Biofilm 3 - Candida Flashcards

1
Q

What specific component distinguishes fungal cell walls from other organisms?

A

Chitin

polysaccharide

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2
Q

What is the most abundant component of fungal cell walls?

A

Glucans

polysaccharide

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3
Q

What are glycoproteins in the fungal cell wall?

A

Carbohydrates associated with proteins

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4
Q

What provides stability and regulates compounds entering and exiting fungal cells?

A

Phospholipids in the cell membrane

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5
Q

What is ergosterol and what is its function?

A

The fungal sterol equivalent of cholesterol; maintains structure and contributes to membrane-bound enzyme functions

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6
Q

What comprises the plaques in pseudomembranous candidiasis?

A

Desquamated epithelial cells, hyphae, and fibrin

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7
Q

In which conditions is pseudomembranous candidiasis common?

A

Immunocompromised patients and corticosteroid use

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8
Q

What key characteristic distinguishes chronic hyperplastic candidiasis from pseudomembranous?

A

White patches that do not wipe away (unlike pseudomembranous which can be removed)

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9
Q

Where does chronic hyperplastic candidiasis typically present?

A

On the buccal mucosa and border of the tongue

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10
Q

What serious condition is chronic hyperplastic candidiasis classified as?

A

Oral potentially malignant disorder (OPMD)

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11
Q

What condition is chronic hyperplastic candidiasis similar to?

A

Leukoplakia lesion

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12
Q

Describe Newton’s type I denture-induced stomatitis.

A

Localized inflammation

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13
Q

Describe Newton’s type II denture-induced stomatitis.

A

Diffuse inflammation

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14
Q

Why are dentures conducive to candidiasis?

A

They provide a solid abiotic surface for Candida to adhere and proliferate on

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14
Q

Describe Newton’s type III denture-induced stomatitis.

A

Granular inflammation

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15
Q

What environmental factors promote denture-induced stomatitis?

A

Sub-optimal hygiene and a protected environment

16
Q

Which is the most common form of oral candidiasis?

A

Pseudomembranous (Thrush)

17
Q

Name three Candida species other than C. albicans that can cause oral infection.

A

Any three of: C. glabrata, C. tropicalis, C. krusei, C. parapsilosis, C. dubliniensis

oppurtunastic

18
Q

Define biofilm according to the lecture.

A

“Matrix-enclosed microbial populations adherent to each other and/or to surfaces or interfaces”

19
Q

What are the four stages of biofilm formation?

A

Adhesio
Initiation (proliferation)
Maturation
Dispersal

20
Q

List three protective benefits that biofilms provide to microorganisms.

A

Immune evasion, antimicrobial resistance, resistance to detergents and antiseptics

21
Q

Besides protection, what other two benefits do biofilms provide?

A

Nutrient sharing/metabolic cooperation and better usage of resources (reduced energy usage)

22
Q

What term describes C. albicans’ ability to exist in multiple forms?

A

Morphogenic yeast

23
Q

What two primary morphological states can C. albicans exhibit?

A

Yeast and hyphal cells

24
List four virulence factors of C. albicans.
Any four of: biofilm formation, adhesion, morphogenesis, secreted proteinases, adaptability/heterogeneity, extracellular matrix (ECM)
25
Name five triggers that can cause morphogenic switching in C. albicans.
Any five of: temperature, serum, pH, nutrient starvation, osmolarity, other stress
26
What is the term for C. albicans' ability to switch between unicellular yeast and filamentous forms?
Polymorphic
27
How does the morphogenic transition affect cell size?
It drastically increases cell size
28
How might hyphal formation exert pressure on tissue?
Tight adhesion allows exerted pressure on tissue (mechanical force)
29
What gene family is key in Candida adhesion?
ALS (Agglutinin-Like Sequence)
30
Describe the key virulence factors of C. albicans.
Biofilm formation, adhesion (ALS gene family), morphogenesis, secreted proteinases (SAPs for tissue invasion/damage), HWP1 (covalent binding to buccal cells), adaptation/heterogeneity, extracellular matrix
31
How does the mycobiome relate to oral health versus disease?
Malassezia mycotype predominates in health; Candida mycotype is selected for in disease; Candida interacts with various bacterial species (not limited to oral cavity)
32
Compare the three main classes of antifungals by their mechanisms and examples.
Azoles (fluconazole, voriconazole): inhibit ergosterol synthesis; Polyenes (nystatin, amphotericin B): bind ergosterol creating membrane pores Echinocandins (caspofungin, micafungin): inhibit β-glucan synthesis
33
Explain three mechanisms of antifungal resistance in Candida.
Overexpression of target components (ergosterol) Mutations in drug targets (e.g., Erg11 in C. glabrata causing azole resistance) Changes in drug transporter expression (CDR/MDR)
34
Why are biofilms naturally resistant to antimicrobials and which antifungals remain effective?
Resistance due to: reduced permeability, matrix protection, persister cells, resource sharing Effective agents: polyenes, echinocandins, chlorhexidine (not azoles)
35
Describe culture-based methods for identifying Candida species.
Media: Sabouraud agar or CHROMagar; Conditions: 30-37°C aerobic (cells remain yeast at 30°C); Identification: microscopic examination (germ tube formation)
36
Compare molecular methods for identifying known vs. unknown Candida species.
Known species: qPCR with specific primers, MALDI-TOF, multi-locus sequence typing; Unknown species: 18S/ITS sequencing or whole genome sequencing