2-32 Fungi II Flashcards

1
Q

What are the four major categories of fungal infection?

A
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2
Q

What are some recurring themes for superficial mycoses?

A

Caused by fungal growth on the 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
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3
Q

What is the pathogenesis of superficial mycoses?

A

Caused by dermatophytes (AKA dermatophytoses)

Infect only superficial keratinized structures

  • Skin
  • Hair
  • Nails

▪ Form chronic infections in warm, humid areas 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 (Athlete’s foot)

▪ Transmitted by fomites or by autoinoculation from other sites on body

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4
Q

How are superficial mycoses diagnosed, treated, and prevented?

A

Exam: itching, redness, history of tight or wet clothing

Microscopic exam

Scraping from affected skin or nail

Treat w/ 10% KOH

Examine remains for hyphae & spores

Culture on Sabouraud’s agar at room temp

Microsporum show fluorescence when examined under Wood’s lamp

Topical antifungal cream

Terbinafine (Lamisil)

Undecylenic acid (Desenex)

Miconazole (Micatin)

Tolnaftate (Tinactin)

Note: treat all affected body sites simultaneously

Alt: oral griseofulvin (Fulvicin)

Keep skin dry and cool

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5
Q

What are some recurring themes for subcutaneous mycoses?

A
  • Introduced by trauma exposing subcutaneous tissue to soil or vegetation
  • Slow spread trauma site → trunk by lymphatics
  • Thermal dimorphism
  • Patient presents with history of ineffective antibiotic treatment
  • Treated with oral azoles
  • In serious cases, may begin with a short course of amphotericin B and surgery
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6
Q

What is an example of an organism that causes a subcutaneous mycosis?

A
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7
Q

What is the pathogenesis of subcutaneous mycoses?

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 corticosteroid use may develop pulmonary symptoms from inhaling the spores; difficult to distinguish from TB or histoplasmosis

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8
Q

How are subcutaneous mycoses diagnosed?

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

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)

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9
Q

How are subcutaneous mycoses treated and prevented?

A

Treatment: 3-6 months itraconazole (Sporanox) or other oral azoles for normal form of disease

For more serious types, admit for Amphotericin B

Prevention: garden gloves

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10
Q

What are some recurring themes in 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
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11
Q

What is an example of an organism that causes systemic mycosis?

A
  • Coccidioides = coccidioidomycosis
  • Coccidioides immitis and C. posadasii
  • Dimorphic: mold in soil, spherule in tissue
  • Grow in the rainy season as mycelia (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 the 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

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12
Q

What is the general pathogenesis of coccidioides?

A

Arthrospores (arthroconidia) are inhaled: Infectious dose can be as low as a single IU, though high dosage is more likely to cause symptoms

Within terminal bronchiole, change form

  • Spherules: highly resistant to eradication by immune sys
  • 30um diameter
  • Thick, doubly-refractive wall
  • Filled with endospores
  • Wall ruptures to release endospores, develop into new spherules
  • Spherules and endospores are not infectious

Symptomatic disease may appear as Valley fever or desert rheumatism

•May affect any organ; primarily seen in bones and meninges

•Induces immune anergy; May be rapidly fatal

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13
Q

What are the phases of coccidioides infection?

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 (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 (~60% exposures = asymptomatic+flulike)

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14
Q

What are risk factors for coccidioides infection?

A

•advanced age, immunocompromise, late-stage pregnancy, occupational high-level exposure (farmers, construction workers, archaeologists), black or Filipino race

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15
Q

How is coccidioides infection diagnosed?

A
  • Workup for pneumonia, meningitis
  • Take biopsies of relevant 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
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16
Q

How is coccidioides infection treated?

A
  • High morbidity but low mortality
  • No treatment required for mild disease (minor pneumonia, asymptomatic nodules); oral azoles may be used, no data indicate faster or better resolution
  • Must treat if predisposed to complications: severe immunosuppression, diabetes, cardiopulmonary disease, (oral azoles) pregnancy (Amphotericin B)
  • Persisting lung lesions or disseminated: Amphotericin B and long-term itraconazole.
  • Minimum of 6 months of drug therapy, followups for at least a year
17
Q

What are some recurring themes for opportunistic mycoses?

A
  • Diseases and severity are widely varied, depending on the patients’ pre-existing conditions
  • Prolonged neutropenia is the most important predisposition
  • Optimal treatment addresses both the infection and the underlying problem
18
Q

Cryptococcus

A
19
Q

What is the pathogenesis of cryptococcus?

A

Transmitted by inhalation

Lung infection may be asymptomatic or lead to pneumonia

Immunosuppression, esp AIDS, is predisposing but not required

for dissemination

Dissemination leads to cryptococcal meningitis w/ skin nodules

Disease is very low-inflammation

Virulence factors: capsule, melanin in cell wall . . .

20
Q

How is cryptococcosis diagnosed and treated?

A

Diagnosis:

  • Exam: meningitis w/ subcutaneous nodules
  • History: steroid use, malignant disease, transplantation, HIV infection
  • Lab: CSF: stain w/ India ink to observe yeast w/ wide capsule
  • Other stains: methenamine silver, periodic acid-Schiff, mucicarmine
  • Culture from spinal fluid for mucoid colonies on agar
  • Serologic tests: “crag” for cryptococcal antigen

Treatment:

  • Amphotericin B (liposomal if kidney issues) plus flucytosine
  • In AIDS patients, use fluconazole for long-term suppression