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Microbiology for Dentists > 21. Oral Fungal Infections > Flashcards

21. Oral Fungal Infections Flashcards

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Biology 101 flashcards
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
Q

How to grow candida in agar?

A
  • 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
Q

Instead of using a microscope to identify candida, how could you?

A
  • biochemical tests
  • e.g carbohydrate utilisation
  • used more for quick and accurate assessments
  • or molecular methods for epidemiology to track clones
25
Q

List types of virulence factors on candida

A
  • morphology - hyphae formation
  • phenotypic switching
  • hydrolytic enzymes
  • candidalysin
26
Q

How is candida morphology a virulence factor?

A
  • 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
Q

How is phenotypic switching a virulence factor for candida?

A
  • ability to rapidly change cell morphology
  • responsive to environment
  • associated with altered gene expression affecting antigenicity, adhesion, phagocytosis and drug susceptibility
28
Q

2 hydrolytic enzymes in candida that aid virulence

A
  • aspartyl proteinases
  • phospholipases
29
Q

Role of aspartyl proteinases in candida

A
  • 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
Q

Role of phospholipases in candida

A
  • hydrolyse phospholipids
  • damage host cells - host cell membrane damage, promoting cell lysis or exposure to receptors to facilitate adherance
31
Q

How is candidalysin a virulence factor for candida?

A
  • peptide toxin
  • candidalysin helps c. albicans penetrate host epithelial cells
32
Q

Human infections caused by fungi are characterised how?

A
  • superficial
  • subcutaneous
  • systemic
33
Q

How do we defend against oropharyngeal candidiasis?

A
  • damage mediated by C. albicans hyphal penetration and secretion of proteolytic enzymes
  • host responds with Th1 and Th17 adaptive immune response
34
Q

How do we defend against hematogenously disseminated candidiasis?

A
  • 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
Q

Intra-abdominal candidiasis is triggered by … and results in …

A
  • C.albicans invasion of abdominal organs
  • formation of abscesses
36
Q

Explain denture stomatitis

A
  • 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
Q

Explain gastro-intestinal candidiasis

A
  • 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
Q

Explain vulvovaginal candidiasis

A
  • 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
Q

What determines the particular form of oral candidosis?

A
  • combination of host factors and microbial factors
40
Q

What is likely to influence proliferation of candida?

A
  • change in environment
  • change in host immunity
41
Q

Local factors that predispose patients to oral candidosis?

A
  • denture wearing
  • inhaled corticosteroids
  • reduced salivary flow
  • carbohydrate rich diet
42
Q

Systemic factors that predispose patients to oral candidosis?

A
  • 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
Q

How to diagnose oral candidosis?

A
  • clinical appearance (size/site, can white plaques be scraped off?)
  • lab tests (blood tests, microbiology - oral rinse and swab - and histology - biopsy)
44
Q

4 primary forms of oral candidosis

A
  • acute pseudomembranous
  • acute erythematous
  • chronic erythematous
  • chronic hyperplastic
45
Q

Acute pseudomembranous candidosis is …

A

oral thrush

46
Q

Acute erythematous candidosis is …

A
  • antibiotic sore mouth/stomatitis
47
Q

Chronic erythematous candisosis is …

A
  • denture stomatitis
48
Q

Management of denture stomatitis

A
  • 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
Q

Chronic hyperplastic candidosis is …

A

candidal leukoplasia

50
Q

List types of secondary oral candidosis

A
  • angular cheilitis
  • median rhomboid glossitis
  • chronic mucocutaneous candidosis
51
Q

Give cause and treatment for angular cheilitis

A
  • infection with candida or staphlo/streptococcus
  • consider cause e.g denture wearer and then miconazole cream or sodium fusidate (fusidic acid) ointment
52
Q

Explain causes of median rhomboid glossitis

A
  • symmetrical-shaped area in midline of dorsum of tongue
  • chronic infection with atrophy of filiform papillae
  • infection linked to smoking and inhaled steroids
53
Q

Explain chronic mucocutaneous candidosis

A
  • skin, mucous membranes and nails
  • associated with rare congenital disorders
  • key predisposing factor impaired cellular immunity against Candida
54
Q

Treatment of oral candidosis

A
  • rectify any local factors, identify risk factors and treat systemic disease
  • antifungal meds like topical (suspension, gel, lozenges) or systemic (tablets)
55
Q

3 main groups of antifungal meds

A
  • polyenes
  • azoles
  • DNA analogues
56
Q

Examples, mode of action and administration of polyenes

A
  • nystatin, amphotericin
  • disrupt fungal cell membrane (interact with ergosterol)
  • topical
57
Q

Examples, mode of action and administration of azoles

A
  • fluconazole, clotrimazole, miconazole, ketoconazole, itraconazole
  • inhibit ergosterol biosynthesis (interfere with lanosterol demethylase)
  • topical or systemic
58
Q

Examples, mode of action and administration of 5-flucytosine

A
  • inhibit DNA and protein synthesis (enter fungal cells through cytosine permease and is converted to %-fluorouracil)
  • systemic (often given with amphotericin)
59
Q

Examples, mode of action and administration of eschinocandins

A
  • caspofungin, microfungin
  • inhibit beta 1,3 D-glucan synthesis
  • intravenous

Microbiology for Dentists (37 decks)

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