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

HISTOPLASMOSISDarling’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 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

CLINICAL SYNDROMES: Normal Host

Asymptomatic or mild flu like illness N exposure

Acute Pulmonary Histoplasmosis H exposure

Rare complications Pericarditis,mediastinal fibrosis

Opportunistic infection Disseminated histoplasmosis

Chronic Pulmonary histoplasmosis

HISTOPLASMOSIS

Laboratory Diagnosis: 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: Amphotericin B

BlastomycosisChicago 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

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

Clinical Syndromes: Primary infection in the lungs- Inapparent Ulcerative lesions of the skin & lytic bone lesion

Laboratory Diagnosis: Serology Microscopic findings

Treatment: Amphoterecin B

Blastomycosis

Blastomycosis

ParacoccidiodomycosisSouth American blastomycosis, Lutz Splendore-

Almeida’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

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

Clinical Syndromes: Primary lung infection- asymptomatic Ulcerative lesions of the buccal, nasal & occasionally GIT

mucosa

Laboratory Diagnosis: Serology Microscopic findings

Treatment : Amphotericin B

CoccidiodomycosisPosada’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

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

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

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

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:

Low virulent fungi

Monomorphic

Causes infection in immunocompromised host

Healthy individual develop high degree of innate resistance to fungal colonization

CrytococcosisBusse-Buschke’s disease, torulosis, and European

Blastomycosis

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

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

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

Treatment: Amphotericin B

Candidiasis

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

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

Etiologic agent: A. fumigatus; A. niger; A. flavus Common in the environment Exogenous source Normal individual not susceptible to systemic aspergillosis

Aspergillosis

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

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

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