Lecture 13: Intro To Mycology

Question 1

The oral mycobiome is predominated by what fungi?
The oral mycobiome in the healthy oral cavity is predominated by what fungi?

Answer 1

-Candida sp.
-Malassezia

can proliferate to cause opportunistic infections

Question 2

Fungi
-size
-grow as
-how many are pathogenic? Oral lesions?
-cell type
-replication

Answer 2

-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

Question 3

What fungal species is most commonly found in the oral micro biome of healthy individuals?

Answer 3

Candida albicans
Malassezia

Question 4

Common fungal colonizer of the oral cavity

Answer 4

-candida (albicans, tropicales, Dubliniensis, parasilosis, krusei, Glabrata)
-cladosporium spp.
-saccharomyces spp (yeast to make bread)
-aspergillus spp.
-cryptococcus spp.
-fusarium spp.

Question 5

How do humans protect against fungi?

Answer 5

-temperature: 37: too hot for all but some tolerate
-low [O2]
-immune cells: innate & adaptive

Question 6

What do these anti fungal drugs target?
Give medication example for each.
What do they share in common?
-polyenes
-azoles
-allylamines
-echinocandins

Answer 6

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

Question 7

Which antivirals binds or inhibit ergosterol?

Answer 7

-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

Question 8

Candida cell wall components and its influence on resistance and virulence

Answer 8

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

Question 9

Cryptococcus cell wall components and influence on resistance and virulence

Answer 9

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

Question 10

Aspergillus cell wall components and its influence on resistance and virulence

Answer 10

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

Question 11

How many subtypes of asexual conidia?

Answer 11

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

Question 12

What are the subdivisions for “sac-less” conidia ?
“Sac-less” conidia are also called?

Answer 12

-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

Question 13

Categories for sexual reproduction

Answer 13

-asco-spore: nuclei fuse in a sac-like ascus
-basidio-spore: formed externally on a base pedestal
-zygo-spore: tips of multinucleate hyphae copulate

Question 14

What are mycoses? Mycoses classification? - 5 groups

Answer 14

Mycoses= chronic infections
-superficial
-cutaneous
-subcutaneous
-systemic
-opportunistic

Question 15

True pathogens are described as?

Answer 15

-invade and grow in a healthy host
-high temp, low oxygen (OBVIOUSLY) = thermal dimorphism
-High pathogenicity
-rare

Question 16

Intermediate pathogens are described as?

Answer 16

-inoculation (open wound or abrasion)
-not inherently invasive

Question 17

Opportunistic infections are described as?

Answer 17

-require compromised host
-low pathogenicity
-do not show thermal dimorphism

Question 18

How can a host detect fungi?

Answer 18

A host can detect a fungi through PRRs.
These PRRs recognize PAMPs
PAMPs include -glucan, mannan, and chitin on the fungal cell surface

Question 19

What factors play a role in Fungal virulence? (8)
-include cell wall antigens

Answer 19

-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)

Question 20

Non-specific HOST defense mechanisms against fungal infections

Answer 20

-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

Question 21

Specific HOST defense mechanisms against fungal infection
-what happens when there’s a depletion of CD4+ T cells?
-what activates and recruits neutrophils?

Answer 21

-humoral immunity
-cell-mediated immunity
-IgA (agglutinate microorganisms)

-leads to aspergillosis or oropharyngeal candidiasis (immunocompromised people)
-Th17 cells/cytokine Interleukin-17 (IL-17))