment.

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4. • Infections that extend deeper into the epidermis, as well as hair and nail
and caused by dermatophytes.
• Dermatophytes infect only superficial keratinized structures but not
deeper tissues.
• They possess keratinases allowing them to utilize keratin as a nutrient &
energy source  colonization  its destruction and inflammation is
caused by host response to fungi & to metabolic by-products.
• Clinical variation of dermatophytes infection depends on:
1. Fungal spp.
2. Stage of infection.
3. Body location.
4. Immune status of the host.

5. THE MAIN 3 GENERA OF DERMATOPHYTES ARE:
1. Trichophyton (abbreviated as "T") infections
on skin, hair, and nails
2. Epidermophyton (“E") - infections on skin and
nails (not the cause of TINEA CAPITIS)
3. Microsporum (“M") infections on skin and
hair (not the cause of TINEA UNGUIUM)

7. 1. Tinea capitis (head)
2. Tinea faciei (face)
3. Tinea barbae (beard)
4. Tinea corporis (body)
5. Tinea manus (hand)
6. Tinea cruris (groin)
7. Tinea pedis (foot)
8. Tinea unguium (nail)

9. • Etymology: L. [caput] head.
• Tinea capitis is the most common pediatric dermatophyte
infection worldwide.
• The age predilection (3 and 7 years of age) is believed to
result from the presence of Malassezia furfur which is part of
normal flora, and from the fungistatic properties of fatty
acids of short and medium chains in postpubertal sebum so
it is rare in adult population.

12. A. Anthropophilic infections: such as T. tonsurans are more
common in crowded living conditions. The fungus can
contaminate hairbrushes, clothing, towels and the backs of
seats. The spores are long lived and can infect another individual
months later.
B. Zoophilic infections: are due to direct contact with an infected
animal and are not generally passed from one person to
another. This produce a much greater inflammatory response
and this often results in a boggy inflammatory swelling known as
a kerion.
C. Geophilic infections: usually arise when working in infected soil
but are sometimes transferred from an infected animal.

17. PATTERNS OF HAIR INVASION BY DERMATOPHYTES
Small spore
Large spore
Arthrosporic
ectothrix
ectothrix
endothrix
Favus
endothrix
Species of
dermatophyte
M. canis,
M. audouinii
T. mentagrophytes,
T. verrucosum
T. tonsurans
T. violaceum
T. schoenleinii
Fungal Growth
& Hair Shaft
affection
Penetrates the surface 
grow downwards until
Adamson’s fringe. The cuticle
of the hair is destroyed
Straight 1ry extrapilary
hyphae
Hyphae invade only the
inside of the hair shaft
(intrapilary hyphae). Cuticle
of the hair remains intact
Inside invasion broad
hyphae and
significant air pockets
Arthroconidia
Small spherical on outer
surface of H. shaft
Larger & arranged in
straight manner
Within hair shaft. No spores
Wood’s Lamp
Examination
Bright green
fluorescence
No fluorescence No fluorescence
Pale green
fluorescence
Clinically
H. Shaft fracture & dry scaling
patch of alopecia (GPTC)
kerion
Damage of H. shaft at skin
surface  Black dots (BDTC)
Scutula  Favus

18. I. Scaly (Gray Patch) Tinea Capitis (GPTC)
II. Black Dot Tinea Capitis (BDTC)
III. Kerion
IV. Favus

19. I. SCALY TYPE/GRAY PATCH TINEA
CAPITIS (GPTC):
• It begins with an erythematous, scaling, well-demarcated
patch on the scalp that spreads
centrifugally for a few weeks or months, ceases to
spread, and persists indefinitely, sometimes for
years.
• Single or multiple patches of scaly (grayish-white)
alopecia are seen where the hairs are broken just
above the level of scalp  short stumps.
• No subsequent scarring alopecia.

21. II. BLACK DOT TINEA CAPITIS (BDTC):
• It is an endothrix infection, so hair become notably
fragile and break easily at the level of the scalp.
• The rest of the infected follicle look like "black dots".
• Variable degrees of scaling.
• Usually begins as an asymptomatic, erythematous,
scaling patch on the scalp, which slowly enlarges.
• Lesions may be single or multiple. Early lesions are
easily overlooked and the disease is not usually
noticed until areas of alopecia become evident.

26. III. KERION:
• Usually zoonotic infection e.g. T. verrucosum.
• Scattered painful pruritic pustular folliculitis generally
associated with regional lymphadenopathy and fever.
• Boggy (soft & watery) swelling studded with broken
hairs and purulent sticky material "kerion" appear.
• Hairs  easily removed when pulled.
• Untreated kerion may result in permanent scarring
alopecia.

28. IV. FAVUS (TINEA FAVOSA):
• Etymology: Favus=L. honeycomb
• Perifollicular erythema on the scalp, which progresses to
the characteristic finding of concave, cup-shaped yellow
crusts called scutula.
• The scutulum develops at the surface of a hair follicle with
the shaft in the center of the raised lesion & formed of
dense masses of mycelium, neutrophils, dried serum and
epithelial debris.
• Removal of scutula reveals an oozing, moist, red base.
• After a period of years, atrophy of the skin occurs leaving
scarring alopecia.
• It has unpleasant smell “mousy odor”.

31. • Uncommon dermatophyte infection (most
commonly T. rubrum) of the face. It does not
include infection of the beard and moustache
area in men.
• While some dermatophyte infections of the face
have classic features of tinea circinata, e.g.
scale, annular configuration, pustules in the
border. It is frequently aggravated by sun
exposure.
• Others infections can be more difficult to
diagnose clinically “tinea incognito” and require
a high index of suspicion.

34. • It is dermatophyte infection of the beard and
moustache areas of the face.
• Currently, it is infrequent around the world.
• Generally affects only adult men.
• The mechanism that causes tinea barbae is similar to
that of tinea capitis but it is less frequently occurring.
• Tinea barbae was observed more frequently in the
past when infection frequently was transmitted by
barbers who used unsanitary razors, so it was termed
BARBER'S ITCH.
• Tinea barbae can result in an id reaction, especially
just after starting antifungal treatment.

35. 1. INFLAMMATORY DEEP TYPE/KERION (T. Barbae Profunda):
• It is the most common clinical presentation of T. barbae.
• Caused primarily by zoophilic dermatophytes mainly T.
verrucosum, T. mentagrophytes. Most often affects farmers
and is due to direct contact with an infected animal.
• Intense reddish inflammation and multiple follicular pustules.
Abscesses, draining sinus tracts, bacterial super-infection and
even kerion-like boggy plaques can develop.
• Most patients show solitary plaques or nodules; however,
multiple plaques are relatively common.
• Usually localized on the chin, cheeks, or neck, involvement of
the upper lip is rare.

36. 1. INFLAMMATORY DEEP TYPE/KERION (T. Barbae
Profunda):
• Surprisingly, it is not excessively itchy or painful.
• Hairs are loose or broken, and depilation is easy
and painless.
• Over time, the surface of the indurated nodule is
covered by exudate and crust.
• This variety of tinea barbae usually is associated
with generalized symptoms, such as regional
lymphadenopathy, malaise, and fever.
• Scarring alopecia may develop.

38. 2. NON-INFLAMMATORY SUPERFICIAL TYPE:
• Caused by anthropophilic dermatophytes. T. rubrum
is usually the causative agent.
• This variety is less common.
• Typically, erythematous patches show an active
border composed of papules, vesicles, and/or crusts.
• Hairs are broken next to the skin.
• Alopecia may be present in the center of the lesion,
but it is reversible.

40. • It is a dermatophyte infection of the skin of the trunk
and extremities, excluding the hair, nails, palms, soles
and groin.
• T. rubrum is the most common infectious agent in the
world followed by T. mentagrophytes & E. floccosum.
• MOI:
1. Anthropophilic: result from direct contact with infected
humans including autoinoculation e.g. from t. capitis or
pedis.
2. Zoophilic: often transmitted by domestic animals,
3. Geophilic.

41. • Predisposing factors include;
1. Occupational or recreational exposure (e.g. Military housing, gymnasiums,
locker rooms, outdoor occupations, wrestling).
2. Contact with contaminated clothing and furniture.
3. Immunosuppression.
• In response to the infection, the active border has an increased epidermal
cell proliferation with resultant scaling.
• This creates a partial defense by way of shedding the infected skin and
leaving new, healthy skin central to the advancing lesion.

43. • Patients can be asymptomatic or pruritic and
burning.
• The typical incubation period is 1 to 3 weeks.
• Infection spreads centrifugally from the point of skin
invasion, begins as an erythematous, scaly, sharply
marginated plaque that may rapidly worsen and
enlarge.
• Central resolution causes the lesion to be annular
but it may be arcuate, oval or discoid.
• Scales, crusts, vesicles, papules and pustules often
develop, especially in the advancing border.

48. • Infections due to zoophilic or geophilic
dermatophytes may produce acute (sudden
onset and rapid spread) more intense
inflammatory response than those caused
by anthropophilic fungi chronic (slow
extension of a mild, barely inflamed
lesion).

49. 1. MAJOCCHI GRANULOMA (Nodular Folliculitis) usually caused
by T. rubrum, is characterized by perifollicular
papulopustules or granulomatous nodules commonly in a
distinct location, which is the lower two thirds of the leg in
females who have t. pedis or onychomycosis and shave their
legs, represents a deep dermatophyte folliculitis in which the
follicular wall is disrupted. Also occur in immunosuppressed.
2. TINEA IMBRICATA (Imbricate= Overlapping) shows distinct scaly
plaques arranged in concentric annular rings.
3. TINEA PROFUNDA results from an excessive inflammatory
response to a dermatophyte (analogous to a KERION on the
scalp). It may have a granulomatous or verrucous.

56. • Dermatophyte infections of the palm.
• It shows different clinical picture due to lack of
sebaceous glands on the palms.
• The typical causative organisms are the same
as those for tinea pedis and tinea cruris: T.
rubrum, T. mentagrophytes and E. floccosum.
• It is an uncommon dermatophytic infection.

57. • The patient may complain from mild itching.
• Presentation is similar to moccasin tinea pedis.
• Chronic erythema, dryness, scaling and
hyperkeratosis of the palms and fingers affecting
the skin diffusely is the commonest variety, and
is unilateral in about half the cases  “TWO
FEET AND ONE HAND SYNDROME”.
• The accentuation of the flexural creases is a
characteristic feature because of scale. An
important clinical clue is tinea unguium of the
involved hand.
• Tinea manuum is usually non-inflammatory.

58. • Other clinical variants include;
1. Vesicular (on the edges of the fingers or palm)
2. Crescentic
3. Circumscribed
4. Discrete
5. Red papular
6. Follicular scaly patches

61. • It is a dermatophyte infection of the inguinal region, in
particular the inner aspects of the upper thighs and crural
folds, with occasional extension onto the abdomen and
buttocks.
• The three most common causative agents are T. rubrum, T.
mentagrophytes and E. floccosum.
• Autoinoculation occurs in 50 % of cases from
onychomycosis or tinea pedis.
• Risk factors for initial infection or reinfection include
infected fomites particularly infected towels, obesity,
excessive perspiration, wearing tight-fitting or wet
clothing or undergarments.
• Tinea cruris is more common in adult men than in women.

63. • Patients complain of pruritus and rash in the
groin. A history of previous episodes of a similar
problem usually is elicited.
• Large patches of erythema with central clearing
are centered on the inguinal creases.
• Sharply demarcated lesions with a raised
reddish, scaly advancing border (usually
downwards) that may contain pustules, pustules
or vesicles.
• The lesion may initially be circinate and then
become serpiginous.

64. • The disease can remain unilateral but
usually become bilateral.
• Lesions may extend to the thighs, lower
abdomen, pubic area & buttocks.
• The penis, scrotum and vulva are typically
spared.

66. • ACUTE INFECTIONS, the rash may be moist and
exudative with a prominent inflammation with
or without pustules. Caused by zoophilic
pathogens e.g. T. mentagrophytes.
• CHRONIC INFECTIONS typically are dry with a
papular annular or arciform border and barely
perceptible scale at the margin sometimes even
leathery and lichenified. Caused by
anthropophilic pathogens e.g. T. rubrum.

67. • Chronic infections may be modified by the
application of topical corticosteroids (tinea
incognito).

69. • It is a dermatophyte infection of the soles and interdigital web
spaces of the feet.
• Tinea pedis is thought to be the world's most common
dermatophytosis. Up to 70% of the population will be infected
with tinea pedis at some time.
• It is more common in adult men as childhood tinea pedis is rare.
• The lack of sebaceous glands in the soles is an important factor
in its development.
• T. rubrum being the most common cause worldwide other
dermatophytes that are typically responsible for tinea pedis are
T. mentagrophytes and E. floccosum.

70. 1. A hot, humid, tropical environment.
2. Prolonged use of occlusive footwear as it is uncommon in
populations that do not wear shoes at all.
3. Certain activities, such as swimming and communal bathing, going
barefoot (locker rooms, gyms, public facilities) may also increase the
risk of infection.
4. Hyperhidrosis.
5. Immunodeficiency.

71. 1. Interdigital type
2. Moccasin type (Chronic hyperkeratotic)
3. Inflammatory (Vesicular) type
4. Ulcerative type

72. 1. INTERDIGITAL TYPE:
• The most common type, with erythema, maceration, fissuring,
and scaling in the web spaces; the two lateral web spaces are
most commonly affected & may be pruritic.
• “DERMATOPHYTOSIS COMPLEX” (fungal infection followed by
bacterial invasion) can develop; The clinical features of
symptomatic athlete's foot are a result of the interaction of
fungi and bacteria.
• The dorsal surface of the foot is usually clear, but some
extension onto the dorsal or plantar surfaces of the foot may
occur.
• May be caused by non-dermatophyte pathogens e.g. S.
dimidiatum or Candida spp.

74. 2. CHRONIC HYPERKERATOTIC TYPE (MOCCASIN)
• Named so because it has a moccasin-like distribution pattern.
• Plantar erythema with slight scaling to diffuse hyperkeratosis
& fissuring but not inflamed that can be asymptomatic or
pruritic.
• Both feet are usually affected.
• Frequently chronic and difficult to cure because of the
thickness of stratum corneum on plantar surfaces and the
inability of T. rubrum to elicit sufficient immune response.
• Typically, the dorsal surface of the foot is clear, but, in severe
cases, the condition may extend onto the sides of the foot.
• May be caused by non-dermatophyte pathogens e.g. S.
dimidiatum.

77. 3. INFLAMMATORY/VESICULAR TYPE:
• Painful, pruritic vesicles, pustules or bullae
usually on the medial anterior plantar surface;
often associated with the id reaction.
• After they rupture, scaling with erythema
persists.
• Cellulitis, lymphangitis and adenopathy can
complicate this type.

80. 4. ULCERATIVE TYPE:
• Typically an exacerbation of interdigital
tinea pedis.
• Ulcers and erosions in the web spaces;
commonly secondarily infected with
bacteria.
• Seen in immunocompromised and
diabetic patients that may show even
osteomyelitis leading to amputation.

82. DERMATOPHYTID (ID) REACTION:
• It is an allergic eruption caused by an inflammatory fungal
infection at a distant site.
• It is associated with vesicular tinea pedis. They develop on the
palmar surface of one or both hands and/or the sides of the
fingers as papules, vesicles, and, occasionally, bullae or pustules
may occur, often in a symmetrical fashion. They mimic
dyshidrosis (pompholyx).
• Scattered follicular lesions mainly affect the trunk usually follows
a kerion (inflammatory tinea corporis or tinea capitis) from a
zoophilic fungus.

83. DERMATOPHYTID (ID) REACTION:
• As it is an allergy or hypersensitivity response to the fungal infection it
contains no fungal elements. The specific explanation of this
phenomenon is still unclear.
• Distinguishing between a dermatophytid reaction and dyshidrosis can be
difficult. Therefore, a close inspection of the feet is necessary in patients
with vesicular hand dermatoses and KOH examination may help.
• The dermatophytid reaction resolves when the kerion or tinea pedis
infection is treated, and treatment with topical steroids can hasten
resolution. Occasionally systemic steroids are required for a few weeks.

87. • TINEA UNGUIUM (Dermatophytic onychomycosis): is
clinically defined as a dermatophyte infection of the nail
plate.
• ONYCHOMYCOSIS: includes all infection of the nail caused
by any fungus, including non-dermatophytes and yeasts.

88. • It affects men more often than women.
• It accounts for 20% of all nail disease.
• Approximately 30% of patients with dermatophyte infections
on other parts of their body also have onychomycosis.
• Toenail infections are more common than fingernail
infections.
• A single nail may be involved, but more commonly, multiple
nails are affected.

89. ONYCHOMYCOSIS CAN BE DUE TO:
1. DERMATOPHYTES (~90% of cases) most commonly T. rubrum, T. mentagrophytes or
E. floccosum.
2. YEASTS such as Candida albicans.
3. MOULDS especially Fusarium species usually indistinguishable from tinea unguium.
PREDISPOSING FACTORS:
1. Trauma
2. Aging
3. Diabetes
4. Poorly fitting shoes
5. The presence of tinea pedis and other nail disorders represent

90. • The patient often complain of discomfort and pain
associated with trimming the nails, running, and other
activities.
• Characteristically, infected nails coexist with normal-appearing
nails.
• In addition, serious complications such as cellulitis can result
from onychomycosis, especially in patients who are diabetic
or immunocompromised.
• Onychomycosis and concurrent diabetes triple a patient’s risk
of toe ulceration, infection and gangrene.

91. 4 MAJOR CLINICAL TYPES OF ONYCHOMYCOSIS:
1. Distal/Lateral subungual onychomycosis
2. White superficial onychomycosis
3. Proximal subungual onychomycosis
4. Candidal onychomycosis

93. 1. DISTAL/LATERAL SUBUNGUAL ONYCHOMYCOSIS:
• It is the most common type and starts by invasion of the
stratum corneum of the hyponychium and distal nail bed.
• Infection moves proximally in the nail bed and invades the
ventral surface of the nail plate.
• Subungual hyperkeratosis results from a hyperproliferative
reaction of the nail bed in response to the infection.
• With further progression of infection, there is yellowing and
thickening of the distal or lateral nail plate as well as distal
onycholysis.
• Eventually, the entire nail bed and plate may become involved
(TOTAL DYSTROPHIC PATTERN). 50% or more of cases of nail
dystrophy are due to onychomycosis.

98. 2. WHITE SUPERFICIAL ONYCHOMYCOSIS:
• Direct penetration into (and usually confinement to)
the dorsal surface of the nail plate often due to T.
mentagrophytes.
• This classic form shows well-delineated discrete
opaque "white islands" on the plate.
• Patches coalesce to involve the entire nail plate. The
nail becomes rough, soft and crumbly.
• Transverse striate bands and deeper invasion of the
nail plate can also occur. These variants are more
likely be caused by T. rubrum or non-dermatophyte
molds.

100. 3. PROXIMAL SUBUNGUAL ONYCHOMYCOSIS:
• It is the least common variant of onychomycosis.
• It starts by fungal invasion of the stratum
corneum of the proximal nail fold and
subsequently the nail plate.
• Yellow spots appear at the lunula.
• Frequently in immunocompromised hosts.

101. 4. CANDIDAL ONYCHOMYCOSIS:
• Candida spp. are often found in association with
chronic paronychia.
• The fingernails are usually affected, with ridging,
yellow discoloration, tenderness and onycholysis.
• The nail fold is swollen and red.
• Candida spp. are a relatively common cause of
onychomycosis in children less than 3 years of age,
and nail involvement also represents a manifestation
of chronic mucocutaneous candidiasis.

103. OTHER TYPES OF ONYCHOMYCOSIS
• Total Dystrophic Onychomycosis
• Endonyx Onychomycosis
– Fungal organisms invade only the nail plate but do not
cause nail bed inflammatory changes.
– This type of onychomycosis is mainly confined to the lower
layers of the nail plate and is characterized by a diffuse
discoloration of the affected nail.
– The nail plate surface and nail thickness are normal and
no subungual hyperkeratosis and no onycholysis.

105. ONYCHOMYCOSIS IS CHALLENGING TO MANAGE DUE TO;
1. Difficulties in diagnosis.
2. The requirement for long treatment periods.
3. Potential side effects of systemic medications.
4. Frequent recurrences.

107. DEFINITION:
• Ringworm infections modified by
systemic or topical corticosteroids
prescribed for some pre-existing
pathology or given mistakenly for
the treatment of misdiagnosed
tinea.

108. • The inflammatory response of tinea may be almost totally
suppressed by corticosteroids, systemic (degree of
modification is often minor) or topical (degree of
modification can be profound) especially strong fluorinated
steroids.
• At the same time, it is probable that the resistance to
infection mediated by the immune response, especially the
cell-mediated response, is diminished by corticosteroids.

109. • The history is characteristic. The patient is
often satisfied initially with the treatment.
Itching is controlled and the inflammatory
signs settle. He or she stops applying the
cream, the eruption relapses, with varying
rapidity. Further applications bring renewed
relief and the cycles are repeated.
• The eruption usually remains localized but,
especially in E. floccosum infections, it
spreads more widely than one would expect in
the unmodified case.

110. • In the groins, the patient may develop few
persistent nodules, which become
unsuppressible by the steroid preparation.
• The usual sites are the groins, lower legs,
face, hands and perianally but tinea circinata
elsewhere may be steroid treated.
• On the face, the picture may be modified by a
superimposed perioral dermatitis with
papules and tiny pustules.

111. • Typically, the raised margin is diminished.
Scaling is lost and the inflammation is reduced
to a few nodules. Often, a bruise-like brownish
discoloration is seen, especially in the groins.
• With chronic use, atrophy, telangiectasia and, in
the groins and axillae, striae are likely to be
observed.
• In some cases, concentric rings of erythema are
seen among the atrophy and telangiectasia.
Presumably, these represent waves of fungal
growth.

112. DIRECT MICROSCOPY AND CULTURE:
• Scrapings and culture may be difficult to obtain in a patient
who is currently applying a steroid cream and may show
very few fungal elements.
• If the patient stops steroid for a few days an upsurge of
inflammation with marked scaling often occurs, making
clinical diagnosis easier and facilitating the taking of
scrapings. In such samples, fungal mycelium is usually
abundant.

116. 1. SKIN:
– Any ointments or other local applications present should first be removed with
alcohol.
– Using a blunt scalpel, 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.
– Skin stripped off with adhesive tape, which is then stuck on a glass slide.
2. HAIR:
– Epilation of short broken hairs with tweezers especially fluorescent hairs with
Wood’s lamp. Hair should be pulled out from the roots.
– Brushings from an area of scaly scalp.
– Swabs from pustular area in kerion.
3. NAILS:
– Nail clippings should be taken from crumbling tissue at the end of the infected nail.
The nail should be pared and scraped using a blunt scalpel until the crumbling white
degenerating portion is reached.
– Any white keratin debris beneath the free edge of the nail should also be collected.
4. MUCOUS MEMBRANES:
– Moistened swabs.

117. The material is examined by microscopy by one
or more of these methods:
1. Potassium hydroxide (KOH) preparation, stained
with blue or black ink.
2. Unstained wet-mount.
3. Stained dried smear.

118. • We add 10-20% KOH on the collected material on
glass slide then it is covered with cover slip.
• The glass slide is gently warmed and left for 20
min.
• Examination under LM may shows;
– Dermatophytes: identified by hyaline septate
branching hyphae and arthrospores. Spores inside a
hair (endothrix) or outside a hair (ectothrix).
– Candida: Budding yeast, pseudohyphae also septate
hyphae may be present.
• Examination under fluorescence microscopy;
– After applying special fluorescent stain e.g. calcoflour
white (it binds to the chitin in the cell walls of the
fungi).

120. • Fungal elements are sometimes difficult to find, especially if
the tissue is very inflamed, so a negative result does not rule
out fungal infection.
• Repeat collections should always be considered in cases of
suspected dermatophytosis with negative laboratory reports.

121. • Specimens should be inoculated onto primary
isolation media, like Sabouraud's dextrose agar
containing; cycloheximide (to suppress environmental
contaminant fungi so it is left out if a mould requires
identification) and chloramphenicol (to suppress
bacterial growth) then incubated at 26-28Co for
duration ranging from 2 days up to 4 weeks. The
growth of any dermatophyte is significant.
– Fast growers: e.g. Candida, M. canis  2-3 d.
– Slow growers: e.g. T. schoenleinii, T. rubrum  2-3 w.
• Identification of fungal spp. is based on both
microscopic & macroscopic appearance.
Raimond Sabouraud

123. A NEGATIVE CULTURE MAY ARISE BECAUSE:
1. The condition is not due to fungal infection.
2. The specimen was not collected properly.
3. Antifungal treatment had been used prior to collection of the
specimen.
4. There was a delay before the specimen reached the laboratory.
5. The laboratory procedures were incorrect.
6. The organism grows very slowly.

124. • This is a source of ultraviolet light from
which most visible light have been
excluded by a Wood’s (9% nickel oxide)
glass filter and allows passage of UV-A of
wavelength ~ 365 nm.

125. USES IN FUNGAL INFECTIONS:
1. Tinea capitis:
i. Large spore ectothrix & Arthrosporic endothrix:
do not fluoresce, so a negative test does not
exclude the diagnosis but may help in screening
to control epidemics.
ii. M. canis, M. audouinii → bright green
fluorescence.
iii. T. schoenleinii → pale green fluorescence.
2. Pityriasis (Tinea) Versicolor:
– Golden yellow fluorescence.

127. OTHER USES OF WOOD’S LAMP:
1. Bacterial infections e.g. Erythrasma, Pseudomonas
2. Infestations  Scabies.
3. Porphyrias
4. Pigmentary disorders
5. Detection of Drugs and chemicals
6. Detection of certain Tumours e.g. SCC
7. Miscellaneous; e.g. PDT, Bromhidrosis

128. IN TINEA CAPITIS:
• Endothrix infections  There is minimal
epidermal response aside from mild
hyperkeratosis. The hyphae extend within the hair
shaft and produce spores. This form is caused by T.
tonsurans, T. violaceum.
• Ectothrix infections  There is also often minimal
inflammatory reaction. The fungal forms coat the
outside of the hair shaft without significant
invasion of the shaft itself. This is typically caused
by M. Canis, M. audouinii.

129. TINEA CERCINATA:
• Typically show foci of parakeratosis with
epidermal acanthosis, spongiosis, and
collections of neutrophils in the upper layers
of the epidermis. The dermis may display
edema and predominantly chronic
inflammatory changes.
• Prolonged topical treatments with
corticosteroids may result in attenuation of
these inflammatory changes and extensive
proliferation of the organisms which become
easy to identify, even with routine H & E
stain.
• Special stains: PAS or GMS stains.

133. I. GENERAL MEASURES
II. TOPICAL TREATMENT
III. SYSTEMIC TREATMENT

134. 1. Good hygiene of the skin, hair and nail.
2. In tinea capitis asymptomatic carriers should be detected and treated (Antifungal shampoo
twice weekly). Surveillance in schools would be helpful. Personal objects, such as combs and
hairbrushes  disinfected or discarded.
3. Avoiding prolonged wetting or humidity of skin and feet.
4. In tinea pedis footwear should be disinfected, and patients should avoid walking barefoot in
public areas such as locker rooms. Other measures to reduce recurrence include controlling
hyperhidrosis with powders and wearing absorbent socks and nonocclusive footwear.
5. Treatment of any associated fungal infection e.g. treatment of tinea pedis helps prevent
onychomycosis.
6. In tinea cruris include wearing clean loose clothing, drying thoroughly after bathing, using
topical powders, weight reduction (if obese), laundering contaminated clothing and linens,
and treating concomitant tinea pedis.

135. A. Topical antifungal
1. Whitfield's ointment (benzoic acid)
2. Undecylenic alkanolamide
3. Topical azoles
i. Clotrimazole (Canesten®)
ii. Ketoconazole (Nizoral®)
iii. Miconazole (Daktarin®)
iv. Tioconazole (Trosyd®)
v. Sertaconazole (Dermofix®)
vi. Econazole (Ecreme®)
4. Allylamine (higher cure rates and more rapid responses than older topical antifungals) Terbinafine (Lamisil®)
5. Ciclopirox olamine (Batrafen®)
6. Thiocarbamates e.g. Tolnaftate
B. Dandruff shampoos: Ketoconazole 2%, selenium sulfide 2.5% , zinc pyrithione 1% to 2% for t. capitis.
C. Mild steroid to  inflammation for short period also in tinea incognito  few applications of topical
steroid to continue until the oral antifungal has begun to take effect. It is wise to use a weaker steroid
than that originally prescribed.

136. 1. Oral antifungals
2. Oral antihistamines
3. Oral antibiotics
4. Oral corticosteroids

137. 1. Oral antifungals
2. Oral antihistamines for symptomatic relief of itching.
3. Oral antibiotics
4. Oral corticosteroids

138. 1. Oral antifungals
2. Oral antihistamines
3. Oral antibiotics for 2ry infection e.g. kerion, ulcerative t. pedis.
4. Oral corticosteroids

139. 1. Oral antifungals
2. Oral antihistamines
3. Oral antibiotics
4. Oral corticosteroids for short period in id reaction & marked
inflammatory tinea capitis.

140. Oral antifungal medications may be required for a fungal
infection if:
1. It is extensive or severe.
2. It resists topical antifungal therapy.
3. It affects hair-bearing areas (tinea capitis and tinea barbae).

141. 1. Griseofulvin*
2. Terbinafine*
3. Itraconazole
4. Fluconazole
5. Ketoconazole

142. 1. DOSE REGIME FOR GRISEOFULVIN:
– Adults: 500 mg to 1 g /day.
– Children: 10-25 mg/kg/day.
– Tinea pedis, Tinea cruris, tinea manuum,
tinea corporis etc. for 2-6 weeks.
– Tinea unguium for 12-18 months until all
signs of nail infection have gone.

143. 2. DOSE REGIME FOR TERBINAFINE:
– The oral dose of terbinafine for adults is 250 mg daily.
– For children, the tablets can be hidden in food – the tablets
taste unpleasant:
• Weight 10-20 kg, 62.5 mg per day
• Weight 20-40 kg, 125 mg per day
• Weight >40 kg, 250 mg per day
– Sometimes, if the fungal infection does not clear, the dose in
children may need to be increased.
– Tinea corporis, tinea cruris, tinea pedis, tinea manuum: 1 to 4
weeks.
– Tinea unguium: for 6-8 weeks (fingernails) or 3-4 months
(toenails).
– Treatment can be repeated if necessary.

144. 3. DOSE REGIME FOR ITRACONAZOLE:
– Tinea corporis, tinea cruris: 200 mg daily
for one week OR 100 mg daily for 2 weeks.
– Tinea pedis, tinea manuum: 200 mg twice
daily for one week OR 100 mg daily for 2-4
weeks.
– Tinea unguium: 200 mg/day for 6-8 weeks
(fingernails) or 3-4 months (toenails), OR
200 mg twice daily for 7 days, repeated
monthly for 2 months (fingernails) or 3-4
months (toenails).

145. 4. DOSE REGIME FOR FLUCONAZOLE:
– Either 50 mg daily or 150 mg once weekly is
taken for two to six weeks.
– Fluconazole is not normally used in children
but doses of 5 mg/kg/day have been safely
prescribed for serious infection.

146. 5. DOSE REGIME FOR KETOCONAZOLE:
– In adults is 200 to 400 mg daily, taken for
two to eight weeks. Nail infections are
treated for up to twelve months.
– The dose in children is usually 50 mg per
day for those weighing less than 20 kg
and 100 mg daily for those 20-40 kg.

147. • In August 2013, the FDA announced that clinicians should no
longer prescribe ketoconazole (Nizoral) tablets as a first-line
therapy for any fungal infection, including Candida and
dermatophyte infections, because of the risk for severe liver
injury, adrenal insufficiency, and adverse drug interactions.
• Ketoconazole tablets were also withdrawn from the market
in the European Union in July 2013.

148. TREATMENT OF TINEA CAPITIS
• Oral antifungal medicines, including Grizofulvin he most effective agent
for infection with Microsporumcanis, terbinafine and itraconazole or
fluconazole for 4 to 6 weeks. Trichophyton infections.

150. 1. Interdigital: Topical antifungal; may require topical or oral
antibiotic if superimposed bacterial infection.
2. Moccasin: Topical antifungal plus product with urea or lactic
acid; may require oral antifungal therapy.
3. Vesicular: Topical antifungal usually sufficient.
4. Ulcerative: Topical antifungal; may require topical or oral
antibiotics if secondary bacterial infection (common).

151. • Recently, non-drug treatment has been developed to treat onychomycosis thus
avoiding the side effects and risks of oral antifungal drugs.
1. Lasers emitting infrared radiation are thought to kill fungi by the production of heat
within the infected tissue. Laser treatment is reported to safely eradicate nail fungi
with one to three, almost painless, sessions. Several lasers have been approved for this
purpose by the FDA and other regulatory authorities.
– Nd:YAG continuous, long or short-pulsed lasers
– Ti:Sapphire modelocked laser
– Diode laser
2. Photodynamic therapy using application of 5-aminolevulinic acid or methyl
aminolevulinate followed by exposure to red light has also been reported to be
successful in small numbers of patients, whose nails were presoftened using urea
ointment for a week or so.
3. Iontophoresis and ultrasound are under investiation as devices used to enhance the
delivery of antifungal drugs to the nail plate.

152. References
• Ihab Younis, M.D. Fungal skin infections (Presentation)
• http://dermnetnz.org
• Google images
• Bolognia 3rd ed.
• http://www.mayomedicallaboratories.com
• Oral Candidiasis by Hemam Shankar Singh
)Presentation(
• Assoc. Prof. Ivan Lambev (Presentation)
• medscape.dermatology.com