Mycology Tutorial Notes

Mycology: the study of fungi Fungi: are eukaryotic, spore-bearing, heterotrophic organisms producing extra cellular enzymes & absorb their nutrition Fungal classification: 900 Mya With four major lineages such as zygomycota, ascomycota(sac), basidiomycota(club), deuteromycota(imperfect) Although less than 1% are pathogenic and cause human infection Deuteromycota: Human pathogens i.e. athletes foot, ring worm, aspergilllus and non pathogens i.e. penicillium, camembert Fungi are eukaryotes that possess rigid cell walls of chitin. However, the cell membrane differs due to the ergosterol that replaces the cholesterol. They can either be uni or multi cellular. Yeasts are unicellular and moulds are multicellular Hyphae: Tubular with hard walls of chitin and cross walls which may form compartments. They are also multinucleat and they grow at tips. Feeding web Spores: Sexual reproduction- fusion of unicellular gametes or specialised hyphae called gametangia or by the fusion of 2 haploid cells to produce a diploid cell Types of spores include: Ascospores an enclosed sac common in bakers yeast i.e. saccharomyces cerevisiae Basidiospores produced on the end of the club-shaped structure Zygospores produced by zygomycetous fungi which are common bread moulds i.e. rhizopus Spores of fungal are not as resistant to heat Yeast: single called fungi adapted to liquids such as Plant saps, water films and most animal tissues i.e. Saccharomyces and candida Yeast reproduction: Moulds: Hyphae are tubular units of construction form mycelium Saprophytic secure nutrients by absorption Reproduction can be both sexual and asexual Fungi pathogenesis: Dermatophytes(skin): microsporum, trichophyton, epidermophyton Candida spp C.albicans thrush, oral candidiasis Aspergilllus spp (RTI) Cryptococcus spp (meningitis) Very few fungi cause primary pathogenesis but healthy individuals have high resistance to fungal infections due to barriers such as skin, mucosal surfaces etc. the pathogenic opportunities increase when host is immunosuppressive such as with HIV or commensalism parameters are altered such as C. Albicans Superficial is mainly cosmetic and rarely induces immune responses and is infection of the outermost layer of skin or hair shaft Dermatophyte/cutaneous have increased invasive properties but do not pass into the deeper skin layers thus, colonising skin hair and nails Subcutaneous produce proteolytic enzymes and can enter via skin trauma (moulds and yeasts) Systemic is the most dimorphic (change from unicellular to mycelial type to evade the hosts immune system vice versa) and enter by inhalation or skin trauma Dermatophytes Are keratin loving organisms that invade keratinised structures such as skin hair and nails, they digest keratin by keratinases and are resistant to cycloheximide I.e. trichophyton- hair skin nails, microsporum- hair skin, epidermophyton- skin nails Tinea infection: T. Corpis or ringworm- microsporum can is, trichophyton mentagophytes T. Pedis or athletes foot- T. Rubrum, t. Mentagophytes, epidermophyton floccosum T. Capitals or head ringworm- m. Canis, t. Tonsurous T. Unguium or nail ringworm- t. Rubrum, t. Mentagophytes, e. Floccosum Candida albicans: Dimorphic, diploids who have no sexual cycle, commensalism mucousal membranes/skin and can invade mucosa superficial i.e. thrush. Can cause systemic infections and are opportunistic Antifungal drugs: As they are eukarya, man y cellular components are the same as humans Antifungal agents work on the same metabolic pathways in fungi as the host which makes them toxic Majority are topical and oral drugs target unique fungal structures Antifungal agents: Ergosterol inhibitors- ergosterol in fungi replaces cholesterol found in the human cytoplasmic membranes Polyenes produced by streptomyces disrupt the membrane integrity and cause permeability Azoles synthetic agents abnormal fungal membranes Allylamines synthetic agent inhibit ergosterol and are topical so not readily taken up by animal cells Echincandins inhibits 1,3 beta-D glucan synthesis, an enzyme that forms glucan polymers in the fungal cell wall