IN FEK S I JA M U R

PA D A PA R U -PA R U

Sistem Respirasi
Rizalinda Sjahril
Bagian Mikrobiologi Fakultas Kedokteran Unhas
2010

 The following fungi cause a variety of

infections, clinical manifestation severity varies.

Distinguished from opportunistic infection by
the ability to cause infection in an otherwise
healthy individuals.
These fungi are:
Cryptococcosis
Blastomycosis
Coccidioidomycosis

Opportunistic deep mycoses:

Aspergillosis
Zygomycosis

Cryptococcosis
Etiology : Criptococcus neoformans.
Replicate by budding new yeast cells 4-6

m, has large characteristic complex

polysacharide capsule (>25 m). Major
components of the capsule is
glucuronoxylomannan (GXM)
Culture appearance in Saboraud Dextrose
agar containing no cycloheximide*: smooth,
creamy, mucoid white colony in 2-3 days
Produce melanin and urease in culture

Cryptococcosis -pathogenesis

Aerosolized spores in soil reach the lung. In

tissue, spores start to produce capsule that

enables to evade immune response.
GXM binds to complement C3 and interfere
with antigen presentation.
Lung lesions: intense granulomatous
inflammation
Staining: methenamin silver or Per acid schif
predisposing conditions: lymphoma,
sarcoidosis or treatment of corticosteroid

Cryptococcosis ClinicalM anifestation

Causes chronic meningitis and pneumonia.
Silent hematogenous spread to the brain

clusters of cryptococci in the perivasc areas

of the gray matter
Symptoms:
Headache, nausea, staggering gait, dementia,

irritability, confusion, blurred vision

Fever, nuchal rigidity often mild

Criptococcal pneumonia is mostly

asymptomatic.
Chest pain (40%), cough (20%)

Cryptococcosis -diagnosis
Cryptococcal meningitis: CSF

increased pressure, pleocytosis,

glucose depression
Isolation of fungi in CSF requires
large volume specimen
because.?
Capsule in CSF can be stained by
China Ink

H istoplasm a
Etiology: Histoplasma capsulatum
Multiply by budding (blastoconidia)
Dimorphic: yeast form 2-4 m at 37oC
Mold phase at 22-25oC
Growth in culture in weeks time
Mycelial produces microconidia and

macroconidia
Diagnostic structure: tuberculate
macroconidium

H istoplasm a ClinicalM anifestation

Most cases are asymtomatic or with fever and

cough
X-ray : mediastinal lymphadenopathy,
infiltrates.
Histoplasmin skin test positive in 3 weeks .
Severe cases: chills, malaise, chest pain,
extensive infiltrates.
Residual nodule may continue to enlarge over
a year and mimic pulmonary neoplasma.
Progressive pulmonary disease resembles
pulmonary tuberculosis

H istoplasm a -Pathogenesis
Reticuloendothelial system is the focus of

infection.
Initial infection is by inhaled microconidia
that changes to yeast form in the host.
Phagocytosed (macrophage and PMNs) and
may grow inside macrophages by
controlling lysosomal pH (increased to
neutral)
Further lymphatic spread and development
of primary lesion is similar to mycobacteria

H istoplasm a diagnosis
Pulmonary histoplasmosis Direct

examination or culture of sputum is low

Disseminated histoplasmosis blood
and bone marrow, staining by Wright
or Hematoxylin Eosin show intracellular
histoplasma, tuberculate
macroconidium and dimorphism
EIA detects Antigen (immunodifusion)
Nucleic acid detection

Blastom yces
Etiologi: Blastomyces dermatitidis
Dimorphic fungus that changes to

mycelial at 25oC. Produces

microconidia, but no macroconidia
Blastomyces is similar to
histoplasma, but larger yeast cells
(8-15 m), and broad base buds and
thick wall.

Blastom yces clinicalm anifestation

Most clinical features are similar to

histoplasmosis (asymtomatic or
cough or mild fever).
Disseminated infection: skin lesions

Blastom yces -pathogenesis

Has surface glucan and glycoprotein

adhesin (BAD1) for binding to host

cells.
Yeast are large cells, thick double
walls, extracellular

Blastom yces Clinicalm anifestation

Pulmonary infection: cough, sputum

production, chest pain, fever.

Hilar lymphadenopathy, nodular
pulmonary infiltrates with alveolar
consolidation resembles
pulmonary tumor, tuberculosis, other
mycosis.
Skin lesions: occur on exposed skin

Blastom yces -D iagnosis

The presence of large yeast cells

with broad-based buds

( blastoconidia) in KOH preparation
Biopsy H & E staining
Culture: grow in weeks, but conidia
not distinctive
Immunodifusion test
Serologic tests mostly negative

Coccidioides im m itis
Dimorphic fungi filaments and spherules
Spherule= large (12-100m), round walled

invasive, multicompartmental structure.

The compartment consists of 200-300 endospores,
each is then capable to become another
spherule
In Culture and in soil : grow in 2-5 days in mold
form regardless of the temperature.
Hyphae are septate and thick walled, barrel
shaped arthroconidia

Coccidioides im m itis
Is restricted to Sonoran Desert
Arthroconidia (2-6 m) are inhaled,

enters the bronchioles.

Arthroconidia has antiphagocytic
action due to the outer portion of the
cell wall
Athroconidia convert to large
spherule

Coccidioides im m itis clinicalaspects

More than 50% infection shows no

symptoms or very mild disease.

Symptomatic: malaise, cough, chest pain,
fever, arthralgia 2-6 weeks (Valley Fever)
Erythema nodosum is common in women
Chronic pulmonary infection forms cavity
Disseminated disease is more common in
men related with racial orientation and
immune status

Coccidioides -D iagnosis
Direct examination for spherule by

KOH prep or biopsy section.

Culture
Skin and serologic test: conversion 14 weeks post infection
Complement fixing test : to measure
the extent of the disease.

Organism

Growth

Culture
25oC

Culture
37oC

Cryptococ
cus
neoforma
ns

Encaps.
Yeast

Encaps.
Yeast

Histoplas
ma
capsulatu
m

te

Blastomyc
es
dermatitid
is
Coccidioid
es immitis

Mold,

Small
Tubercula yeast
Macroco
nidia
Mold

Tissue

Source

Encaps.
Yeast

Environm, Pnie
worldwide

Small
intracell
yeast

Environm,
US
midwest

Environm,
Us
Spherule midwest
Mold,
(spherule s
arthroco )
Environm,
n.
Sonoran
desert
Mold

Primary
Disease

Dissemi
nated
Disease

Chronic
meningiti
s

Pnie,
hilar
RES
adenopat enlargem
h
nt

Yeast

Yeast,
mltiple

Environm,
latin

Pnie
Valley
fever

Pnie

Skin and
bone
lesion
Pnie,
meningiti
s, skin,
bone

Aspergillus
Aspergillus spp. are molds with

branching septate hyphae and

characteristic conidia arrangement on
he conidiophore.
Flufy colonies 1-2 days 5 days full
pigmented growth covering plate
Most frequent spp:
Aspergillus fumigatus
Aspergillus flavus
Aspergillus niger

Aspergilosis
Occurs in immunocompromised

individuals, rapid progression to

death.
The only sign and symptom may be
fever and dry cough.
Conidia is small enough to enter the
lung
Adherence with fibrinogen and
laminin.
Extracellular elastase, proteinase,

Invasive aspergillosis
Occurs in the presence of preexisting

pulmonary disease( bronkhiectasis,

bronkhitis, asthma, Tb) or
immunosuppression.
Aspergillus invade tissues by forming
branching septate hyphae fungus
ball = aspergilloma within
preexisting cavity.
Invasion into blood vessels
hemopthysis

Aspergillus -D iagnosis
Isolation and identification
Rapid growth, frequently as

contamination
Specimen: lung aspiration, biopsy
and bronkhoalveolar lavage

Zygom ycosis
Zygomycosis(mucormycosis) is

caused by any of zygomycetes

(Absidia, Rhizopus, Mucor).
Saprophyts
Immunocompromised hosts with
diabetes are infected
Pulmonary disease is similar to other
fungi
Pathologic finding in tissue:
ribbonlike non septate hyphae.