fungi
TRANSCRIPT
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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)
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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)
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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
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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
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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
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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
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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
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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)
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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.
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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
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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
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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
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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
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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
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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
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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)
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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)
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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
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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
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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
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Opportunistic Mycoses
• 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
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Opportunistic Mycoses
• 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
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Opportunistic Mycoses
• 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
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Opportunistic Mycoses
• 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)
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Opportunistic Mycoses
• 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
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Opportunistic Mycoses
• 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