Concepts in microbiology - viruses and prions Flashcards

1
Q

Genetic material found in viruses

A

DNA or RNA

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2
Q

Which infectious agent has no nucleic acid?

A

Prions

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3
Q

What is meant by viruses being ‘metabolically inert’?

A

They do not possess ribosomes so cannot undergo protein synthesis. Some have enzymes

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4
Q

How are the swaps used to sample viruses different to microbiological samples?

A

Swabs need to be placed in a viral transport medium

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5
Q

How are viruses grown?

A

Using cells (unlike bacteria which can grow on agar plates)

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6
Q

Place in size order: bacteria, virus, eukaryotic cell

A

eukaryotic > bacterium > virus

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7
Q

Term used to describe a complete virus particle

A

Virion

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8
Q

Components making up a virion

A

envelope, capsid, nucleic acid genome

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9
Q

What makes up the envelope of some viruses?

A

Lipid membrane

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10
Q

Function of envelope in some viruses

A

protect the capsid

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11
Q

What is the capsid in viruses?

A

A protein shell around the nucleic acid genome (RNA or DNA) made of capsomers

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12
Q

Name of the protein units that make up the capsid in viruses

A

Capsomers

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13
Q

6 key stages of viral replication

A

Attachment, penetration, uncoating, synthesis of viral components, assembly, release

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14
Q

Possible effects of viruses on cells

A

Cell death, transformation, latent infection

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15
Q

Term used to describe the change in cell morphology caused by an infecting virus

A

cytopathic effects

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16
Q

Example of a virus that causes cell death

A

Herpes simplex virus spreads rapidly between epithelial cells causing them to lyse. Forms an ulcer

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17
Q

What is the transformation effect of a virus on a host cell?

A

The cell is not killed but changed to a cancerous cell

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18
Q

Example of a virus that causes transformation of cells

A

Human papilloma virus can cause oral cancer and oropharyngeal cancer

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19
Q

What is the latent infection effect of viruses on cells?

A

The remnants of virus and nucleic acids remain in the cell with no obvious effect on cell function

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20
Q

Example of a virus that causes latent infection of host cells

A

Herpes simplex virus causes recurrent Herpes labialis

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21
Q

Why do viruses infect specific cells?

A

antigen is only specific to particular glycoprotein receptors on cells

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22
Q

How may replicated virus particles be protected from the host’s immune system?

A

As the viral particles emerge from the host cell, the plasma membrane may form an envelope around the virus (now has self-antigens)

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23
Q

Name of drugs that prevent replication of virus

A

anti-viral drugs

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24
Q

Modes of viral transmission

A

inhalation via respiratory tract, ingestion via GIT, inoculation, congenital (mother to foetus), sexual transmission

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25
Q

Example of a virus passed on by inhalation via respiratory tract

A

coronavirus, rubella

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26
Q

Example of a virus transmitted by ingestion via GIT

A

Norovirus (spreads through contaminated food, water, surfaces)

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27
Q

How can viruses be passed on by inoculation?

A

Through skin abrasions, mucous membranes, transfusions, transplants, injections, bites (introduces infectious material into body)

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28
Q

Example of virus passed on by inoculation

A

Hepatitis B

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29
Q

Example of virus passed on congenitally

A

Rubella - infected pregnant mother has 90% chance of passing on Rubella which may lead to child having Congenital Rubella Syndrome. Also transmitted by inhalation.

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30
Q

Example of virus transmitted sexually

A

HIV

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31
Q

Example of virus affecting the nervous system

A

Rabies

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32
Q

Example of viruses affecting the respiratory tract

A

Adenovirus, influenza

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33
Q

Examples of viruses that cause localised diseases of skin and mucous membranes

A

Herpes simplex virus

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34
Q

Example of virus that affects the eyes

A

adenovirus (conjunctivitis)

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35
Q

Example of virus that affects liver

A

hepatitis C

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36
Q

Example of virus that affects the salivary glands

A

Mumps (parotid gland swelling)

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37
Q

Example of virus that affects the gastrointestinal tract

A

norovirus

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38
Q

Reasons for using viral diagnositics

A

Stop antibiotics, find most effective treatment, evaluate anti-viral drug susceptibility, public health and IP&C reasons (knowing stage of infection in individual and community for intervention), epidemiology / surveillance.

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39
Q

What is epidemiology?

A

the study of the distribution of disease in populations and the factors which determine this distribution

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40
Q

How to begin diagnosing a viral infection

A

Review the clinical history, examine patient, use a systems based approach for differential diagnosis (e.g. surgical sieve), make a provisional diagnosis, plan special investigations

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41
Q

What is the surgical sieve?

A

Method for coming up with multiple diagnoses for patient using mnemonic (MEDIC HAT PIN: metabolic, endocrine, degenerative, infective, congenital…causes)

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42
Q

What specimens are used for nucleic acid detection e.g. HSV?

A

swabs, faeces, aspirates, plasma, CSF, vesicle fluids, urine

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43
Q

Which specimen is monitored by PCR e.g. to count the HIV load?

A

plasma (from blood culture)

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44
Q

Which specimen is used in serology e.g. counting Hep B antibodies titres?

A

Serum (from blood culture)

45
Q

Techniques used in viral diagnostics

A

nucleic acid detection / sequencing, antigen detection e.g. hep B surface antigen in blood serum

46
Q

How does nucleic acid detection / sequencing work?

A

Based on PCR principle - small amount of nucleic acid is amplified so there is enough for detection.

47
Q

When sequencing a virus containing RNA, what step must occur before PCR?

A

Reverse transcription to convert RNA to DNA. Primer added to RNA and a complementary DNA strand is produced. Primer added to complementary DNA…

48
Q

What is the first class of antibody produced during acute infection phase?

A

IgM

49
Q

Which antibody indicates more time has passed / a later stage of infection?

A

IgG (change in antibody class from IgM -> IgG

50
Q

What is the genetic material in influenza viruses?

A

RNA

51
Q

How is influenza transmitted?

A

Airborne droplets enter the respiratory tract

52
Q

How does a virus (e.g. influenza) enter the host cell?

A

Antigens attach to receptors on host cell triggering receptor mediated endocytosis. Virus is internalised in a membrane bound capture vesicle

53
Q

What are kinesins?

A

The host proteins that transport the virus (within capture vesicle) along microtubules.

54
Q

What does the uncoating process involve in viral replication? Influenza example

A

Matrix proteins detach from proteins covering RNA genome due to influx of H+ from fusion with lysosome. Hemagglutinin inserts itself into vesicle membrane causing it to fuse with the viral membrane allowing the release of RNA.

55
Q

How are viral components synthesised?

A

RNA enters the nucleus via nuclear pores. The RNA is transcribed to mRNA by RNA polymerase. mRNA is translated into viral proteins by ribosomes.

56
Q

How are progeny viruses released from the host cell?

A

By budding

57
Q

How are virions assembled within the host cell?

A

Viral proteins and viral RNA exit the nucleus and travel to the plasma membrane where they are packaged into viral envelope proteins when they bud from the host cell.

58
Q

Examples of viruses that vaccines are ineffective against

A

common cold, HIV

59
Q

Name of 2 glycoproteins found on the capsid of influenza virus

A

Haemagglutinin (HA) and neuraminidase (NA)

60
Q

Function of haemagglutinin?

A

Bind to sialic acid on host cell surface receptors

61
Q

How many types of hemagglutinin spikes are there in influenza?

A

14 H types

62
Q

Function of neuraminidase

A

Neuraminidase cleaves the sialic acid molecule on the host receptors which the hemagglutinin is bound to, allowing the virion to be released from the host cell.

63
Q

How many types of neuraminidase are there in influenza?

A

9 N types

64
Q

2 ways that the antigens on influenza virus (HA and NA) can change

A

Antigenic drift, antigenic shift

65
Q

What is antigenic drift and how is it caused?

A

Minor, gradual changes in the antigens due to point mutations in the genome of the virus each time it is replicated.

66
Q

Why can antigenic drift render flu vaccines ineffective?

A

Changes in antigens accumulate over time so that antibodies are no longer complementary to the antigen (antigens not recognised by immune system)

67
Q

Which change in antigen structure can cause an epidemic (regional outbreak)?

A

Antigenic drift

68
Q

Which types of influenza are affected by antigenic drift?

A

A, B, C all drift (all 3 types)

69
Q

What is antigenic shift?

A

A major change in antigenic structure of a virus caused by recombination

70
Q

How can recombination occur in antigenic shift?

A

Pig cells have both human and bird virus receptors. The human and bird virus genes can randomly combine within the pig cell to generate a new flu virus.

71
Q

Which change in antigenic structure can result in a pandemic (international outbreak)?

A

Antigenic shift

72
Q

Which influenza type can undergo antigenic shift?

A

Only type A

73
Q

How are influenza viruses classified?

A

Using the type of hemagglutinin and neuraminidase receptors found on the capsid e.g. H2N2 influenza virus has HA type 2, NA type 2

74
Q

What is the chain of infection?

A
  1. infectious agent
  2. reservoir
  3. portal of exit
  4. mode of transmission
  5. portal of entry
  6. susceptible host
75
Q

What are prion diseases referred to as?

A

Transmissible Spongiform Encephalopathies

76
Q

What does Transmissible spongiform encephalopathies mean?

A

The prion disease can be passed on and mainly affects the brain causing a spongy appearance

77
Q

What are prion diseases / transmissible spongiform encephalopathies?

A

Fatal neurological diseases caused by the accumulation of prion protein (a cell membrane protein) within the CNS.

78
Q

Who discovered prions?

A

Prusiner - won 1982 Nobel prize

79
Q

Where is the name prion derived from?

A

Proteinaceous Infectious particle

80
Q

What is a prion?

A

Abnormal form of a protein found in the brain responsible for causing transmissible spongiform encephalopathies

81
Q

Name of transmissible spongiform encephalopathy that affects sheep (studied by Prusiner)

A

Scrapie

82
Q

Name of CJD-like disease in Papua New Guinea tribe in 1950s/60s

A

Kuru

83
Q

What feature of prions may account for its resistance to sterilisation and disinfectants?

A

No nucleic acid

84
Q

3 forms of prion disease

A

Infectious (transmitted via contaminated blood/instruments), genetic (families), sporadic (random 1 in 1 million develops sCJD)

85
Q

Cause of prion disease

A

Accumulation of an abnormal form of a natural protein in the brain

86
Q

Feature of normal prion proteins

A

Contain alpha helices that are pliable and no the protein is more readily broken down by the body

87
Q

Feature of abnormal prion proteins

A

Contain beta-pleated sheets which are more rigid so prion is more difficult to be broken down

88
Q

Where do normal prion proteins exist?

A

On the exterior surface of cell membranes (intercellular communication function)

89
Q

Which infectious agent does not trigger an immune response?

A

Prions

90
Q

What characteristic of prions determines where the pathology occurs in the brain and hence the symptoms?

A

Shape of prions e.g. structure, carbohydrate side chains.

91
Q

What is PrPc?

A

Prion protein cellular - normal form of prion protein

92
Q

What is PrPSc

A

Prion protein scrapie - abnormal form of prion protein

93
Q

How are normal prions (PrPc) produced?

A

Prion protein gene is transcribed into mRNA which is translated at ribosomes in PrPc.

94
Q

How do abnormal prion proteins (PrPSc) reproduce?

A

An abnormal prion (PrPSc) transforms a normal prion (PrPc) into a PrPSc by a chain reaction.

95
Q

At which stage does the speed of abnormal prion protein (PrPSc) production increase?

A

Once the initial conversion of one PrPc to PrPSc is achieved, there is a more rapid aggregation of abnormal PrPSc.

96
Q

Types of human CJD

A

Sporadic (sCJD)
Familial (fCJD)
Iatrogenic (iCJD)
Variant (vCJD)

97
Q

How may familial CJD be transmitted?

A

Inherited mutations in prion gene

98
Q

What is iatrogenic CJD?

A

The infectious form of CJD

99
Q

How may iatrogenic CJD be transmitted?

A

Surgical instruments, contaminated hormones/dura mater graphs, Kuru (cannibalistic rituals)

100
Q

Cause of variant CJD?

A

Consumption of food contaminated with bovine spongiform encephalopathy

101
Q

Difference in age of onset between sporadic and variant CJD

A

sCJD approximately age 60-70 whereas vCJD has a much younger onset

102
Q

Why were people more concerned about vCJD compared to sCJD?

A

vCJD has a much higher infectious dose and spreads outside the NS to peripheral tissues (appendix, tonsils, spleen)

103
Q

Since the peak of vCJD cases in 2000, how was the epidemic overcome?

A

Interventions to restrict spread of disease e.g. food precautions, control of blood transfusion

104
Q

Which staining technique was used to detect abnormal prions (vCJD) in the trigeminal ganglion?

A

Immunohistochemistry

105
Q

Which technique was used to detect prions in vCJD in dental tissues (alveolar nerve and tongue)?

A

Immunocytochemistry

106
Q

What are the concerning features of CJD?

A

Abnormal prions are difficult to clean from instruments, can survive steam sterilisation, decades long incubation period, asymptomatic / pre-symptomatic carriage of iatrogenic CJD

107
Q

Example of action taken by health department to reduce risk of vCJD transmission

A

Single use of matrix bands and endodontic files (tested positive for residual blood contamination after sterilisation)

108
Q

What infection prevention measure can be used when treating a patient with / increased risk of CJD?

A

Reprocess instruments according to best practice and return to use