MEDICAL

MYCOLOGY
Prof. Carl Jay Bregente, RMT, MPH, MSc.
SWU PHINMA – School of Medicine and College of Medical Technology
 FUNGI
- eukaryotic organisms (true nucleus, 80s ribosomes, mitochondria)

1. Fungal cells have cell walls (CW).

a. Fungal cell walls protect cells from osmotic shock, determine
cell shapes, and have components that are antigenic.
b. Fungal cell walls are composed primarily of complex
carbohydrates such as chitin with glucans and mannoseproteins.
c. The CW glucan (not found in humans) is the antifungal target
of the echinocandins like caspofungin.

2. Ergosterol is the dominant fungal membrane sterol - targeted by

imidazoles, triazoles, and polyenes antifungals
 Fungi include organisms called molds,
mushrooms, and yeasts.
HYPHAE are filamentous (tubelike) cells of
molds (also known as the filamentous fungi)
and mushrooms.
- Septae or septations are cross walls of
hyphae and occur in the hyphae of the
great majority of the disease-causing fungi.
- Nonseptate or aseptate hyphae lack
regularly occurring cross walls. These cells
are multinucleate and are also called
coenocytic
- Hyphae may be dematiaceous (dark
colored) or hyaline (colorless).
- Fluffy surface masses -mycelia.
 FUNGI
YEASTS are single-celled fungi, generally
round to oval shaped. (blastoconidia).

• PSEUDOHYPHAE (hyphae with sausage-like

constrictions at septations) are formed by
some yeasts when they elongate but remain
attached to each other.
-Ex: Candida albicans
 FUNGI
THERMALLY DIMORPHIC FUNGI are fungi capable of
converting from a yeast or yeast-like form to filamentous
form and vice versa. (Yeast in the heat; mold in the cold)
- include the major pathogens:
o Sporothrix
o Blastomyces
o Histoplasma
o Coccidioides
o Paracoccidioides
FUNGAL SPORES are formed either asexually or by
a sexual process involving nuclear fusion and then
meiosis.
- Conidia are asexual spores of filamentous fungi

(molds) or mushrooms
- Blastoconidia are the new yeast ‘‘buds’’

- Arthroconidia are conidia formed by laying down

joints in hyphae followed by fragmentation of the

hyphal strand
 Fungal Environment:
¨ SAPROBES / SAPROPHYTES live on dead organic material.
¨ COMMENSAL COLONIZERS generally live in harmony on
humans, deriving their nutrition from compounds on body surfaces.
¨ PATHOGENS infect the healthy but cause more severe disease in
the compromised hosts
Overview of Fungal Disease
A. FUNGAL ALLERGIES
sick building syndrome, farmer’s lung, silo worker’s disease, allergic
bronchopulmonary aspergillosis (Aspergillus fumigatus)

B. MYCOTOXICOSES
- may result from ingestion of fungal-contaminated foods ( e.g., St.
Anthony’s fire from ergot-contaminated bread or aflatoxin
- ingestion of psychotropic (Psilocybe) or toxic (Amanita) mushrooms.

C. FUNGAL INFECTIONS (MYCOSES)

- range from superficial to overwhelming systemic infections hat are
rapidly fatal in the compromised host.
Lab Diagnosis of Fungi
¨ Microscopic examination- rapid methods
1. KOH mount – dissolve human cells.
2. Nigrosin or India ink – capsule
3. Giemsa or Wright’s stain
4. Calcofluor white stain – blue-white appearance
(fungus)
Lab Diagnosis of Fungi
Histologic staining – special fungal stains for fixed
tissues
¨ Gomori methenamine-silver stain: fungi are dark
gray to black
¨ Periodic acid-Schiff (PAS): fungi are hot pink to
red.
¨ Gridley fungus stain: fungi are purplish rose with a
yellow background
¨ Immunofluorescent stains are available for some
fungal pathogens
 Lab Diagnosis of Fungi
¨ DNA probes – for some systemic pathogens.
¨ Cultures (e.g., Sabouraud’s dextrose medium),
enriched media (e.g., blood agar)
¨ Fungal antigen detection. (Antibodies are available
for Histoplasma and Cryptococcus).
¨ Serologic testing
Antifungal therapy
 MYCOSES
Credit to: Marvi G. Dulnuan – Niog, MD, FPSP
Mycoses
¨ Definition - Fungal infections

Ø Rarely serious unless the immune system is weakened,

usually by drugs or disorders.
Ø Fungal infections usually progress slowly.

¨ Most pathogenic fungi are exogenous

Ø Normal biota – Dermatophytosis
– Candidiasis
Risk Factors for Developing Fugal Infections

Use of drugs that suppress the Disorders that suppress the

immune system immune system

ü Cancer chemotherapy drugs üAIDS

ü Corticosteroids üBurns, if extensive
ü Drugs to prevent rejection of an üDiabetes
organ transplant, such üHodgkin lymphoma or other
as azathioprine, methotrexate üLymphomas
and cyclosporine üKidney failure
üLeukemia
üLung disorders, such as emphysema
Classification
¨ Basis of clinical nomenclatures used for the mycoses
:
1. site of the infection

2. route of acquisition of the pathogen,

3. type of virulence exhibited by the fungus.

1. Based on Site
 Based on Site
1. Superficial üstratum corneum
üessentially elicit no inflammation
2. Cutaneous üinvolve the integument and its
appendages, including hair and nails.
üInfection may involve the stratum
corneum or deeper layers of the
epidermis.
üInflammation of the skin is elicited by
the organism or its products.
3. Subcutaneous üInfection of the subcutaneous tissues
usually at the point of traumatic
inoculation.
üAn inflammatory response develops
in the subcutaneous tissue frequently
with extension into the epidermis.
4. Deep Mycoses üinvolve the lungs, abdominal viscera,
(Systemic) bones and or central nervous system.
 2. Based on Route of Acquisition

Mode of Transmission
Exogenous infecting organism
may be transmitted
by airborne,
cutaneous, or
percutaneous routes
Endogenous acquired from
colonization or
reactivation of a
fungus from a latent
infection.
3. Based on Virulence
Primary Infections Opportunistic
can establish infections in normal hosts cause disease in individuals with
compromised host defense mechanisms.
SUPERFICIAL
MYCOSES
Superficial Mycoses
Infection Etiology
Pityriasis Versicolor 1. Malassezia furfur complex
2. Malassezia globosa
3. Malassezia restricta

Tinea Nigra Hortaea (Exophilia) wernickii

Piedra Piedraia hortae

Trichosporon ovoidis
Trichosporon inkin
 Superficial Mycoses
Pityriasis Versicolor

q Chronic mild superficial infection of Malassezia spp

the stratum corneum - Lipophylic yeast
q No inflammation - Short unbranched hyphae
(pseudohyphae) and spherical cells
q Discrete, serpentine, hyper- or (spores)
hypopigmented maculae on the skin; “spaghetti and meat balls”
dundruff

“Fawn-colored liver spots”

Superficial Mycoses
Tinea Nigra (Tinea Nigra Palmaris/Plantaris)
q Superficial chronic and asymptomatic
infection of the stratum corneum; no
inflammation
q More prevalent in warm coastal
region; among young women
q Dark brown discoloration, often on
the palm
Hortaea (Exophiala) werneckii
- Dematiaceous fungus – darkly
pigmented
- Branched septate hyphae and budding
yeasts (blastoconidia) with melanized
cell walls.
“annelloconidia”
 Superficial Mycoses
Piedra endemic in tropical countries
¨ BLACK PIEDRA
Ø Dark brown gritty nodules firmly
attached to hair shaft.
Ø Nodules consists of asci/ascus (sack
like structures) with 8 ascospores
Ø Caused by Piedraia hortae
¨ WHITE PIEDRA
Ø Larger softer, nodules on the hair shaft
Ø Caused by Trichosporon ovoidis
& Trichosporon inkin
Ø Presence of both arthroconidia and
blastoconnidia
 Superficial Mycoses
Diagnosis and Treatment

MYCOSES Diagnostic Tool Treatment

1. Ptyriasis Topical Selenium
Versicolor fulfide
Oral Azoles

Direct examination
of skin scraping
2. Tinea Nigra ü 10-20% KOH
üCalcaflour white Kertolytic solutions
üWood’s lamp – Salicylic acid
lesion fluoresce Azole antifungal
drugs

3. Piedra
SUBCUTANEOUS
MYCOSES
 Subcutaneous Mycoses

¨ Usually follow trauma or any kind of

injury

¨ In field workers

¨ Lesions develop at the site of

implantation of the etiological agent in
the subcutaneous tissue.
Types of Subcutaneous Mycoses
Types Etiology
1. Chromoblastomycosis Dematiaceous fungi
Chromomycosis Phialophora verrucosa Fonseccae pedrosoi
Rhinocladiella aquaspersa
Fonseccae compactum
Cladophialophora carrionii
2. Mycetoma Pseuddallescheria boydii
Acremonium falciforme
Madurella mycetomatis
M. Grisea Exophiala jeanselmi
3. Sporotrichosis. Sporothrix schenkii
4. Phaeohyphomycosis Exophiala spp
E. dermatitidis
5. Rhinosporidiosis Rhinosporidium seeberi
6. Lobomycosis Lacazia loboi
MYCETOMA
¨ Chronic, slowly progressive
granulomatous infection of skin &
subcutaneous tissues with the
involvement of underlying fascia &
bones commonly affecting the
extremities.

¨ Reported by Gill from Madurai,

S.India.

¨ Maduramycosis or Madura foot.

Classification of Mycetoma
¨ Based on the causative agent
¤ Fungi : Eumycetoma
¤ Bacteria (actinomycetes) : Actinomycetoma

¨ Based on the colour of grains

¤ Bacterial agents : white to yellow grains except
Actinomadura pelletieri (red or pink)
¤ Fungal agents : black as well as white grains.
Colour of grains in Mycetoma of various etiology

White to yellow Brown to black Red

Pseudollescheria boydii Madurella Actinomadura
mycetomatis madurai

Acremonium falciforme Madurella grisea

Exophiala
jeanselmei
Mycetoma: Epidemiology

¨ More prevalent in developing countries, especially

in the rural areas.

¨ Field workers, farmers – prone to thorn prick injury

& trauma.

¨ Prevalence in world : Eumycetoma (40%)

Actinomycetoma (60%)
Mycetoma: Pathogenesis
¨ Entry of pathogen into the injured site, mostly foot.

¨ Lesion begins as a small subcutaneous swelling of the injured

site

¨ Enlargement of the lesion & burrowing into deeper tissues

¨ Formation of multiple sinuses on the surface discharging

viscid, seropurulent fluid containing granules or grains which
are microcolonies of the causative agent.
Mycetoma: Clinical features

¨ Characterized by a triad of
clinical features:

1. Tumefaction – tumor like

swelling

2. Multiple draining sinuses

3. Presence of grains or granules

in sinuses.
 Mycetoma: Direct Examination
¨ KOH mount – after crushing the
grains
Eumycetoma : 2-6µ, wide
interwoven hyphae with large,
swollen cells (chlamydospores)
at the margin of the lesion.

Actinomycetoma : filaments with

a diameter of 0.5 - 1µ, coccoid
to bacillary forms.

If hyphae seen on KOH mount,

use special stains.
Mycetoma: Culture
¨ Different sets of media – both possibilities of fungi &
bacteria
Ø When Actinomycetoma is suspected on direct examination -
wash grains several times with NS & then inoculate on SDA
without antibiotics, BA, LJ & BHIA.
Ø When Eumycetoma is suspected – wash grains several times
in NS with antibiotics (Pn) & inoculate it on SDA with
antibiotics.
- actidione not added.
- incubated at 25° & 37°C
 Mycetoma: Treatment & prophylaxis

¨ Eumycetoma – Oral Ketoconazole & Itraconazole

.

¨ Actinomycetoma – Sulfonamides, Tetracyclines,

Streptomycin, Amoxycillin, Clavunate & Amikacin

¨ Protracted case – Surgery (debridement with skin graft)

SPOROTRICHOSIS
¨ Caused by Sporothrix schenckii, a dimorphic
fungus.

¨ Most common in USA.

¨ Associated with a variety of plants grasses, trees, sphagnum

moss, rose bushes

¨ Cause - thorn pricks or other minor injuries

¨ Mostly involves upper limbs
Sporothicosis: Pathogenesis & pathology

¨ Spreads from primary site to the

regional lymph nodes through
lymphatics

¨ Pyogranulomatous reaction

¨ Clinical features - Nodules on the

skin, subcutaneous tissue and in
the LNs which later soften &
ulcerate.
¨ Elicit delayed skin test – Lymphocutaneous sporotrichosis
“sporotrichin”
Laboratory Diagnosis

¨ Specimens
– pus, exudate & aspirate from nodules.
- curettage or swabs from open lesions.

Direct Examination
¨ Gram’s stain – gram +ve, irregularly stained yeast
cells.
Sprotrichosis: Direct Examination

¨ Tissues –
¤ organisms appear as cigar shaped
bodies (yeast cells) 3-5µ in
diameter.

¤ “Asteroid bodies” in the lesion:

central fungus cell surrounded by a
refractile eosinophilic halo, called “
Splendore-Hoeppli ” phenomenon :
due to immune complex deposition
around the rganism.
 Sprotrichosis: Culture

¨ Inoculated on 2 sets of SDA,

BHIA

¨ Incubated at 25°& 37°C

¨ Smear from Culture

Ø septate hyphae - very thin &
carry flower like clusters of small
conidia on delicate sterigmata
RHINOSPORIDIOSIS

¨ Caused by a hydrophilic protist,

Rhinosporidium seeberi

¨ 1st identified in Argentina, but majority of cases

occur in India and Sri Lanka.

¨ High incidence among people who frequently bath

along with domestic animals in ponds, tanks, lakes
RHINOSPORIDIOSIS: Clinical Features
¨ Chronic, recurrent granulomatous disease of mucous
membrane.

¨ Characterised by the development of friable

polyps in the nose, mouth or eye.

¨ Miscellaneous forms –
Buccal cavity,vagina,
vulva, penis, urethra
or rectum
Rhinosporidiosis: Laboratory Diagnosis

¨ Cannot be cultured

Direct Examination
¨ FNAC, Biopsy of lesion, Nasal washing
- Contains sporangia
filled with thousands of
sporangiospores(6-9µ)
embedded in a stroma
of connective tissue &
capillaries
Rhinosporidiosis: Treatment & Prophylaxis
¨ Radical Surgery:- Excision/ Electrocautery

¨ Medical therapy :- not useful

DDS (dapsone - widely used)

¨ Recurrences common
CHROMOBLASTOMYCOSIS
¨ Caused by dematiaceous (pigmented) fungi

¨ Confined to subcutaneous tissue of the feet &

lower legs
¨ Commonly seen in barefoot agricultural workers
& wood cutters.
¨ Commonest fungi - Phialophora verrucosa
Cladosporium sp.

¨ Also called as Verrucous dermatitis - Warty

cutaneous nodules which resembles flouts of
cauliflower

¨ Frequently ulcerates
CHROMOBLASTOMYCOSIS:
Laboratory Diagnosis
Direct Examination
Specimen - Dry crusty material from
the surface of the lesions
KOH
- dark brown, multicellular
structures, 5-12μ in diameter that
divide by transverse septation.

- Called sclerotic bodies, medlar

bodies, copper-pennies bodies or
muriform cells
Chromoblastomycosis: Direct examination

Histopathology

Ø Specimen - Tissue biopsy

Ø Stains - HE, Giemsa &
Fontana- Masson
Ø Sclerotic bodies very well
Sclerotic/ Medlar bodies - characteristic tissue
seen form facilitates survival of organism in host
tissues.
Treatment & Prophylaxis
¨ Poor response to available therapies.

¨ Cryotherapy, Thermotherapy, Laser therapy,

Chemotherapy and Surgery.

¨ Flucytosine (commonly used drug)

*Relapses are frequently seen

PHAEOHYPHOMYCOSIS
¨ Also caused by dematiaceous (pigmented) fungi
¨ Causes infection mainly in debilitated & immunodeficient hosts.
¨ Can cause cutaneous, subcutaneous as well as deep infections
¨ Clinical types:
1. Brain abscess

2. Subcutaneous or intramuscular lesions - abscess or cysts

3. Cutaneous lesions

• Diagnosis : KOH mount of cyst aspirates/ abscess – pigmented

hyphae

• Treatment - Local excision , I.V. AMB + Oral Flucytosine.

LOBOMYCOSIS
¨ Caused by Lacazia loboi
(Hydrophilic fungus) : exists only as
yeast cells.

¨ Involves exposed parts

¨ Presence of macule, papule, keloid,

verrucous, nodular lesions or plaques
& tumors.

¨ Lesions are painless with slight pruritis

¨ Treatment – excision/ cryosurgery

Laboratory Diagnosis
¨ Direct Examination of
curettage / biopsy -crushed
a. KOH w / m
b. CFW
- yeast-like cells
- form chain with cells joined by
bridges.
c. HE stain – may show
‘asteroid bodies’

• Culture – cannot be cultured

END.
Subcutaneous and Deep Mycoses will be discussed by Dr. Yee-Morata
To be discussed by:
Dr. Yee-Morata
CUTANEOUS
MYCOSES
DERMATOPHYTOSIS OR DERMATOMYCOSES
Cutaneous Mycoses
¨ Caused by fungi (Dermatophytes) that infect only
keratinized tissues – SKIN, HAIR and NAILS

¨ Secrete keratinase-degrades keratin

¨ Infections extends deep

into the epidermis.

q Rarely invade deeper tissue

 Ecology of Dermatophytes
To determine the source of infection
Anthropophilic üAssociated with humans only.
üPerson -to-person transmission through contaminated
objects (comb, hat, etc.)
üElicit relatively mild and chronic infections
üProduce few in conidia in culture
Zoophilic üAssociated with animals.
üDirect transmission to humans by close contact with animals.
üProduce more acute inflammatory infections that tend to
resolve quickly
Geophilic üUsually found in soil.
üTransmitted to humans by direct exposure.
üProduce more acute inflammatory infections that tend to
resolve quickly

Geographic Distribution : WORLDWIDE

 Common Etiology
Genera Site of infection
restricted to non-viable skin; unable to grow at 370C or in the presence of serum
Dermatophytes
1. Trichophyton
T. rubrum T. tonsurans
T. mentagrophytes T.equinum (horse) Hair, skin and nails
T. verrocosum (cattle)

2. Miscrosporon
M. gypseum (most common) Hair and skin
M. canis (dogs and cats)
M. gallinae (fowl)
M. nanum (pigs)
3. Epidermophyton Skin and nails
E. floccosum

Dermatomycoses
üare cutaneous infections due to other fungi
üCandida spp – most common
Morphology and Identification

¨ Common dermatophytes identified due to colonial

appearance and microscopic morphology

¨ Growth for 2 weeks at 250C on Sabouraud’s

dextrose agar (SDA)
Trichophyton species
T. mentagrophytes T. rubrum
Colonies are cottony to granular Colonies are white and cottony surface & deep
red non-diffusable pigment

T. tonsurans
Flat, powdery to velvety colony;
reddish brown on reverse
 Trichophyton species
T. mentagrophytes T. rubrum T. tonsurans

Makes both macroconidia and
microconidia
üMicroconidia – globose and
in clusters “grapelike” or
engrape
üMacroconidia – thin walled,
smooth and cigar-shaped.
üProduce 4-8 celled cylindrical üMacroconidia are variable
macroconidia in shape
üClavate or peg-shaped Club-shaped
macroconidia, side of hyphae
“Birds on fence”
Microsporum species
Macroconidia
Microsporum gypseum

üPowdery granular colonies

üFusiform, moderately thick-

walled conidia, rounded tips

Microsporum canis

üFluffy and white colonies

with the reverse side
forming lemon-yellow
pigment
üSpindle shaped
macroconidia with
echinulate thick-walled; with
tapering spiny distal end.
Epidermophyton floccosum
Produces only macroconidia, smooth walled, clavate
Flat velvety colonies, with tan to olive 2-4 celled, and formed small clusters
green tinge Macroconidia only
Clinical Features
Mycoses Location of Lesions Clinical Features Fungi Responsible
Tinea corporis Non-hairy, smooth Circular patches with üTrichopyton
skin advancing red, rubrum
vesiculated border & üEpidermophyton
central scaling, pruritic floccosum

Tinea pedis Interdigitate spaces Acute- itching, red üTrichopyton

(Athletes foot) on feet of persons vesicular; rubrum,
wearing shoes Chronic – itching, üTrichopyton
scaling and fissures mentagrophytes
üEpidermophyton
floccosum
Clinical Features
Mycoses Location of Lesions Clinical Features Fungi Responsible
Tinea cruris Groin Eryhtematous üTrichopyton
“jock itch” scaling lesion in rubrum,
intertriginous area; üTrichopyton
pruritic mentagrophytes
üEpidermophyton
floccosum

Tinea capitis Scalp, hair. Circular bald üTrichopyton

üEndothrix: patches with short mentagrophytes
fungus inside hair stubs or broken üTrichopyton
hair shaft hair within hair tonsurans
üEctothrix: fungus follicles. Kerion rare üMicrosporum
on surface of canis
hair Microsporum –
infected hair
fluoresce
Clinical Features
Mycoses Location of Lesions Clinical Features Fungi Responsible
Tinea barbae Beard hair Erythematous lesions üTrichopyton
rubrum,
üTrichopyton
mentagrophytes
üEpidermophyton
floccosum

Tinea ungium Nail Nails thickened or üTrichopyton

“Onychomycosis” crumbling distally; rubrum,
discolored; lusterless. üTrichopyton
Usually associated mentagrophytes
with Tinea pedis. üEpidermophyton
floccosum
Diagnosis

¨ Microscopic examination
¤ 10-20% Potassium Hydroxide (KOH)
¤ Calcaflour white

¤ Wood’s Light

¨ Culture
¤ Sabouraud’s agar slants
¤ Mold agar

¤ Incubated for 1-4 weeks at room temperature

Treatment
Disease /condition Treatment
Tinea capitis üOral administration of Griseofulvin or
Terbinafine for weeks
üFrequent shampoos
üMiconazole cream and other topicals for weeks
- Ketokonazole, Itraconazole

Tinea corporis, Tinea pedis, Related üTopicals for 2- 4 weeks

infections - Itraconazole, Terbinafine
- Miconazole nitrate, Tolnaflate,
Cotrimazole
üOral Griseofulvin

Tinea ungium üOral Itraconazole or terbinafine for months

üSurgical removal of nail
DEEP (SYSTEMIC)
MYSCOSES
Deep Mycoses
¨ Deep within the body:
Ø Affects a number of organs or tissues

¨ Usually soil fungi

¨ Route of transmission – Spore Inhalation

Ø Starts in the lungs à spread to other body tissues

q Not Contagious
Deep Mycoses

Primary/Endemic Opportunistic
¨ establish infection in a ¨ require a compromised host
normal/healthy host in order to establish
infection
¨ usually gain access to the
host via the respiratory ¨ invade via the respiratory
tract tract, alimentary tract, or
intravascular devices.
 Primary/Endemic Mycoses
Geographically restricted to specific areas of endemicity

Primary/Endemic Mycoses Etiology Ecology Geographic Distribution

Coccidioidomycosis üCoccidioides Soil, rodents üSemi-arid regions;

Posadassii Soutwest United
üCoccidioides States, Mexico,
immitis Central and America
Histoplasmosis üHistoplasma Avian and bat üGlobal; endemic Ohio,
“most prevalent” capsulatum habitats (guano); Missouri and
alkaline soil Mississippi River
Valleys; Central and
South America
Blastomycosis üBlastomyces Unknown ü Mississippi, Ohio and
dermatitidis Riverbanks? St. Lawrence River
Valleys
Paraccocidioidomycosis üParaccocidioides Unknown üCentral and South
brasielinese Soil? America
Primary/Endemic Mycoses

¨ Caused by Dimorphic fungi

n Fungal dimorphism is the morphological and physiological conversion of certain
fungi from one phenotype to another when such fungi change from one
environment to another.

¨ Infection is initiated in the lungs following inhalation of the

conidia.

¨ Mostly asymptomatic or mild and resolve without treatment.

¨ Not transmissible among humans or other animals.

Coccidioides posadasii
 Etiology Disease Caused Morphology & Dissemination
Identification
Coccidioides -“Valley Fever”, üWhite to tan cottony ümay suffer dissemination to the
posadasii/ -San Joaquin colony brain, bone, and other sites
Coccidioides Valley Fever” üHyphae form chains of
immitis -“Desert arthroconidia
Rheumatisms” (arthrospores)
üSpherules with
endospores
Histoplasma Histoplasmosis üHyaline septate that üto hilar and mediastinal lymph
capsulatum produce large nodes, spleen, liver, bone marrow,
spherical and brain
macroconidia with
peripheral projections.
Blastomycosis Pyro-granulomatous Branching hyhae bearing üDissemination occurs most
dermatitides leaiona spherical, ovoid to pyriform commonly to the skin, bone, and, in
conidia à slender terminal males, prostate.
or lateral conidiophore;
thick walled multinucleated
, broad base blastoconidia
Parracocidioid Yeast with multiple buds üto skin and mucocutaneous tissue,
es brasiliense “pilots wheel”. LN, Liver, Spleen, liver, adrenal etc
 Coccidioimycoses Histoplasmosis Blastomycosis Paracoccidioidomy
cosis
Specimen CSF, Exudates from Soutum, urine, scrapings Sputum, pus, Putum, exudates,
lesions, Urine Sputum, from skin lesion, bone exudates, urine and tissue biopsies
Blood and Tissue marrow aspirates tissue biopsies

Tests 1. Microscopic ID 1. Microscopic ID 1. Microsopic ID 1. Microscopic ID

KOH and Calcaflour Gomori Methenamine 2. Culture 2. Culture
White - Identification Stain (GMS), Periodic 3. PCR for specific 3. Serology for
of endospores and Acid Schiff (PAS), DNA sequence antibodies
spherules Calcaflour White, 4. Skin test
2. Culture on SDA Giemsa Paracoccidioidin
3.Serology for 2. Culture
antibodies 3.PCR for specific DNA
4. Skin tests sequences
Coccidioidin/ 4.Serology for antibodies
Spherulin 5. Skin test Histoplasmin

Treatment Supportive treatment Supportive treatment Itraconazole Itraconazole,

Oral itraconazole Itraconazole Amphotericin B Ketoconazole &
Amphotericin B Amphotericin B Trimethoprim –
Surgical Resection sulfameta-xazole
Amphotericin B
References:
¨ Jawetz, M. A. (2013). Medical microbiology (26th ed). United States
of America: TheMcGraw-Hill Companies.
¨ Murray, P R, Rosenthal, K and Pfaller, M.A. (2021). Medical
microbiology (9th ed). USA: Elsevier
¨ Torok, M.E., Moran, E, & Cooke, FJ. (2017). Oxford handbook of
infectious diseases and microbiology (2nd ed). United Kingdom:
Oxford University Press
¨ Anon. (nd). Ultimate reviewer in microbiology and parasitology for
physician licensure examination
END of MYCOLOGY
Credits: Dr. Marvi G. Dulnuan-Niog and Prof. Carl Jay B. Bregente