Dermatomycosis

Dermatovenerology Co-Assistant
July 12th-25th 2021
Introduction
 Introduction
● Dermatomycoses are fungal diseases of the skin.

● Worldwide distribution with high prevalence in most developing

countries.

● Common Risk Factors of dermatomycosis:

○ Environmental and geographical factors (climate, humidity)
○ Human factors (population mobility, personal hygiene, abusive antifungal
drug use)
○ Economic factor (poverty)

Ngatu NR. Common Environmental Dermatomycoses. Occupational and Environmental Skin Disorders: Springer; 2018. p.
119-31.
 Introduction
● Classification according to the fungal agents natural habitat:
○ “Anthropophilic” dermatophytes: they are parasitic organisms that infect
humans.
○ “Zoophilic” dermatophytes: those that infect animals.
○ “Geophilic” dermatophytes: they are fungi found in the soil.

● Classification according to the cite of infections:

○ Superficial dermatomycosis
○ Intermediate dermatomycosis
○ Deep-seated dermatomycosis (Deep dermatomycosis)

Ngatu NR. Common Environmental Dermatomycoses. Occupational and Environmental Skin Disorders: Springer; 2018. p. 119-31.
Mochizuki T, Tsuboi R, Iozumi K, Ishizaki S, Ushigami T, Ogawa Y, et al. Guidelines for the management of dermatomycosis (2019). The Journal
of Dermatology. 2020;47(12):1343-73.
 Introduction

Mochizuki T, Tsuboi R, Iozumi K, Ishizaki S, Ushigami T, Ogawa Y, et al. Guidelines for the management of
dermatomycosis (2019). The Journal of Dermatology. 2020;47(12):1343-73.
Introduction
Superficial Dermatomycosis

Dermatophytosis Non - Dermatophytosis

● Tinea Capitis ● Pityriasis Versicolor
● Tinea Facialis ● Piedra
● Tinea Barbae ● Tinea Nigra
● Tinea Corporis ● Otomycosis
● Tinea Cruris
● Tinea Manus
● Tinea Pedis
● Tinea Unguium
Introduction
Intermediate Dermatomycosis

Candidiasis
● Candidal Intertrigo
● Interdigital candidiasis
● Generalized candidiasis
Introduction

Deep Dermatomycosis
● Chromomycosis
● Sporotrichosis
● Mycetoma
 Superficial
Dermatomycosis
● Tinea (capitis, facialis, barbae, corporis,
cruris, manus, pedis, unguium)
● Pityriasis Versicolor
● Piedra
● Tinea Nigra
● Otomycosis
 TINEA CAPITIS
Tinea capitis is a Risk factors → poor hygiene and
dermatophyte infection sanitation, high humidity and hot
of the hair and scalp
climate, contact with animal such
characterized by local
alopecia with scaling. as cat or dog

Etiology :
Dermatophytes :
1. T. rubrum
2.. T. mentagrophytes
3. M. gypseum
4. M. Canis
5. M. audoini
Paller AS., Mancini AJ. Skin Disorders due to
Fungi. In: Hurwits Clinical Pediatric Dermatology.
4th ed. New York: Elsevier Saunders. 2011.p.
390- 415.
TINEA CAPITIS

Pathophysiology

Causative agent ⇒ present in non living cornified layers of skin and its appendages, then
invading stratum corneum, and then fungal hyphae grow centrifugally and continues downward
growth into the hair.
Invaded keratin ⇒ extends upwards at the rate at which hair grows and visible by days 12-14.

Infected hairs are brittle, and by the third week, broken hairs are evident.

Trovato MJ, Schwartz RA, Janniger CK. Tinea capitis: current concepts in clinical practice. Cutis. 2006 Feb. 77(2):93-9.
TINEA CAPITIS
There are three types of hair invasion :

1. Ectothrix invasion on the exterior of the hair shaft, cuticle of the hair is destroyed,
and fluoresce a bright greenish-yellow color under a Wood lamp. In ectothrix infection,
only arthroconidia are found on the surface of the hair shaft, although hyphae are also
present in the hair shaft and damage the hair cuticle.
2. Endothrix invasion within the hair shaft only. The cuticle of the hair remains intact
and infected hairs do not fluoresce under a Wood lamp ultraviolet light. In endothrix
infection, arthroconidia and hyphae are found in the hair shaft where the cuticle and
cortex remain intact.
3. Favus produces favus-like crusts or scutula and corresponding hair loss. Favus is
characterized by dense hyphae arranged longitudinally and there are air cavities in the
hair shaft, arthroconidia generally not found.

Puri N, Puri A. A study on tineacapitis in the pre School and school going children. department of
dermatology and venereology, Punjab Health Systems Corporation, India. 2013;4(2): 157-160
 DIAGNOSIS TINEA CAPITIS
Diagnose ⇒ Physical examination
⇒ Anamnesis
● Black dot ringworm
● 7 sacred and fundamental 4 (especially
previous recurrence, long term
medicine, immunological status, and risk
factor).
● Patient may experienced itching,
burning sensation, scaling hair with
patchy hair loss lesion, gray hair
❏ Mostly caused by T. tonsurans and T.
discoloration, baldness, black dot
violaceum which caused 2 type of hair
baldness, sometimes there a pain
invasion (endothrix and ectothrix). Hair
redness lesion with pus, and wet lesion
become fragile and vulnerable to break
with stink odor.
right on scalp surface that leaving
Fuller LC, Child FJ, Midgley G, Higgins EM. Diagnosis and management of scalp ringworm. BMJ. black dots in the area of alopecia.
2003 Mar 8. 326 (7388):539-41.
❏ Sometimes diffuse scale can be seen,
Jain N, Doshi B, Khopkar U. Trichoscopy in alopecias: diagnosis simplified. Int J Trichology. 2013
Oct. 5(4):170-8 surrounding hair color become hazy.
TINEA CAPITIS
Physical examination

Gray Patch Ringworm Kerion Celsi Tinea Favosa

Localised swelling that form
- Hair follicles prone
some small papules with
to break easily
skuama, pustular folliculitis,
- Circular gray patches
of alopecia lesion furuncles or kerion with
scaling. (Itchy, pain)
- Scutula : a bowl shaped
crust with red yellowish
colour which develops to a
yellowish-brown colour
- If the crust is removed,
there is a red wet sunken
bottom with mousy odor
 TINEA CAPITIS
Additional examination
Wood lamp examination
The fluorescent substance appears to be produced by
the fungus only in actively growing infected hairs.
- M canis, M rivalieri, and M ferrugineum → a bright
green to yellow-green color
- T schoenleinii → a dull green or blue-white color
Microbiology analysis
- Direct microscopy and culture of skin
rubbings, skin scrapings, or hair pluckings
from lesions.
- Examination of 10-20% KOH solution ->
hyphae or spores
- Culture on Sabouraud agar -> gross colony
 TINEA CAPITIS
Differential Diagnoses In ectothrix infection (M.
Microsporum infections
canis, M. audouinii,)
- Alopecia areata Griseofulvin 20-25 mg/kg/day in
Oral steroids may help reduce
- Dermatitis seborrheic single or two divided doses for
the risk for and extent of
- Bacterial folliculitis microsized or 15-20 mg/kg/day
permanent alopecia in the
- Subacute Cutaneous in single dose or two divided
Lupus Erythematosus treatment of kerion. Avoid
doses for ultramicrosized.
using topical corticosteroids
during the treatment. (a longer
The duration of treatment should
duration of therapy may be
be between 4 and 6 weeks.
Treatment required)
Determined by the
species of fungus For topical treatment can be
Trichophyton infections used : Selenium Sulfide 1% or
concerned, degree of Terbinafine tablets at doses 2.5% 2-4 times a week or
inflammation, the of 3-6 mg/kg/d for 2-4 ketoconazole 2% for 2-4
immunologic and weeks, times a week
nutritional status
TINEA FACIEI
Definition
A superficial dermatophyte infection limited
to the glabrous skin of the face. (the
mustache and the beard areas of the adults
men are excluded)

Etiology:
Trichophyton rubrum
Trichophyton mentagrophytes
Microsporum canis
Trichophyton tonsurans
Microsporum audouinii
Chalmers, R., Bleiker, T., Creamer, D. (2016). Rook's Textbook of Dermatology, 4 Volume Set. United Kingdom: Wiley.
 TINEA FACIEI
Diagnosis Clinical Features
Anamnesis
● Annular erythematous, slightly
● Patients may complaints of
itching, burning and exacerbation scaling, and indistinct borders
after sun exposure may be present at the periphery of
● A history of exposure to animals the lesions
● Simple papular lesions and
completely flat patches of
erythema, also occur in some
cases

Chalmers, R., Bleiker, T., Creamer, D. (2016). Rook's Textbook of Dermatology, 4 Volume Set. United Kingdom: Wiley.
Neuhaus, I., Treat, J. R., Rosenbach, M. A., James, W. D., Elston, D. (2019). Andrews' Diseases of the Skin E-Book: Clinical Dermatology. Netherlands: Elsevier Health Sciences.
 TINEA FACIEI
Examination Treatment
● Scrapings from the lesion(s) are placed in a
Most cases of tinea faciei are curable with topical
drop of KOH and examined under a
antifungal agents.
microscope for the presence of fungal hyphae.
● Terbinafine 1% cream once or twice daily 1-2
● Fungal culture can be performed as a
weeks
confirmatory test if results from a KOH stain
● Miconazole 2% cream twice daily for 1-2
are inconclusive. Scrapings extracted from
weeks
affected areas are placed on Sabouraud’s
● Clotrimazole 1% cream twice daily for 1-2
medium
weeks

Differential Diagnosis Oral antifungal treatment is an option if severe or

extensive disease is present or if topical treatment
● is failed.
Discoid Lupus Erythematosus
● Seborrheic dermatitis ● Griseofulvin (child : 10-25 mg/KgBW/day,
● Rosacea adult 0.5-1 g/day, for 2-4 weeks)
Huckerby C. Guidelines For The Prescribing Of Topical Antifungal Agents Guidelines For The Prescribing Of Topical Antifungal Agents. 2020
Neuhaus, I., Treat, J. R., Rosenbach, M. A., James, W. D., Elston, D. (2019). Andrews' Diseases of the Skin E-Book: Clinical Dermatology. Netherlands: Elsevier Health Sciences.
TINEA CORPORIS
Definition

is a superficial fungal skin infection of the body

caused by dermatophytes. Called ringworm
because the rash usually circular with clearer
middle

Predilection: Trunk, abdomen, back, neck, arms

and legs

Etiology:
Trichophyton rubrum
Epidermophyton floccosum
Microsporum
Chalmers, R., Bleiker, T., Creamer, D. (2016). Rook's Textbook of Dermatology, 4 Volume Set. United Kingdom: Wiley.
TINEA CORPORIS

Clinical Finding
Anamnesis :
● Skin rash demarcated , erythematous and scaly
● Itchy, especially when sweating

Physical Exam :
Single or multiple lesions are usually circular or ovoid
in appearance with patches and plaques. These
annular lesions demonstrate sharp marginations with a
raised erythematous scaly edge which may contain
vesicles.
TINEA CORPORIS
Examination Differential Diagnosis
● Scrapings from the lesion(s) are placed in a
● Morbus Hansen (TT/BT) : erythematous
drop of KOH and examined under a
macular appearance with slightly
microscope will reveal septate and branching
active margins
long narrow hyphae
● Pityriasis Rosea : erythematous
● Fungal culture can be performed as a macular appearance with slightly
confirmatory test if results from a KOH stain raised margins, papules, scales.
are inconclusive. Scrapings extracted from
affected areas are placed on Sabouraud’s ● Circumscribed Neurodermatitis :
medium erythematous macular appearance
with well-defined borders

Huckerby C. Guidelines For The Prescribing Of Topical Antifungal Agents Guidelines For The Prescribing Of Topical Antifungal Agents. 2020
Neuhaus, I., Treat, J. R., Rosenbach, M. A., James, W. D., Elston, D. (2019). Andrews' Diseases of the Skin E-Book: Clinical Dermatology. Netherlands: Elsevier
Health Sciences.
TINEA CORPORIS

Therapy
Systemic
Topical - Adult
● Itraconazole 100mg/day (1 week)
● Clotrimazole 1% cream/ ointment/solution ●
Fluconazole 150-300 mg/day
2x/day ● Griseofulvin 500 mg/day
● Ketoconazole 2% cream
/shampoo/gel/foam 1x/day - Children
● Miconazole 2% ● Itraconazole 5 mg/Kgbw/day ( 1week)
cream/ointment/solution/lotion/powder ● Griseofulvin 10-20 mg/Kgbw/day
2x/day
● Naftifine 1% cream/gel 1-2x/day
● Terbinafine 1% cream/gel/spray solution 1-
2x/day
 TINEA CRURIS
- Definition
Tinea cruris is dermatophytosis that often found on the skin of the groin,
genital, pubic, perineal and perianal
- Etiology → Trichophyton rubrum & Epidermophyton floccosum
- Transimision → another fungal infection fomites such as towels and
sheets other humans, animals, soil
- Risk Factors and Predispositions → Mal, Excessive sweating, Tight
clothing, Improper hygiene, DM, Immunocompromised, Obesity,
Lower socioeconomic status, Sharing clothing
PATHOPHYSIOLOGY OF TINEA CRURIS
● The most common etiologic agents for tinea cruris include
Trichophyton rubrum and Epidermophyton floccosum; less commonly
Trichophyton mentagrophytes and Trichophyton verrucosum are
involved.
● Tinea cruris is a contagious infection transmitted by fomites, such
as contaminated towels or hotel bedroom sheets
● The etiologic agents in tinea cruris produce keratinases, which
allow invasion of the cornified cell layer of the epidermis. The
host immune response may prevent deeper invasion. Risk factors
for initial tinea cruris infection or reinfection include wearing
tight-fitting or wet clothing or undergarments.
CLINICAL
FEATURES TINEA ANAMNESIS
CRURIS TINEA CRURIS
•Red, itcy rash in upper Patients with tinea cruris report
thigh pruritus and rash in the groin. A
•Pruritic history of previous episodes of a
•Annular plaque with a similar problem usually is elicited.
Additional historical information in
raised leading edge and
patients with tinea cruris may
central healing include recently visiting a tropical
•Papules, vesicles climate, wearing tight-fitting
•Extends outward with clothes (including bathing suits)
centrifugal spread for extended periods, sharing
•Can spread into perineum clothing with others, participating
and gluteal cleft in sports, or coexisting diabetes
mellitus or obesity.
PHYSICAL
EXAMINATION
Large patches of erythema with
central healing are centered on the
inguinal creases and extend distally
down the medial aspects of the
thighs and proximally to the lower
abdomen and pubic area.
ADDITIONAL
EXAMINATION
Macroscopic → wood lamp → is used
to rule out other diagnosis of
erythrasma. Interpretation of wood lamp
test for erythrasma may show red coral
fluoroscence.
Microscopic → Potassium hydroxide
(KOH) → branched septate hyphae
 TREATMENT OF TINEA CRURIS
Topical
● Drugs of choice : Terbinafine topical, 4 weeks
● Alternative : Miconazole, Ketoconazole, Clotrimazole twice a day, 4-
6 weeks

Systemic (extensived lesions, chronic lesions)

● Drug of choice:
Terbinafine 250 - 500 mg/day, 2 weeks
Itraconazole 100 - 200 mg/day, 2-4 weeks
● Alternative :
Itraconazole 2x100mg/day, 2 weeks
Griseofulvin 500mg/day or 10-25 mg/kg/day, 2-4 weeks
Ketoconazole 200mg/day
TINEA MANUUM
Definition
Superficial dermatophtye infection of the palmar, dorsum, or interdigital areas of one or both
hands.

Etiology
Most common: Tricophyton rubrum
Others: Tricophyton (Tricophyton verrocosum, Tricophyton interdigitale, Tricophyton
mentagrophytes), Epidermophyton (Epidermophyton floccosum), Microsporum (Microsporum
canis and Micropsorum gypseum)

Risk Factors
Male, High Humidity (Hyperhidrosis), DM, Hypertension, Immunocompromised, Atherosclerosis,
Communal Bathing/sport facilities, Farmworkers or pet owners, Picking toenails infected with
tinea, and repeated hand trauma.
TINEA MANUUM
Pathophysiology
● Dermatophyte infection defensive mechanism is related to cell mediated immune response.
Increased susceptibility of tinea infection in immunocompromised individuals.
● Mannan glycoprotein (T. rubrum cell wall) assist the adherence of dermatophtyes to the epithelial
tissue of the host that contains keratin and protease digest the keratin network to facilitate
penetration. It has also been shown to suppres lymphocyte response.
● Dermatophytes invade and infect the stratum corneum and may persist there.
● The skin responds to the infection through the increase proliferation of keratinocytes and the
production of scales or epidermal hyperkeratosis.
TINEA MANUUM
Diagnosis
History Taking
● Patients complain of thickened skin or pruritis in one/both hands or redness and scaling on the
dorsum of the hands.
Physical Examination
● “Two-foot, One hand syndrome” : most common clinical presentation
● Red plaque with an active vesicular, scaly border, and a centrifugal growth in the dorsum hands
● Concentric rings might be seen
● Palmar surfaces usually dry and have a scaling appearance
TINEA MANUUM
Diagnosis
Mycological Confirmation with Triple Confirmation
● Clinical Exam
● KOH 10% : branched septate hyphae
● Culture : positive cultures (2 weeks) with SDA
● Microscopic Fluorescent Staining : bright-green/apple green fluorescence
● Dermoscopy : white scales localized in the skin furrows
Differential Diagnosis

Psoriasis Dyshidrotic eczema Contact Dermatitis

TINEA MANUUM
Treatment
● Avoid Transmission
● Keep the skin dry
● Treat dermatophyte infection of feet/nails (if there is coexisting infection)
● Topical: imidazole creams (clotrimazole, miconazole, ketoconazole, etc), allylamine lotion
(terbinafine cream) 1-2x/day for 1-2 weeks
● Systemic:
Terbinafine 250 mg tablet/day (2 weeks)
● Alternatives:
Itraconazole 200 mg daily (7 days)
Fluconazole 150-200 mg tab daily (2-4 weeks)
 01

02

03

Tinea Pedis 04

05

06
 Tinea Pedis
Definition
Tinea pedis, athlete’s foot or foot ringworm is an infection of the feet affecting soles,
interdigital clefts of toes, and nail with a dermatophyte fungus.

Etiology
- Tricophyton rubrum → 70%
- Tricophyton interdigitale
- Epidermophyton floccosum
Pathophysiology
The skin of soles has a thick keratinized
layer & numerous eccrine sweat gland

Risk factors
- a hot and humid environment Combination of abundant keratin,
sweat, and occlusion with shoes creates
- prolong wearof occlusive footwear
a perfect environment for dermatophyte
- Prolong exposure to water infection
- Excess sweating
 Diagnosis
Patient’s History
- Itching and persistent scaling or less commonly blisters usually on the plantar surface
or in the toe webs
- May lasts for months to years to lifetime and often with prior history of tinea pedis or
other form of tinea

Physical Examination
Depends on the type:
- Chronic intertriginous (interdigital)
- Chronic hyperkeratotic
- Vesiculo-bullous
- Acute ulcerative
 Interdigital Tinea Pedis
- Most common form
- Predominantly caused by T. Rubrum
- Characterized by interdigital erythema, scaling,
maceration, and fissuring
- Lesions are typically located between 4th - 5th
toes
- On several conditions, infection may spread to
sole and dorsal part of feet
- Occlusion and co-infection with bacteria may
Scale and small fissures can be seen
cause maceration, pruritus, and malodor
(complex dermatophytosis)
 Chronic Hyperkeratotic Tinea Pedis
- Known as moccasin-type
- Most common pathogen are T. rubrum,
followed by E. floccosum and T. interdigitale
- Characterized by diffuse or localized squama.
Few vesicles may appear, leaving a squama
with diameter less than 2 mm
- Commonly seen in lateral of sole and around
sole area
- Associated with unilateral tinea manum
which known as two feet-one hand syndrome Subtle diffuse scale bilaterally
 Vesicobullous Tinea Pedis
- Typically caused by zoophilic strains of
T. interdigitale
- Characterized by tight vesicles with
diameter > 3 mm, vesiculopustular or
bullae around area with less thick skin
(sole and periplantar)
- Rarely seen in kids

Vesiculobullous pattern tinea pedis

Vesicles on the instep of the foot with
cellulitis
 Acute Ulcerative Tinea Pedis

- Commonly caused by Trichophyton

interdigitale
- At risk of co-infection with gram-negative
bacteria
- Characterized by vesiculopustular lesion and
purulent ulceration in wide area of plantar
surface
- Followed by cellulitis, lymphangitis,
Purulent Ulceration can be seen
lymphadenopathy, and fever
 Laboratory Findings
- KOH examination → needed to distinguish from dermatitis. Branched septate hyphae
can be seen
- Dermatophyte Test Medium culture → positive between 2 weeks

Segmented, branched hyphae are visible on this KOH preparation

 Differential Diagnosis

Interdigital Hyperkeratotic Vesicobullous

- Erosio - Dyshidrosis - Dyshidrosis

interdigitalis - Psoriasis - Contact
blastomycetica - Contact dermatitis
- Erythrasma dermatitis - Pustular psoriasis
- Bacterial - Atopic
coinfection dermatitis
 Treatment
Recurrence prevention
- Keep the skin dry & clean
- Treat any coexisting nail infection
Topical Agents
- Topical Allylamine (terbinafine, butenafine cream) once a day for 1-2 weeks
- Azole cream (Miconazole, Imidazole) twice a day for 4-6 weeks
- Ciclopirox Olamine (ciclopirox gel 0,77% or cream 1%) twice a day for 4 weeks for
tinea pedis & tinea interdigitalis
Systemic (oral) Agents
May be required for patients who have failed with topical antifungal therapy
● Terbinafine 250 mg/day for 2 weeks (pediatric dose -> 5 mg/kgBW)
● Itraconazole 100 mg twice a day for 3 weeks or 100 mg/day for 4 weeks
Tinea Ungium
Tinea Ungium
Definition
It’s a common fungal or dermatophyte infection of the nails. Usually invade healthy nails, it may
also invade dystrophic nails especially in elderly patients.

Etiology
Trichophyton rubrum & Trichophyton interdigitale → 90%
Trichophyton tonsurans
Epidermophyton floccosum

Risk Factor
● Immunocompromised
● Contact with the source of infection
● Nail disease or injury
● Modern life : wearing a shoes, particularly fashionably tight shoes, high-heels shoes,
sharing shoes → increasing the humidity.
Tinea Ungium
Physical Examination
➔ DLSO : subungual hyperkeratosis or crumbling. Discoloration, thickening and
subungual debris of the distal nails.
➔ PSO : overlying the nail matrix. Discoloration and thickening of the proximal
nail.
➔ WSO : irregular opaque white patches on various parts of the nail plates.
➔ TDO : total nail destruction
➔ MDO : mixed
Tinea Ungium
Diagnosis
➔ Mycological laboratory confirmation
➔ KOH stain
➔ Nail clip biopsy
➔ Culture on sabouraud dextrose agar

Differential Diagnosis
➔ Nail psoriasis : most common, usually bilateral and symmetrical
➔ Nail Trauma
➔ Onychogryphosis
Management
ORAL (SYSTEMIC)
➔ Terbinafine 250 mg / day, 6 weeks to 3 months for finger nails and 3-6 months for toenails
➔ Itraconazole 200 mg x 2, for 2 weeks with repeated doses after 21 days. Fingernail
infections need to be repeated up to 2 times, and 3 times for toenail infections
➔ Antibiotics for secondary infection
TOPICAL
➔ Locetar nail polish (Amolorphine Group)
➔ Loprox nail polish (Ciclopirox olamine)
DOSAGE
➔ 1st Month : 3x / week
➔ 2nd Month : 2x / week
➔ 3th Month : once / week
(by cutting the nails beforehand)
Management
Education
➔ Maintain cleanliness of toenails and hand
➔ Wearing loose shoes, keeping nails short, and stopping a range of potentially risky
behaviors (going barefoot in public places, wearing open sandals, wearing other
people’s shoes, and exposing feet or hands to damp environments)
➔ Antifungal powders should be used once a week to help keep shoes free from
pathogens
Pityriasis
Versicolor
Pityriasis Versicolor
● Pityriasis versicolor or previously known as tinea versicolor is a mild chronic superficial
fungal infection of the skin, mainly characterized by hypopigmented or hyperpigmented
macules to patches caused by Malassezia yeasts.

Etiology Pathophysiology

Malassezia species, mainly Malassezia metabolizes various fatty acids

M.giobosa, M.sympodialis, and → azelaic acid → inhibits tyrosinase →
M.furfur reduce melanin production →
hypopigmentation

● Malassezia changes from saprophytic yeast to parasitic mycelial form which invades
stratum corneum due to predisposing factors.
● Predisposing factors include warm, humid environment, hyperhidrosis, oral
contraceptive, pregnancy, systemic corticosteroids, Cushing’s disease,
immunosuppression, and malnutrition.
Clinical Manifestation
1
● Asymptomatic to mildly pruritic. The major
concern is its appearance.
● Severe pruritus may present in warm and humid
conditions, such as sweating.
● Distribution : predilection in seborrheic area,
including upper trunk, upper arms, neck, abdomen,
axilla, groins, thighs, genitals, facial, or scalp.
● Morphology : multiple, well-defined oval to round 2
patches to thin plaques with mild, fine scale.
● Color : the color of the scales may vary (versicolor):
1. Brown to pinkish (hyperpigmented in untanned white
skin)
2. White-ish (hypopigmented in suntanned or dark skin)
Diagnosis
Wood's light examination (365 nm) may show an
orange-yellowish fluorescence in the involved
skin, suspected to be due to pteridine.

Clinical findings are confirmed by positive KOH

examination findings, we can see the form of
round yeast and elongated pseudohyphae, which
are called spaghetti and meatball
DIFFERENTIAL DIAGNOSIS

Often found Infrequent

-Pityriasis alba -Vitiligo

-Pityriasis rosea -Psoriasis gutata
-Seborrheic dermatitis -Pityriasis rubra pilaris
-Dermatophyte infections -Morbus hansen
-Leukoderma
 TREATMENT
TOPICAL

-Ketoconazole shampoo 2% is applied on affected areas and left for 5 minutes prior to rinsing; this
treatment is repeated for three consecutive days (A,1)
-Selenium sulfide lotion 2.5%, which is applied to affected areas for 15-20 minutes prior to rinsing
for 3 days and repeated a week later. (B, 1)
-Zinc pyrithione 1% shampoo is applied all over the infected area/whole body, 7-10 minutes before
bathing, once/day or 3-4 times a week.

SYSTEMIC

-Ketoconazole 200 mg/day for 10 days

-Itraconazole 200 mg/day for 7 days or 100 mg/day for 2 weeks (B, 1)
-Fluconazole 400 mg single dose (B, 1) or 300 mg/week for 2-3 weeks (A,1)
Piedra
Piedra (trichomycosis nodularis)
Definition
- an asymptomatic superficial fungal infection of the hair shaft.
- The term “Piedra” means “stone” (in Spanish),reflecting the fungal elements’ to one
another toform nodules along the hair shaft.

Transmission
Direct Contact

Classification
 Black Piedra White Piedra

Etiology Piedraia hortae Trichosporon sp.

- T. asahii
- T. ovoides
- T. inkin
- T. mucoides
- T, asteroides
- T. cutaneum
 Black Piedra White Piedra

Predilection : scalp hair Predilection : scalp, ayelash, eyebrow,

bard, axillary, pubic hair

Dark nodular concretion around 4-8 on Multiple, tiny white dots on and around
the distal half of the hair several hair shaft. The white dots can
merge and form a sheath

Attached strongly on hair Attached weakly on hair

Clinical Weaken the hair shaft → hair breakage Broken hairs are less common than in
Features black piedra
 Black Piedra White Piedra

Microscopy KOH Examination Microscopy KOH Examination

Nodules are composed of closely packed brown Non-dematiaceous hyphae, arthroconidia 2-4 pm
thick-walled, septate hyphae held in a mass by a in diameter, and budding blastoconidia.
viscous or cement-like substance.

Diagnosis
Culture Culture
Colonies: Rapidly-growing. Soft, moist, creamy and
Slowly-growing. Compact, domed, black. Not wrinkled, and sometimes mucoid (yeast-like).
inhibited by cycloheximide. Most species are inhibited by cycloheximide
Microscopy: (should be excluded from the culture medium).
Hyphae and chlamydoconidia.
Differential Diagnosis
 Piedra (trichomycosis nodularis)
Treatment
- Clipping off the hair of affected areas
- Wash the hair with antifungal shampoo
- High relapse rates, as well as evidence for intrafollicular organisms in white piedra,
some advice the use of a systemic antifungal agent such as itraconazole.

Black Piedra
White Piedra
Application such poly antimycotic agents as
Daily application of either classical 1 : 2000 bichloride
clotrimazole, miconazole, and haloprogin (but
of mercury solution, povidone- iodine, or one of the
their application is uneasy and must be continued
new yeast inhibiting preparations (nystatin,
for a long period of time)
amphotericin B, clotrimazole, or miconazole).
 TINEA
NIGRA
A rare superficial fungal infection of stratum corneum, usually found on palm
and soles that is caused by Hortaea werneckii or Stenella araguata

Infection is believed to occur as a result of inoculation from a contamination

source (soil, sewage, wood, or compost) subsequent to trauma in the affected
area.

Risk Factor:
Poor hygiene, Hot-humid climate, Hyperhidrosis, Age (children and
younger adults)
Clinical Features
● Asymptomatic, but sometimes it feels little itchy
● Hyperpigmented (brown to black) macule
● Sharply marginated
● The lesions are typically solitary, although more than one lesion
can be present.
● The shape of the lesion varies: oval, round, or irregular
● The size may range from a few millimeters to several centimeters
in diameter, depending on the duration of the infection.
Diagnosis

Wood’s Lamp: SDA culture: KOH skin scrapping: HE skin scrapping:

Greenish yellow fluorescence visible fungal septated and freely spores and hyphae can
growth branched hyphae, be seen in the
brown/olive epidermis, no
Differential diagnosis:
inflammation
● Melanoma
● Syphilis
● Addison disease
 Treatments
● Ointments containing 3-5% salicylic acid and 5-10% benzoic acid
● 1-2% imidazole preparations in creams or ointments.
● Tinea nigra responds readily to topical therapy with a keratolytic (Whitfield ointment, 2% salicylic
acid), tincture of iodine, or topical antifungal.
● Treatment should be continued for 2 to 4 weeks after clinical resolution to prevent relapse.
● Although oral ketoconazole, itraconazole, and terbinafine are also effective, systemic therapies are rarely
indicated
Otomycosis
Otomycosis
Definition
Otomycosis is an ear sub-acute or chronic infection caused by a fungus. It’s affects
the outer ear canal and tympanic membrane. It’s also known as fungal otitis externa.

Aetiology:
Risk Factors:
Aspergillus sp. , Mucor sp. and
Female. humid climate, swimming/diving,
Penicillium sp
increased use of topical antibiotics/steroid,
immunocompromised host, and those who
wear hearing aids with occlusive ear mold
Otomycosis
General Complains:
- Itchy - Discomfort
- Hearing loss - Tinnitus
- Aural fullness - Otalgia
- Discharge

Signs:
● Persistent white or colorless otorrhea with tympanum
perforation
● Grayish-black or yellow dots surrounded by cotton-like
fungal spores will form in your ear canal indicated infection
usually caused by Aspergillus sp.
● Edema, erythema of the meathal epithelium of the auditory
canal and tympanic membrane
 Otomycosis
Diagnosis
● History Taking
○ The symptoms are often indistinguishable. However pruritus is almost frequent
characterisstics for mycotic infections and also discomfort, hearing loss, tinnitus, aural
fullness, otalgia and discharge.
○ Also history of activity in water such as swimming or diving.
○ Patients have typically been tried on topical antibacterial agents with no significant response.

● Physical Examination
○ The auditory canal may be erythematous and fungal debris may appear white, gray, or black.
○ The diagnosis can be confirmed by identifying fungal elements on a KOH preparation or by a
positive fungal culture.
Otomycosis
Treatment
- Ear toilet, which is an important treatment in otomycosis.
- Antifungal preparations can be divided into non specific and specific types. Non specific
antifungals included acidic and dehydrating solutions such as:
- Boric acid is a medium acid and often used as a antiseptic and insecticide. Boric acid can be
used to treat yeast and fungal infection caused Candida albicans.
- Gentian violet is prepared as a low concentrate solution (eg. 1%) in water. It has been used to
treat otomycosis as it is an aniline dye with antiseptic, antiseptic, antiinflamatory, antibacterial
and antifungal activity. It is still use in some countries and FDA approved. Studies report an up
to 80% efficacy.
- Castellani’s paint (acetone, alcohol, phenol, fuchsin, resocinol) - Cresylate (merthiolate, M-
cresyl acetate, propylene glycol, boric acid and alcohol).
- Merchurochrome, a well known topical antiseptics, antifungal. With merthiolate (thimerosal),
merchurochrome is no longer approved by FDA because they contains mercury.
 Otomycosis
Spesific antifungal therapies consist of:
● Nystatin is a polyene macrolide antibiotic that inhibits sterol synthesis in cytoplasmic membrane. Nystatin can be
prescribed as cream, ointment or powder. With efficacy rates up to 50- 80%.
● Azoles are synthetic agents that reduced concentration of ergosterol an essential sterol in normal cytoplasmic
membrane.
● Clotrimazole is most widely used as topical azole. Clotrimazole has a bacterial effects and this is advantage when
clinician treats mixed bacterial-fungal infections. Clotrimazole has no ototoxic effects and available as powder,
lotion and solution.
● Ketoconazole and fluconazole have a broad spectrum activity. Efficacy of ketoconazole reported 95-100% against
Aspergillus species and Candida albicans. Topical fluconazole has been reported effective in 90% cases.
● Miconazole cream 2% has also demonstrated at efficacy rate up to 90%.
● Bifonazole. The potency of 1% solution is similar to clotrimazole and miconazole.
● Itraconazole is also has invitro and in vivo effects against Aspergillus species.
M

Intermediate
Dermatomicosis
Intermediate Dermatomicosis

Candidal Interdigital
01 Intertrigo 02 Candidiasis

Generalized
03 Candidiasis
 Candidal
01 Intertrigo
Intertriginous
Candidiasis
Definition
Intertrigo is a clinical inflammatory condition that
develops in opposing skin surfaces in response to
friction, humidity, maceration, or reduced air
circulation.

Etiology

Candida albicans
Intertriginous Candidiasis
❑ Risk factors

1. Humid and hot weather

2. Tight underclothes
3. Occlusive wearings
4. Poor hygiene
Intertriginous Candidiasis

History
Patients complaint of redness and itching in body fold
areas (moist conditions), mild itching and sharp pain may
be present

Diagnosis
The diagnosis is made by clinical examination in
addition to fungal culture and KOH testing
 Intertriginous
Candidiasis
Predilection
• Neck and Nuchal
• Inframammary
• Axillary
• Abdominal folds
• Genitocrural folds
• Gluteal
Intertriginous
Candidiasis
Clinical Presentation
Pruritic, erythematous, macerated skin areas are
observed in intertriginious areas with satellites
vesicopustules.

The characteristic : pustulae rapidly rupture 🡪

formation of collarette type erythematous surface,
from which the necrotic epidermis may be easily
removed
Intertriginous Candidiasis
Differential Diagnosis

01 Allergic contact dermatitis

02 Irritant contact dermatitis

03 Seborrheic dermatitis

04 Atopic dermatitis
Intertriginous Candidiasis
Treatment

Identification and correcting predisposising factors

Topical administration of nystatin and azole group

antifungal
 Interdigital
02 Candidiasis
 Interdigital
Candidiasis
Risk factors
1. Occupational wet work
2. Diabetes mellitus
3. Immunocompromised state
Definition 4. Recent use of systemic antibiotics or
Interdigital candidiasis / Erosio interdigitalis corticosteroids
blastomycetica is a superficial yeast infection that
affects the interdigital web spaces, most frequently of
the hands

Etiology
Candida yeast
 Interdigital Candidiasis
Clinical Presentation
Central erythematous erosion surrounded by a rim of white macerated
skin involving at least one interdigital web space
Diagnosis
The diagnosis is made by clinical examination in addition to fungal
culture and KOH testing

Differential diagnosis
Allergic Contact Dermatitis, Irritant Contact Dermatitis, Tinea manuum
Treatment
Topical azole antifungal creams. Recurrence can be prevented by controlling any risk factors
 Generalized
03 Candidiasis
Generalized
Candidiasis
Definition
Generalized candidiasis is when infection due to
fungi of genus Candida causes lesions that appear
throughout many parts of the patient’s skin,
particularly skin folds.
Candidiasis is opportunistic in nature, in which it
naturally occurs as part of the normal microbial
flora until an imbalance in the local environment
occurs and Candida becomes infectious

Etiology
Candida albicans
Generalized
Candidiasis
Clinical Presentation
● Capable of manifesting in both children and adults
● Vulvoaginal candidiasis can be passed on from
mother to child and cause congenital generalized
candidiasis

Physical Examination
● Erythematous damp rashes surrounded by satellite
lesions (papules, vesicles and pustules)
● Pruritus with increased severity in genitocrural
folds, axilla, extremities
● Onychomycosis → “drumstick” fingers
Generalized
Candidiasis
Laboratory Examination
● Direct smear = specimen procured from swabbing
the lesion, stained with Gram/KOH → presence of
pseudohyphae
● Microbial culture = Sabouraud Dextrose Agar
(SDA) as growth medium → incubation at 37 C =
fungal colony appears with smooth surface, yeast
odor, yellowish coloration
● Sugar fermentation test = Species identification →
incubation in urea, lactose dextrose, sucrose,
maltose and trehalose
● Germ tube test = incubation in serum, results in
sprout-like growth
 Generalized Candidiasis

Treatment
● Keeping the skin dry (particularly skinfolds)
● Topical nystatin powder, clotrimazole, or miconazole twice daily
● Mild topical corticosteroid (if needed)
● In the event of extensive infection, fluconazole (100 mg PO for 1-
2 weeks) or itraconazole (100 mg PO for 1-2 weeks) may be
prescripted
 Deep
Dermatomycosis

1. Chromoblastomycosis
2. Sporotrichosis
3. Mycetoma
 Chromoblastomycosis
Chromoblastomycosis (also known as
chromomycosis) is a chronic cutaneous and
subcutaneous fungal infection caused by traumatic
inoculation of a specific group of dematiaceous fungi
(usually Fonsecaea pedrosoi, Phialophora verrucosa,
Cladosporium carrionii, or Fonsecaea compacta)
through the skin

Incident :
● Age of 30 – 50 years old, infrequently occur in
children or teenagers
● Men > Women (occupational factor -> higher
probability of trauma)

Arguello-Guerra L, Gatica-Torres M, Dominguez-Cherit J. Chromomycosis. BMJ Case Reports. 2016.

Queiroz-Telles F, de Hoog S, Santos DWCL, Salgado CG, Vicente VA, Bonifaz A, et al. Chromoblastomycosis. Clin Microbiol Rev. 2017;
 Chromoblastomycosis

Etiology :
Chromoblastomycosis is caused by dematiceous fungi ;
● Fonsecaea pedrosoi -> most often
● Fonsecaea compacta
● Phialophora verrucosa
● Cladosporium carrion
● Rhinnocladiella aquaspersa

Queiroz-Telles F, de Hoog S, Santos DWCL, Salgado CG, Vicente VA, Bonifaz A, et al. Chromoblastomycosis. Clin Microbiol Rev. 2017
de Hoong GS, Guarro J, Gené J, and Figueras MJ. 2000. Atlas of clinical fungi, 2nd ed, p 645–896. Centraalbureau voor Schimmelcultures, Utrecht, The Netherlands
 Chromoblastomycosis
Clinical features
Cutaneous lesion :
● Nodule
● Tumorous
● Verrucous
● Plaque
● Cicatrical
● Mixed form

Predilection
Feet, knees, lower legs, and hands are the most
common sites, but infections of other regions, such as
the trunk, nose, ears, eyelids, shoulders, and buttocks,
have also been reported

Queiroz-Telles F, de Hoog S, Santos DWCL, Salgado CG, Vicente VA, Bonifaz A, et al. Chromoblastomycosis. Clin Microbiol Rev. 2017
 Chromoblastomycosis
Clinical classification

Type of lesion Description of lesion

Moderately elevated, fairly soft, dull to pink

violaceous growth; surface is smooth, verrucous, or
Nodular
scaly; over time, lesions may gradually become
tumorous

Hyperkeratosis is the outstanding feature; warty dry

Verrucous lesions; frequently encountered along the border of
the foot

Tumor-like masses, prominent, papillomatous,

sometimes lobulated; “cauliflower like”; surface is
Tumorous
partly or entirely covered with epidermal debris and
crusts; more exuberant on lower extremities

Queiroz-Telles F, de Hoog S, Santos DWCL, Salgado CG, Vicente VA, Bonifaz A, et al. Chromoblastomycosis. Clin Microbiol Rev. 2017
 Chromoblastomycosis
Clinical classification

Type of lesion Description of lesion

Nonelevated lesions that enlarge by peripheral extension

with atrophic scarring, while healing takes place at the
Cicatricial center; may expand centrifugally, usually with an
annular, arciform, or serpiginous outline; tend to cover
extensive areas of the body

Least common type; slightly elevated with areas of

infiltration of various sizes and shapes; reddish to
Plaque violaceous, presenting a scaly surface, sometimes
showing marked lines of cleavage; generally found on
the higher portions of the limbs, shoulders, and buttocks

Association of the seven basic types of lesions; usually

Mixed formj observed in patients showing severe and advanced stages
of the disease

Queiroz-Telles F, de Hoog S, Santos DWCL, Salgado CG, Vicente VA, Bonifaz A, et al. Chromoblastomycosis. Clin Microbiol Rev. 2017
 Chromoblastomycosis (A) Dark brown, velvety colony
on sabouraud dextrose agar culture
Diagnosis

● Diagnosis is mainly based on clinical and epidemiological suspicion in endemic areas,

and must be confirmed by microbiological in clinical samples.
● Present inside the tissues are oval-shaped, dark brown, thick-walled fungal cells 4-12
μm in diameter, called copper pennies or muriform cells (sclerotic or fumagoid cells or
medlar bodies) that can be found singularly or in groups
● Direct microscopy using potassium hydroxide (KOH) 10-20% or KOH/DMSO reveals
muriform (sclerotic) bodies (A) and dematiaceous hyphae (B), pathognomonic of CBM
regardless of the causative species
● Skin biopsies of scraping must be performed on fungal media containing antibiotics, such
as Saboraud’s dextrose agar. Should be taken from the surface of the lesion where "black
dots" may be visible.
● Histopathology will demostrate pseudoepitheliomatous hyperplasia, hyperparakratosis,
and dermis with edema and granulomatous inflamatory infiltrate (A) and muriform cells
in the stratum corneum with transdermsl elimination (B)

Arguello-Guerra L, Gatica-Torres M, Dominguez-Cherit J. Chromomycosis. BMJ Case Rep. 2016;2016:bcr2016215391. Published 2016.
doi:10.1136/bcr-2016-215391
Brito AC, Bittencourt MJS. Chromoblastomycosis: an etiological, epidemiological, clinical, diagnostic, and treatment update. An Bras Dermatol.
2018;93(4):495-506. doi:10.1590/abd1806-4841.20187321
 Chromoblastomycosis
Differential Diagnosis
1 Verrucous tuberculosa cutis

Verrucous paracoccidiomidomycosis
2

3 Verrucous sporotrichosis

4 Verrucous leishmaniasis

5 Squamous cell carcinoma

Brito AC, Bittencourt MJS. Chromoblastomycosis: an etiological, epidemiological, clinical, diagnostic, and treatment update. An Bras Dermatol. 2018;93(4):495-506.
doi:10.1590/abd1806-4841.20187321
 Chromoblastomycosis
Treatment

Antifungal Drugs

● Antifungal drugs, often used before surgery to downsize the lesion and later to avoid risk of relapse.
● The antifungals that have shown the greatest efficacy are itraconazole (200-400mg/day) and
terbinafine (500-1000mg/day) for at least 6-12 months → In the event of widespread presentation,
intravenous amphotericin B (1mg/kg/day) can be used.
● Antifungal drugs, often combined with physical treatments like surgery, cryotherapy, and
thermotherapy.

Brito AC, Bittencourt MJS. Chromoblastomycosis: an etiological, epidemiological, clinical, diagnostic, and treatment update. An Bras Dermatol.
2018;93(4):495-506. doi:10.1590/abd1806-4841.20187321
Rositawati A, Suyoso S. Chromomycosis Treatment With Combination Of Itraconazole And Terbinafine. 2017;29(2):168–73.
Sporotrichosis
 Sporotrichosis
● Also known as “rose gardener’s disease”
● An infection caused by a fungus called Sporothrix
● This fungus lives throughout the world in soil and on plant matter such as sphagnum moss,
rose bushes, and hay.
● Inoculation of soil, plants, and organic matter contaminated with the fungus
● People get it by coming in contact with the fungal spores
● Cutaneous (skin) infection is the most common form of the infection.
● It occurs when the fungus enters the skin through a small cut or scrape, usually after someone
touches contaminated plant matter.
● Skin on the hands or arms is most commonly affected.
● Presents as papules or pustules that form ulcerated nodules involving local lymphatics.

Sizar O, Talati R. Sporotrichosis. [Updated 2020 Jun 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK532255/?report=classic
 Sporotrichosis
● Sporotrichosis was first thought to be caused by a single
organism but is now known to contain several species
including S. brasilienis, S. globosa, and S. Mexicana, so
it has been renamed S. schenckii complex or S.
schenckii senu lato.
● Sporotrichosis has been reported in most mammals
including cats, dogs, swine, horses, rats, and
armadillos.
● Results from traumatic implantation of an intact skin by
organic materials (e.g., soil, plant debris)
● Sporadic, but occupational exposure may occur
● Not transmissible from person-to-person
● Animal transmission and zoonotic transmission

Sizar O, Talati R. Sporotrichosis. [Updated 2020 Jun 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK532255/?report=classic
 Sporotrichosis
Types of sporotrichosis:
● Cutaneous (skin) sporotrichosis
● Pulmonary (lung) sporotrichosis
● Disseminated sporotrichosis
Risk Factors:
1. Occupation. Rose gardeners, farmers, miners, horticulturists, and armadillo
hunters have an increased risk of infection
2. Animals. Infection may also occur during animal transmission and zoonotic
transmission which is associated with scratches or bites from infected cats

Sizar O, Talati R. Sporotrichosis. [Updated 2020 Jun 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK532255/?report=classic
 Sporotrichosis
Sporotrichosis has an incubation period of several days to 3 months after exposure

A. Cutaneous (Skin) Sporotricosis

● Lesions are erythematous papulonodular lesions that may be smooth or verrucous
● Involve lymphatic channels
● Lesions are typically painless even after ulceration.
In this syndrome, the patient will not have systemic symptoms, and laboratory
exams will be normal.

Sizar O, Talati R. Sporotrichosis. [Updated 2020 Jun 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532255/
Conceição-Silva F, Morgado FN. Immunopathogenesis of Human Sporotrichosis: What We Already Know. Journal of Fungi. 2018; 4(3):89. https://doi.org/10.3390/jof4030089
 Sporotrichosis
B. Pulmonary (Lung) Sporotrichosis
● Symptoms include a cough, low-grade fever, or weight loss
● Risk factors include chronic pulmonary issues, alcohol abuse or
have a history of steroid use, diabetes mellitus, sarcoidosis, and
immunocompromised state
● Gram stain or sputum culture will help in diagnosis

B. Disseminated Sporotrichosis
● Typically occur in immunocompromised patients
● Occurs with lung abscess, liver and spleen involvement, and
fungemia

Sizar O, Talati R. Sporotrichosis. [Updated 2020 Jun 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532255/
do Monte Alves M, Pipolo Milan E, da Silva-Rocha WP, Soares de Sena da Costa A, Araújo Maciel B, Cavalcante Vale PH, et al. (2020) Fatal pulmonary sporotrichosis caused by Sporothrix brasiliensis in Northeast Brazil. PLoS Negl Trop Dis
14(5): e0008141. https://doi.org/10.1371/journal.pntd.0008141
 Sporotrichosis
Diagnosis
The gold standard for the diagnosis of sporotrichosis is the
isolation and the identification of the Sporothrix species,
samples include:
● Tissue biopsy or pus from lesions (direct microscopy made
with potassium hydroxide (KOH) preparations) Tissue
biopsy reveals cigar-shaped yeast cell when stained using
Gomori-methenamine silver (GMS). Some more specific
staining for fungi such as Grocott’s metamine-silver (GMS)
or periodic acid-Schiff (PAS) may reveal so-called “asteroid
bodies”
● Sputum culture (pulmonary sporotrichosis)
● Urine, blood, and synovial fluid analysis (disseminated
sporotrichosis)

Arenas R, Sánchez-Cardenas CD, Ramirez-Hobak L, Ruíz Arriaga LF, Vega Memije ME. Sporotrichosis: From KOH to Molecular Biology. J Fungi (Basel). 2018;4(2):62. Published 2018 May 23. doi:10.3390/jof4020062
Sizar O, Talati R. Sporotrichosis. [Updated 2020 Jun 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532255/?report=classic
 Sporotrichosis
Treatment
● Itraconazole
-100 to 200 mg/day orally for cutaneous forms
- 400 mg/day orally should be used for pulmonary forms
- Children weighing up to 20 kg, 5 to 10 mg/kg/day is recommended
Before the introduction of azole compounds in the 1990s, potassium iodide was the
treatment of choice. Due to adverse effects of this drug, itraconazole is the first
treatment of choice
Itraconazole cannot be used in patients who are pregnant
● Amphotericin B
- Can be used by pregnant woman after 12 weeks
- For disseminated and pulmonary forms, particularly in
immunocompromised patients

Sizar O, Talati R. Sporotrichosis. [Updated 2020 Jun 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK532255/?report=classic
Mycetoma
● Mycetoma is a chronic, progressively destructive infectious disease of the
subcutaneous tissues, affecting skin, muscle and bone.
● Mycetoma is a chronic disease usually of the foot but any part of the body
can be affected.
● Mycetoma was first reported in the mid-19th century in Madurai, India, and
hence was initially called Madura foot.

Risk Factor
● Barefoot walking people in tropic countries
● Low socioeconomic status and health education level
● Prior penetrating wounds by thorns or splinters

Hay R, Denning DW, Bonifaz A, et al. The Diagnosis of Fungal Neglected Tropical Diseases (Fungal NTDs) and the Role of Investigation and Laboratory Tests: An Expert Consensus Report. Trop Med Infect
Dis. 2019;4(4):122. Published 2019 Sep 24. doi:10.3390/tropicalmed4040122
 Mycetoma

Caused by

Bacteria (actinomycetoma) Fungi (eumycetoma)

● Nocardia (N.brasilensis; ● Maurella mycetomatis
N. ateroides; N.otitidis- (70%)
caviarum; ● Madurella grisea
N.transvalensis) ● Scedosporium
● Streptomycessomaliensis apiospermum
● Actinomadura
(A.madurae;A.pelletien)

Reis CMS, Reis-Filho EGM. Mycetomas: an epidemiological, etiological, clinical, laboratory and therapeutic review. An Bras Dermatol. 2018;93(1):8-18.
doi:10.1590/abd1806-4841.20187075
Transmission
● Transmission occurs when the causative organism enters the
body through minor trauma or a penetrating injury,
commonly thorn pricks.
● People living in or travelling to endemic areas should be
advised not to walk barefoot, as footwear and clothing in
general can protect against puncture wounds.

Reis CMS, Reis-Filho EGM. Mycetomas: an epidemiological, etiological, clinical, laboratory and therapeutic review. An Bras Dermatol. 2018;93(1):8-
18. doi:10.1590/abd1806-4841.20187075

https://www.cdc.gov/fungal/diseases/mycetoma/index.html
Symptoms and Sign
● The typical clinical presentation is a painless subcutaneous mass of slow progression forming
multiple sinuses that drain pus and clusters of bacterial and fungal called "grains"
● The bacteria are represented by delicate filaments of about 1μm or less, which are known as
actinomycotic grains,
● While fungi are formed by thicker and coarser filaments, measuring 2μm or more in
diameter, known as eumycotic grains.
● It usually spreads to involve the skin, deep structures and bone, resulting in destruction,
deformity and loss of function, which may be fatal.
● ● Mycetoma commonly involves the extremities, back and gluteal region but any other part of
the body can be affected.

Reis CMS, Reis-Filho EGM. Mycetomas: an epidemiological, etiological, clinical, laboratory and therapeutic review. An Bras Dermatol. 2018;93(1):8-
18. doi:10.1590/abd1806-4841.20187075
 Diagnosis

● Early phase mycetoma

Clinical Presentation ● Late phase mycetoma

Identification of the
● Laboratory
etiological agents in
● Imaging
the tissue

● Emmanuel P, Dumre SP, John S, Karbwang J, Hirayama K. Mycetoma: a clinical dilemma in resource limited settings. Ann Clin Microbiol Antimicrob.
2018;17(1):35. Published 2018 Aug 10. doi:10.1186/s12941-018-0287-4
● Ahmed AA, van de Sande W, Fahal AH. Mycetoma laboratory diagnosis: Review article. PLoS Negl Trop Dis. 2017;11(8):e0005638. Published 2017 Aug 24.
doi:10.1371/journal.pntd.0005638
Diagnosis ( Clinical Presentation)
Early phase mycetoma Late phase mycetoma

● a papule, a nodule, an abscess or just an ● Classical characteristic triad of a painless

induration lacking a clear margin can be subcutaneous mass, multiple sinus, and
seen. discharge containing grains.

● The epidermis may become hypo- or ● Vital structures such as tendons and nerves
hyperpigmented and the nodules which are usually well preserved until late in the
increase in size eventually rupture along disease course due to adequate supply of
fascial plains to form secondary nodules. blood in mycetoma.

● These ruptured nodules continue as a sinus ● Regional lymph nodes may enlarge as a
tract discharging fluid which contains result of superimposed bacterial infection or
grains, Pain is hardly felt at this stage. immune complex deposition.

● Emmanuel P, Dumre SP, John S, Karbwang J, Hirayama K. Mycetoma: a clinical dilemma in resource limited settings. Ann Clin Microbiol Antimicrob.
2018;17(1):35. Published 2018 Aug 10. doi:10.1186/s12941-018-0287-4
Diagnosis (identification of the causative organisms)
a) Grain Myctemoma Macroscopic
Size ● large grains → Madurella mycetomatis, A.
madurae
● small grains → Nocardia brasiliensis, N.
cavae, and N. asteroids grains

● Eumycetoma → Black grain (Madurella spp.,

Color Myctemoma Macroscopic
Grain
Leptosphaeria spp., Curvularia spp.)
● Actinomycetoma → Pale, white, yellow grains
(Actinomadura madurae, Nocardia spp.
Photography of surgical biopsy showing a
well encapsulated eumycetoma lesion with
numerous black grains.
Consistency The consistency of most grains is soft, except
Streptomyces somaliensis and M. mycetomatis are
quite hard.
● Ahmed AA, van de Sande W, Fahal AH. Mycetoma laboratory diagnosis: Review article. PLoS Negl Trop Dis. 2017;11(8):e0005638. Published 2017 Aug 24.
doi:10.1371/journal.pntd.0005638
Diagnosis (identification of the causative organisms)
b) Grain direct Microscopic
KOH 10% ● The grains can be directly examined under light
microscope using 10% potassium hydroxide
(KOH)
● Presence of the hyphae and spores.
● Actinomycetes → show branching filaments,
abundant aerial mycelium, and long chains of
spores
Grain Myctemoma Macroscopic
Gram staining ● Actinomycetoma → gram-positive, consist of
fine, branching filaments, about 1 micron thick.
● Eumycetoma → gram-negative, composed of
septate hyphae 4–5 microns thick.

Ziehl–Neelsen (ZN) ● Superior in discriminating between

staining Actinomycotic agents; KOH wet mount direct microscopic
● Nocardia spp. → ZN (+) examination of M. mycetomatis grains
showing its hyphal structure.
● A. madurae and S. somaliensis → ZN (-)
Diagnosis (identification of the causative organisms)
c) Grain Culture
● Sabouraud Dextrose Agar
● Modified Sabouraud agar supplemented with 0.5%
yeast extract, blood agar, brain–heart infusion agar,
and Löwenstein agar are the commonly
recommended media.
● Fungi is sometimes difficult and time consuming,
culture usually takes about 3 weeks to give an
accurate result, and accidental contamination may
give a false positive result

Photograph showing M. mycetomatis

growth in Sabouraud agar media.

● Ahmed AA, van de Sande W, Fahal AH. Mycetoma laboratory diagnosis: Review article. PLoS Negl Trop Dis. 2017;11(8):e0005638. Published 2017 Aug 24.
doi:10.1371/journal.pntd.0005638
Diagnosis (identification of the causative organisms)
d) Fine-needle aspiration cytology (FNAC)
● In smears stained with haematoxylin and eosin (H&E), the M. mycetomatis grains appeared
rounded or oval in shape and black with a green tinge of colour or occasionally brownish.
● Actinomycetes grains are homogeneously eosinophilic in H&E. In Geimsa-stained smears, the
grain appears homogeneously blue in the centre, while in the periphery it consists of fine
granules and radiating pink filaments.

e) Molecular-PCR
● This technique provide an accurate identification of the causative agents of mycetoma.
● Expensive, not readily available in endemic areas, only available in tertiary facilities
IMAGING used to assess the extent of lesions and planning the clinical management, including plain
x-ray, ultrasonography, computed tomography (CT), and nuclear magnetic resonance imaging (MRI)

● Ahmed AA, van de Sande W, Fahal AH. Mycetoma laboratory diagnosis: Review article. PLoS Negl Trop Dis. 2017;11(8):e0005638. Published 2017 Aug 24.
doi:10.1371/journal.pntd.0005638
Treatment

Actinomycetoma
❏ Rifampisin 600 mg/daily (10 mg/kg daily) and Co-trimoxazole 2x2 tablet (2x1 tablet forte)
❏ Streptomycin sulphate (14 mg/kg daily) IM 1 month combined with Co-trimoxazole (14 mg/kg
twice daily)

Alternative:
❏ Combination of Streptomycin with dapson (100 mg/kg daily) or Rifampicin (4,3 mg/kg daily)
or Sulfadoxin-pirimetamin (500 mg/ twice weekly)
❏ Amikacin sulphate (15 mg/kg) twice daily in three weeks and Co-trimoxazole (8/40 mg/kg
daily) in five weeks (1 cycle).

● Fahal AH. Tropical Infectious Diseases: Principles, Pathogens and Practice (Third Edition), CHAPTER 83 - Mycetoma, Pages 565-568, W.B.
Saunders, 2011, SBN 9780702039355, https://doi.org/10.1016/B978-0-7020-3935-5.00083-5.
● Perhimpunan Dokter Spesialis Kulit dan Kelamin Indonesia (PERDOSKI). Panduan Praktik Klinis bagi Dokter Spesialis Kulit dan Kelamin di
Indonesia. Jakarta: PERDOSKI; 2017.
Treatment

Eumycetoma
Combined surgery and antifungal drugs.
❏ Ketoconazole: doses 400-800 mg/daily or itrakonazol: 400 mg/daily.
❏ Terbinafin 2x500 mg/daily in weeks.
❏ Combination of terbinafin 500 mg/daily and itrakonazol 400 mg/daily.
❏ Before surgery: combination of terbinafin 500 mg/daily dan itrakonazol 400 mg/daily in 1-3
months to prevent diseminata.
❏ After surgery: continue combination treatment of terbinafin dan itrakonazol in 3-6 months to
prevent relaps.

● Fahal AH. Tropical Infectious Diseases: Principles, Pathogens and Practice (Third Edition), CHAPTER 83 - Mycetoma, Pages 565-568, W.B.
Saunders, 2011, SBN 9780702039355, https://doi.org/10.1016/B978-0-7020-3935-5.00083-5.
● Perhimpunan Dokter Spesialis Kulit dan Kelamin Indonesia (PERDOSKI). Panduan Praktik Klinis bagi Dokter Spesialis Kulit dan Kelamin di
Indonesia. Jakarta: PERDOSKI; 2017.
Thank You
For your attention.