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PVS > Microbiology 3 > Flashcards

Microbiology 3 Flashcards

1
Q

Describe the viral replication cycle

A
  • Virus binds to cell via receptor, enters cell (e.g. via endosome)
  • Initiates reverse transcription
  • cDNA produced, inserted into chromosome
  • cDNA produces RNA strands via transcription of host chromosome
  • RNA exits nucleus to produce viral proteins
  • Assembled and released as new virus
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2
Q

What stages of the viral replication cycle can be targeted by drugs?

A
  • Every stage
  • Entry
  • Uncoating
  • Replication
  • Release
  • Immune Response
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3
Q

Give the 3 classes of antiviral therapy

A
  • Drugs which target viral proteins (safe) e.g. inhibit viral replicative enzyme
  • Drugs which target host proteins e.g. block receptors
  • Drugs which enhance host defences e.g. interferons
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4
Q

What is meant by antiviral selectivity?

A

The difference between the dose of the drug which inhibits viral protein over any similar cellular protein

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5
Q

Which class of antiviral has the highest specificity?

A

Drugs targeting viral proteins that have no host analogues, may have absolute specificity. very safe

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6
Q

What are the targets to inhibit attachment and entry be inhibited?

A
  • Viral proteins

- Host cell receptors

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7
Q

Give an example of a antiviral that inhibits viral uncoating

A
  • Influenza A: hydrogen ions cause HA to fuse with membrane, and ions enter virion via M2 channels stimulating release of the nucleoprotein from the virus core
  • Amantidine blocks M2, preventing influx of H+ and thus inhibiting release of nucleoproteins
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8
Q

How may viral genome replication be inhibited by antiviral drugs?

A
  • Inhibition of viral polymerase (e.g. herpesvirus DNA polymerase, retrovirus reverse transcriptase)
  • Nucleotide analogues
  • Antiretroviral drugs
  • Integrase inhibitors (HIV)
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9
Q

Explain how nucleotide analogies can inhibit genome replication

A
  • Typically need to be activated by cellular or viral enzymes
  • Nucleotide analogue incorporation prevents elongation of DNA and no functioning DNA produced
  • e.g. acyclovir (herpesviridae), zidovudine (HIV)
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10
Q

Explain how antiretroviral drugs inhibit genome replication

A
  • Non-nucleotide reverse transcriptase (RT) inhibitors e.g. nevirapine
  • Bind near catalytic site of RT
  • highly specific
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11
Q

Explain the mechanism of action of integrase inhibitors for HIV

A
  • Bind to viral integrase to prevent viral cDNA from being inserted into the host genome
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12
Q

Describe the mechanism of action of protease inhibitors

A
  • Inhibit virus assembly
  • If viral proteins are produced as polyproteins and require cleavage this is a good drug target
  • Immature (uncleaved) viruses are inactive
  • e.g. HIV, hepatitis C in man
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13
Q

Describe the mechanism of action of antivirals that inhibit viral release

A
  • e.g. Neuraminidase inhibitors
  • Prevent release of influenza virus from cells
  • Haemaglutinin (binds to sialic acids) important for getting virus into the cell
  • Neuraminidase destroys sialic acids on cell allow release of virus
  • Neuraminidase inhibitors prevent this destruction and so the virus cannot escape
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14
Q

Outline the use of antivirals in veterinary medicine

A
  • Generally not done in farm/food production animals, often have secondary bacterial infections, expensive, MRLs a concern
  • Few antivirals licensed in veterinary species, vaccines are main method
  • Biosecurity important for production animals
  • Treatment typically requires supportive therapy
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15
Q

Outline antiviral therapy in cats

A
  • Feline interferon omega, nucleotide analogues, human interferon alpha used to treat FeLV and FIV
  • Lymphocyte T cell immunomodulator for FeLV (USDA approved but not licensed in UK
  • Feline interferon omega for FIP
  • trifluorothymidine can be used to treat FIP, also acyclovir ointment, oral acyclovir, oral famicyclovir, L-lysine but these have little proof
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16
Q

List some problems with antiviral therapy

A
  • Drug resistance due to fast development of viral mutants

- More of a worry in RNA viruses due to inherently higher mutation rate

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17
Q

Outline the use of multidrug antiviral therapy

A
  • Combining drugs improves antiviral effect

- But increases complexity and cost, reduces compliance

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18
Q

What are superficial mycoses?

A

Fungal infections of the skin, hair and nails, mucosal surfaces in upper respiratory tract

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19
Q

What are subcutaneous mycoses?

A

Fungal infections affecting muscle and connective tissue, below the skin

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20
Q

What are systemic (invasive) mycoses?

A

Fungal infections of internal organs, may be primary or opportunistic and often relate to immune suppression or other issues

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21
Q

What are some challenges of antifungal therapy?

A
  • Low susceptibility/high resistance
  • Time take for drugs to show effect
  • Environmental fomites leading to reinfection or cross infection
  • Specificity issues/side effects
  • Lack of vaccine
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22
Q

List the main groups of antifungal agents

A
  • Polyenes
  • Allylamines
  • Azoles
  • Echinocandins
  • Pyrimidine analogues
  • Antimitotics
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23
Q

What is the mechanism of action of polyenes?

A
  • Bind to and disrupt fungal membranes
  • Preferentially bind to ergosterol
  • Binding alters membrane osmotic regulation, leads to leakage of intracellular potassium and other small molecules
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24
Q

Describe the structure of polyenes

A
  • Composed of hydrophilic polyhydroxyl chain on one side

- Lipophilic polyene hydrocarbon chain on the other

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25
Q

Name some examples of polyenes and their use

A
  • Amphotericin B: systemic infections

- Nystatin: topical and oral (mucosa and GI superficial infections)

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26
Q

What is the main limitation of polyenes?

A

Toxicity

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27
Q

Describe the formulation of most polyenes

A
  • Poorly soluble in water

- Most formulations are lipid based, reduces intrinsic toxicity of compound

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28
Q

What is the mechanism of action of azoles?

A
  • Interferes with ergosterol synthesis (membrane sterols)
  • Fungistatic
  • Inhibit 14-alpha-demethylase which depletes ergosterol over time, causes accumulation of methyl-ergostadiene-diol
  • Methyl-ergostadiene-diol is toxic
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29
Q

What are the 2 groups of azoles?

A
  • Imidazoles (ketoconazole, clotrimazole)

- Triazoles (Fluconazole, intraconazole)

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30
Q

Describe the rate of action of azoles

A

Slow, require several generations to act

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31
Q

What fungi are affected by azoles?

A
  • Dimorphic
  • dermatophytes
  • Aspergillus only susceptible to triazoles, not other azoles
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32
Q

Describe the mechanism of action of allylamines

A
  • Inhibit squalene epoxidase to reduce ergosterol production
  • Interfere with ergosterol synthesis (membrane sterols)
  • Accumulation of toxis squalene
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33
Q

Describe the spectrum of activity of allylamines

A
  • Broad

- Especially active against dermatophytes

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34
Q

Name some allylamines

A

Terbinafine, butenafine

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35
Q

Describe the mechanism of action of echinocandins

A
  • Inhibit glycan synthesis
  • Affect hyphae growing tips and branching points
  • Affect yeasts so that buds fail to separate from mother cell
  • Also lead to osmotically sensitive fungal cells
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36
Q

Name examples of echinocandins

A
  • Capsofungin
  • Micafungin
  • Anidulafungin
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37
Q

Outline resistance to echinocandins

A
  • Intrinsic resistance in some fungal genera/species where other glycans predominate
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38
Q

Describe the mechanism of action of antimitotic antifungals

A
  • Binds to tubulin and interferes with microtubule function

- Thus inhibits mitosis

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39
Q

Name an antimitotic antifungal

A

Griseofulvin

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40
Q

Describe the administration and distribution of griseofulvin

A
  • Oral dose only, topically inactive

- Drug reaches site of action only when hair or skin replaced by keratin-griseofulvin complex

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41
Q

What is a contraindication for the use of griseofulvin?

A

Teratogenic, so contraindicated in pregnant animals

42
Q

Describe the mechanism of action of pyrimidine analogues

A
  • Deaminated in fungal cells by cytochrome deaminase
  • Produces fluoorodeoxyuridine monophosphate (FdUMP) and 5-fluorouridine tri-phosphate (FURTP) produced
  • FURTP incorporates into fungal RNA in place of uridylic acid, leading to inhibition of protein synthesis
  • FdUMP inhibits thymidylate synthetase leading to inhibition of DNA synthesis
43
Q

Outline the administration of pyrimidine analogues

A

Parenteral administration, oral rare and only under specific ordering

44
Q

Give an example of a pyrimidine analogue antifungal agent

A

Flucytosine

45
Q

Describe the spectrum of activity of topically administrated azoles

A

Broad (dermatophytosis, candidiasis, Malassezia and aspergillosis)

46
Q

Describe the spectrum of activity of orally or IV administrated azoles?

A

Broad

47
Q

Which azoles are administered topically?

A

Clotrimazole (imidazole) and enilconazole

48
Q

Which azoles are mainly administered orally or IV?

A
  • (Can also be administered topically)

- Ketoconazole (imidazole), fluconazole (triazole), intraconazole (triazole)

49
Q

Describe the spectrum of activity of flucytosine

A
  • Narrow

- Yeasts, cryptococcossis, candidiasis

50
Q

Give an example of synergistic antigfungals

A

Flucytosine and amphotericin B

51
Q

Describe the spectrum of activity of allylamines

A
  • Narrow

- Dermatophytosis, particularly for oncychomycosis in humans

52
Q

Outline the use of antifungals in horses

A
  • Dermatophytosis usually self-limiting
  • Treatment rare due to cost (may be used to reduce spread, shorten infection time, where animals move a lot, in case of non-self limiting disease)
  • Azole wash e.g. imaverol
  • Griseofulvin oral treatment
53
Q

What are the most important control methods for fungal infections of horses?

A

Cleaning of fomites (tack and self)

54
Q

What are the key side effects of griseofulvin?

A

Toxicity - liver damage and carcinogenicity

55
Q

Outline the use of antifungals in cows

A
  • Rare
  • Ringworm common and usually self limiting
  • Treat if: serious condition or show animal
  • Treatment usually restricted to washes e.g. iodine washes
56
Q

Outline the use of antifungals in pigs

A

Very rare

Ringworm very self-limiting, usually no treatment used

57
Q

What factors may lead to antifungal therapeutic failure?

A
  • Wrong diagnosis and use of wrong antifungal
  • Net state of immunosuppression
  • High burden of fungus at initiation of treatment
  • Strain acquisition of increased virulence
  • Pharmacokinetics and/or pharmacodynamics
  • Site of infection
  • Length of treatment and/or compliance
  • Underlying disease
58
Q

Give potential mechanisms for azole resistance

A
  • Increased efflux
  • Altered target
  • Upregulation of target
  • Development of bypass pathways
59
Q

Explain why the upregulation of a target would lead to antifungal resistance

A

More drug required to inhibit the target

60
Q

Compare the acquisition of resistance in fungi and bacteria

A

Slower in fungi due to slower growth rate and growth dynamics

61
Q

What is a potential mechanism for polyene resistance?

A

Alteration in balance of sterol types so the impact of the drug is less (acts on ergosterol)

62
Q

What are potential side effects of membrane disrupting antifungals?

A
  • Neuropathy
  • GI upset
  • Renal damage
  • Liver failure
  • Rash
63
Q

Why are fungal membranes good antifungal targets?

A

Sterols different in fungi and animals

  • In fungi: ergosterol
  • In animals: cholesterol
64
Q

Describe the mechanism of action of glucan/chitin synthesis inhibitors

A
  • Lipo-peptide based drug
  • Inhibits 1,3-beta-glucan synthase by non-competitive inhibition
  • Fungicidal and non-toxic
  • Glucan depletion weakens the cell wall
65
Q

Describe nikkomycins-

A
  • New, chitin targeting
  • Nucleoside-peptide antibiotics produced by Streptomyces spp, with antifungal activities
  • Structural similarities to natural chitin synthase substrate, uridine diphosphate-N-acetylglucosamine
  • Acts as competitive inhibitor
66
Q

What factors may lead to non-compliance to treatment regimens?

A
  • Regimen complexity
  • Side effects
  • Method/frequency of administration
  • Other lifestyle factors
  • Length of time regimen is used
  • Cost
  • Practical barriers
67
Q

What is meant by viral fitness?

A

The ability of a virus to replicate in a given environment

68
Q

What are the Protect guidelines??

A

Guidelines for the responsible use of antimicrobials

69
Q

According to the Protect guidelines, which antibiotics should not be used in veterinary practice?

A
  • Imipenem
  • Linezolid
  • Teicoplanin
  • Vancomycin
70
Q

Describe the primary antibiotics group under the Protect guidelines?

A
  • Narrow spectrum
  • Older
  • No less efficacious than newer antibiotics
71
Q

Describe the secondary antibiotics group under the Protect guidelines

A
  • Broad spectrum
  • Newer
  • More important in treatment of serious or often resistant infections in humans
  • Only to be used where indicated by culture and sensitivity testing
72
Q

Describe the tertiary antibiotic group under the Protect guidelines

A
  • Broad spectrum
  • Very important for human and animal health care
  • Efficient against more resistant bacteria
  • Only to be used in clinically important infections, shown to be resistant to all primary and secondary drugs
73
Q

Describe the prohibited antibiotic group under the protect guidelines

A
  • Significant clinical value to human medicine

- Essential for treating resistant infections in humans

74
Q

Give examples of primary/first line antibiotics

A
  • Penicillin
  • 1st gen cephalosporins
  • Amoxicillin and clavulanate
  • Trimethoprim + sulphonamides
  • Tetracyclines
  • Lincosamides
75
Q

Give examples of secondary/second line antibiotics

A
  • Aminoglycosides
  • Medtronidazole
  • Macrolides
  • Chloramphenicol
  • Fluoroquinolones
  • Cefeovecin
76
Q

Give examples of tertiary/third line antibiotics

A
  • 3rd and 4th gen cephalosporins
  • Rifampicin
  • Fosfomycin
77
Q

Define minimum selective concentration

A
  • The lowest concentration of an antibiotic that still selects for a given resistance mutation
  • The lowest concentration of an antimicrobial that gives the resistant strains a competitive advantage based on growth inhibition of non-resistant strains
78
Q

Give general methods used in disease control

A
  • Accurate identification of infected animals
  • Restriction on movement
  • Lab testing for diagnosis
  • Vaccination, chemophylaxis where appropriate
  • Cleaning of environment
79
Q

What factors affect the survival of a pathogen in the environment?

A
  • The environmental conditions i.e. dry, wet, presence of organic material
  • The bacterial sensitivity to the environment, stress, spore formation
80
Q

Compare the environmental sensitivity of Mycoplasmas, some enveloped viruses vegetative bacteria, non-enveloped viruses, endospores of bacteria, prions

A
  • Mycoplasmas (and some enveloped viruses) tend to have poor environmental survival rates
  • Average vegetative bacteria and non-enveloped viruses have average survival rates and may persist for months
  • Endospores of bacteria and prions survive a long time, years
81
Q

What factors promote pathogenic persistence in the environment?

A
  • Poor general cleaning routine
  • Surface structure i.e. crevices, surface joins
  • surface characteristics e.g. absorbent, smooth, rough etc
  • Weather
  • Local environment i.e. soil pH, faecal contamination
82
Q

Name the possible methods of sterilisation of media and small equipment

A
  • Filtration
  • Heat inactivation
  • Irradiation
  • Chemical
83
Q

Describe filtration sterilisation

A
  • Liquids
  • Use of filters in the um size can remove pathogens
  • Ultrafiltrations using reverse osmotic filters can remove ions, producing ultra-pure water
84
Q

Describe heat inactivation sterilisation

A
  • Liquids and solids
  • Depends on solutions e.g. glucose solutions may caramelise
  • Compounds can degrade
  • Temperature range of material
  • Disinfection (removes residues)
  • Some solid substances may clog filters
85
Q

What is irradiation sterilisation used for?

A

Medical field plastics and some sensitive material

86
Q

What is chemical sterilisation used for?

A

Surface decontamination

87
Q

What pathogens are killed by a normal autoclave cycle?

A
  • Bacteria
  • Viruses
  • Parasites
88
Q

Define disinfection

A

Destruction of micro-organisms by physical or chemical methods on surfaces or objects

89
Q

Define antisepsis

A

Destruction of microorganisms on tissues by chemicals which are non-toxic and non-irritating to the tissue

90
Q

List the features of the ideal chemical disinfectant

A
  • Broad activity
  • Safe
  • Stable
  • Long shelf life
  • Soluble in water
  • Compatible with wide range of other chemicals
  • Active in organic matter
  • Non-corrosive to metal/surfaces
  • Active over range of temperatures
  • Absence of tainting of food products
  • Good price
  • Non-polluting/biodegradable
91
Q

List the groups of chemical disinfectants used in veterinary medicine

A
  • Acids
  • Alcohols
  • Aldehydes
  • Alkalis
  • Biguanides
  • Halogen compounds
  • Chlorine compounds
  • Iodine compounds
  • Phenolic compounds
  • Quarternary ammonium compounds
92
Q

List the potential modes of action of disinfectants

A
  • Damages nucleic acids
  • Direct action on organism surface
  • Coagulation of cytoplasmic components
  • Affect cell membrane
  • Target cell components
  • Interaction with essential enzymes
93
Q

Describe the mode of action of alcohol disinfectants

A

Denature proteins causing membrane damage

94
Q

Describe the use of alcohol disinfectants

A
  • Broad action
  • Ethyl alcohol and isopropyl based most common
  • Rapid activity against vegetative bacteria and some viruses
  • Needs to be between 70-90% concentration (water required)
95
Q

What are some problems with alcohol disinfectants?

A
  • Flammable
  • Limited activity in presence of organic material
  • Ca damage some plastics and rubber
  • Minor irritation to try cracked skin
  • Not active against spores or small non-enveloped viruses
96
Q

What are some practical benefits of alcohol disinfectants?

A
  • Evaporates quickly leaving no residue

- Can be used or combined with other anti-microbial compounds

97
Q

List the pathogenic groups against which alcohol disinfectants are active

A
  • Mycoplasmas
  • Gram +ve and -ve
  • Enveloped viruses
  • Some fungal spores
  • Acid fast bacteria
98
Q

Describe the mode of action of acid disinfectants

A
  • Function related to pH
  • Low pH inhibits growth
  • Destroy nucleic acid bonds and precipitate proteins
  • Change pH and therefore activity of enzymes etc.
99
Q

Describe some problems with acid disinfectants

A
  • Concentrated acids can be caustic
  • Causes burns
  • Caustic fumes with strong acids
  • Toxic at high concentrations in air
  • Reactive, can damage surfaces
100
Q

Outline the main uses of acid disinfectants

A
  • Organic acids used in food industry
  • Household products
  • Cleaning alkaline deposits in machinery such as milking machines
  • HCl can destroy endospores
101
Q

List the microbes against which acid disinfectants are active

A
  • Mycoplasmas
  • Gram +ve and -ve bacteria
  • Enveloped viruses
  • Some fungal spores
  • Some bacterial spores

PVS (23 decks)

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