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Flashcards in 2-32 Fungi II Deck (20):

What are the four major categories of fungal infection?


What are some recurring themes for superficial mycoses?

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


What is the pathogenesis of superficial mycoses?

Caused by dermatophytes (AKA dermatophytoses)

Infect only superficial keratinized structures




▪ 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


How are superficial mycoses diagnosed, treated, and prevented?

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


What are some recurring themes for subcutaneous mycoses?

  • 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


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


What is the pathogenesis of subcutaneous mycoses?

▪ 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


How are subcutaneous mycoses diagnosed?

▪ 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)


How are subcutaneous mycoses treated and prevented?

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


What are some recurring themes in 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


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

•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


What is the general pathogenesis of coccidioides?

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


What are the phases of coccidioides infection?

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)


What are risk factors for coccidioides infection?

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


How is coccidioides infection diagnosed?

•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


How is coccidioides infection treated?

•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



What are some recurring themes for opportunistic mycoses?

  • 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




What is the pathogenesis of cryptococcus?

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 . . .


How is cryptococcosis diagnosed and treated?


  • 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


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