Fungi II Flashcards
- What are superficial mycoses (i.e. dermatophytosis) caused by?
- Do superficial mycoses require thermal dimorphism?
- What are the symptoms and how are they treated?
- Fungal growth on the superficial skin
- No, often growing on cool exterior as hyphae
- Itch or discoloration, treated with topical azoles, alt oral griseofulvin
- What causes dermatophytosis?
2. What does it infect?
- Dermatophytes
- Only superficial keratinized structures - skin, hair, nails, produce keratinases that allow invasion of the cornified cell layer
- What does dermatophytosis look like?
- How is it transmitted?
- What will some patients have?
- Chronic infections in warm, humid areas on body surfaces - inflamed circular border of papules and/or vesicles - it is named ofr the affected body part : Tinea capitis (head), etc.
- Transmitted by fomites or autoinoculation from other sites on body
- Hypersensitive dermatophytid (“id”) reactions: vesicles on fingers - caused by hypersensitivity to circulating fungal antigen - the vesicles do not contain live fungus
- How do you diagnose dermatophytosis?
2. Treatment
- Itching, redness, history of tight or wet clothing. On microscopic exam, examine for hyphae and spores. Culture on Sabouraud’s agar at room temperature. Microsporum show fluorescence when examined under Wood’s lamp.
- Topical antifungal cream - treat all affected body sites simultaneously, alternatively - oral griseofulvin and keep skin dry and cool
- How do you get subcutaneous mycoses (i.e sporotrichosis)?
- Is there thermal dimorphism?
- What are some indications to look for?
- How do you treat?
- Introduced by trauma exposing subcutaneous tissue to soil or vegetation - slow spread from trauma site to trunk by lymphatics
- Yes
- Patient presents with history of ineffective antibiotic treatment
- With oral azoles, in serious cases, may begin with short course of amphotericin B and surgery
- Where is sporotrichosis found?
- How does it manifest?
- What to look for in lab diagnosis?
- Treatment?
- On vegetation, often seen in gardeners - thermally dimorphic
- 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 corticosteroid use may develop pulmonary symptoms from inhaling the spores - difficult to distinguish from TB or histoplasmosis
- Round or cigar-shaped budding yeasts -hard to see, culture pus at room temp = hyphae with oval conidia in clusters at tip of slender conidiophores
- 3-6 months itraconazole or other oral azoles for normal fowm of disease - for more seirous admit for amphotericin B
Major themes in systemic mycoses:
- Environmental?
- Thermal dimorphism?
- What is the range of severity?
- Yes - spores/fungi in soil, inhaled into lungs
- Yes
- Wide, from asymptomatic clearance to death - not person-to-person transmissible - coccidioides/histoplasma/blastomyces: mimic TB
Coccidioides (systemic mycoses)
1. Dimorphic?
- yes, mold in soil, spherule in tissue - in the dry season, forms hyphae with alternating arthrospores and empty cells - when disturbed by wind or excavation, readily release arthroconidia (infectious) - spores carried by wind, inhaled by humans
Pathogenesis of coccidioides:
1. How large is the infectious dose?
- Can be as low as a single IU, though high dosage is more likely to cause symptoms - spherules are highly resistant to eradication by immune system in terminal bronchiole, filled with endospores, walls rupture to release endospores and develop into new spherules. Spherules and endospores are not infectious
What the acute phase of coccidioides?
What is the chronic phase?
Innate immunity (macrophage response) attempts to clear infection: often successful.
Innate immunity inadequate for clearance; lymphocytes and histiocytes initiate granuloma and giant cell formation (containment)
If CMI is healthy, infection is contained in granulomas in lung; many eventually cleared asymptomatically
many patients who become ill have nonspecific flulike symptoms that resolve at home
symptomatic disease may appear as Valley fever or desert rheumatism - fever, arthralgias, erythema nodosum, erythema multiforme, chest pain
What happens if you are immunosuppressed and have coccidioides?
Disseminated infection both by intracellular travel in macrophages and hematogenous spread. Risk factors - advanced age, immunocompromise, late-stage pregnancy, occupational high-level exposure (farmers, construction workers, archaeologists), black or Filipino race - may affect any organ; primarily seen in bones and meninges - induce immune anergy; may be rapidly fatal
How can you diagnose in lab?
Biopsies of tissues, CSF, blood, urine, stain with H&E or fungal stains; examine microscopically for spherules
Cultures on Sabouraud’s agar at 25C: cottony white mold composed of hyphae with arthrospores: cultures are infectious! handle in biosafety level 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
No treatment required for mild disease
Must treat if predisposed to complications (immunosuppression, diabetes, cardiopulmonary disease, pregnancy)
With persisting lung lesions or dissemination: Amphotericin B and long-term itraconazole - minimum of 6 months of drug therapy, folloup for year
Themes in opportunistic mycoses
- Disease and severity are widely varied, depending on the patients’ pre-existing conditions
- Optimal treatment addresses both the infection and underlying problem
Cryptococcosis
what temp do they grow at?
C. neoformans, C. gatti, 5 serotypes. cryptococcal meningitis
C. neoformans is environmental, found worldwide in soil contaminated with bird droppings, esp pigeons, oval yeasts with narrow-based bugs and wide polysaccharide capsules
37C, not thermally dimorphic; does have a moldlike sexually reproducing form in environment
No human-to-human transmission except organ transplantation or needle sticks (localized cutaneous disease)
C. meningitis rare before 1946, use of steroids, survival with malignancy and AIDS have dramatically increased caseload.
Disseminated disease was inevitable fatal prior to amphotericin B
