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Slide 1 - Title

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Slide 2 - What is Mycology?

• Mycology is the study of fungi, which are eukaryotic organisms (they have a nucleus, unlike bacteria).
• There are over 100,000 species of fungi, but only about 200 are pathogenic (disease-causing) to humans and animals.
• Over the past decade, serious fungal infections have been increasing in frequency, especially in:
  • Healthcare settings (hospital-acquired infections)
  • People with compromised immune systems (immunocompromised patients)

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Slide 3 - Types of Fungi: Yeasts and Molds

• Hyphae can be:
  • Septate - have transverse walls (cross walls between cells)
  • Nonseptate (coenocytic) - no cross walls, multinucleated
• Hyphal growth occurs at the tip of the filament, not by cell division all along it

• Some medically important fungi change form depending on temperature:
  • 25°C (environment/room temp): grow as molds
  • 37°C (body temp in human tissues): grow as yeasts
• This is called thermal dimorphism and is key to how they infect humans.

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Slide 6 - Physiology & Cell Structure of Fungi

• Most fungi are obligate aerobes (need oxygen); some are facultative anaerobes; none are obligate anaerobes.
• They need a preformed organic carbon source - hence their association with decaying matter.
• They use ammonium or nitrate ions as a nitrogen source.
• Most fungi live in the environment, except Candida albicans, which is part of normal human flora.

1. Cell wall - made of CHITIN (not peptidoglycan like bacteria)
   • This is why antibiotics like penicillins, cephalosporins, and vancomycin do NOT work against fungi - they target peptidoglycan.
2. Cell membrane - contains ERGOSTEROL (not cholesterol like human cells)
   • This difference is exploited by antifungal drugs:
     • Amphotericin B binds ergosterol directly
     • Azoles (fluconazole, ketoconazole) inhibit ergosterol synthesis
   • Human cell membranes use cholesterol, so these drugs are selective for fungi.

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Slide 7 - Anamorph

• Anamorph refers to the mitotic or asexual reproductive state of a fungus (as opposed to the teleomorph, which is the sexual state).

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Slide 9 - Pathogenesis of Fungal Infections

1. Entry - via inhalation (e.g., Aspergillus spores), skin/mucosal breach, or commensal overgrowth (e.g., Candida overgrowth after antibiotic use)
2. Adherence - fungi attach to epithelial cells using adhesins and form biofilms (e.g., Candida)
3. Invasion - via hyphal penetration, enzyme secretion (e.g., proteases), or dimorphic switching (e.g., Histoplasma converts to yeast at body temperature)
4. Immune Evasion - using capsules (e.g., Cryptococcus), biofilms, and antigenic variation
5. Host Damage - through tissue destruction, inflammation, and systemic spread (especially in immunocompromised hosts)

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Slide 10 - Fungal Toxins & Allergies (Mycotoxins)

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Slide 11 - Types of Fungal Infections in Humans

1. Superficial Mycoses - affect only the outermost layers of skin (stratum corneum) or hair cuticle; cosmetic problem only, rarely trigger immune response
2. Dermatophyte Infections - affect nails, hair, and skin; caused by dermatophytes
3. Subcutaneous Mycoses - fungi enter through traumatic skin implantation; low infectivity, spread to subcutaneous tissue
4. Systemic Mycoses - the most serious; only 5 specific fungi can cause these: Histoplasma capsulatum, Blastomyces dermatitidis, Paracoccidioides brasiliensis, Coccidioides immitis, and Penicillium marneffei. The primary site of infection is the respiratory tract.

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Slide 13 - Immune Response to Fungi

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Slide 14 - Laboratory Diagnosis

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Slide 15 & 16 - Antifungal Agents

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Slides 19-20 - Superficial Fungal Infections

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Slides 21-23 - Cutaneous Fungal Infections (Dermatophytoses)

• KOH prep → branched hyphae
• Wood's light (UV at 365nm) → Microsporum species fluoresce brilliant green

• First-line: topical imidazoles; keep skin dry
• Tinea capitis & unguium: oral griseofulvin (incorporates into newly synthesized keratin, clears as old keratin is replaced)

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Slides 24-25 - Subcutaneous Fungal Infections

• Occupational hazard for gardeners (found in soil, hay, moss, plant surfaces)
• Entry: thorn prick → subcutaneous nodule → necrosis → ulceration → new nodules spreading up the arm along lymphatic tracts
• Dimorphic: yeast at 37°C, branching hyphae at 25°C
• Treatment: oral potassium iodide or amphotericin B

• Copper-colored soil fungi on rotting wood
• Entry via puncture wound → violet wart-like lesions → clusters resembling cauliflower
• KOH prep → copper-colored sclerotic bodies
• Treatment: itraconazole + local excision

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Slides 26-29 - Systemic Fungal Infections (Dimorphic Triad)

• Histoplasma & Blastomyces: endemic to Mississippi River drainage basin (central US)
• Coccidioides: endemic to southwestern US (Arizona, New Mexico, southern California) and northern Mexico; 2nd most common opportunistic infection in AIDS patients in Arizona

1. Asymptomatic (majority)
2. Pneumonia (mild to severe; can become chronic cavitary pneumonia with weight loss, night sweats, fever)
3. Disseminated (rare; meningitis, bone lesions, skin ulcers - mainly in immunocompromised)

• Acute pulmonary histoplasmosis/coccidioidomycosis: often no treatment needed
• Chronic/disseminated: itraconazole or amphotericin B for months
• All Blastomyces: aggressive amphotericin B or itraconazole

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Slides 30 & 32 - Cryptococcus neoformans (Cryptococcosis)

• A polysaccharide-encapsulated yeast (NOT dimorphic)
• Found in nature, especially in pigeon droppings
• Inhaled → lung infection (usually asymptomatic) → spreads via blood to brain
• No geographic clustering (unlike the dimorphic triad)
• ~75% of cases in immunocompromised; nearly 100% of AIDS patients develop cryptococcosis

• Symptoms: headache, nausea, confusion, staggering gait, cranial nerve deficits
• Fatal without treatment (cerebral edema → brainstem compression)

• Lumbar puncture + CSF analysis
• Cryptococcal antigen test (detects polysaccharide antigens in CSF) - most sensitive
• Culture confirms diagnosis

• Amphotericin B + flucytosine for up to 6 months
• AIDS patients may require treatment for life

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Slides 33-34 - Candida albicans (Candidiasis)

1. Esophagitis - extension of thrush; burning substernal pain worsened with swallowing
2. Disseminated candidiasis - bloodstream invasion, every organ possible; check retina (white fluffy patches); isolation from blood is always abnormal and must be treated

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Slides 35-36 - Aspergillus (Aspergillosis)

1. Allergic reaction (in normal hosts): Type I (IgE-mediated, bronchospasm, eosinophilia) AND Type IV (cell-mediated) hypersensitivity → Allergic bronchopulmonary aspergillosis (ABPA) - treated with systemic corticosteroids
2. Aspergilloma (fungal ball): In pre-existing lung cavities (from TB or malignancy), Aspergillus grows into a ball - can be as large as a golf ball; may require surgical removal
3. Invasive aspergillosis (in immunocompromised): Pneumonia with bloody sputum due to blood vessel wall invasion by hyphae; can disseminate

• Aspergillus flavus produces aflatoxin - contaminates peanuts, grains, rice worldwide
• Causes liver cancer; 50% of cancers south of the Sahara are liver cancers, and 40% of screened foods contain aflatoxins - a significant global health threat

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Slide 37 - Recommended Books

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Summary of the Entire Lecture

1. Basic biology of fungi (structure, physiology, dimorphism)
2. Pathogenesis - how fungi enter, invade, and evade the immune system
3. Toxins and allergies caused by fungi
4. Classification of infections by anatomical depth (superficial → systemic)
5. Immune response to fungi
6. Diagnosis methods (KOH, culture, serology, DNA probes)
7. Antifungal drugs and their targets (ergosterol, cell wall, enzymes)
8. Detailed coverage of key pathogens: Malassezia, Sporothrix, Histoplasma, Blastomyces, Coccidioides, Cryptococcus, Candida, and Aspergillus