Fungi 2 Flashcards
1
Q
Fungal Molds vs Yeasts
A
- Molds:
- asexual or sexual reproduction with spores
- multicellular: not very mobile in the body
Yeasts:
- asexual by budding
- single celled: can circulate resistant to phagocytosis
Other:
-dimorphs- thermal dimorphs
2
Q
Four categories of Fungal Infections (Mycosis)
A
- 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
3
Q
Themes of Superficial Mycoses
A
- 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
4
Q
Superficial Mycoses: Dermatophytosis
A
- caused by dermatophytes
- infect only superficial keratinized structures- skin, hair, nails
- produce keratinases that allow invasion of cornified cell layer
5
Q
Pathogenesis of Dermatophytosis
A
-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
6
Q
Hypersensitive dermatophytid reactions
A
- 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
7
Q
Diagnosis of Dermatophytosis
A
- 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
8
Q
Dermatophytosis: Treatment and Prevention
A
- 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
9
Q
Themes in Subcutaneous Mycoses
A
- 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
10
Q
Sporotrichosis
A
- Sporothrix schenckii and other species
- thermally dimorphic
- found on vegetation
- often seen in gardeners, particularly of roses (thorns)
11
Q
Pathogenesis of Sporotrichosis
A
- 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
12
Q
Exam of Sporotrichosis
A
- 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
13
Q
Diagnostic Lab of Sporotrichosis
A
- 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)
14
Q
Treatment and Prevention of Sporotrichosis
A
- 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
15
Q
Recurring Themes of Systemic Mycoses
A
- 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
16
Q
Coccidioides
A
- 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
17
Q
Pathogenesis of Coccidioides
A
- 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
18
Q
Phases of Coccidioides Pathogenesis
A
- 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
19
Q
Valley fever
A
- coccidioides symptomatic disease may appear as Valley Fever or desert rheumatism
- fever
- arthralgias
- erythema nodosum
- erythema multiform
- chest pain
20
Q
Risk factors for cocidioides
A
- 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
21
Q
Coccidioides Lab Diagnosis
A
- 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
22
Q
Treatment of Coccidioides
A
- 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
23
Q
Opportunistic Mycoses Themes
A
- diseases and severity are widely varied, depending on the patients’ pre-existing conditions
- optimal treatment addresses both the infection and the underlying problem
24
Q
Crytococcosis
A
-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
25
Q
Crytococcosis Pathogensis
A
- 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
26
Q
Diagnosis of Cryptococcosis
A
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
27
Q
Lab for Cryptococcosis
A
- 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
28
Q
Treatment of Cryptococcosis
A
- pulmonary cryptococcosis may not need treatment
- Amphotericin B plus flucytosine if meningitis
- In AIDS use fluconazole for long term suppression
- examine CSF weekly
