Transcript Slide 1

Ma. Rosario L. Lacandula, MD, MPH
Department of Microbiology & Parasitology
College of Medicine
Our Lady of Fatima University
General Characteristics:
 True Pathogenic fungi- causes infection in normal host
 Highly virulent organism
 MOT: Inhalation; Respiratory droplet
 Primary site of infection- LUNGS, 90% of infection is asymptomatic
or they resolved spontaneously accompanied by high degree of
specific resistance to infections
 Causes dissemination to other sites
 Geographically restricted
 Dimorphic
 25 C- grows as filamentous mold
 37C- yeast cell
HISTOPLASMOSIS
Darling’s disease, Reticuloendothelial cytomycosis,
Cave disease & Spelunker’s disease
Thin branching hyphae that
produce microconidia and
tuberculate macroconidia
Small budding yeast 2-5 um
in diameter and found inside
macrophages
Histoplasmosis
Histoplasmosis
Histoplasmosis
Histoplasmosis
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Etiologic agent: H. capsulatum var. capsulatum, H. capsulatum var
duboisii
Natural reservoir: grows in soil with high nitrogen content especially
areas contaminated by excreta of bats and birds( starlings &
chicken)
High endemicity- Ohio & Mississippi Valley regions of the United
States
 Southern provinces of Ontario & Quebec in Canada
 Scattered areas of Central & South America
 Cases- Europe & Asia
 Africa- H. capsulatum var. duboisii
HISTOPLASMOSIS
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CLINICAL SYNDROMES:
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Normal Host
Asymptomatic or mild flu like illness
Acute Pulmonary Histoplasmosis
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Rare complications
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Opportunistic infection
N exposure
H exposure
Pericarditis,mediastinal fibrosis
Disseminated histoplasmosis
Chronic Pulmonary histoplasmosis
HISTOPLASMOSIS
Laboratory Diagnosis:
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Serologic Test- complement fixation- standard test – (+) later in
the disease 6 weeks or longer after symptoms, fourfold rise
Immunodiffusion- detects H & M antigens, more specific but less
sensitive
Microscopic examination of infected tissue
Skin test- Histoplasmin test- ( +) after 2 weeks of exposure, no
diagnostic value
Treatment:
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Amphotericin B
Blastomycosis
Chicago Disease,Gilchrist’s disease, North American
blastomycosis
Mold phase – typical pyriform
microconidia 2-4 um in
diameter
Tissue phase – 8-15 um in
diameter; buds are produced
singly & attached to parent cell
by a broad base
Blastomycosis
Blastomycosis
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Etiologic Agent: Blastomyces dermatitidis
North America Continent & parts of Africa
Endemicity overlaps with histoplasmosis
Other endemic areas: Minnesota, Southern Manitoba, & Southwest
Ontario
Epidemics- Wisconsin, Minnesota, Illinois, Eastern State of Virginia
& North Carolina
Natural reservoir : not known, rarely cultured from soil of endemic
areas
Infection can also occur among dogs and horses
Blastomycosis
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Clinical Syndromes:
 Primary infection in the lungs- Inapparent
 Ulcerative lesions of the skin & lytic bone lesion
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Laboratory Diagnosis:
 Serology
 Microscopic findings
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Treatment: Amphoterecin B
Blastomycosis
Blastomycosis
Paracoccidiodomycosis
South American blastomycosis, Lutz SplendoreAlmeida’s disease
No typical pattern of
sporulation
Yeast with several budding
cells attached to a parent cell;
“pilot’s wheel”; 2-3 um in
diameter
Paracoccidiodomycosis
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Etiologic Agent: P. brazieliensis
Central & South America & has high incidence in Brazil, Venezuela
& Colombia
Natural reservoir: isolated in soil that have high humidity & average
temperature of 23 C
Equal distribution among males & females, but clinical disease is
about 9X higher in males
Transition of fungi from mold to yeast can be induced in vitro by
raising the temperature of 25 C to 37 C
M-17-beta- estradiol inhibits transformation of the fungi
Testosterone,corticosterone & 17 alpha estradiol had NO inhibitory
on the transformation
Paracoccidiodomycosis
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Clinical Syndromes:
 Primary lung infection- asymptomatic
 Ulcerative lesions of the buccal, nasal & occasionally GIT
mucosa
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Laboratory Diagnosis:
 Serology
 Microscopic findings
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Treatment : Amphotericin B
Coccidiodomycosis
Posada’s Disease, San Joaquin Valley fever &
Desert rheumatism
Mycelia fragment to produce
cylindrical arthroconidia
Spherule; multinucleated
structure that undergoes internal
cleavage to produce endospore
Coccidioidomycosis
Coccidioidomycosis
Coccidioidomycosis
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Etiologic Agent: Coccidiodes immitis
“ New World”- North, Central & South American Continents
Highest endemicity- San Joaquin Valley in California, Maricopa &
Pima Countries in Arizona, Texas
Endemic- Northern states of Mexico, parts of Venezuela, Paraquay
& Argentina
Isolated in soil samples during summer
Inhibited by P. jantheniluem & B.subtilis during rainy season
Coccidioidomycosis
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Clinical Syndromes
 60 % asymptomatic
 40 % develop symptomatic pulmonary infection.Most common
symptoms of primary disease are cough, fever, and chest pain.
Night sweats and joint pains are not unusual
 Primary infections usually self limited
 Dissemination mainly in the meninges and/or skin
 HLA A9, Type B blood, do not develop toxic erythemas
 Blacks/ Asian are susceptible
Coccidioidomycosis
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Laboratory Diagnosis
 Complement fixation and tube precepitin
 Latex agglutination and agar immunodiffusion- two lines of
precipitation appear to be significant
 2 sources of antigen, both cell-free culture filtrates
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Coccidiodin
Spherulin
Treatment: Amphotericin B, ketoconazole
Coccidioidomycosis
Ma. Rosario L. Lacandula, MD, MPH
Department of Microbiology & Parasitology
College of Medicine
Our Lady of Fatima University
Opportunistic mycoses
General Characteristic:
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Low virulent fungi
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Monomorphic
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Causes infection in immunocompromised host
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Healthy individual develop high degree of innate resistance to fungal
colonization
Crytococcosis
Busse-Buschke’s disease, torulosis, and European
Blastomycosis
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Etiologic agent: Crytococcus neoformans
Monomorphic
Encapsulated- inhibits phagocytosis
Phenoloxidase- converts phenolic compounds to melanin
Lungs- Primary site of infection
High predilection for systemic spread to the brain- leading cause of
fungal meningitis
Cryptococcosis
Cryptococcosis
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Survive well in dessicated, alkaline, nitrogen rich, and hypertonic
environment- recovered from excreta and debris of pigeons
Organism that not cause infection of pigeons
Worldwide distribution
Clinical Syndromes:
 Primary pulmonary infection-asymptomatic detected as an
incidental finding on routine chest X ray- solitary nodule
 Symptomatic pneumonia-diffuse pulmonary infiltrates
 Skin cryptococcosis, Cryptococcal meningitis, osteolytic bone
lesions
Cryptococcosis
Cryptococcosis
Cryptococcosis
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Laboratory Diagnosis
 Detection based on the presence of antigen
 Latex agglutination test for detection of the capsule
 Rapid test- use of India Ink preparation of CSF- seen as clear
halo
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Treatment: Amphotericin B
Candidiasis
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Etiologic agent: Specie of Candida
Endogenous normal flora
Major disease problem of immunocompromised host
Clinical disease ranges from superficial skin infection to systemic
life threatening disease
Rarely isolated from the surface of human skin except from certain
intertrigenous areas
Organs involved- lungs, spleen,kidney,liver,heart and brain
Pseudohyphae & septate hyphae
Candidiasis
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Clinical Syndromes
 CMC Chronic mucocutaneous candidiasis- heterogenous group
of clinical syndromes characterized by chronic, treatment
resistant superficial Candida infections of the skin, nails and
oropharynx
 No dissemination seen in visceral organs
 Defect in CMI
Laboratory Diagnosis
 Rapid diagnosis- germ tube test
 Budding yeast cells, pseudohyphae and septate hyphae
Treatment: Amphotericin B , 5-fluorocytosine, ketoconazole and
fluconazole
Development of germ tubes by Candida albicans yeast
cells after incubation in serum x 2 hours @ 37oC
Candidiasis (Moniliasis)
Candidiasis (Moniliasis)
Aspergillosis
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Etiologic agent: A. fumigatus; A. niger; A. flavus
Common in the environment
Exogenous source
Normal individual not susceptible to systemic aspergillosis
Aspergillosis
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Clinical syndromes
 Mycotoxicosis- ingestion of contaminated peanuts
 Allergic aspergillosis- allergic bronchopulmonary disease
 Secondary Colonization- fungal colonization of pre existing
cavity ( e.g. pulmonary abscess) w/o invasion.
 Fungus ball- spherical mass of intertwined septate branching
hyphal elements
 Systemic disease- Invasive disease involving multiple organs
Laboratory Diagnosis: septate hyphae that branch at regular
intervals seen in clinical specimens
Mucormycosis
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Susceptibility to the fungi- metabolic acidosis, DM, leukopenis and
hyperglycemia
Grows rapidly on all laboratory media
Form coenocytic hyphae
Ubiquitous in the environment and encountered as contaminants
Clinical Syndromes
 Rhinocerebral zygomycosis-most common-originate in the
paranasal sinuses can involve the ocular orbit and palate with
extension to the brain
 Lungs, GIT, subcutaneous tissue
Mucormycosis
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In severely burned patients- colonize the damaged tissues and tend
to become invasive.
In disseminated disease- predilection for invading major bood
vessel. Clot that result can cause ischemia and necrosis of adjacent
tissues.
Laboratory Diagnosis:
 Microscopic findings
Mucormycosis
Mucormycosis