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262A Oral Biology > Microbiology - RC > Flashcards

Microbiology - RC Flashcards

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1
Q

What are the features of an “ideal” antimicrobial?

A

L4

  • selective toxicity against microbial target
  • minimal toxicity to the host
  • no adverse drug interactions
  • long plasma half-life
  • good tissue distribution
  • cidal activity
  • low binding to plasma proteins
  • oral and parenteral preparations
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2
Q

What are the pathogenicity factors of C. albicans?

A

L7

  • adhesion
  • dimorphism
  • secretion hydrolytic enzymes
  • interaction with immune system
  • toxin production: candidalysin
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3
Q

How is adhesion a pathogenicity factor in C. albicans?

A

L7

adhesion allows the cell to overcome the clearance function of the innate immune system

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4
Q

How is dimorphism a pathogenic factor in C. albicans?

A

L7
= yeast and hyphae growth
hyphae can penetrate tissue + burst out of macrophages
(strains that are defective in mycelial formation are less virulent)

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5
Q

What are the secreted hydrolytic enzymes of C. albicans and how are they pathogenic factors?

A

L7

  • secreted aspartic proteinases: degrade sIgA, promote adhesion + aid tissue penetration/destruction
  • phospholipase: degrades phospholipids = destroy cell membranes + aid tissue penetration
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6
Q

How is interaction with immune system a pathogenic factor in C. albicans?

A

L7

  • grow out of phagocytes after being engulfed
  • secreted proteinases may degrade antibodies
  • hyphae secrete a substance that inhibits polymorphonuclear leukcyte (neutrophil, basophil etc.) degranulation (release of cytotoxic molecules + prevents phagocytosis
  • supress T-cell proliferation
  • bind C3b + C3d complement proteins which masks cell from phagocytes
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7
Q

How is candidalysin toxin production a pathogenic factor in C. albicans?

A

L7

- permeabilises the host cell membrane

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8
Q

What are the predisposing factors of developing oral candidosis?

A

L8

  • prosthesis
  • low saliva flow
  • antibiotics
  • malignancies + cytotoxic therapy
  • corticosteroids
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9
Q

Why does prosthesis predispose for oral candidosis?

A

L8

  • tissue trauma breaches barrier component of innate immune system
  • compromised saliva flushing function
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10
Q

Why does low saliva flow contribute to developing oral candidosis?

A

L8

  • reduced flushing action of saliva
  • innate immune system
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11
Q

Why are antibiotics a predisposing factor for oral candidosis?

A

L8

  • reduce microbial competition by inhibiting bacteria
  • causes increased number of candidda
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12
Q

Why are malgnancies and cytotoxic therapy predisposing factors for oral candidosis?

A

L8

  • impair phagocytosis by neutrophils + macrophages
  • affects cell mediated and acquired immunity
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13
Q

Why are corticosteroids a predisposing factor in oral candidosis?

A

L8

  • immunosuppressive
  • used by asthmatics + absorbed into oral mucosa which increased the chance of fungal infections
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14
Q

What are the types of oral candidosis?

A

L8

  • pseudomembranous candidosis (oral thrush)
  • acute and chronic erythematous candidosis
  • plaque-like/nodular candidosis
  • angular cheilitis
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15
Q

Who is likely to get oral thrush (pseudomembranous candidosis)?

A

L8

  • infants
  • elderly
  • immunocompromised (HIV + AIDS patients)
  • asthmatics using steroid inhalers
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16
Q

What is the clinical presentation of oral thrush (pseudomembranous candidosis)?

A

L8

  • creamy-white plaques
  • can be removed with a swab
  • bleeding mucosa underneath plaques
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17
Q

What forms the pseudomembranes seen in oral thrush (pseudomembranous candidosis)?

A

L8

desquamated epithelial cells + Candida hyphae

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18
Q

When does acute erythematous candidosis occur?

A

L8

  • often follows course of broad spectrium antibiotic
  • occurs due to loss of competition
  • thus also called “antibiotic sore tongue” and “acute atrophic candidosis”
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19
Q

What is the clinical presentation of acute erythematous candidosis?

A

L8

  • reddeninh of tissue
  • inflammation
  • painful
  • papillae not evident due to inflammation of tongue: looks smooth
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20
Q

What is the factor that leads to chronic erythematous candidosis?

A

L8

  • affects denture wearers
  • is the most common form of candidosis
  • also called “denture-induced candidosis” and “denture sore mouth”
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21
Q

What is the clinical presentation of chronic erythematous candidosis?

A

L8

- inflamed palatal mucosa

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22
Q

What are the other names for plaque-like/nodular candidosis?

A

L8

  • chronic hyperplastic candidosis
  • candidal leukoplakia
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23
Q

What is the clinical presentation of plaque-like/nodular candidosis?

A

L8

  • irregular white plaques that cannot be removed by scraping
  • liable to undergo malignant transformation
24
Q

What can angular cheilitis be caused by?

A

L8

  • can be caused by bacteria such as staphylococci
  • can also be caused by Candida
25
Q

What is the clinical presentation of angular cheilitis?

A

L8

  • inflammation
  • ulceration
  • crusting
26
Q

What are some anti-fungal drug types and their sites of action?

A 
L8
5-fluorocytosine: DNA RNA synthesis
polyenes: membrane integrity
azoles: sterol synthesis
echinocandins: wall synthesis
27
Q

What is the mode of action of 5-fluorocytosine?

A

L8

  • fungicidal
  • administered as a prodrug which is metabolised in fungal cell to active metabolite
  • metabolite interacts with RNA and DNA synthesis = abnormal RNA + proteins
28
Q

What examples of polyene antifungal drug?

A

L8

- nystatin + amphotericin B

29
Q

What is the mechanism of action for nystatin and amphotericin B?

A

L8

  • fungicidal
  • insert and aggregate with ergosterol in cell membrane
  • form channel with pore
  • cause H+ and K+ ion leakage
  • cell death
30
Q

What is an example of a azole antifungal drug?

A

L8

- fluconazole

31
Q

What is the mode of action for fluconazole?

A

L8

  • fungistatic
  • inhibits an enzyme in the pathway to ergosterol production
  • results in loss of membrane integrity
  • causes cell lysis
32
Q

Why is fluconazole not toxic to humans?

A

L8

  • ergosterol is equivalent to cholesterol found in mammals
  • different production pathway so able to target this difference
33
Q

What preparations are available for nystatin + amphotericin B, and fluconazole?

A 
L8 
nystatin + amphotericin B:
- topical: suspension, pastilles, lozenges, and ointment
fluconazole:
- systemic: capsules
34
Q

What are the possible drug resistance mechanisms for Candida?

A

L8

  1. alteration in metabolic pathway (5-FC + polyenes)
  2. over-expression of drug target (azoles)
  3. mutation in drug target (azoles)
  4. over-expression of drug pumps (azoles)
35
Q

How does drug resistance affect 5-FC (antifungal)?

A

L8

  • mutations in UMP pyrophosphorylase enzyme
  • partially resistance strains can acquire full resistance
36
Q

What is the mechanism of polyene drug resistance in fungi?

A

L8

  • changes in the sterol composition of the plasma membrane
  • if no sterols present, then polyenes cannot interact to form pores
37
Q

What is the mechanism of azole antifungal drug resistance?

A 
L8
C. albicans can acquire azole drug resistance by:
- over-expression of drug target
- mutation of drug target
- energy-dependent drug efflux
38
Q

Resistance to which antifungal drug is a problem to some patients?

A

L8

  • azole resistance
  • problem to AIDS patients with oropharyngeal candidosis
39
Q

What are the reasons for the recurrence of fungal infections?

A

L8

  • patients have another endogenous source of Candida for re-infection
  • impaired immune system
  • used a fungistatic drug
40
Q

What is an example of viral latency?

A

L5

e. g. Herpes Simplex Virus (HSV)
- primary herpetic gingivostomatitis
- secondary herpes labialis (cold sore)
e. g. Varicella Zoster Virus (VZV)
- primary chicken pox
- secondary shingles

41
Q

Describe the latency of HSV?

A

L5

  • virus remains latent in sensory neurons in trigeminal ganglion
  • reactivation: virus migrates down peripheral nerve
  • causes lesions on mucocutaneous junction of the lip
42
Q

What are the stages involved in virus replication?

A

L5

  • adsorption
  • penetration
  • nucleic acid replication
  • viral assembly and release
43
Q

How does viral adsorption occurs?

A

L5

- specific interaction between viral protein and host receptor

44
Q

How does the viral penetration stage occur?

A

L5

  • translocation (diffusion)
  • endocytosis
  • fusion of membranes
45
Q

What occurs during the viral nucleic acid replication stage?

A

L5

  • ssDNA: replicated to make complementary template which is used to make more copies
  • dsDNA: replicated
  • ssRNA: viral transcriptase to form complement (-ve or +ve sense) then again to form copy
46
Q

What is a retrovirus?

A

L5

- a ssRNA virus with a DNA intermediate

47
Q

What is the replication cycle of retroviruses?

A

L5

  • receptor binding + entry
  • nucleoprotein complex
  • reverse transcription = DNA
  • DNA integration into host genome = provirus (viral latency)
  • transcription = mRNA + pre-genome RNA
  • mRNA translation = proteins
  • proteins + pre-genome RNA = virus
48
Q

What is involved during the viral assembly and release stage?

A

L5

  • intracellular assembly and maturation = requires cell lysis for release
  • enveloped virus: viral membrane proteins into cell membrane, capsid assembles intracellularly + associates with membrane proteins = virus buds from cell (e.g. HIV)
  • nucleocapsid assembly occurs in nucleus (e.g. herpes)
49
Q

What kind of virus is HIV?

A

L6

- enveloped RNA retrovirus

50
Q

What is the time course of HIV disease?

A

L6
- immune system detects the HIV virus and starts producing anti-HIV antibodies
- HIV affects white blood cells = decrease CD4 WBC count
- antibodies initially effect so cause a decrease in the amount of virus
- WBC are destroyed so cannot produce antibody anymore
- amount of virus increases
= immunodeficient

51
Q

What are some anti-viral drugs?

A

L6

  • acyclovir: HSV + VZV
  • abacavir: HIV
  • lamivudine: HIV
  • ritonavir: HIV
52
Q

What is the mechanism of action for acyclovir antiviral?

A

L6

  • prodrug
  • activated by phosphorylation by viral thymidine kinase
  • potent inhibitor of viral DNA polymerase
53
Q

What is the mechanism of action for abacavir + lamivudine antivirals?

A

L6

  • nucleoside analogues
  • inhibit retroviral reverse transcriptase
54
Q

What is the mechanism of action for Ritonavir?

A

L6

  • proteinase inhibitor
  • aspartic proteinase required by HIV to cleave viral protein precursors
55
Q

What resistance problems is there in antiviral drugs?

A

L6

  • influenza significantly resistant to Amantadine
  • HIV resistance to reverse transcriptase and proteinase inhibitors
56
Q

What are the components of the innate immune system?

A 
L10
- physical barriers: skin
- flushing action: saliva
- biological components: enzymes, phagocytosis, complement, inflammation, 
nutrient privation 
- microbial competition

262A Oral Biology (4 decks)

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