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Flashcards in Fungi 2 Deck (28)

Fungal Molds vs Yeasts

-asexual or sexual reproduction with spores
-multicellular: not very mobile in the body

-asexual by budding
-single celled: can circulate resistant to phagocytosis

-dimorphs- thermal dimorphs


Four categories of Fungal Infections (Mycosis)

-Superficial mycoses- minor infections or overgrowth on skin surface

-Subcutaneous mycoses- granulomatous infection of lower dermal layers, slow spread from periphery toward trunk

-Systemic mycoses- potentially-dangerous infection spreading from inhaled spores

-Opportunistic mycoses- cause a variety of disease predicted on the patents' preexisting conditions


Themes of Superficial Mycoses

-caused by fungal growth on superficial skin layer
-does not require thermal dimorphism: often growing on cool exterior as hyphae
-very common, but symptoms are minor: itch or discoloration
-treated with topical azoles, alt oral griseofulvin


Superficial Mycoses: Dermatophytosis

-caused by dermatophytes
-infect only superficial keratinized structures- skin, hair, nails
-produce keratinases that allow invasion of cornified cell layer


Pathogenesis of Dermatophytosis

-form chronic infections in warm, humid areas in on body surface
-inflamed circular border of papules and/or vesicles, broken hairs, thickened, broken nails
-skin within border may be normal
-named for affected body part:
tinea capitis- head
tinea corporis- ringworm
tinea cruris- Jock itch
tinea pedis- Athletes's foot
-transmitted by fomites or by autoinoculation form other sites on body


Hypersensitive dermatophytid reactions

-vesicles on fingers
-caused by hypersensitivity to circulating fungal antigen
-vesicles do not contain live fungus or spores
-tinea is very common: accounts for 10-20% of visits to US dermatologists
-no morbidity results from the primary infection, but prolonged itch can lead to bacterial superinfection


Diagnosis of Dermatophytosis

-exam: itching, redness, history of tight or wet clothing
-microscopic exam: scraping from affected skin or nail, treat with 10% KOH, exame for hyphae and spores
-culture on Sabouraund's agar at room temp
-may show fluorescence when examined under Wood's lamp


Dermatophytosis: Treatment and Prevention

-topical antifungal treatment: Terbinafine (Lamisil), Undecylenic acid (Desenex), Miconazole (Micatin), Tolnaftate (Tinactin)
-treat all affected body sites simultaneously

alternate: oral griseofulvin (Fulvicin)
-keep skin dry and cool


Themes in Subcutaneous Mycoses

-introduced by trauma exposing subcutaneous tissue to soil or vegetation
-slow spread from trauma site toward trunk by lymphatics
-thermal dimorphism
-patient presents with history of ineffective antibiotic treatment
-treated with oral azoles
-in serious cases, may begin with short course of amphoterin B and surgery



-Sporothrix schenckii and other species
-thermally dimorphic
-found on vegetation
-often seen in gardeners, particularly of roses (thorns)


Pathogenesis of Sporotrichosis

-introduced into skin by thorn puncture
-yeasts grow at site and form painless pustule or ulcer
-draining lymphatics form suppurating subcutaneous nodules
-symptoms wax and wane over years
-may progress to disseminated disease and meningitis if immunosuppressed
-patients with COPD and long term corticosteriod may develop pulmonary symptoms from inhaling the spores; difficult to distinguish from TB or histoplasmosis


Exam of Sporotrichosis

-painless pustule or ulcer on hand or arm: reddish, necrotic, nodular papules may extend along lymphatic from initial injury site
-history of gardening, farming, landscaping, berry-picking
-history of ineffective antibiotic treatment
-in AIDS, may see nodules disseminated over whole body
-in COPD+ alcoholism, respiratory distress


Diagnostic Lab of Sporotrichosis

-tissue biopsy: round or cigar shaped budding yeasts- hard to see
-culture at room temp from pus, biopsy: hyphae with oval conidia in clusters at tip of slender conidiophores (resembles a daisy)


Treatment and Prevention of Sporotrichosis

-treatment: 3-6 months itraconazole or other oral azoles for normal form of disease
-for more serious types, admit for Amphotericin B
-prevention: garden gloves


Recurring Themes of Systemic Mycoses

-environmental: spores/fungi in soil
-inhaled into lungs
-thermal dimorphism
-wide range of severity: asymptomatic clearance to death
-not person to person transmissible
-coccidioides/histoplasma/blastomyces: mimic TB
-History: American dirt, not foreign crowds



-coccidioides= coccidioidomycosis
-coccidioides immitis and C. posadasii
-dimorphic: mold in soil, spherule in tissue
-grow in the rainy season as mycelial (noninfectious)
-in the dry summer, forms hyphae with alternating arthrospores and empty cells
-when disturbed by wind or excavation, readily release arthroconidia (infectious)
-spores are carried by wind, inhaled by humans
-endemic in southwest US and Latin America; may travel home in returning patient or arrive in contaminated shipped material
-caseload has spiked in this century as endemic areas have become geriatric population centers: Phoenix, Tucson, Fresno, El Paso
-symptomatic disease can keep a previously healthy person out of school or work for a month
-80% of residents in endemic areas develop positive skin test within 5 years


Pathogenesis of Coccidioides

-arthrospores are inhaled: infectious dose can be as low as 1U, though high dosage is more likely to cause symptoms
-within terminal bronchiole change form:
-spherules: highly resistant to eradication by immune system
-30um diameter
-thick, doubley refractive wall
-filled with endospores
-wall ruptures to release endospores, develop into new spherules
-spherules and endospores are not infectious
-depends a lot of exposure and healthy or immunosuppressed


Phases of Coccidioides Pathogenesis

-Acute phase- innate immunity (macrophage response) attempts to clear infection: often successful

-Chronic phase: innate immunity inadequate for clearance; lymphocytes and histiocytes initiate granuloma and giant cell formation (containmnet)

-if CMI is healthy, infection is contained in granulomas in lung; many eventually cleared asymptomattically
-many patients who become ill have nonspecific flulike symptoms that resolve at home (~60% exposures = asymptomatic and flulike


Valley fever

-coccidioides symptomatic disease may appear as Valley Fever or desert rheumatism
-erythema nodosum
-erythema multiform
-chest pain


Risk factors for cocidioides

-if immunosuppressed, disseminated infection both by intracellular travel in macrophages and hematogenous spread
-risk factors: advanced age, immunocompromised, late-stage pregnancy, occupational high-level exposure ( farmers, construction workers, archeaologists), black or Filipino race
-may affect any organ; primary seen in bone and meninges
-induced immune anergy; may be rapidly fatal


Coccidioides Lab Diagnosis

-take biopsies of relevant tissues, CSF, blood, urine, stain with H and E or funal stains; examine microscopically for spherules
-cultures on Sabourand's agar at 25C: cottony white mold composed of hyphae with arthrospores: cultures are infectious! Handle in Biosafety 3
-Serology for exposure, titers: IgG from blood and/or CSF titer spikes if disseminating. Positives are very reliable, but some false negatives occur


Treatment of Coccidioides

-high morbidity but low mortality
-no treatment required for mild disease
-must treat is predisposed to complications: severe immunosuppression, diabetes, cardiopulmonary disease, (oral azoles), pregnancy ( Amphotericin B)
-persisiting lung lesions or disseminated: Amphotericin B and long term itraconazole
-minimum of 6 months drug therapy, follow ups for at least a year


Opportunistic Mycoses Themes

-diseases and severity are widely varied, depending on the patients' pre-existing conditions
-optimal treatment addresses both the infection and the underlying problem



-crytococcus neoforms and C. gattii form 5 serotypes, A,D, and AD are neoforms, B and C are gattii

-crytococcosis, esp cryptococcal meningitis
-C. neoformans is environmental, found worldwide in soil contaminated w/ bird droppings, esp pigeon

-oval yeasts with narrow based buds and wide polysaccharide capsule

-pathogenic strains grow at 37C
-not thermally dimorphic
-no human to human transmission
-polysaccharide capsule
-disseminated disease fatal before Amphotericin B


Crytococcosis Pathogensis

-transmitted by inhalation: pigeon droppings may be contagious for years
-lung infection may be asymptomatic or lead to pneumonia
-can be intracellular infection in alveolar macrophages
-immunocompentent hosts restrict infection to lungs
-successful hosts raises Helper Ts, skin test conversion, antibodies to capsule
-deficient CMI, esp AIDs predisposing for dissemination
-dissemination- crytococcal meningitis w/ skin nodules

Virulence factors: capsule, melanin in cell wall (antiphagocytic), Phospholipase B for invading tissue


Diagnosis of Cryptococcosis

History: steriod use, malignant disease, transplantation, HIV
Skin: biopsy
Pulmonary: range from symptomatic to ARDS, cough and chest pain common
with HIV: fever, cough, headache, weight loss, positive cultures in blood, CSF, urine
CNS: subacute meningitis, antifungal needed to live


Lab for Cryptococcosis

-CSF: stain with India ink to observe yeast with wide capsule
-Biopsy: stain with methenamine silver, periodic acid-Schiff, mucicarmine
-Culture: at 37C for CSF, blood, urine, sputum for mucoid colonies on Sabourand agar, will produce melanin in culture on special media
-Serology: crag for crytococcal antigen in blood and CSF
-Routine bloodwork may be normal


Treatment of Cryptococcosis

-pulmonary cryptococcosis may not need treatment
-Amphotericin B plus flucytosine if meningitis
-In AIDS use fluconazole for long term suppression
-examine CSF weekly