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OPPORTUNISTIC
MYCOSES

Prof.Dr.Demet KAYA
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• Advances in medicine have resulted in

increase in fungal infections!!!
• Opportunistic mycosis; is a fungal disease
occurring in human’s with a compromised immune
system.
• Some opportunistic organisms are members of
microbiota, that become pathogenic only when
the host's immune defences are altered, as
• in immunosuppressive therapy,
• in a chronic disease, such as diabetes mellitus,
• during steroid or antibacterial therapy that
upsets the balance of bacteria in microbiota in
the body.
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Common Opportunistic Fungi

1. Candida spp. (Candidiasis)

2. Cryptococcus neoformans (Cryptococcosis)
3. Aspergillus fumigatus (Aspergillosis)
4. Mucor, Rhizopus spp. (Zygomycosis)
5. Penicillium, Fusarium, Geotrichum spp.
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CANDIDIASIS
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CANDIDA

1. C. albicans
2. C. tropicalis
3. C. krusei
4. C. pseudotropicalis
5. C. stellatoidea
6. C. parapsilosis
7. C. (Torulopsis) glabrata
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CANDIDA SPP.

• Important cause of opportunistic fungal infections

(Candidiasis)
• Members of microbiota (oral, vaginal,
gastrointestinal tract, skin in 20 % of normal
individuals)
• As Candida is present in all humans, it has many
opportunities to cause endogenous infections in
compromised host - so, Candida infections
continues to most frequent opportunistic fungal
infection.
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• Can cause mycoses in the presence of

predisposing factors.
• Cause of superficial,opportunistic and systemic
mycoses (infect skin, mucosa, or organs)
• Member of Fungi imperfecti (Deuteromycotina)

***Most common patogenic species is; C. albicans.

Others are; C.tropicalis, C.glabrata, C.krusei
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Predisposing factors:
• Immunosupression (Corticosteroids, HIV,…)
• Recipients with organ transplantation
• Broad spectrum antibiotics (prolonged usage)
• Diabetes mellitus
• Infancy – Old age – Pregnancy
• Malnutrition (dietary protein deficiency, zinc
and iron deficiencies)
• Obesity
• Skin humidity
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Morphology

• Ovoid shape (2-5µm x 5-7µm),

• Gram (+) yeast,
• Non capsulated,
• Aerobic,
• Blastospore forming (budding)
cells,
• Produces pseudomycelium
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Culture:

• Sabouraud Dextrose agar (SDA),22°C- 37 °C

• Grow predominantly in yeast phase
• White, cream colored, smelling “S” colonies

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Differential diagnosis of
C. albicans:

• Germ tube formation: 37°C- 2h.in human sera

• Chlamydospore formation (Corn-meal agar)
• Biochemical tests(Fermentation and Assimilation
tests)
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Clinical Manifesitations:
1. Oral candidiasis:

Superficial WHITE PATCHES on mucosal

surface/skin.
(Poor oral hygiene, dietary protein deficiency, poorly
fitted dentures, mouth burns from hot food or
drinks or conditions that affect the entire body,
such as medications, allergic reactions, radiation
therapy, or infections)
• Infants and old persons are affected

• In immunocompromised /AIDS-commonly seen

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Moniliasis :Oral thrush produced by

Candida albicans
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• Stomatitis: Tongue, cheeks, gums, lips, throat, roof

or floor of the mouth
• Angular Stomatitis: Irritation and fissuring in the
corners of the lips is termed ''angular stomatitis''

Angular Stomatitis
Stomatitis
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2. Vulvo-vaginitis:
• White patches on vaginal mucosa
• Causes itching, soreness, white discharge
• Common in pregnancy
• Majority experience one episode in a life time

Vulvo-vaginal
candidiasis
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3. Skin( axillar, submamillar,interdigital,anal ) &

Nails (onychomycosis)

Submamillar candidiasis Anal candidiasis

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Interdigital candidiasis

Onychomycosis
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4. Organ candidiasis: Pulmonary (common),

gastrointestinal, urinary, disseminated)

Gastrointestinal candidiasis

5. Chronic Mucocutaneous Candidiasis:

Disseminated infection in patients with
cellular immun deficiencies
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Diagnosis
• Specimen:Skin scrapings, mucosal
scrappings,vaginal secretions, blood and other body
fluids

1. Microscopy: Gram, KOH (Gram + yeast

cells,blastospore and pseudohyphea)
2. Culture: SDA
Identification: Germ tube production,
Chlamydospore formation, Biochemical tests
(Fermentation and Assimilation tests)
3. Serology: Latex aglutination, ELISA
4. Skin test: Candidin
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Treatment

• Local • Systemic
Nystatin Ketaconazole
Miconazole Amphotericin-B
Flucytosine
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CRYPTOCOCCOSIS
 Cryptococcus neoformans

• A sporadic disease in the past.

• Most common infection in AIDS
patients.
• Found in wild / domesticated birds.
Birds do not get infected
• Pigeons harbors the C.neofromans
in nature.
• Inhalation (pigeon droppings)

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Morphology:

• A capsulated yeast

• 4 – 10 microns, round

• Negative staining (India

Ink,Nigrosin)

• KOH preparations (Sputum and

other tissues)

• PAS,Mucicarmine staining (for

confirmation)
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Pathogenesis

• Enters through lungs - Inhalation of spores of

C. neoformans
• Enters deep into lungs,
• Self limiting in most cases,
• Pulmonary infections can occur.
• Present as separate nodules - Cryptococcoma.
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Life cycle of C.neoformans

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Clinical Manifesitations: Pulmonary infection,

meningitis, granulomatous lesions

• Abnormalities of T lymphocyte function

aggravates, the clinical manifestations.
• In AIDS, 3- 20% develop cryptococcosis.
• Present with chronic meningitis , meningo
encephalitis: – headache, low grade fever,visual
abnormalities ,coma – fatal
• Disseminated form: Involvement of skin,
mucosa, organs, bones.
• Treatment reduces the morbidity and cure in
non immunosupressed patients.
Diagnosis

• Specimen: Sputum, CSF

• Microscopy: India ink, FAT
• Culture: 37°C (Creamy, white,
yellow, brown colored colonies
• Urease test (confirming the
isolate)
• Serology:
Ag detection: Latex ag., FAT
Ab detection: IFA, CFT,
Hemaglutination
• Skin test: Cryptococcin
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Treatment

• Immune competent - Fluconazole, Itraconazole

• Immune deficient – Amphotericin, Flucytosine
• AIDS patients are not totally cured
• Relapses are frequent with fatal outcome.
• Rapid resistance with fluconazole.
• Prevention-Avoid contact with birds
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ASPERGILLOSIS
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Aspergillosis
• In nature > 100 Aspergillus species
• Few are important as human pathogens
• Fungal spores enters through respiratory tract
• An opportunistic pathogen in immunosupressed
patients (AIDS)

1. A.fumigatus
2. A.niger
3. A.flavus
4. A.terreus
5. A.nidulans
Morphology

• Mycelial fungus
• Separate hyphae with
distinctive sporing
structures
• Spore bearing hyphae
– conidiophores
terminates in a
swollen cell vesicle
surrounded by one or
two rows of cell
chains (asexual
conidia)
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A.fumigatus
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A.niger A.flavus
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Clinical Manifesitations

Allergic Aspergillosis –

• Atopic individuals, with elevated IgE levels

• 10-20% of asthmatics react to A.fumigatus
• Follows particularly heavy and repeated exposure
to larger number of spores
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Aspergilloma –

•A fungal ball, fungus colonize preexisting

cavities in the lung (tuberculosis ) and form
compact ball of mycelium which is later
surrounded by dense fibrous wall presents
with cough, sputum production
•Haemoptysis occurs due to invasion of blood
vessels
Invasive Aspergillosis
• Occurs in immunocompromised patients with
underlying disease
• Neutropenia most common predisposing factor
• In bone marrow recipients leads to high mortality
• A.fumigatus is the most common infecting species
• Fungus invades blood vessels, causes thrombosis
septic emboli
• Can spread to kidney and heart(endocarditis) .
• Paranasal granulomas: a rare presentation
(may invade paranasal sinuses spread to bone, orbit
of the eye, and brain)

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Diagnosis

Microscopy:
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Culture: SDA
(Grey, green,black colonies )
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ZYGOMYCOSIS
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Zygomycosis
• Also called as Mucormycosis or Phycomycosis
• Major causative agents Rhizopus,
Mucor,
Absidia.
• Saprophytic mold
• Spread from nasal mucosa
• Spread to paranasal sinuses , orbit, brain & lungs
• Leads to fatal outcome,
• Improved with anti fungal treatment.
Morphology

• Majority are with

broad aseptate
mycelium with many
number of asexual
spores inside a
sporangium which
develops at the end
of the aerial hyphae

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Mucor

Microscopy
• Non septate hyphae
• Having branched
sporangiophores with
sporangium at terminal
ends

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Mucor
 Rhizopus

Microscopy
• Shows non septate
hyphae
• Sporangiophores in
groups
• They are above the
rhizoids

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Rhizopus
 Clinical Manifestations
• Patients may manifest with
«Rhinocerebral zygomycosis»
• Associated with diabetus mellitus,
leukemia or lymphomas
• Spread from nasal mucosa to bone,
paranasal sinuses orbit and brain
• Causes extensive cellulitis and tissue
destruction
• Rapidly fatal if untreated
• Severe immunocompromised may manifest
as primary cutaneous lesions
• Rarely infects burns patients 51
 Diagnosis
• Nasal discharges, sputum,
rarely contain many fungal
elements
• Histopathology (Biopsy)
more reliable than culturing
• Histological sections: contain
‘non septate hyphae’ in
thromboses vessels or sinuses
surrounded by leukocytes or
giant cells

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Microscopy
• KOH preparation
shows broad aseptate
branching mycelium,
and distorted hyphae
• Methenamine silver
staining is more
sensitive.
Culture
SDA

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Treatment

• Early diagnosis highly essential for effective

cure
• High doses of IV Amphotericin B
• Surgical interventions
• Control of underlying disease a basic
requirement for better clinical outcome
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OTHER OPPORTUNISTIC
MYCOSES

1. Penicillum
2. Fusarium
3. Geotrichum
4. Paecilomyces
5. Bipolaris
6. Curvilaria
7. Alternaria
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Penicillum

Fusarium
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Geotrichum