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Microbiology for Dentists > 21. Oral Fungal Infections > Flashcards

21. Oral Fungal Infections Flashcards

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1
Q

Fungi are simple …
Some can form …
And some transition between …

A
  • eukaryotes
  • multicellular structures like mushrooms, pin moulds
  • yeast and hyphal forms (e.g candida spp.)
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1
Q

Yeasts are … with … bodies

A
  • unicellular
  • spherical or ovoid
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2
Q

Hyphae are what?

A
  • thread-like tubes containing fungal cytoplasm and organelles `
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2
Q

Moulds are … with a variety of …

A
  • mutlicellular
  • specialised structures to perform specific functions
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3
Q

Define ‘mycelium’

A

mass of hyphae that forms mould colony

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4
Q

Fungi are …, … cells
With what two defining components?

A
  • larger, eukaryotic cells
  • with membrane-bound nucleus and mitochondria
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5
Q

Fungi for medicine are classified into …

A
  • yeasts
  • filamentous fungi
  • dimorphic fungi
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6
Q

Diameter of fungi
Relation to animal and bacteria

A
  • around 3-6 micrometres
  • smaller than animal, larger than bacteria
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7
Q

Fungi are slow/fast growing
Hetero/homotrophic?

A

slow
hetero

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8
Q

Fungi have a similarity with … cells of human host

A

mammalian

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9
Q

Fungi cell walls have what main component?

A

chitin

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10
Q

Cell walls in fungal cells

A
  • thick and rigid surrounding plasma membrane
  • two layers
  • contains ergosterol instead of cholesterol
  • outer amorphous layer of glycoproteins, carbohydrates, mannans
  • inner layers of polysacchardies e.g glucans/chitins
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11
Q

Role of fungal cell walls

A
  • antigenicity
  • adherance to host cells
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12
Q

Are fungi normally in mouth?

A

yes
- part of normal oral microbiota

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13
Q

Incidence of oral Candida carriage?

A

35-80% in healthy individuals

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14
Q

What’s the most predominant fungi in mouth?

A

candida species

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15
Q

Explain the genus ‘Candida’

A
  • over 400 species
  • mainly non-pathogenic
  • C.albicans over 90% of oral isolates
  • carried naturally but overgrowth can be infection (enumeration is important)
  • dimorphic fungi (yeasts and hyphaes)
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16
Q

Specifications about candida albicans

A
  • typically grows as spherical to oval budding yeast cells 3-5 x5-10 micrometres in size
  • indigenous to oral cavity, GI tract, female genital tract and skin
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17
Q

Explain the yeast to hyphae transition

A
  • hyphal form invades epithelia
  • certain cell surface receptors are only present in hyphae
  • morphotype switching is under complex regulation circuit
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18
Q

What controls the morphotype switching of yeast to hyphae?

A
  • osmotic shock
  • temp fluctuations
  • pH
  • nutrients
  • cell density
  • salivary factors like statherin
  • oral bacteria
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19
Q

How does oral bacteria interact with candida albicans?

A
  • grow alongside each other in mixed community
  • oral bacteria modulate morphology and physiology of C.albicans
  • some species synergistic whilst others tend to compete with Candida spp.
  • on the whole, oral strep benefit from candida but lactobacillus spp. tend to inhibit
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20
Q

List candida species that cause infection?

A
  • albicans
  • glabarta
  • krusei
  • topicalis
  • guilliermondii
  • kefyr
  • dubliniensis
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21
Q

How does the genus candida go from normal to infectious?

A
  • normal, harmless commensal
  • change in env or systemic conditions
  • conditions favour candida prolieferation
  • pathogenic disease causing infection
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22
Q

Candida infections are … and depends on …

A
  • opportunistic
  • underlying predisposition (sometimes termed ‘disease of the diseased’)
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23
How to grow candida in agar?
- culture on Sabouraud Dextrose agar (sometimes with antibiotics) - selects candida over bacteria due to low pH - microscopy used to identify (e.g germ tube test, chlamydospore production)
24
Instead of using a microscope to identify candida, how could you?
- biochemical tests - e.g carbohydrate utilisation - used more for quick and accurate assessments - or molecular methods for epidemiology to track clones
25
List types of virulence factors on candida
- morphology - hyphae formation - phenotypic switching - hydrolytic enzymes - candidalysin
26
How is candida morphology a virulence factor?
- can be dimorphic or polymorphic - C.albicans and C.dubliniensis can grow as yeast cells, pseudohyphae and hyphae - hyphae formation promotes oral epithelium invasion, reduces likelihood of phagocytosis, allows phagocytosed yeast to escape phagocyte - mutants unable to form hyphae are less virulent - responds to environment for example producing hyphae in response to elevated temp, CO2 conc, alkaline pH, presence of serum, limited nutrients
27
How is phenotypic switching a virulence factor for candida?
- ability to rapidly change cell morphology - responsive to environment - associated with altered gene expression affecting antigenicity, adhesion, phagocytosis and drug susceptibility
28
2 hydrolytic enzymes in candida that aid virulence
- aspartyl proteinases - phospholipases
29
Role of aspartyl proteinases in candida
- expressed under different conditions (10 genes) - some expressed during hyphal development - nutrition - adapting cell morphology - break down tissue barrier - cleave immune proteins - facilitate adherance - host cell and extracellular matrix damage
30
Role of phospholipases in candida
- hydrolyse phospholipids - damage host cells - host cell membrane damage, promoting cell lysis or exposure to receptors to facilitate adherance
31
How is candidalysin a virulence factor for candida?
- peptide toxin - candidalysin helps c. albicans penetrate host epithelial cells
32
Human infections caused by fungi are characterised how?
- superficial - subcutaneous - systemic
33
How do we defend against oropharyngeal candidiasis?
- damage mediated by C. albicans hyphal penetration and secretion of proteolytic enzymes - host responds with Th1 and Th17 adaptive immune response
34
How do we defend against hematogenously disseminated candidiasis?
- induced by biofilm formation on tissue or abiotic surfaces - damage is mediated by C.albicans hyphal invasion and secreted proteolytic enzymes - host responds with Th1 and Th17 adaptive immune response
35
Intra-abdominal candidiasis is triggered by ... and results in ...
- C.albicans invasion of abdominal organs - formation of abscesses
36
Explain denture stomatitis
- induced by C. albicans formation on dentures - damage is initiated by hyphal invasion of host tissue - further damage is mediated and propagated by host innate immune response, mainly neutrophils
37
Explain gastro-intestinal candidiasis
- induced by C. albicans overgrowth in GI tract - in immunocompromised hosts, damage is mediated by mucosal invasion and disruption of epithelial barrier - at other end of host response spectrum, C. albicans overgrowth can be a predisposing dactor for inflammatory diseases of Gi tract like colitis
38
Explain vulvovaginal candidiasis
- onset initiated by C. albicans hyphal transition and subsequent invasion of vaginal mucosa - triggers innate immune response - damage is mediated and propagated by host innate immune response, mainly neutrophils
39
What determines the particular form of oral candidosis?
- combination of host factors and microbial factors
40
What is likely to influence proliferation of candida?
- change in environment - change in host immunity
41
Local factors that predispose patients to oral candidosis?
- denture wearing - inhaled corticosteroids - reduced salivary flow - carbohydrate rich diet
42
Systemic factors that predispose patients to oral candidosis?
- systemic corticosteroids, immunosuppressants, cytotoxics, broad-spectrum antibiotics - extremes of age - endocrine disorders (like diabetes) - anaemia - patients with nutritional deficiencies - salivary gland hypofunction - immunosuppression (and from linked conditions like leukaemias, malignancy or HIV)
43
How to diagnose oral candidosis?
- clinical appearance (size/site, can white plaques be scraped off?) - lab tests (blood tests, microbiology - oral rinse and swab - and histology - biopsy)
44
4 primary forms of oral candidosis
- acute pseudomembranous - acute erythematous - chronic erythematous - chronic hyperplastic
45
Acute pseudomembranous candidosis is ...
oral thrush
46
Acute erythematous candidosis is ...
- antibiotic sore mouth/stomatitis
47
Chronic erythematous candisosis is ...
- denture stomatitis
48
Management of denture stomatitis
- clean dentures thoroughly - soak them in chlorhexidine mouthwash or sodium hypochlorite for 15 mins twice daily - chemical and mechanical cleansing of dentures twice daily - leave them out as often as possible - denture replacement or adjustment - antifungal therapy if continues
49
Chronic hyperplastic candidosis is ...
candidal leukoplasia
50
List types of secondary oral candidosis
- angular cheilitis - median rhomboid glossitis - chronic mucocutaneous candidosis
51
Give cause and treatment for angular cheilitis
- infection with candida or staphlo/streptococcus - consider cause e.g denture wearer and then miconazole cream or sodium fusidate (fusidic acid) ointment
52
Explain causes of median rhomboid glossitis
- symmetrical-shaped area in midline of dorsum of tongue - chronic infection with atrophy of filiform papillae - infection linked to smoking and inhaled steroids
53
Explain chronic mucocutaneous candidosis
- skin, mucous membranes and nails - associated with rare congenital disorders - key predisposing factor impaired cellular immunity against Candida
54
Treatment of oral candidosis
- rectify any local factors, identify risk factors and treat systemic disease - antifungal meds like topical (suspension, gel, lozenges) or systemic (tablets)
55
3 main groups of antifungal meds
- polyenes - azoles - DNA analogues
56
Examples, mode of action and administration of polyenes
- nystatin, amphotericin - disrupt fungal cell membrane (interact with ergosterol) - topical
57
Examples, mode of action and administration of azoles
- fluconazole, clotrimazole, miconazole, ketoconazole, itraconazole - inhibit ergosterol biosynthesis (interfere with lanosterol demethylase) - topical or systemic
58
Examples, mode of action and administration of 5-flucytosine
- inhibit DNA and protein synthesis (enter fungal cells through cytosine permease and is converted to %-fluorouracil) - systemic (often given with amphotericin)
59
Examples, mode of action and administration of eschinocandins
- caspofungin, microfungin - inhibit beta 1,3 D-glucan synthesis - intravenous

Microbiology for Dentists (37 decks)

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