Fungi

Fungi

• Mycology: the study of fungi– Fungi are widespread in nature; ~200,000

species identified– Most fungi involved in decomposition of

organic matter & play important role in recycling organic compounds in nature

– Fungi are Eukaryotic organisms• Unicellular morphology (=Yeast) or

Mulitcellular morphology (= Mold)

Fungi

• Yeasts (Unicellular morphology)– Single, oval or spherical fungal cell– Reproduction: Asexual by budding– Budding

• Division of nucleus• Passage of one nucleus to a bud the “balloons” out from the mother

cell• Formation of wall between the bud and mother cell• Daughter cell = bud or blastospore• Daughter cell initially smaller than mother cell; but, it will increase in

size & produce own buds

• Molds (Filamentous morphology)– Multicellular – filamentous or tubular structures– Reproduction: asexual or sexual (main discriminating feature)

Fungi

• Growth of mold– Germination of Condium (=asexual reproductive unit in fungi) –

send out a filament that grows by elongation @ its tip– Hyphae – elongated filament; the basic structure of growing

molds– Mycelium – multiple branches of hypae; mass of hypae– Many nuclei located w/in each hypae– Formation of Septae = “cross-walls” w/in hypae– Conidia – terminal ends of hyphae; “seeds” for new colonies;

molds reproduce by developing conidia on the hyphae• Sexual reproduction

– 2 reproductive bodies connect & haploid cells fuse to form diploid cells (spores) – meiosis

– Resulting diploid cells become Spores = reproductive elements formed from sexual reproduction

– Rare among the human fungal pathogens

Fungi

• Dimorphic Fungi– Dimorphism: the property of having 2 morphological

shapes; dimorphic fungi have capability of 2 distinct forms – dependent on temperature

• Temperature Dependent1. Yeast form: 37°C2. Mold or mycelial form: 25°C

• General characteristics– Cell wall: rigid & thick; NO PG– 1° component is presence of sterol in cell wall– No locomotion: non-motile

• Distinguishing Morphological Characteristics– Size, presence of a capsule, cell wall thickness, spores or

conidia production

Fungi

• Growth Conditions– Molds: aerobic– Yeasts: facultative anaerobes– Acid pH (4.0 → 6.0)– Selective Laboratory Media

• Sabouraud’s Dextrose Agar (SDA) – low pH• Dermatophyte Test Media (DTM) – turns red in presence of all

dermatophytes• Birdseed Agar – specific for ID of Cryptococcus neoformans ( agar

turns brown); all other Crytpococcus spp – turn it white– Minimal Media

• Corn Meal Agar (ID of spore formation: production of terminal conidia)– Slide cultures – undisturbed growth– Colonial Morphology

• Molds – dry, cotton-like masses• Yeast – moist, opaque, creamy colonies

Mycoses (Fungal Diseases)

1. Superficial Mycoses• “surface infection”• Fungal diseases that grow on surface of skin & nails

2. Cutaneous Mycoses or Dermatomycoses• Fungal infections of keratinous structures – outer layers of

skin, nails, in hair shafts

3. Subcutaneous Mycoses• Infections that penetrate below the skin & involve the

subcutaneous CT and bone tissue

4. Systemic or Deep Mycoses• Infections of internal organs – from disseminated disease

5. Opportunistic Mycoses• Infections in compromised or immunosuppressed

Dermatomycoses

• ONLY contagious fungal infection/disease in humans; not associated w/ death, just uncomfortable symptoms and characteristic lesions

• Dermatophytes – fungi that invade keratinized & cutaneous areas of the body– Nails, hair and skin

• 3 Major Genera– Microsporum– Tichophyton = m/c dermatophyte fungus– Epidermophyton

Dermatomycoses

• Mode of Infection– Hyphae grows into keratinized tissues of epidermis, into hair

shaft, or into finger/toe nail– Growth outward from infection site in concentric circles– Enzyme production – keratinase, elastase and collagenase

• Clinical Infections1. Tinea capitis (ringworm of scalp) – Trichophyton &

Microsporum spp.– Initial Sx: inflammation & itching of the scalp– Mode of Infection: hypae spread into keratinized areas of scalp &

hair follicle → fungal growth weakens the hair → breakage @ shaft → ALOPECIA (hair loss): localized & spotty

– Associated mostly w/ children (high transmission)

Dermatomycoses

• Clinical Infection2. Tinea Barbae (ringworm of the beard)

– Infection site – bearded areas– Superficial lesion – scaly– Severe infection – development of deep pustules– Result – permanent hair loss

3. Tinea pedis (ringworm of the foot, “Athlete’s Foot”) – m/c in adolescents & adults

– Trichophyton rubrum, Trichophyton mentagrophytes, Epidermophyton floccosum

– Sx’s – foot lesions– Mode of infection – growth between toes of small fluid-filled

vesicles → vesicles rupture → development of shallow lesion that itch; may become infected with bacterial (2° bacterial infection)

– Predisposing conditions – public showers, swimming pools, failure to dry between toes.

Dermatomycoses

• Clinical Infections4. Tinea curis (ringworm of the groin, “Jock Itch”)

– E. floccosom & T. rubrum– Sx’s – lesions in groin or perianal area → red, scaly, itchy and

often dry– Predisposing factors – moisture in the groin area; wet bathing

suits, athletic supporter, tight fitting pants/slacks and obesity5. Tinea corporis (ringworm of the body)

– E. floccosum, spp. of Trichophyton & Microsporum– Infection site – non-hairy areas of the body– Sx’s – lesions are reddened, scaly, w/ papular eruptions

6. Tinea unguium (ringwom of nails - onychomycosis)– T. rubrum– Infection sites – fingernails and toenails– Initial Sx’s – superficial white patches on nail beds: puffy & chalky– Later Sx’s – thickening of the nail, accumulation of cheesy debris,

cracking and discoloration of the nail

Dermatomycoses

• Diagnosis– Clinical signs and symptoms– Microscopic ID from tissue scraping samples: presence of

hyphae• Tissue scraping + 10% KOH (heated, then stain added) → presence

of septate hyphae visible under microscope– Macroscopic ID

• Culture: Dermatophyt Test Media (DTM) – turns RED• Culture: Sabouraud’s Dextrose Agar (SDA)

• Treatment– Non-Rx: salves/ointments – for symptomatic relief– Good hygiene– Oral antibiotic therapy– Topical antifungal agentNote: re-infection may occur over & over => not good host immune

response

Subcutaneous Mycoses

• Fungal source = normal inhabitants of soil or organic matter

• Introduction to host – wound or abrasions of skin• Deeper infection – penetration to below skin• Clinical Infections

1. Sporotrichosis (“Rose Gardner’s Disease”)– Causative agent = Sporothrix schenckii– Mode of infection – traumatic implantation of fungus into skin →

painless papule @ inoculation site → enlargement to form ulcerated lesion → then possible spread to regional lymph nodes = Lymphocutaneous sporotrichosis

2. Lymphocutaneous Sporotrichosis– Mode of infection – fungus form multiple nodules after being

spread by draining lymph node channels → nodules may ulcerate → untreated lesions last for years

– Occupational Risk Groups = horticulturists, foresters, gardeners, farmers & basket weavers

Systemic Mycosis

• “True pathogens” – infect normal, healthy individuals• “Opportunisitic pathogens” – infect debilitated +/or

immunocompromised individuals• Mode of Infection – inhalation of spores → lower

respiratory tract → germinate into yeast → asymptomatic or 1° pulmonary infection that parallels TB → disseminated to other organs d/t compromised defense mechanism

• NO person-to-person transmission; only airborne route to humans from fungal spores– Fungi growing in soil or on an. droppings produce conidia that be

aerosolized and carried by air-borne route to humans

Systemic Mycosis

• Clinical Diseases1. Coccidioidomycosis

– Chronic, necrotizing mycotic infection of the lungs; resembles TB pathologically

– Begins as a bronchopneumonia w/ its inflammatory infiltrate

– Disseminated to many site in immunocompromised pt’s: skin, bones, meninges, liver, spleen

– Causative agent: Coccidiodes immitis• Dimorphic fungus that grows in soil of SW US• Spore = Arthrospores – inhaled into alveoli and terminal

bronchi, where they enlarge into “spherules”• Spherules fill w/ endospored, which are released to form more

spherules• In Arizona – 50% chance (after 10 yrs) person w/ (+) serology

to this b/c of exposure, NOT necessarily the disease

Systemic Mycosis• Clinical Diseases

1. Coccidioidomycosis– Epidemiology

SW US, particularly San Joaquin and Sacramento Valley of California, areas around Tucson and Phoenix in Arizona

High incidence of infection & disease may follow dust storm Coccidioidomycosis = Valley Fever = San Joaquin Valley Fever =

Desert Rheumatism– Pathogenesis

Inhalation of arthroconidia leads to 1° infection• Asymptomatic in 60% individuals• 40%: self-limiting influenza-like illness – fever, malaise, cough,

arthralgia, HA– Laboratory DX

1. Culture: specimen from sputum; exudate from cutaneous lesions; CSF, blood, urine, tissue biopsies

2. Serology – IgM Ab detection w/ latex agglutination3. Coccidioidin Skin Test (+)4. Chest X-Ray analysis – hilar lymphadenopathy along w/ pulmonary

infiltrates, pneumonia, pleural effusions or nodules

Systemic Mycosis

• Clinical Diseases2. Histoplamosis

– m/c fungal disease in US– Acute, necrotizing, caseous granuloma of the lungs– Causative agent = Histoplasma capsulatum

Dimorphic fungus found in nature Multiplies extensively in areas where bird feces accumulate

– Fungus grows in soil → formation of conidia → airborne → inhalation into the lungs → germination into yeast-like cells → engulfed by alveolar macrophages

– Infection – acute, but benign and self-limiting; or chronic, progressive and fatal Usu. Self-limiting flu-like syndrome (fever, chills, myalgia, HA, non-

productive cough– Dissemination = rare; but can occur – to reticuloendothelial

tissues (liver, spleen, BM lymph nodes)

Systemic Mycosis

• Clinical Diseases2. Hitoplasmosis

– Laboratory Dx Culture – specimens include sputum, urine, scrapings from

superficial lesions, BM aspirates Microscopic examination of fungus in macrophages Serology – Tests for Ab’s to Histoplasmin Ag or yeast cells Skin Test – Histoplasmin (+)

– Epidemiology most prevalent in Ohio & Mississippi River Valleys,

including Central and Eastern States KC = high risk area Reservoir = Soils laden w/ bird, chicken, or bat droppings =

rich sources of the fungus (natural habitat)

Systemic Mycosis

• Clinical Diseases3. Blastomycosis

– Chronic granulomatous and suppurative disease of the lungs, resulting in small areas of consolidation

– Causative agent = Blastomyces dermatitidis– Fungus produces microconidia in soil, which become

airborne and inhaled in lungs Germination into yeast cells Dissemination is rare, but can occur – skin, bone, GU tract

– M/c in South Central and South Eastern US– M/c clinical presentation = pulmonary infiltrate w/ fever,

malaise, cough, myalgia, night sweats

Opportunistic Mycoses

• Endogenous type infection – caused by normal flora of respiratory tract, mouth, intestinal tract and vagina

• Opportunistic Infection– Overgrowth of normal flora → inflammation of

epithelial surfaces (m/c = oral cavity and vagina) → dissemination to internal organs

Opportunistic Mycoses• Clinical Diseases

1. Cryptococcosis– 1° disease of lungs w/ granulomas and consolidation– Rapidly spreads to the meninges and brain, causing

meningoencephalitis– Etiological agent = Cryptococcus neoformans

Only systemic fungus that is NOT dimorphic Only true yeast unicellular pathogen of humans

– Epidemiology Occurs worldwide in nature; found in very large #’s in dry pigeon feces Usually associated w/ immunosuppression – AIDS, malignancy 2nd m/c fungal dis in AIDS pts (after candidiasis) Reservoir = decomposing plant materials (soil) w/ high N content from

pigeon feces– Pathogenesis

Inhalation of yeast cells (encapsulated, dry, easily aerosolized) Influenza-like illness follows Immunosupressed: yeast cells multiply and disseminated to CNS

• YEAST CELLS FOUND W/IN CSF


• Clinical Diseases1. Cryptococcus

– S/sx’s: MAJOR clinical manifestation = chronic meningitis w/ spontaneous remissions and exacerbations

– Pt presentation HA Stiff neck Disorientation Lesions in skin, lungs

– Laboratory Dx CSF pressure and protein [ ] ↑ WBC count ↑ Glucose [ ] normal or low

– Diagnosis Specimens from CSF, sputum, blood, urine, exudates Culture Serology


• Clinical Diseases2. Candidiasis (candidiosis)

– Causative agent = Candida albicans Normal flora of skin, vagina, and intestines Considered a yeast, but is Dimorphic (forms a true mycelium)

– Cutaneous Infections arise d/t host’s condition – diabetes, immunological

deficiencies, exposure of skin to moist environment Mode of infection

1. Adherence to epithelial surfaces

2. Fungal proliferation

3. Invasion of epithelial tissue


• Cutaneous Infection w/ C. ablicans1. Thrush or Oral Candidiasis = Most Common Candidiasis

– Symptomatic appearance: white, adherent patches (pseudomembranes) attach to epithelial membranes of tongue, gums, cheeks, or throat – FUNGAL MAT formation

– Pseudomembrane composition = yeast, hyphae, epithelial debris– Increased susceptibility: Newborns– Transmission: Vertical - Mother→Child

2. Vaginal Candidiasis = m/c form of vaginal infection– Sx’s: yellow to white milky discharge, inflammation, painful

ulcerations & itching– Candidal overgrowth – related to increased glucose content of

vaginal secretions– Assoc’d w/ - diabetic ♀, pregnant ♀, broad spectrum antibiotic tx


• Cutaneous Infection w/ C. ablicans3. Esophageal Candidiasis

– Complication of AIDS patients– Sx’s: painful bleeding, ulcerations, nausea,

vomiting

4. General Candidiasis Infections– Infections of epidermal tissue – folds of skin on

obese people (usual sites =upper legs, underarms); tissue that remains wet (dishwashers); skin covered by wet diapers (diaper rash)


• Disseminated infection w/ C. albicans– Cutaneous infection → mutisystem disease– Iatrogenic – use of catheters of prosthetic devices

• Diagnosis– Clinical symptoms– Microscopic examination– Macroscopic examination – culture

• SDA (white- to cream-colored colny, pasty w/ a yeasty odor• Corn Meal Agar – visualization of spores

• Treatment: Antifungals


• Clinical Diseases3. Asperigellosis

– Causative agent = Aspergillus fumigatus– Acute, invasive infection of lung – dissemination to brain, GIT,

other organs– Non-invasive lung infection gives rise to aspergilloma (Fungal

Ball) – a mass of hyphal tissue that can form in lung cavities produced by other diseases, like TB

4. Pneumocystis Pneumonia– Causative agent = Pneumocystis jiroveci

Pneumocystis carnii– Acute interstitial pneumonia w/ plasma cell infiltrates– As disease progresses, pt. experiences weakness, dyspnea, and

tachypnea leading to cyanosis; Death can result from asphixiation

– m/c cause of DEATH in AIDS pts from Pneumocystis carinii pnuemonia

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Fungi