1.

Morfologi Fungi
 Dinding sel: mengandung chitin
 Membran sel: mengandung ergosterol
 Mikroskopik: memiliki 2 macam morfologi:
 yeast – berbentuk bulat-oval
 hyphae – berbentuk filamen , disebut juga:molds
 Beberapa fungi mempunyai kedua fase tersebut
 disebut sbg fungi dimorphic
Dimorfisme dipengaruhi suhu:
 37oC  Yeast
 25oC  Mold / hifa

2
 Yeast
Uniseluler
Nonfilamentous
biasanya berbentuk oval/spheris.
Bereproduksi secara mitosis.
Hyphae / Molds
 jamur berfilamen, multiseluler
 Hiphae:
 Hifa bersepta
 Hifa tidak bersepta
 Mycelium: Gabungan dari hifa
Morfologi Hiphae / Molds
Mycelium: Large, Visible Mass of Hyphae
Sifat Fungi
 heterotrophic
 Mayoritas tidak membahayakan, hidup
secara saprofit pada tumbuhan atau hewan
yang mati
 Optimal growth temperature 20o-40oC
 Beberapa mrpkn parasit yang hidup pada
jaringan organisme lain  infeksi jamur
mycoses

7
 Klasifikasi Infeksi Jamur Secara Klinis:
Superficial Cutaneus Subcutaneus Sistemic Opportunistic
•Pityriasis •Tinea pedis •Chromoblastomy •Aspergillosis •Aspergillosis
versicolor •Tinea cosis •Blastomycosis •Candidosis
•Tinea niegra unguinum •Sporothricosis •Candidosis •Cryptococcosis
•Piedra •Tinea corporis •Mycetoma •Coccidioido •Zygomycosis
•Tinea cruris mycosis •Pneumocystosis
•Tinea manus •Histoplasmosis
•Tinea capitis •Cryptococcosis
•Tinea barbae •Paracoccidioido
mycosis
•Zygomycosis
1. Superfisial mycosis
Disease Causative organisms Incidence Clinical Manifestation
Pityriasis
Malassezia furfur Hipopigmented
versicolor Common
macule

Exophiala
Tinea nigra Rare black macules
werneckii
Cream colored nodule on
White piedra Trichosporon beigelii Rare
hair shaft
Black nodules on hair
Black piedra Piedraia hortae Rare
shaft
2. Cutaneus Mycosis

Disease Causative organisms Incidence

Dermatophytosis
Dermatophytes (Microsporum,
Ringworm of the scalp, Common
Trichophyton, Epidermophyton)
glabrous skin and nails.

Candidiasis of skin and Candida albicans and related

Common
and nails. species.
Dermatophytosis

Disease Symptoms
Tinea capitis ringworm lesion of scalp

Tinea corporis ringworm lesion of trunk, arms, legs

Tinea manus ringworm lesion of hand

Tinea cruris "jock itch" ringworm lesion of groin

Tinea pedis"athlete's foot" ringworm lesion of foot

Tinea barbae (barber itch) Ringworm of the beard

Tinea unguium infection of nails

Ectothrix infection of hair shaft surface

Endothrix infection of hair shaft interior

 Ringkasan
Organisme Manifestasi klinik
Penyakit
penyebab
Sporothrix Nodule pada temat inokulasi yang
Sporotrichosis
schenckii mengikuti aliran limfe
Fonsecaea, Nodule verrucous / plaque/cauliflower
Chromoblastomycosis
Phialophora, nodul pada tempat inokulasi
Cladosporium etc.
Pseudallescheria, sinus yang mengeluarkan nanah dan
Madurella, granul / grains seperti butiran pasir
Mycotic mycetoma
Acremonium, yang mengandung kuman
Exophiala etc.
Polip pada hidung, infeksi kelenjar air
Rhinosporidium mata, rectum dan vagina
Rhinosporidiosis
seberii

Bentukan nodul atau keloid pada fase

Loboa loboi atau awal nodul tidak terfiksir  nodul
Lobomycosis
Lacazia meluas dan membesar secara perlahan
4. Systemic Mycoses
Disease Causative organisms Incidence
Histoplasma
Histoplasmosis capsulatum Rare*
Histoplasma dubosii
Coccidioidomycosis Coccidioides immitis Rare*
Blastomyces
Blastomycosis Rare*
dermatitidis
Paracoccidioides
Paracoccidioidomycosis Rare*
brasiliensis
Sporotrichosis Sporothrix schenkii Rare

*more common in endemic areas.

Infeksi Oportunistik
Disease Causative organisms Incidence

Candida albicans and

Candidiasis Common
related species.

Cryptococcosis Cryptococcus neoformans Rare/Common

Aspergillosis Aspergillus fumigatus etc. Rare

Rhizopus, Mucor,
Zygomycosis
Rhizomucor, Rare
(Mucormycosis)
Absidia etc.

Pneumocystosis Pneumocystis carinii Rare

CANDIDA
 Epidemiology
Normal flora of the skin, mucous membranes, and
gastrointestinal tract
MOST COMMON invasive fungal infection in
immunocompromised patients.
4th most common cause of nosocomial blood stream infection.
Species implicated in human disease most often:
– C. albicans
– C. tropicalis
– C. parapsilosis
– C. krusei
– C. glabrata
– C. lusitaniae
2
Morphology
• Oval budding yeast cells
(3–6 µm in size)
• Pseudohyphae
buds that continue to grow but fail to detach,
producing chains of elongated cells that are pinched
or constricted at the septations between cells.
• C. albicans : in addition to yeasts and pseudohyphae,
it can also produce true hyphae
• C. glabrata is unique only yeast cells and no
pseudohyphal forms.
 Predisposing Factors (Immunologic)
Cancer (esp. hematological malignancy)
Organ Transplantation (bone marrow, liver,
lung, kidney)
Cellular Immune Dysfunction (AIDS)

5
 Predisposing Factors
(Non-Immunologic)
• Chemotherapy (cytotoxic) - mucosal damage
of GI, respiratory, GU tracts
• Antibiotics - Broad spectrum; loss of normal
flora
• Invasive devices - breach skin/mucosal
defences, i.e. intravenous lines, urinary
catheters, tracheostomies
• Invasive procedures - surgery
6
 Pathogenesis of Candida albicans

Surface galactomannan on the yeast may bind to fibronectin covering the epithelial cell or
to elements of the extracellular matrix (ECM) when the epithelial surface is lost or when
the candida invade beyond it. Invasion is associated with formation of hyphae and
production of proteinases, which may digest tissue elements.
 Pathogenesis
• Shift from yeast to hyphae is associated with
invasion
• Hwp 1 (hyphal wall protein)  binds to epithelial
cells (found only on the surface of germtube and
hyphae)
• Hyphae produce proteinase and phospholipase
 digest tissue.
• Antimicrobial and immunosuppresion increase
risk
• Receptors bind C3 in an antiopsonic manner
 Clinical Manifestation
• Mucous membrane infections
– Thrush (oropharyngeal)
– Esophagitis
– Vaginitis
• Cutaneous infections
– Paronychia (skin around nail bed)
– Onychomycosis (nails)
– Diaper rash
– Chronic mucotaneous candidiasis
• children with T-cell abnormality

9
 Mucosal candidiasis

Oral thrush
Vaginal candidiasis
10
Cutaneous candidiasis

11
Cutaneous candidiasis

Onychomycosis and paronychia

13
 Clinical Manifestation
• Urinary tract infection
• Fungemia
• Disseminated (systemic, invasive) infection
– Immunocompromised patients
– Liver and spleen, Kidneys, Skin, Brain, Lungs,
Bone

15
 Laboratory Diagnosis
• Specimens : Blood, tissue (biopsy or autopsy),
sterile fluid, urine, CSF, skin, respiratory
secretions
• Microscopy (direct on specimen)
– Gram stain, Calcofluor, KOH
• Histopathology (tissues)
– H E - stain poorly
– GMS - stain well

16
Candida species

Top: Calcofluor White x400: Yeast

and pseudohyphae

Bottom: Gram stain x1000: Yeast

and pseudohyphae

17
Pathology of disseminated candidiasis

Yeast cells and septate hyphae

(GMS staining)
18
Pathology of disseminated candidiasis

Blastoconidia and pseudohyphae

(PAS staining)
19
 Laboratory Diagnosis
• Culture
– Colony morphology
• White, smooth, creamy
– Laboratory identification
• Unique color on chromagar
• Chlamydospore production (terminal vesicle) on nutritionally deficient
media (Cornmeal Tween 80/Oxgall agar)  C. albicans (+)
• Germ tube production (in horse serum)
– beginning of true hypha (no constriction)
» C. albicans - Germ tube positive
» Other Candida - Germ tube negative
• Carbohydrate assimilation and fermentation (API 20C, Vitek2, RapID and
reference)

20
 SDA Chrom Agar

Morphology:
Creamy white yeast,
may be dull
Yeast Identification:
Carbohydrat Assimilation (API 20 C AUX)

22
 Germ tube test

inoculation of yeast in horse serum

incubated at 370C for 2 to 3 hours

 Germ Tube: Positive

Germ tube is a continuous filament
germinating from the yeast cell without
constriction at the point of attachment.
e.g. C. albicans, C. dubliniensis

 Germ Tube: Negative

Shows constriction at the attachment site
e.g. other Candida species
23
GERM TUBES

GERM TUBES
 Candida albicans

 Oxgall Agar
large round and thick
walled chlamydospores

x400 x1000

25
 Laboratory Diagnosis

• Candida antigen, antibody and

metabolite detection
– NOT useful in routine practice
– Low sensitivity and specificity

26
 Treatment
• Antifungal therapy
– Amphotericin B
– Azoles (fluconazole, itraconazole, voriconazole,
posaconazole)
– Flucytosine
– Echinocandins (caspofungin, micafungin)
• Remove infected intravenous lines
• Primary (inherent) resistance
– C. lusitaniae (amphotericin B)
– C. glabrata (fluconazole)
– C. krusei (fluconazole)

27
Pneumocystis jiroveci
 Introduction
• Spores morphologically resemble protozoa
• Cell wall is thin, but glucan and chitin
elements are present
• rRNA and mitochondrial gene sequences are
homologous with fungi
• Lack of ergosterol  insensitive to antifungal
drug that target ergosterol biosynsthesis
 Life cycle
(two stages: trophic form and cystic form)
 Epidemiology
• Worldwide distribution in humans and
animals (rats, mice, dogs, cats, rabbits).
• P. jiroveci is the human species (P. carinii is found
only in rats)
• Antibodies are common
• Primary infection, reinfection, reactivation.
• Pneumonia is a complication of
immunodeficient states
• Airborne transmission is probable
 Pathogenesis and Pathology
• Low virulence seldom produce disease in host with
normal T-lymphocyte function. Low CD4+ T
lymphocyte counts (<200 cells/mm3) increase the risk
in AIDS
• P jiroveci is an extracellular pathogen. Growth in the
lung is limited to the surfactant layer above alveolar
epithelium
• Major Surface Glycoprotein (MSG) on surface of P.
carinii attaches to pneumocytes
• Alveoli are filled with foamy exudate (consist of:
desquamated alveolar cell, organism, monocytes and
fluid)  blockage oxygen exchange  cyanosis
 Clinical Manifestation
• Low grade fever
• Nonproductive cough, dyspnea, and cyanosis
• Alveolar infiltrates
• Extrapulmonary lesions are seen in AIDS
 Diagnosis
• Specimen:
– Sputum  low diagnostic yield
– BAL
– lung biopsy tissue
• Organism can not be cultured
• Staining: Giemsa, toluidin blue, HE, silver stain
(GMS), Immunohistochemistry.
In smear of rat lung, cyst containing intracystic bodies is seen. The wall of the
cyst is not stained with Giemsa, but the intracystic bodies are clearly seen
(Giemsa stain, 1000x).
Cyst of Pneumocystis carinii (Toluidine blue stain, 1000x).
 An HE stain of a rat lung infected with P. carinii. It does not show any
organisms, but shows the proteinaceous exudate (Honeycomb appearance)
which results from Pneumocystis infection, and ultimately causes reduced gas
exchange
Cluster of Pneumocystis cysts (methenamine silver stain,
× 1250).
Cyst of Pneumocystic Carinii in alveolar cast stained with
immunohistochemistry method
 Treatment and Pevention
• Trimetoprim-sulfametoxazole is treatment of
choice
• Prophylactic treatment if CD4 count is low
(<200)
CRYPTOCOCCAL INFECTIONS
(CRYPTOCOCCOSIS)
Microbiology of Cryptococcus
• Encapsulated yeast
• Cryptococcus spp., possess urease, an enzyme that hydrolyzes urea to
ammonia and increases the ambient pH.
• Patogenic species: 5 serotypes (A-D and AD)
• C. neoformans (may posses serotype A,D, or AD)
• C. gattii (may posses serotype B or C)
• Life cycle
• Asexual: yeast that reproduce by budding
• Human infections
• Sexual: only seen in the laboratory
Ecology and Epidemiology
• World wide
• C. neoformans associated with bird droppings
• C. gatti not associated with birds, associated with eucalyptus trees
• Generally an infection of immunocompromised but can cause clinical
disease in healthy persons
• Decreased Cell-mediated immunity
• AIDS – CD 4 usually < 100
• Prolonged corticosteroids
• Organ transplant
• The pathogenesis of cryptococcosis is determined by three broad
factors:
(1) the status of the host defenses;
(2) the virulence of the strain of C. neoformans;
(3) the size of the inoculum
Pathogenesis
• susceptible host inhalation of infectious propagules from
environment contact the alveolar macrophages in alveoli recruit
other inflammatory cells through cytokines or chemokines, Th1
response  elicit granulomatous inflammation.
• The infection can then take one of three pathways:
1. In an immunosuppressed host, the yeast continues to proliferate and
disseminate, causing clinical disease.
2. The effective immune response completely eliminates the yeast from the
host.
3. The yeasts produce a small lung–lymph node complex and remain dormant in
tissues but are not dead (common occurrence)
Pathogenicity
• Capsule – polysaccharide
• Melanin  act as antioxidant, support cell wal integrity, protection
from temperature, interference T-cell response,abrogation antibody-
mediated phagocytosis
• High temperature growth (37ºC)
Clinical Presentations
• Pulmonary
• Asymptomatic nodule
• Symptomatic: not distinguishable from other causes
• History, Physical Examination, routine laboratory testing does not produce features
peculiarly suggestive of cryptococcal infection
Cutaneous
Disseminated disease
Looks similar to molluscum contageosum
Clinical Presentations
• Cryptococcal Meningitis
• Typical
• Subacute onset of fever and headache
• Photophobia and/or meningeal signs in only 25%
• Less typical
• Seizures
• Confusion
• Progressive dementia
• Visual or hearing impairment
Summary of Diagnostic Options

• Culture
• White mucoid colonies within 48hours
• Blood cultures often (+) in immunosuppressed patients

• Tissue
• Silver or mucicarmine stain
• India Ink for CSF Indian ink
• Cryptococcal antigen (capsular antigen)
• can be performed on cerebrospinal fluid, serum and urine.
• The latex slide agglutination test or enzyme immunoassay
positive in 90% of patients with cryptococcal meningitis

Silver stain
Antifungal theraphy
DERMATOPHYT INFECTION
(DERMATOPHYTOSIS)
DERMATOPHYTOSIS
(=Tinea = Ringworm)
• Infection of the skin, hair or nails caused
by dermatophytes
Dermatophyte Skin Hair Nails

Microsporum X X

Trichophyton X X X

Epidermophyton X X
DERMATOPHYTES
• Digest keratin by their keratinases
• Resistant to cycloheximide
• Classified into three groups depending on their usual
habitat
Epidemiology
• Anthropophilic
• Man : Trichophyton rubrum
• Zoophilic
Animals:
• Microsporum canis: cats and dogs
• Microsporum nanum: swine
• Trichophyton verrucosum: horse and swine
• Geophilic
• Soil : Microsporum gypseum
DERMATOPHYTOSIS
Pathogenesis and Immunity
• Contact and trauma
• Moisture
• Crowded living conditions
• Cellular immunodeficiency (chronic inf.)
DERMATOPHYTOSIS
Clinical Classification
• Infection is named according to the
anatomic location involved:
a) Tinea barbae
b) Tinea corporis
c) Tinea capitis
d) Tinea cruris (Jock itch)
e) Tinea pedis (Athlete’s foot)
f) Tinea manuum
g) Tinea unguium
Clinical classification of Dermatophytosis

Tinea cruris Tinea barbae

Tinea Unguinum Tinea corporis

DERMATOPHYTOSIS
Clinical manifestations
Skin:
• Circular, dry, erythematous, scaly, itchy lesions
Hair:
• Typical lesions,”kerion”, scarring, “alopecia”
Nail:
• Thickened, deformed, friable, discolored nails, subungual
debris accumulation
Favus (Tinea favosa)
• characterized by scutula
 Clinical manifestationof Dermatophytosis
Tinea capitis: kerion, grey patch, black dot

"Kerion" : T. verrucosum & T .mentagrophytes Grey patch: M. canis.

Black dot: T. tonsurans dan T. violaceum Tinea favosa (Favus): T. schoenleinii

Tinea capitis
• Hair
• Ectothrix
• Endothrix
Transmission
• Close human contact
• Sharing clothes, combs, brushes,
towels, bedsheets (Indirect)
• Animal-to-human contact (Zoophilic)
Laboratory Diagnosis
• Specimen collection
• Direct examination
• Culture
• Identification
Laboratory Diagnosis: Specimen Collection

• Hair
• Plucked, not cut, from edge of lesion
• Skin
• Wash, scrape from margin of lesion
• Nails
• Scrapings from nail bed or infected area
• Transport in sterile petri dish
Laboratory Diagnosis
Direct Examination
• Examine specimen for fungal elements
• 10% KOH
preparation
• Calcofluor
white stain
Laboratory Diagnosis
Specimen processing
• Hair
• Cut into short segments
• Nails
• Mince into small pieces
Laboratory Diagnosis
Culture Media

• Select two media types

• General purpose – Sabouraud’s agar Sabouroud
• Selective – Mycosel agar, Dermatophyt Test Medium agar

• Antibiotics
• Gentamicin: inhibits normal bacterial flora
• Cycloheximide: inhibits saprophytic fungi

DTM
Laboratory Diagnosis
Culture Growth Requirements

• Place specimen pieces on culture media

• Incubate at 30°C in ambient (room) air
• Growth at 3 days to 3 weeks
• Examine plates frequently for 4 weeks
Laboratory Diagnosis
Identification
• Colony morphology
• Microscopic morphology
Laboratory Diagnosis
Identification

• Physiologic tests
– Rice grain media
• Urea hydrolysis
• Hair perforation – Vitamin requirements
Microscopic examination: Microsporum,
Epidermophyton, and Trichophyton species

• Microsporum has numerous thick-walled macroconidia with

RARE microconidia
• Epidermophyton has numerous club-shaped macroconidia
hanging out in groups of 2-3 with NO microconidia
• Trichophyton has thin-walled macroconidia and MANY
microconidia.
Identification: Microsporum species

Characteristic appearance of the macroconidia, and the

general appearance of the hyphae (such as pectinate
bodies). As a group, Microsporum have few to absent
microconidia.
Microsporum canis
• Colony Microscopic
morphology:
morphology:
spinde shape
macroconidia,
rough surface
especially on
the knob

surface reverse
 Microsporum gypseum

Colony morphology: • Microscopic

morphology:
 Microsporum audouinii
• Microscopic morphology:
• Colony comblike hyphae / pectinate
morphology: hyphae
 Epidermophyton floccosum

Microscopic morphology:
Colony morphology: No microconidia, clubshape macrononidia with
rounded end
Trichophyton rubrum

Microscopic morphology:
Colony morphology:
Teardrop-shaped microconidia (2-
3x3-5 µm)
Trichophyton rubrum
• Physiological tests
• Urea: negative
• Hair perforation: negative
Trichophyton mentagrophytes
• Colony morphology:

Downy Granular Velvet

Trichophyton mentagrophytes
• Microscopic
morphology:
spiral hyphae
Trichophyton mentagrophytes
• Physiologic tests:
• Urea: positive
• Hair perforation:
positive
DERMATOPHYTOSIS
Treatment

• Topical
Miconazole, clotrimazole,
econazole, terbinafine...
• Oral
Griseofulvin
Ketaconazole
Itraconazole
Terbinafine
SUPERFICIAL MYCOSIS
 1. Superfisial mycosis

Fungal infection on superficial of the skin or

hair shaft (stratum corneum)
No living tissue is invaded
No inflamation or cellular response
Patients are often unaware of their condition
 Pityriasis versicolor
• Chronic mild superficial infection of the
stratum corneum
• Caused by: Malassezia furfur
• Host responses (scaling, inflammation, and
irritation) are minimal.
• Discrete, serpentine, hyper- or
hypopigmented maculae occur on the skin,
usually on the chest, upper back, arms, or
abdomen.
• Species of Malassezia are considered part of
the microbial flora  can be isolated from
normal skin and scalp.
• They have been implicated as a cause of or
contributor to seborrheic dermatitis, or
dandruff.
 LABORATORY DIAGNOSIS
• 1. Clinical material: Skin scrapings from
patients with superficial lesions, blood from
patients with suspected fungaemia.
• 2. Direct Microscopy:
• Skin scrapings  10% KOH, glycerol and
Parker ink solution  spagety and meat ball
(yeast and pseudohyphae)
• Culture preparations are usually not
necessary.
M. furfur on skin scrapping specimen with GMS staining
(left) and KOH staining (right):
spagety and meatballs appearance
Culture
• only necessary in suspected fungaemia
• M. furfur is a lipophilic yeastin vitro growth must
be stimulated by natural oils or other fatty
substances.
• Medium:
– Sabouraud's dextrose agar with olive oil
– or Dixon's agar (contains glycerol mono-oleate)
• Rapid growth
(best growth 37 C, 3 days)
 Tinea Nigra (Tinea Nigra Palmaris)
• A superficial chronic and asymptomatic infection
of the stratum corneum
• caused by: the dematiaceous fungus Hortaea
(Exophiala) werneckii.
• More prevalent in warm coastal regions and
among young women.
• The lesions appear as a
dark (brown to black)
discoloration, often on
the palm.
 Hortaea (Exophiala) werneckii
• a common saprophytic fungus
• believed to occur in soil, compost, humus and
on wood in humid tropical and sub-tropical
regions.
 LABORATORY DIAGNOSIS
• Diagnosis:
– Specimen: Skin scrapings
– Staining KOH
Branched, septate hyphae and budding yeast cells
(2-celled yeast cells) with melaninized cell walls.
– Cultur: not necessary
 Black piedra
• Nodular infection of the hair shaft
• Caused by Piedraia hortai
• Axillary, pubic, beard, and scalp hair may be
infected.
• Treatment :
– removal of hair
– topical antifungal
agent
 LABORATORY DIAGNOSIS
• Specimen: hair with hard black nodule
• Staining with 10%KOH
• Culture: hair shaftSabouraud’s dextrose
agar  2-3 weeks black to brown colony
microscopic : septate hyphae with
chlamydoconidia appearance.
 White piedra
• larger, softer, yellowish nodules on the hairs
• Caused by: Trichosporon species
 LABORATORY DIAGNOSIS
• Specimen: hair with soft white nodule
• Staining with 10%KOH
• Culture: hair shaftSabouraud’s dextrose
agar  2-3 weeks yellowish to deep cream
colored, smooth coloniesmikros: hifa,
pseudohifa, arthroconidia, blastoconidia
 RANGKUMAN
Disease Causative organisms Incidence Clinical Manifestation
Pityriasis
Malassezia furfur
versicolor Common Hipopigmented macule

Tinea nigra Exophiala werneckii Rare black macules

Cream colored nodule on
White piedra Trichosporon beigelii Rare
hair shaft
Black piedra Piedraia hortae Rare Black nodules on hair shaft
Subcutaneus mycosis
 Infeksi jamur pada jaringan subkutan.
 Disebabkan oleh jamur saprofit yang hidup pada
tanah atau tanaman.
 Infeksi terjadi karena masuknya spora atau
micelium pada luka kulit.
 Dapat menyebar melalui pembuluh limfe.
SUBCUTANEUS MYCOSIS
 Sporotrichosis
 Chromoblastomycosis
 Mycetoma
 Rhinosporidiosis
 Lobomycosis
SPOROTRICHOSIS
 Penyebab: Jamur Sporotrix schenckii (jamur dimorfik)
 Disebut juga Rose gardener disease
 Manifestasi klinik:
 Cutaneus sporotrichosis (sering)
 Biasanya menyerang pada pekerjaan yang berhubungan dengan
tanah (misal: berkebun dan bercocok tanam)

 Systemic sporotrichosis (jarang)

 Dpt terjadi penyebaran ke tulang, meningen dan paru paru. Terjadi
pada pasien dgn faktor resiko, misal: DM, HIV, peminum alkohol.
Manifestasi klinik

Ciri khas: nodul subkutan yang mengikuti aliran limfe

Diagnosis Laboratorium
 Spesimen: biopsi
 Diagnosis
 Histopatologi jaringan
 Kultur: tumbuh dalam waktu 4 hari
 Suhu 25–30 C: fase mycelium
 Suhu 35-37 C : fase yeast
Histopatologi
Kultur
Chromoblastomycosis
 Penyebab: Fonsecaea pedrosoi, Fonsecaea compacta,
Phialophora verrucosa, Cladosporium carrionii
 Manifestasi klinik:
 Nodule verrucous atau plaque
 Sering terjadi di daerah tropis yang lembab
 Kebanyakan pada kaki, didahului dgn luka ( bisa pada
bagian tubuh lain)
 Walaupun jarang, dapat menyerang otak (menyebar
secara hematogen)
Manifestasi klinik

Tampak nodul verucous

Diagnosis Laboratorium
 Spesimen : kerokan kulit dan/atau biopsi jaringan
 Diagnosis:
 Pewarnaan langsung: KOH 10% & tinta parker,
calcofluor white stain
 Histopatologi : HE, PAS, GMS
 Kultur : Sauboroud dextrose agar pada suhu ruang
Pewarnaan langsung

Pewarnaan langsung dari kerokan kulit menunjukkan

sclerotic bodies yang berwarna coklat
Histopatologi

Pada Jaringan tampak gambaran sclerotic bodies , yg mrpkn gambaran khas

chromoblastomycosis.
Scerotic bodies adalah sel yang single/berkelompok , berdinding tebal. Pada
pewarnaan HE (kiri): berwarna coklat, pewarnaan GMS(kanan): berwarna hitam
Kultur
 Identifikasi dilakukan dengan mengamati morfologi
makroskopik dan mikroskopik (tipe konidia)
 Matur : 14 – 28 hari
Type Cladosporium
Type Rhinocladiella
Type Phialophora
Cladosporium carionii
Mycetoma (Madura foot)
 Penyebab:
 Jamur (Eumycotic mycetoma)
 Madurella mycetomatis
 Exophiala jeanselmei
 Pseudallescheria boydii
 Madurella grisea
 Kuman yang mirip jamur (Actinomycotic mycetoma)
 Nocardia
 Actinomadura madurae
 Streptomyces somaliensis
 Gx klinis:
 infeksi subkutan yang membengkak seperti tumor dan adanya sinus
yang mengeluarkan nanah dan granul / grains seperti butiran pasir
yang mengandung kuman
 Ditemukannya granule/grains sangat penting untuk diagnosa
 bbrp jamur/bakteri penyebab mycetoma dapat di isolasi dari tanah/
pohon.
Manifestasi klinik
Mycetoma showing numerous draining
Excised mycetoma showing a
sinuses. There is destruction of bone,
draining sinus (cut open in
distortion of the foot, and hyperplasia at the
this preparation) containing
openings of the sinus tracts. (Courtesy John
black grains.
Rippon USA).
Diagnosis Laboratorium
 Spesimen
 cairan sinus yang mengandung granule
 Biopsi jaringan atau eksisi sinus

 Pemeriksaan:
 Histopatologi: HE, PAS, GMS
 Kultur : Sabouroud dextrose agar, suhu ruang
Histopatologi GMS 1000x
HE 450x

GMS 450x

Hyphae dan Chlamydoconidia

baru terlihat pada perbesaran
1000x
Rhinosporidiosis
 Penyebab: Rhinosporidium seberii
 70 % menginfeksi hidung
 Dapat juga menginfeksi conjunctiva, kelenjar air mata,
larinx, mukosa mulut, kulit, vagina dan rectum.
 Banyak di dapatkan di daerah tropis
 Mekanisme penyebarannya tidak diketahui
Gambaran klinik
 Berupa polip yang menggantung pada kedua lubang
hidung. Pada pengamatan yang teliti, ada titik-titik
putih pada polip. Titik-titik putih adalah sporangium.
 Infeksi pada kelenjar air mata akan membuntu saluran
air mata  air mata keluar terus
 Infeksi pada vagina dan rectum  menyerupai
kondiloma, hemoroid dan polip rektum.
Diagnosis Laboratorium
 Tidak dapat di kultur
 Pemeriksaan histopatologi
Histopatologi: Pewarnaan HE

Catatan:
Sporangium immatur berukuran 10-100um, tdp satu nucleus di tengah,
sitoplasma berbentuk granuler
Sporangium matur berukuran 100-300um dan didalamnya terdapat spora
Setelah sporangium matur ->mengeluarkan sporamjd sporangium collapse
Histopatologi: Pewarnaan GMS-HE
Lobomycosis (Lobo disease)
 Jamur penyebab: Loboa loboi atau Lacazia
 Menginfeksi manusia dan lumba-lumba
 Mrpk infeksi kronis yang didahului oleh trauma pada
kulit dan jaringan subkutan.
 Insiden 90% laki-laki ( >>petani)
 Manifestasi klinis :
 Bentukan nodul atau keloid pada fase awal nodul
tidak terfiksir  nodul meluas dan membesar secara
perlahan
Manifestasi klinis

Tampak nodul pada lesi kulit

Diagnosis laboratorium
 Tidak dapat dikultur
 Mikroskopis lansung (KOH)
 Pegecatan jaringan

Pengecatan GMS jaringan: darkly

pigmented yeast-like cells, susunan
berantai, 9-12 um .
HE GMS GMS-HE
 Ringkasan
Organisme Manifestasi klinik
Penyakit
penyebab
Sporothrix Nodule pada tempat inokulasi yang
Sporotrichosis
schenckii mengikuti aliran limfe
Fonsecaea, Nodule verrucous / plaque/cauliflower
Chromoblastomycosis
Phialophora, nodul pada tempat inokulasi
Cladosporium etc.
Pseudallescheria, sinus yang mengeluarkan nanah dan
Madurella, granul / grains seperti butiran pasir
Mycotic mycetoma
Acremonium, yang mengandung kuman
Exophiala etc.
Polip pada hidung, infeksi kelenjar air
Rhinosporidium mata, rectum dan vagina
Rhinosporidiosis
seberii

Bentukan nodul atau keloid pada fase

Loboa loboi atau awal nodul tidak terfiksir  nodul
Lobomycosis
Lacazia meluas dan membesar secara perlahan
Referensi
 CD Rom Mikologi Kedokteran (Dr. Arthur Pohan K,
dr,Mkes, SpMK(K) )
 Clinical Mycology, The Human Opportunistic Mycosis
(David H. Ellis)
 www.mycologyonline.com
 Description of medical important fungi(David H.
Ellis)
ZYGOMYCOSIS
Merupakan infeksi yang disebakan
oleh jamur dari kelas zygomycetes
 Medically important zygomycetes
1. Ordo Mucorales  penyebab Mucormycosis
– Genus: Rhizopus, Absidia, Rhizomucor, Mucor,
Cunninghamella, Saksenaea, Apophysomyces,
Cokeromyces, and Mortierella
2. Ordo Entomophthorales  penyebab
Entomophthoromycosis
– Genus: Conidiobolus, Basidiobolus
 Mucormycosis
• Organisme penyebab: banyak ditemukan di
tanah,udara, makanan dan debu
• Manifestasi klinis: >> infeksi rhinocerebral dan
paru (30-50%)
• Predileksi: ≈ aspergillus, invasi ke vaskular 
trombosis, infark dan nekrosis pada jaringan.
• Onset demam dan necrosis cepat
• >> menyebabkan kematian
Pathogenesis of invasive
mucormycosis
 MANIFESTASI KLINIS MUCORMYCOSIS

(Adapted from Roden MM, Zaoutis TE, Buchanan WL, et€al. Epidemiology and outcome of
zygomycosis: A review of 929 reported cases. Clin Infect Dis. 2005;41:634-653.)
 Sino-orbital involvement of mucormycosis. A, Orbital
involvement in cancer patient. Note the periorbital ecchymosis and
sanguineous discharge from the eye. B, Orbital involvement with ecchymosis
and necrosis of the right turbinate. C, Necrotic eschar on the hard
palate of a cancer patient with rhinocerebral mucormycosis
 Cutaneous presentation of mucormycosis. A: Chronic,
nonhealing ulcer with necrosis following traumatic inoculation. B: Cutaneous
ecthyma gangrenosum lesions on the neck
 Diagnosis Laboratorium
Spesimen:
• Kerokan dari lesi kulit
• Sputum dan biopsi dari lesi paru
• Nasal discharge (cairan dari hidung)
• Kerokan dan aspirat sinus pada infeksi
rhinoserebral
• Biopsi jaringan gastrointestinal pada infeksi
gastrointestinal dan infeksi sistemik
 Pemeriksaan
• Pemeriksaan mikroskopik langsung
• Histopatologi
• Kultur
 Direct Microscopy
• Kerokan, sputum, eksudat  KOH 10% dengan
tinta parker atau pewarnaan dengan
Calcofluor
• Evaluasi adanya hifa yang tipis lebar dan septa
yang jarang, dengan adanya dilatasi lokal
membentuk bulbus dan percabangan yg
irregular
 Histopatologi
Dengan pewarnaan HE, PAS, GMS
Tampak hifa yang lebar, berdinding tipis, tidak bersepta/septa yg jarang dan tidak
teratur
H&E stain demonstrating invasion of a vessel wall by Rhizopus
and pyogenic response in pulmonary mucormycosis.
 Kultur
• Sabouraud’s dextrose agar
• Sensitive terhadap cycloheximide

 Evaluasi pertumbuhan koloni yangcepat (fast growing),

warna putih sampai abu-abu atau kecoklatan, dengan
permukaan berbulu halus (downy).

• Evaluasi mikroskopik dari kultur:

– Susunan sporangiospor
– Bentuk, warna dan ada/tidaknya columellae dan apophyses
– Susunan sporangiophor
– Ada/tidaknya rhizoid
• primitive coenocytic hyphae  hifa menjadi
nonviabel selama proses tissue grinding
tidak tumbuh pada kultur

• Hasil pemeriksaan langsung yg positif

(khususnya pada daerah yang normal steril),
walaupun hasil kultur negatif  signifikan
 Interpretasi isolasi zygomycetes dari
kultur
• Pasien dengan faktor predisposisi atau adanya
gejala klinis  isolasi zygomycetes dari
spesimen apapun harus dipertimbangkan
sebagai hal yg signifikan
• Pasien tanpa faktor predisposisi isolasi
zygomycetes dari daerah tidak steril (misal:
kulit atau sputum)  interpretasi harus hati-
hati, khususnya jika direct smear negatif 
mungkin kontaminasi di laboratorium !!
Illustration of the major differentiating morphologic features of three of the most
common agents of mucormycosis.
Note the presence and location of the rhizoids and columella, and the shape of
the sporangia. The infectious spores reside within the sporangia
GMS stained tissue section from a lung showing typical
zygomycete hyphae and by chance a sporangium of
Mycocladus (Absidia) corymbifera.
 ENTHOMOPHTOROMYCOSIS
• Agen infeksi: Basidiobolus, Conidiobolus
• Karakteristik : kronik, slowly progressive,
terbatas pada jaringan subkutan
• Invasi vaskular (-)
• production of a prolific chronic inflammatory
response, often with eosinophils and
Splendore-Hoeppli phenomena around the
hyphae.
 H&E stained section of infected tissue showing broad,
infrequently septate, hyphae surrounded by an eosinophilic
sheath (Splendore-Hoeppli) phenomena
 BASIDIOBOLUS
• >> di tanah mengandung feces kelelawar
• Menginfeksi pada kulit yang terluka
• Inflamasi kronis  Nodul/granuloma terbatas
pada subkutan  mengeras , painless 
melekat pada kulit, tidak terfiksasi pada
jaringan dibawahnya namun melekat pada
kulit hiperpigmentasi
• Hiperpigmentasi kulit (+)
• Insiden >> pada anak
 CONIDIOBOLUS
• Infeksi terjadi karena menghirup spora
Conidiobolus
• Klinis:
– Inflamasi kronis  Nodul/granuloma/polip pada
submukosa nasal  dapat terjadi progressive
pada sinus paranasal  facial swelling
– Obstruksi nasal,perdarahan hidung, nyeri sinus
• Insiden: >> dewasa, >> laki-laki
Zygomycosis caused by Conidiobolus
(a) Sporophore and conidia and (b) zygospores of Basidiobolus ranarum
Spherical conidia with hair-like appendages (villae) and prominent papillae
characteristic of Conidiobolus coronatus.
 Referensi
• CD Rom Mikologi Kedokteran (Dr. Arthur
Pohan K, dr,Mkes, SpMK(K) )
• Description of Medical Fungi (David H. Ellis)
• Clinical Mycology, The Human Opportunistic
Mycosis (David H. Ellis)
 DEFINISI
• Sporangium
Bentukan kantong yang berisi sporangiospore
• Sporangiospores
Spora aseksual yang diproduksi di dalam sporangium
• Sporangiophores
Hifa yang pada ujungnya terdapat sporangium
• Columellae
Dome like structure (bentukan kubah) pada ujung sporangiophore atau di
dalam sporangium
• Apophyses
Bagian dari sporangiophore yang terletak dibawah columellae yang
berbentuk seperti corong.
• Rhizoid
Hifa yang berbentuk seperti akar