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Year 1 MCD > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What are the shapes bacteria can take?

A

Cocci (spherical), Bacilli (capsule) and Spirilli (spiral, worm-like)

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2
Q

What does Gram staining involve?

A

Bacteria are stained with a violet die and iodine, then rinsed in alcohol before being stained with a weaker red dye.

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3
Q

How does Gram staining differentiate between the two types of cell wall?

A

Violet dye resides in the peptidoglycan layer of the Gram positive membrane, and on the outer membrane on the Gram negative membrane. Alcohol dissolves this outer membrane, leaving the Gram positive membrane colourless. The weaker red dye is more visible in the Gram positive bacteria.

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4
Q

What colour would a Gram positive and negative bacteria stain?

A

Gram positive - violet

Gram negative - red

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5
Q

Why does Gram staining have pathological significance?

A

Gram negative bacteria have LPS (Lipopolysaccharide) on their outer membrane which act as a PAMP

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6
Q

What bacteria are neither Gram negative nor positive?

A

Mycobacteria, as they posses a complex waxy lipid as their cell wall.

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7
Q

What must a microorganism be able to do to be considered a pathogen?

A 
Colonise
Persist
Replicate
Disseminate
Cause disease
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8
Q

How do intracellular bacteria survive inside after being phagocytosed?

A

1) Survive in lysosome after modifying vesicle so its not bound to degradation
2) Survive in phagolysosome
3) Escape from vesicle

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9
Q

What two protein machines does a bacterium need to invade a cell?

A

Type III Secretion System and Flagella

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10
Q

How are flagella formed?

A

A co-ordinated assembly of ring and rod proteins. The structures protrude through the membrane, and the rotation causes movement.

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11
Q

What do Type III secretion systems do?

A

Injects virulence proteins into host cells.

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12
Q

What type of bacteria have Type III secretion systems?

A

Gram negative

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13
Q

Give an example of an organism that uses a Type III secretion system to invade a cell.

A

Salmonella use Type III secretion systems to inject protein that causes cytoskeletal actin to polymerise - pushing the membrane to engulf the salmonella behind it. (Bacterial internalisation)

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14
Q

Give an example of a bacterium that uses the cell’s cytoskeleton to move around.

A

Listeria causes actin polymerisation behind it, pushing it forward - allowing it to swim around in the cell.

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15
Q

What are the general properties of bacterial genomes?

A

Code for 500-4500 proteins. Made of core genes (40%) present in all strains of the species, and accessory genes (60%) which vary considerably between the different strains.

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16
Q

How do bacteria replicate?

A

Binary Fission - duplication of it’s chromosome followed by cell division.

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17
Q

Differentiate between bacterial vertical and horizontal gene transfer

A

Vertical gene transfer happens through binary fission. Horizontal gene transfer is transferring genes to and from the environment / other bacteria

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18
Q

What are the mechanisms for horizontal gene transfer?

A
  • Transformation (uptake of naked DNA from environment, recognised and integrated into chromosome)
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19
Q

What are the mechanisms for horizontal gene transfer?

A
  • Transformation (uptake of naked DNA from environment, recognised and integrated into chromosome)
  • Transduction (mediated by bacteriophages, which cut bacterial DNA into small pieces when replicating, taking it into capsule. The bacteria it infects may incorporate it into its chromosome)
  • Conjugation (transfer of plasmid between two bacteria using pilli)
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20
Q

What is a pathogenicity island?

A

A section of the chromosome that contains pathogenic genes derived through horizontal gene transfer. Possible to tell by looking at base composition.

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21
Q

What are the two sources of infection?

A

Intrinsic (from within the body) and Extrinsic (from outside, entering through portals of entry)

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22
Q

What does the upper respiratory tract include?

A
  • Mouth
  • Nose
  • Nasal cavity
  • Sinuses
  • Trachea
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23
Q

What pathogens often infect the upper respiratory tract?

A

Viruses: Influenza, Rhinoviruses, Measles
Bacteria: Neisseria meningitidis and Staphylococcus aureus

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24
Q

What are the consequences of bacterial infection acquired via the upper respiratory tract?

A
  • Pharyngitis
  • Tonsilitus
  • Sinusitis
    If speaks to lower respiratory tract:
  • bronchitis
  • pneumonia
  • pneumonitis
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25
Q

What does the urogential tract include? Where do most infections originate from?

A

The urotract and genital tract. Most infections are intrinsic and original from the large intestine.

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26
Q

What pathogens often infect the urogenital tract?

A 
Intrinsic:
- E.coli
- Group B Strep (Strep. agalactiae)
Extrinsic:
- Nosocomial (urinary catheters)
- Sexually transmitted
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27
Q

What are the consequences of bacterial infection acquired via the urogenital tract?

A 
Urethritis
Pelvis inflammatory disease
Tubo-ovarian abscess
Neonatal group B strep infection
Neonatal gonococcal conjuctivitis
Maternal endometritis
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28
Q

How does broken skin usually occur?

A

Surgery, Insects, Injective Drug Use (IDU), pre-existing skin breaches (e.g varicella)

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29
Q

What infections usually target broken skin?

A

Staphylococcus aureus, Streptococcus pyogenes, MRSA

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30
Q

What are the consequences of bacterial infection acquired via broken skin?

A 
Superficial infection
Abscess
Cellulitis
Fascitis
Myositis
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31
Q

What pathogens often infect the urogenital tract?

A 
Intrinsic:
- E.coli
- Group B Strep (Strep. agalactiae)
Extrinsic:
- Nosocomial (urinary catheters)
- Sexually transmitted
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32
Q

What pathogens often infect the gastro-intestinal tract?

A

E. coli
Shigella spp
Listeria

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33
Q

What are the consequences of bacterial infection acquired via gastro-intestinal tract?

A

Vomiting, Diarrhoea, Dysentry. If bacteria leaves gut often causes Typhoid, Listerosis, Salmonellosis

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34
Q

What is pathogenicity?

A

The ability of a pathogen to cause disease.

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35
Q

What is the difference between true and opportunistic pathogens?

A

True pathogens cause disease in fit people

Opportunistic pathogens need a compromised host to establish infection.

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36
Q

What are bacteria that are not pathogens called?

A

Commensals

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37
Q

What are the factors affecting pathogenicity?

A 
Infectivity:
- transmission
- ability to colonise and replicate
- ability to evade immune system
Virulence:
- toxin production
- interruption of normal host processes
- complete immune evasion
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38
Q

What is an infectious dose?

A

The number of bacteria required to initiate an infection.

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39
Q

Give examples of bacteria that have low and high infectious doses?

A

Low:

  • Mycobacterium tuberculosis
  • Shigella

High:
Vibrio Cholerae

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40
Q

How does Vibrio Cholerae cause diarrhoea?

A

Uses flagella to penetrate mucus and binds to galgliosides on gut. This triggers cAMP and chloride efflux, so Na+ and water follow.

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41
Q

Give examples of Gram+ and Gram- opportunistic bacteria

A

Gram-
Pseudonomas aeruginosa
Acinetobacter baumanii

Gram+
Staphylococcus epidermis
Enterococcus faecalis

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42
Q

What is an antibiotic?

A

An antimicrobial agent produced by a microorganism that kills or inhibits other microorganisms.

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43
Q

What is an antimicrobial?

A

A chemical that selectively kills or inhibits microbes

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44
Q

What is a bactericidal?

A

A chemical that kills bacteria

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45
Q

What is a bacteriostatic?

A

A chemical that stops bacteria growing

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46
Q

What is an antiseptic?

A

A chemical that kills or inhibits microbes usually applied topically.

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47
Q

What is the antibiotic breakpoint?

A

The maximum clinically achievable concentration of antibiotic that can be administered.

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48
Q

When are microorganisms considered resistant to an antibiotic?

A

When the organism can replicate above the breakpoint.

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49
Q

Why is antibiotic resistance problematic in healthcare?

A
  • Increased time of therapy
  • Additional approaches have to be sued
  • More toxic and expensive drugs may be used
  • Less effective ‘second choice’ antibiotics may have to be deployed.
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50
Q

What is the name of the process given to the fact that antibiotics target processes that are different or don’t occur in humans?

A

Selective toxicity

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51
Q

Give examples of drugs that exploit selective toxicity

A

Penicillins, Cephalosporins, Bacitracin and Vancomycin: inhibit cell wall synthesis
Chloramphenicol, erythromycin, tetracyclin, streptomycin: Inhibit protein synthesis

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52
Q

Describe the mechanism and use of Penicillins and Methicillins

A

These are beta-lactams. They interfere with the synthesis of the peptidoglycan component of the cell wall by binding to penicillin-binding proteins.

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53
Q

Describe the mechanism and use of Tetracycline

A

This is an example of a broad spectrum bacteriostatic. It inhibits protein synthesis by binding to the 16S component of the 30S ribosomal subunit, preventing the binding of amino acid/tRNA complexes.

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54
Q

Describe the mechanism and use of Cloramphenicol

A

This is an example of a broad-spectrum bacteriostatic. It inhibits protein synthesis by binding to the 50S ribosomal subunit, blocking the pepidyl transfer step.

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55
Q

Describe the mechanism and use of Quinolones

A

These are synthetic broad-spectrum bactericidals which target DNA unwinding.

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56
Q

Describe the mechanism and use of Sulphonamides

A

These are synthetic bacteriostatics. They are used to treat UTIs and RTIs. They target more than one crucial element for bacteria.

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57
Q

Describe the mechanism and use of Animoglycosides.

A

These include Gentamicin and Streptomycin. They are bactericidal. Targets RNA proofreading.

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58
Q

Describe the mechanism and use of Macrolides

A

An example is erythromycin. These target Gram+ infections - targeting 50S ribosomal subunit, preventing amino-acyl transfer.

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59
Q

What are the four mechanisms in which a bacterium can become resistant? Give examples of such bacteria where appropriate.

A
  • Change of target site for the antibiotic (MRSA encodes an alternate penicillin binding protein, and Streptococcus pneumoniae is resistant to erythromycin through acquisition of erm gene, encoding an enzyme that methylates the target antibiotic site)
  • Inactivate antibiotic
  • Alter its metabolism
  • Change accumulation of antibiotic in cell (e.g by use of pumps)
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60
Q

What are the different sources from which bacteria can acquire antibiotic resistance?

A

Plasmid, Transposons, Naked DNA, Bacteriophages

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61
Q

What are possible non-genetic mechanisms for resistance?

A
  • Biofilms
  • Intracellular location
  • Slow growth (don’t need targets blocked by antibiotics)
  • Spores
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62
Q

What are possible non-genetic mechanisms for resistance?

A
  • Biofilms
  • Intracellular location
  • Slow growth (don’t need targets blocked by antibiotics)
  • Spores
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63
Q

What are the reasons antibiotic treatment mat fail?

A
  • Inappropriate choice of antibiotic for organism
  • Poor penetration of antibiotic
  • Inappropriate dose
  • Inappropriate administration
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64
Q

How can antibiotic resistances be identified clinically?

A

Swabs of infection are streaked out onto a diagnostic agar to identify causative organism. The pathogen is then streaked over a plate containing antibiotic test strips.

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65
Q

Why are hospitals more prone to developing antibiotic resistant strains?

A

Hospitals provide a very strong selective pressure for resistance as there are large numbers of infected people receiving very high doses of antibiotics.

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66
Q

Give examples of hospital-acquired infections

A

MRSA, C. difficile, VISA

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67
Q

How can antibiotic resistance be addressed?

A
  • Prescribing strategies
  • Reduce use of broad-spectrum antibiotics
  • Quicker identification of infections caused by resistant strains
  • Combination therapy
  • Knowledge of local strains
  • Modification of exiting medications
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68
Q

What fungal phylum accounts for 90% of serious fungal infections?

A

Ascomycota

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69
Q

Why are fungi dangerous?

A

They are saprophytes, secreting hydrolytic enzymes that breakdown biopolymers - they digest us from the inside.

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70
Q

What are the types of illnesses caused by fungi?

A
  • Allergies
  • Mycoses
  • Mycotoxicoses
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71
Q

How do fungi cause allergic diseases?

A

Through fungal spores being inhaled/irritating

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72
Q

Give examples of allergic diseases caused by fungi

A
  • Rhinitis
  • Dermatitis
  • Asthma
  • Allergic broncho-pulmonary aspergillosis
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73
Q

Give examples of allergic diseases caused by fungi

A
  • Rhinitis
  • Dermatitis
  • Asthma
  • Allergic broncho-pulmonary aspergillosis
74
Q

What is mycotoxicosis?

A

A toxic reaction caused by the ingestion of inhalation of a mycotoxin.

75
Q

What is a mycotoxin?

A

Secondary metabolites of moulds.

76
Q

What are the symptoms of a mycotoxicosis? How may they be treated?

A

Breathing problems, dizziness, vomiting, diarrhoea, dehydration, hepatic and renal failure.
Treated by gastric lavage or liver transplant

77
Q

What is the most carcinogenic natural compound?

A

Aflatoxin produced by Aspergillus flavus. It causes 28% of worldwide hepatocelullar carcinoma.

78
Q

How are mycoses classified?

A

By the level of tissue affected:

  • Superficial
  • Cutaneous
  • Subcutaneous
  • Systemic
79
Q

Give an example of a superficial mycosis

A

Dandruf is an infection caused by Malassezia globosa

80
Q

What are the types of fungi that cause cutaneous mycoses?

A

Dermatophytes (skin) and Keratinophillic (nails) produce extracellular keratinises that hydrolyse keratin.

81
Q

What are the most common paediatric dermatophyte infections?

A

Tinea capitis (head), pedis (feet), corporis (body), cruris (groin), unguium (finger/toenails)

82
Q

What are the most common paediatric dermatophyte infections?

A

Tinea capitis (head), pedis (feet), corporis (body), cruris (groin), unguium (finger/toenails)

83
Q

What are the properties of subcutaneous mycoses?

A

Chronic, localised infections of the skin and subcutaneous tissue following traumatic implantation of etiologic agent.

84
Q

What are the types of systemic mycoses?

A

Primary (able to establish infection in a normal host) or Opportunistic (require a compromised host)

85
Q

What are the types of systemic mycoses?

A

Primary (able to establish infection in a normal host) or Opportunistic (require a compromised host)

86
Q

What are the types of systemic mycoses?

A

Primary (able to establish infection in a normal host) or Opportunistic (require a compromised host)

87
Q

Why has there been a increase in systemic mycoses?

A

This is due to more people becoming immunosuppressed, either through diseases or treatments.

88
Q

What infections are usually developed by Candida?

A

Candida are found in the skin, GI tract and genito-urinary tract. Superficial candida infections occur in these areas.
Candida are opportunistic fungi. Systemic candida infections are associated with high mortality rates. Risk factors include chemotherapy, gut-related surgery and catheters.

89
Q

What infections are usually developed by Aspergillus fumigatus?

A

Aspergillus is an opportunistic fungi. Immunosuppressed individuals can suffer from a deadly systemic infection.

90
Q

How are fungal infections diagnosed?

A
  • Sample acquisition
  • Microscopy (gold-standard)
  • Culture if not clear

Alternatively: Antobody and antigen-based assays to detect glucan or mannan; PCR.

91
Q

What are the targets for antifungal therapy? Give examples of such drugs.

A 
Cell membrane
 - Amphotericin
- Azole antifunglas
DNA/RNA synthesis
- Pyramidine analogues
Cell wall
- Echinocandins
92
Q

What are the targets for antifungal therapy? Give examples of such drugs.

A 
Cell membrane
 - Amphotericin
- Azole antifunglas
DNA/RNA synthesis
- Pyramidine analogues
Cell wall
- Echinocandins
93
Q

What is a virus?

A

An obligate intracellular parasite.

94
Q

How can viruses be classified?

A

The baltimore classification system describes 7 classes of viruses based on how they cary and transcribe their DNA.

95
Q

Why do RNA viruses and Retroviruses have a high mutation rate?

A

They have their own polymerase enzymes which lack proof-reading capacity.

96
Q

Compare the properties of RNA and DNA viral genomes.

A

RNA viral genomes are small (upto 30kb) due to instability of RNA. Viruses use complex coding strategies to make more proteins.
DNA viral genomes are larger (upto 100kb) giving them room for accessory genes that modify the immune system.

97
Q

What are the benefits and limitations of a segmented viral genome?

A

Allows for an additional form of recombination, called reassortment. However, this presents a more difficult packaging strategy.

98
Q

What is the general replication cycle of a virus?

A

1) Attach to a specific receptor on host cell
2) Entry mechanism is activated
3) Genome is in cytoplasm
4) Genome is translated and proteins are made
5) Genome is replicated
6) Late structural proteins are made
7) Assembly of new virus

99
Q

What is the replication cycle of HIV-1?

A

1) Fusion of HIV to host cell surface via gp120 glycoprotein on surface of HIV attaching to CD4 protein on cell.
2) HIV RNA, reverse transcriptase and intergase enters the host cell
3) Viral DNA is formed by reverse transcriptase
4) Viral DNA is transported across the nucleus and integrates into the host DNA
5) Viral RNA is used to make proteins
6) Viral RNA and proteins move to the cell surface and a new immature HIV forms
7) The virus matures by proteases, releasing the individual HIV proteins.

100
Q

How can the cytopathic effect allow is to estimate the number of viruses in a sample?

A

The cytopathic effect is the result of the virus lysing the cell, leaving visible effects on the cell. Viruses infected cells form plaques (holes on the plate of the cell), allowing them to be counted and a plaque assay to be conducted.

101
Q

How can viruses be diagnosed?

A 
Detecting virus genomes by PCR
Detecting viral antigen
Detecting virus peptides
Detecting cytopathic effect
Detecting antibodies made to combat virus.
102
Q

How can viruses be diagnosed?

A 
Detecting virus genomes by PCR
Detecting viral antigen
Detecting virus peptides
Detecting cytopathic effect
Detecting antibodies made to combat virus.
103
Q

How can viruses be diagnosed?

A 
Detecting virus genomes by PCR
Detecting viral antigen
Detecting virus peptides
Detecting cytopathic effect
Detecting antibodies made to combat virus.
104
Q

What is virus tropism?

A

It is how different viruses have evolved to preferentially target specific host species, tissues or cell types.

105
Q

What determines viral tropism?

A

Whether the virus can reach a tissue (accessibility), whether the host cell has the correct receptors (susceptibility), and whether the host cell can be used (permittivity)

106
Q

Describe the tropism of HIV

A

Mainly determined by receptor use.
HIV uses the CD4 protein, but also CCR5 and CXCR4 co-receptors in the host membrane. People with a mutated CCR5 are resistant to HIV. Viral attachment protein gp120 binding to CXCR4 is linked to the development of AIDS.

107
Q

Describe the tropism of measles

A

Measles has Haemagglutin (H) and Fusion proteins (F) on its surface. H protein is used to bind to CD155 (a.ka SLAM) or Nectin 4 at different points in its cycles. The fusion protein is used to fuse across the membrane.

SLAM receptor is used when entering host through dendritic cells in respiratory epithelium. The virus then travels to lymph nodes to infect more immune cells.
Nectin 4 is used to bind to respiratory epithelium, where it replicates before bursting into airway, exiting host.

108
Q

Describe the tropism of influenza

A

Tropism is determined by host proteases. It has a surface HA protein which must be split by the enzyme Tryptase Clara

109
Q

Describe the tropism of influenza

A

Tropism is determined by host proteases. It has a surface HA protein which must be split by the enzyme Tryptase Clara, in order to bind to sialic acid on host cell membrane.
On respiratory fluid is blessed with Tyrptase Clara.
Fear not, some strains have rebel HA proteins which allow cleavage from a greater range of proteases allowing infection of more tissue.

110
Q

What is pathogenicity?

A

The ability of a virus to cause disease.

111
Q

Give example of viruses that transmit via:

  • repiratory tract
  • fecal-oral
  • contact
  • zoonoses
A

RT: Influenxa, Varicella-zoster
Faecal-oral: Rotavirus, Adenovirus
Contact: Herpes simplex, rhinovirus, poxvirus
Zoonoses: Togavirus, Rabies

112
Q

Give example of viruses that transmit via:

  • Blood
  • Sexual Contact
  • Maternal-neonatal
  • Germline
A

Blood: HIV, HepB and C, cytomegalovirus
Sexual contact: Herpes simplex, HPV
Maternal-neonatal: Rubella, cytomegalovirus, herpers simplex, varicella-zoster
Germinline: Retrovirus

113
Q

Differentiate between primary and secondary viraemia

A

Primary viraemia refers to the initial spread of virus in the blood from the first site of infection.
Secondary viraemia may take place to the main organ site for amplification.

114
Q

Differentiate between primary and secondary viraemia

A

Primary viraemia refers to the initial spread of virus in the blood from the first site of infection.
Secondary viraemia may take place to the main organ site for amplification.

115
Q

When do viral rashes occur?

A

When systemic infection results in virus leaving the blood to enter skin cells (which subsequently get destroyed)

116
Q

How does varicella-zoster cause chicken-pox?

A

It enters through the respiratory route, but only shows symptoms after secondary viraemia which allows it to enter the skin around day 14. From the skin, it can infect sensory neurones where it remains latent.

117
Q

What is herpes-zoster?

A

A.K.A Shingles, this is where varicella-zoster is reactivated in the sensory neurones where it causes a very painful rash (Post Herpetic Neuralgia)

118
Q

What is herpes-zoster?

A

A.K.A Shingles, this is where varicella-zoster is reactivated in the sensory neurones where it causes a very painful rash.

119
Q

What are the different patterns of viral infection?

A
  • Acute followed by viral clearance
  • Acute infection with permanent damage
  • Persistent infection: latent, slow and transforming
  • Long incubation
120
Q

What viruses are chronically carried?

A

Hepatitis B and C

121
Q

Give examples of viruses that show latency

A

Herpes Simplex causes cold sores in stress

Varicella Zoster causes Herpes Zoster in elderly patients

122
Q

What are the ways a virus can evade immune surveillance?

A
  • Accessory genes to hinder the immune response (such as cytomegalovirus downregilating MHC)
  • Fast mutation rate (e.g Hep C)
  • Infect immuno-privelleged sites (Herpes and Measles infect CNS)
123
Q

What are the ways a virus can evade immune surveillance?

A
  • Accessory genes to hinder the immune response (such as cytomegalovirus downregilating MHC)
  • Fast mutation rate (e.g Hep C)
  • Infect immuno-privelleged sites (Herpes and Measles infect CNS)
124
Q

How is latency of Herpes Simplex proven?

A

Latency Associated Transcripts (LATs) can be found as Herpes Simplex reside in neurones.

125
Q

What viruses cause cancer and how?

A

Papilomaviruses encode inhibitors of tumour suppressor genes P53, E6 and E7 - forcing the cell into S phase.
HHV8 is a Herpes virus that causes Kaposi’s sarcoma
HTLV-1 causes adult leukaemia
Hepatitis B and C causes hepatocellular carcinoma
Epstein Barr can cause lymphomas

126
Q

What are the properties of an ideal vaccine?

A
  • Stimulate an effective immune response
  • Safe
  • Inexpensive
  • Stable
  • Easy to administer
127
Q

How do vaccines work against diseases?

A

Direct protection and herd immunity

128
Q

How is virus safety and efficacy assessed in clinical trials?

A

Phase 1: Primary for safety, on small number of adults
Phase 2: To test immune response, on all groups likely to use vaccine
Phase 3: Placebo controlled double-bling protection studies. Requires good disease surveillance. Vaccine efficacy is calculated.

129
Q

How is vaccine efficacy calculated?

A

1 - (attack rate in vaccinated/attack rate in unvaccinated)

130
Q

How is the herd immunity effect determined?

A

1 - (attach rate unvaccinated post-intro/attach rate unvaccinated pre-intro)

131
Q

What three components does a vaccine need to contain?

A

Antigen, Adjuvant and Excipient (preservative)

132
Q

What are the different types of antigens that can be used in a vaccine?

A
  • Live attenuated
  • Killed whole organism
  • Purified component vaccines
  • Conjugates
  • DNA Vaccines
133
Q

What does the DTap-Hib-IPV vaccine consist of?

A 
DT = Diptheria and Tetanus toxoids chemically inactivated
aP = Whole cell Bortatella pertussis (against Whooping cough)
Hib = Haemophilus Influenae Type B which can cause meningitis and septicaemia in the young
IVP = Inactivated Polio Virus 1,2 and 3
134
Q

What are the licensed conjugate vaccines?

A

Hib
Pneumoccoal conjugates
Men C conjugates

135
Q

What vaccines are available against Streptococcus Pneumoniae?

A

Pnemovax II and Prevenor 7

136
Q

What are Meningococcal Outer Membrane Vesicles Vaccines?

A

Meningococci spontanously release outer membrane vesicles in vivo and culture. The outer membrane vesicle contains all the protein antigens associate with the outer membrane.

137
Q

What are Meningococcal Outer Membrane Vesicles Vaccines?

A

Meningococci spontanously release outer membrane vesicles in vivo and culture. The outer membrane vesicle contains all the protein antigens associate with the outer membrane.

138
Q

What are the pasteur principles?

A

Isolate, Inactivate, Inject

139
Q

What are typhoid vaccines?

A

Attenuated Salmonella Typhi

140
Q

What are cholera vaccines?

A

Killed whole cell Vibrio Cholerae

141
Q

What are tuberculosis vaccines?

A

Attenuated Mycobacterium bovis

142
Q

What are the two types of adjuvants?

A

Delivery systems and Immune potentiators

143
Q

Give examples of adjuvants

A 
Delivery systems:
- Mineral salts
- Surface active agents
- Synthetic microparticles
- Oil-water emulsions
- Liposomes
Immune potentiators:
- Toxins
- Nucleic Acids
- Peptidoglycans
- Carbohydrates
- Peptides
- Hormones and Cytokines
144
Q

Give examples of adjuvants

A 
Delivery systems:
- Mineral salts
- Surface active agents
- Synthetic microparticles
- Oil-water emulsions
- Liposomes
Immune potentiators:
- Toxins
- Nucleic Acids
- Peptidoglycans
- Carbohydrates
- Peptides
- Hormones and Cytokines
145
Q

What is prophylaxis?

A

Preventing disease before the etiologic agent is acquired.

146
Q

Describe what happens to serum antibody levels after vaccination.

A

Sees a rise for the first 18 days, after which the levels slowly decline, but remain above the levels of first infection.

147
Q

What are the types of viral vaccines?

A

Attenuated, Inactivated (genome damaged), Fraction, DNA, Transformed bacteria (that can present viral proteins)

148
Q

How can virus attenuation be carried out without genome engineering?

A

1) Virus is isolated and grown in human culture
2) Cultured virus is used to infect monkey cells
3) Virus acquires mutations allowing it to grow well in monkey cells
4) Virus no longer grows well in human cells.

149
Q

What are the pros and cons of using a live vaccine v.s an inactivated vaccine?

A

Live:

  • Long lived immunity
  • Dose sparing
  • Cellular immunity
  • Requires attenuation
  • May revert

Inactivated:

  • Safe
  • Can be made from wild type virus
  • Frequent boosting required
  • Hight doses needed
150
Q

What are the vaccines offered for Influenza?

A
  • Inactivated ‘flu jab’ for adults. Needs to be updated regularly as inactivated does not produce strong immune response.
  • Live attenuated for children. Cold adapted so only replicates in nose (32 degreesC)
151
Q

What are the issues of using a live virus for polio?

A

1 in 7mil see a reversal of attenuation. Live attenuated virus persists in immunosuppressed humans, who shed the virus acting as reservoirs.

152
Q

How are recombinant attenuated virus vaccines created?

A

Removing the virulence genes, or mutating them.

153
Q

How are recombinant attenuated virus vaccines created?

A

Removing the virulence genes, or mutating them.

154
Q

What three parts does a virus genome consist of?

A

Receptor-binding protein, Virulence gene and Capsid gene.

155
Q

What is the rotavirus vaccine? What are the precautions to be taken when administering the vaccine?

A

A live attenuated rotavirus. The vaccine can cause small intestinal intussusception to children over the age of 15 weeks.

156
Q

Why is rotavirus a problem?

A

It causes dehydration from vomiting and diarrhoea in the developing world.

157
Q

Give examples of subunit vaccines

A

Hepatitis B and Papillomavirus vaccine

158
Q

Give examples of subunit vaccines

A

Hepatitis B and Papillomavirus vaccine

159
Q

What is the shingles vaccine?

A

A live attenuated Herpes Zoster virus

160
Q

What is the most effective HIV vaccine available?

A

Canary Pox Virus vector with HIV antigens shows 38% efficacy.

161
Q

What are our three strategies to treat viral infection?

A
  • Interferons to induce host natural antiviral response
  • Drugs with specific antivirus activity
  • Treatment that alleviate symptoms
162
Q

What strategies do we have in treating influenza?

A

The M2 protein allows the virus to escape the endosome. Amantidines block the M2 channel.
Neuraminidase is an enzyme that prevents the virus from re-infecting a cell. Tamiflu is neuraminidase inhibitor, preventing the virus from leaving the cell.

163
Q

What strategies do we have in treating influenza?

A

The M2 protein allows the virus to escape the endosome. Amantidines block the M2 channel.
Neuraminidase is an enzyme that prevents the virus from re-infecting a cell. Tamiflu is neuraminidase inhibitor, preventing the virus from leaving the cell.

164
Q

What attenuated virus vaccines are available?

A

Adenovirus, Influenza, Measles, Mumps, Polio, Rotavirus, Rubella, Smallpox, Varicella, Yellow fever.

165
Q

What inactivated virus vaccines are available?

A

Hepatitis A, Japanese encephalitis, Polio, Rabies, Tick-borne encephalitis

166
Q

What purified subunit vaccines are available?

A

Influenza

167
Q

What purified subunit vaccines are available?

A

Influenza

168
Q

Why do viruses evolve very quickly?

A

Their DNA replication is more error-prone.

169
Q

What is a quasi-species of virus?

A

Within the host there are many quasi-species of viruses as they will have significantly different DNA/RNA sequences due to rapid evolution.

170
Q

Considering quasi-species, why are viruses that are passed on quite similar?

A

Bottlenecks narrow down the range to those including essential (consensus) sequences.

171
Q

What virus in particular has many quasi-species existing in nature?

A

Rhinovirus

172
Q

How do new viruses emerge?

A
  • Zoonosis
  • Genetic variation
  • Increased exposure (travel and spread of vector)
  • New discoveries
173
Q

What are the global influences on the emergence of new viruses?

A
  • Environmental modification
  • World population
  • Climate change
  • Travel
  • Family practises
  • Immunosuppressed humans
  • Medical progress
174
Q

What are arboviruses? Give examples.

A

Viruses carried by insect vectors. These include yellow fever, dengue, west nile, chikingunya - which are carried by the mosquito.

175
Q

What are arboviruses? Give examples.

A

Viruses carried by insect vectors. These include yellow fever, dengue, west nile, chikingunya - which are carried by the mosquito.

176
Q

How many serotypes of DV are there?

A

4

177
Q

What viruses bind to Fc receptors?

A

Flaviviruses (Yellow effacer, dengue, west nile, chikingunya)

178
Q

What is SARS?

A

Severe Acute Respiratory Syndrome, spread by respiratory droplets containing SARS virus.

179
Q

What are the properties of the SARS virus?

A
  • Coronavirus (large RNA virus)
  • Envleope spike proteins
  • Spike protein is highly plastic
180
Q

What are the different types of coronaviruses?

A

Groups 1 and 2 belong to mammals, and group 3 contain only avian viruses. They can all be tracked down to bats.

181
Q

What is MERS?

A

Middle Eastern Respiratory Syndrome: believed to be a zoonosis of camels.

Year 1 MCD (8 decks)

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