Lecture 13: Intro To Mycology Flashcards
The oral mycobiome is predominated by what fungi?
The oral mycobiome in the healthy oral cavity is predominated by what fungi?
-Candida sp.
-Malassezia
can proliferate to cause opportunistic infections
Fungi
-size
-grow as
-how many are pathogenic? Oral lesions?
-cell type
-replication
-3-6 um = bigger than bacteria and virus (light microscope)
-hyphae (mold) or yeast
-150 pathogenic, handful cause oral lesions (candidiasis)
-eukaryotic
-sexually or asexually
What fungal species is most commonly found in the oral micro biome of healthy individuals?
Candida albicans
Malassezia
Common fungal colonizer of the oral cavity
-candida (albicans, tropicales, Dubliniensis, parasilosis, krusei, Glabrata)
-cladosporium spp.
-saccharomyces spp (yeast to make bread)
-aspergillus spp.
-cryptococcus spp.
-fusarium spp.
How do humans protect against fungi?
-temperature: 37: too hot for all but some tolerate
-low [O2]
-immune cells: innate & adaptive
What do these anti fungal drugs target?
Give medication example for each.
What do they share in common?
-polyenes
-azoles
-allylamines
-echinocandins
will target cell wall
-polyenes = AMPHOTERICIN B = binds to ergosterol. target resembles cholesterol
-azoles = KETOCONAZOLE = inhibits ergosterol. Synthesis through cytochrome p450
-allylamines = TERBINAFINE = inhibits ergosterol. Synthesis via squalene epoxidase (fungi specific enzyme)
-echinocandins = MICAFUNGIN =targets b-glucans (unique to fungal wall) - fewer side effects
Which antivirals binds or inhibit ergosterol?
-polyenes = AMPHOTERICIN B (cholesterol) bind to ergosterol
-azoles = KETOCONAZOLE (cytochrome p450) inhibit ergosterol
-allylamines = TERBINAFINE (fungi-specific enzyme) inhibits ergosterol
exception
-echinocandins = MICAFUNGIN (cell wall) target b-glucans
Candida cell wall components and its influence on resistance and virulence
B-1,3 glucan/B-1,6 glucan
Ergosterol = “cholesterol”
Chitin
Mannoproteins = on the surface to metabolize ion exchange
hides and resistance to anti fungal stress
Cryptococcus cell wall components and influence on resistance and virulence
B-1,3/B-1,6 glucan
Ergosterol
Chitin
A-1,3-glucan
Chitoson
Melanin
CAPSULE
hides and resistance to anti fungal stress
*Th2/Th1 (activation of no response from immune) RAISE TH2
*dissemination
Aspergillus cell wall components and its influence on resistance and virulence
B-1,3/B-1,3-1,4/B-1,6 -glucan
A-1,3-Glucan
Ergosterol
Chitin
Melanin
GALACTOSAMINOGALACTAN
GALACTOMANNAN
RODLET
hides and th2/th1
Th2/Th1= activates of no protection from immune
On the cell wall we can have either:
-galactosaminogalactan
Or
-melanin + rodlet
How many subtypes of asexual conidia?
Conidia = spores
2 subtypes of Asexual conidia
-sporangiospore = in a sac called a sporangium
-conidiospore = “sac-less.” produced at the tips and sides of hyphae
What are the subdivisions for “sac-less” conidia ?
“Sac-less” conidia are also called?
-micro- small conidia
-macro- large conidia
-phialo- vase-shaped
-poro- conidia growing through small pores
-blasto- budding from parent
-chlamydo- w/n hyphal segment by thickening or formed terminally
-arthro- fragmentation of septate hyphae
Add-conidia
Sac-less conidia are called conidiospore
This is 1/2 subtypes of asexual conidia
Categories for sexual reproduction
-asco-spore: nuclei fuse in a sac-like ascus
-basidio-spore: formed externally on a base pedestal
-zygo-spore: tips of multinucleate hyphae copulate
What are mycoses? Mycoses classification? - 5 groups
Mycoses= chronic infections
-superficial
-cutaneous
-subcutaneous
-systemic
-opportunistic
True pathogens are described as?
-invade and grow in a healthy host
-high temp, low oxygen (OBVIOUSLY) = thermal dimorphism
-High pathogenicity
-rare
Intermediate pathogens are described as?
-inoculation (open wound or abrasion)
-not inherently invasive
Opportunistic infections are described as?
-require compromised host
-low pathogenicity
-do not show thermal dimorphism
How can a host detect fungi?
A host can detect a fungi through PRRs.
These PRRs recognize PAMPs
PAMPs include -glucan, mannan, and chitin on the fungal cell surface
What factors play a role in Fungal virulence? (8)
-include cell wall antigens
-thermal dimorphism (high temp, low O2)
-conversion to yeast form (more invasive than hyphae)
-mannoproteins (cándidas) (adherence)
-mannan (allows more persistent and chronic infection b/c circulates in body and slow epidermal cell turnover)
-melanin (in aspergillus & Cryptococcus) protects against oxidative burst of neutrophils and macrophages)
-capsule (in cryptococcus)
-fungal mycotoxins (allergens & psilocybin)
-extracellular enzymes (protease, lipases, keratinase, elastases)
Non-specific HOST defense mechanisms against fungal infections
-barrier function: mucosa, saliva (histatins)
-complement system
-initial response: recognition of fungal PAMPs by our PRRs on APCs (APCs = macrophages)
TLR2 and TLR4 recognize mannans (mannans = cell wall antigen- circulates in body, slow epidermal turnover)
c-type lectin receptor dectin 1 recognize surface B-glucan
Specific HOST defense mechanisms against fungal infection
-what happens when there’s a depletion of CD4+ T cells?
-what activates and recruits neutrophils?
-humoral immunity
-cell-mediated immunity
-IgA (agglutinate microorganisms)
-leads to aspergillosis or oropharyngeal candidiasis (immunocompromised people)
-Th17 cells/cytokine Interleukin-17 (IL-17))
