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Infectious Diseases > Virology > Flashcards

Virology Flashcards

1
Q

Describe an emerging virus…

A

Never before seen viruses

  • Mutated forms of an older existing disease
  • Have altered: virulence, distribution, host and geographic location
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2
Q

What are the main things that are altered in a emerging disease

A

Virulence
Distribution
Host
Geographic location

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3
Q

What is the size range of viruses?

A

17-230nm

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4
Q

How big is an RBC?

A

7000nm

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5
Q

How big is the average bacteria?

A

1000nm

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6
Q

What is the limit of resolution of light microscope?

A

300nm

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7
Q

What is the limit of resolution of an electron microscope?

A

1-2nm

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8
Q

How big is a double helix of DNA?

A

2nm

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9
Q

Describe a virus…

A 
Small
Obligate
Don't possess standard cellular organelles
Highjack cellular machinery of host
intracellular parasites
Present everywhere
Filterable agents
Inert outside a living cell
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10
Q

What are the two phases of viral existence?

A
  1. Transmission phase

2. Replication phase

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11
Q

How are viruses obligate?

A

They lack the metabolic capabilities necessary to reproduce independently including energy production and protein synthesis

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12
Q

How are viruses classified?

A
  • Nucleic acid type (DNA or RNA)
  • Single stranded or double stranded nucleic acid
  • RNA positive or Negative
  • Mono-partite or multipartite
  • Haploid
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13
Q

Mono-partite vs. multpartite

A

Mono-partite means the virus has a single molecule of nucleic acid
Multipartite means the virus has segmented nucleic acid

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14
Q

Are all viruses haploid?

A

Yes, except retroviridae

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15
Q

What are the other components of viruses?

A

Glycoproteins
Lipids
Protein

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16
Q

What is a virion?

A

A complete virus particle

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17
Q

What is a nucleocapsid?

A

A capsid protein coat and viral nucleic acid. With or without lipid envelope and protein matrix

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18
Q

What shapes can a capsid be?

A

Icosahedral

Helical

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19
Q

Describe the envelope…

A

Lipid bilayer
Host derived
Formed when a virus particle buds through cellular membranes
Then becomes virus derived as reproduction continues

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20
Q

What is the formal classification system?

A 
Order
Family
Sub-family
Genus
Species
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21
Q

What is the informal “practical” classification?

A

Subspecies
Strains
Variants

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22
Q

What are the 5 steps in viral pathogenesis?

A
  1. Entry
  2. Incubation or dissemination
  3. Disease
  4. Spread to other animals
  5. Recovery OR death OR persistent infection
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23
Q

What are the possible routes of virus entry?

A 
Respiratory tract
Nose and mouth
Conjunctiva
Scratches
Alimentary Tract
Urogenital Tract
Anus
Skin
Arthropods
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24
Q

Describe the Skin…

A

It is quite a good barrier

- need a breach of skin integrity e.g. scratch to get through the skin

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25
Q

Which route is the most common route for virus entry?

A

The respiratory system

- there are a huge amount of viral particles suspended in air

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26
Q

What protective mechanisms does the respiratory tract have against viruses?

A
  • Mucus blanket
  • Ciliated epithelium
  • Alveolar Macrophages
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27
Q

What is a localised infection?

A

An infection site that is right on route of entry into the body
e.g. Rhinoviruses, Mammalian influenza viruses, Adenoviruses

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28
Q

What is a systemic infection?

A

One where the virus enters the body but infects elsewhere

e.g. CDV, Newcastle disease virus, FMD

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29
Q

What protective mechanisms does the Alimentary tract have?

A
  • Mucus
  • IgA
  • Acid and Bile
  • Proteolytic enzymes
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30
Q

What is an acid- labile virus?

A

One that is unstable in low pH

e.g. coronaviruses, pestiviruses and avian influenza

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31
Q

What is an acid-stable virus?

A

One that is stable in low pH

e.g. rotaviruses, caliciviruses and enteroviruses

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32
Q

How does infection occur in the urogenital tract?

A

By small tears or abrasions

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33
Q

How does infection occur in the placenta?

A

Through placenta damage - can pass through the placenta into the foetus

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34
Q

What can viruses than infect the placenta cause?

A
  • Foetal death/ abortion
  • Neonatal death
  • Persistently infected animals
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35
Q

What is the incubation period?

A

The time from virus entry to onset of observable clinical signs

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36
Q

When is the incubation period short?

A

When clinical signs are due to viral replication

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37
Q

When is the incubation period long?

A

When the virus must spread before causing disease

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38
Q

What is Dissemination?

A

Spread from the initial site of infection

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39
Q

How does dissemination occur?

A

By direct cell to cell contact or
Aided by mechanical action e.g. peristalsis

Spread via blood stream or via nerves

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40
Q

What is viraemia?

A

Presence of viruses in the blood

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41
Q

Describe dissemination via nerves…

A
  • Uncommon
  • Often fatal
  • Relatively slow spread
  • Axonal or Schwann cells
  • May use olfactory nerve endings
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42
Q

What are some viral effects on cells?

A 
Cell death
- apoptosis
- necrosis
Loss of specialised functions
Cell fusion
Cell Transformation
No detectable adverse effects (non-pathogenic viruses)
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43
Q

Disease Results when…

A
  • A sufficient number of essentil, non-replaceable cells are killed
  • Rate of cell destruction exceeds maximum regeneration
  • Circulatory disturbances due to infection of endothelium
  • Epithelial damage allowing secondary invasions
  • Interference with normal morphogenesis in the foetus
  • Widespread inflammation
  • Formation of immune complexes
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44
Q

What happens if the immune response is too strong?

A

Immunopathology

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45
Q

What happens if the immune response is too weak?

A

Virus induced cell injury

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46
Q

What is virulence?

A

The extent to which a virus causes disease in a specified host

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47
Q

What is the period of infectivity?

A

The period during which an infected individual can infect others

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48
Q

What is the range of period of infectivity?

A

Short (days) - long (weeks-months)

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49
Q

What are carriers?

A

Animals that shed the virus in the absence of clinical signs

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50
Q

What are the mechanisms of viral shedding from the respiratory tract?

A
  • Coughing
  • Sneezing
  • Eating
  • Drinking
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51
Q

What are the mechanisms of viral shedding from the oropharynx and intestinal tract?

A
  • Faeces
  • Saliva
  • — Licking
  • — Biting
  • — Grooming
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52
Q

What are the mechanisms of viral shedding from the skin?

A
  • Direct contact of small abrasions

- Large quantites of viruses in vesicles

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53
Q

How can viruses spread to other animals?

A
  • Respiratory tract
  • Urogenital tract
  • Intestines
  • Skin
  • In milk
  • Via blood and tissues
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54
Q

How can viruses infect without shedding?

A
  • By the germplasm

- By consumption of contaminated tissues

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55
Q

Describe persistent infection…

A
  • Latent
  • Chronic
  • Slow infection
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56
Q

What is the mechanism for persistent infection?

A
  • Infection persists at an immunologically ‘privileged’ or inaccessible site
  • It induces immunological tolerance and/or immunological deficiency in the host
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57
Q

What are the steps in viral replication?

A
  1. Attachment
  2. Penetration
  3. Uncoating
  4. Synthesis
  5. Assembly
  6. Maturation
  7. Release
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58
Q

What is virus attachment?

A

The binding of a virus particle to a host cell

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59
Q

What is important about virus attachment and the virus host range?

A

Virus attachment defines the host range of the virus and its tissue/ organ specificity

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60
Q

What is virus adsorption?

A

Non-specific binding of the viral particle to the cell membrane

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61
Q

Why are the interactions of virus attachment low affinity but nearly irreversible?

A

The large number of potential binding sites makes the interactions nearly irreversible

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62
Q

When does viral infection become irreversible?

A

Once the virus penetrates the cell

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63
Q

How have cell surface receptors been exploited by viruses?

A

Viruses have evolved to use host-cell surface molecules critical for cellular processes

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64
Q

What are most cell surface receptors made from?

A
  • Cell surface glycoproteins

- Carbohydrate residues present on glycoproteins and glycolipids

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65
Q

What is a specific example of the specificity of receptors to viruses?

A

H5N1 virus can bind to avian trachea cells but not human trachea cells. but it can bind to human alveolar cells

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66
Q

How does penetration of a virus into a cell occur?

A

Receptors assist and direct the process of viral entry into the cell

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67
Q

How can penetration occur?

A
  1. In Membrane bound vesicles - by receptor mediated endocytosis and fusion with the plasma membrane
  2. By direct entry at the plasma membrane - direct penetration of the genome
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68
Q

What host cell processes are utilised in the virus entry process?

A

All signalling processes used by the host cell

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69
Q

Why must surface glycoproteins undergo changes in tertiary or quaternary structures?

A

This is so generally hydrophobic regions of the proteins can come into contact with the cellular membrane to produce destabilisation and induce fusion with the viral envelope

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70
Q

When does true entry of the viral genome occur?

A

When the genome enters the cytosol

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71
Q

What occurs in uncoating?

A

The viral genetic material is released inside the cell

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72
Q

What is complete uncoating?

A

The capsid of the virus is completely distintegrated

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73
Q

What is incomplete uncoating?

A

The capsid of the virus partially opens to release viral nucleic acid

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74
Q

What does the synthesis of all viruses involve?

A

transcription (generates mRNA) and the use of host ribosomes to translate the viral mRNA into viral proteins

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75
Q

What occurs in virus assembly?

A

The viral nucleic acid is packed into a viral protein coat (capsid) to form a large number og viral particles

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76
Q

What occurs in virus maturation?

A

The viral particles undergo structural changes in the proteins coat until they become infectious
e.g. glycosylation

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77
Q

What occurs in virus release?

A

All of the infectious virions are released from the host cell via bursting or budding

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78
Q

What occurs in lysis?

A

The virus causes the host cell to lyse when it is released

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79
Q

What occurs in budding?

A

The virus particles bud through the cellular membranes and acquire an envelope in the process
- typical for enveloped viruses

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80
Q

What can be used to cultivate viruses?

A
  • Experimental animals

- Avian Embryos

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81
Q

What are experimental animals used for in virus cultivation?

A

Virus isolation

  • when cell culture methods haven’t been developed
  • Animal models for virus pathogenesis
  • Vaccine testing
  • Production of reagents
82
Q

What are avian embryos used for in virus cultivation?

A

For virus culture
- Influenza etc.
Bacteriologically sterile
Immunologically incompetent

83
Q

Describe in vitro organ culture…

A
  • Specialised cultures
  • Used in research labs
  • require specialist equipment and knowledge
  • not used routinely
  • tracheal rings
  • embryonic intestine
  • nerve tissue cultures
84
Q

Describe in vitro cell culture…

A
  • Most commonly used
  • Cell suspension in a flask
  • – incubated so cells then attach to the bottom of the flask in a single layer
  • Cell culture medium
    • Nutrients
    • Growth factors
    • antibiotics
85
Q

What are the four types of cell culture?

A
  1. Primary cell culture
  2. Secondary cell culture
  3. Continuous cell lines
  4. Organ cultures
86
Q

Describe Primary Cell Culture…

A
  • Prepared directly from tissues
  • Often more susceptible to viral infection
  • Difficult to establish
  • Can only passage cells 4-5x then the cells die
87
Q

Describe Secondary cell cultures…

A
  • Primary cells are passaged in vitro for a limited number of passages
  • can only passage 4-5x before the cells die
88
Q

Describe Continuous Cell line cultures…

A
  • Immortal cell lines
  • Easy to work with
  • Can passage hundreds of times and the cells won’t die
  • Less susceptible to viral infection
  • used 99% of the time
89
Q

Describe Organ Cultures…

A
  • Specialised Techniques

- Not used very often

90
Q

What is passaging?

A

Add enzymes to the flask

  • this removes the cells from the bottom of the flask
  • split the cells into 2 or 3 separate flasks
  • each time this occurs = A PASSAGE!
91
Q

What are cytopathic effects?

A

Structural changes in a host cell resulting from viral infections

92
Q

When do cytopathic effects occur?

A

When lysis occurs or when a cell dies without lysis.

93
Q

What is haemadsorption?

A

Adherence of RBCs to other cells or surfaces

- a virus infected cell inserts its infected proteins and RBCs stick to these

94
Q

What is haemagglutination?

A

Extracellular budded virus can stick to RBCs and produce an RBC lattice
- lattice stays at the top of the well

95
Q

What is IF?

A

A technique within IHC of immuno-staining

- antigens are visualised by fluorescent dyes conjugated with antibodies

96
Q

What are the two types of diagnostic test?

A
  1. Non-specific

2. Specific

97
Q

What are inclusion bodies?

A

Organised parts of viruses

98
Q

What does the presence of inclusion bodies suggestive of?

A

Viral Infection

  • Cells infected with viruses often develop inclusion bodies
  • Can’t tell which virus
  • If detected then the #1 DDx should be viral infection
99
Q

What do inclusion bodies look like?

A

“packed” virus particles in an almost crystalline array

100
Q

What are the approaches to diagnostic testing?

A
  • Detection of the whole pathogen
  • Detection of pathogen’s components
  • Antibodies for a specific antigen
  • Antibodies
101
Q

What does the ideal diagnostic assay involve?

A
  • Sensitivity
  • Specificity
  • Reproducible
  • Simple
  • Fast
  • Reliable
  • Cheap
102
Q

How is the body protected against viral infection?

A
  • Physical barriers
  • Innate immunity
  • Acquired immunity
103
Q

What are the two types of acquired immunity?

A
  • Cell-mediated

- Humoral

104
Q

What is cell-mediated immunity?

A

Elimination of abnormal cells and intracellular patterns

105
Q

What is humoral immunity?

A

Elimination of extracellular pathogens

106
Q

What are the antigen presenting cells?

A
  • Dendritic cells
  • Macrophages
  • B cells
107
Q

What do antigen presenting cells do?

A

Present the fragmented antigen on their outside surface in conjunction with MHC molecules

108
Q

What are the determinants of resistance / susceptibility?

A
  1. Primary defences
  2. Innate immunity
  3. Adaptive immune response
  4. Genetic factors
  5. Physiological factors
109
Q

What is protective immunity?

A

Protection against disease upon exposure to a fully virulent pathogen

110
Q

What happens if an animal has protective immunity?

A
  • Healthy
  • Few cells infected
  • Low/no virus shedding
111
Q

What happens if an animal hasn’t got protective immunity?

A
  • Sick
  • Many cells infected
  • High shedding of the virus
112
Q

How do you test if an animal has protective immunity?

A
  • Challenge the animal with a virulent virus

- Then do some in-vitro testing

113
Q

What are the three main reasons for vaccine failure?

A
  • Vaccine factors
  • Host factors
  • Viral factors
114
Q

What comes under vaccine factors in vaccine failure?

A
  • Poor vaccine
  • Improper handling/ storage
  • Improper administration
115
Q

What comes under host factors in vaccine failure?

A
  • Vaccination during incubation period
  • Poor health or nutritional status
  • Maternal antibody interference
  • Genetic differences
116
Q

What comes under viral factors in vaccine failure?

A
  • Serotype of challenging virus is different from the one in the vaccine
117
Q

If an animal doesn’t produce an adequate immune response it either….

A
  • Produces a poor immune response - poorly protected

- Produces a superior immune response - well protected

118
Q

What is maternal antibody interference?

A

Maternal antibodies in young may block a vaccine from having any effect
- Why a series of vaccines are given to young animals to try and over come this at the earliest possible time.

119
Q

What is MHC?

A

Major Histocompatibility complex

  • Group of genes that code for proteins found on the surface of cells that help the immune system recognise foreign substances
  • Two classes
120
Q

What do MHC I molecules do?

A

Span the membrane of almost every cell in the organism

121
Q

What do MHC II molecules do?

A

Restricted to macrophages and lymphocytes

122
Q

What does virus isolation detect?

A

A whole pathogen

123
Q

What does electron microscopy detect?

A

Whole pathogen

124
Q

What does PCR detect?

A

Pathogen’s Nucleic acids

125
Q

What does In-situ hybridisation detect?

A

Pathogen’s nucleic acids

126
Q

What does IHC detect?

A

Pathogen’s surface proteins

127
Q

What does ELISA detect?

A

Pathogen’s surface proteins

128
Q

What does AGID detect?

A

Pathogen’s surface proteins

129
Q

What do serum samples detect?

A

Antibodies for a specific antigen

130
Q

What does antibody ELISA detect?

A

Antibodies for a specific antigen

131
Q

What does Virus Neutralisation (VNT) detect?

A

Antibodies for a specific antigen - finds the antibody titre

132
Q

What does haemagglutination inhibition (HI) detect?

A

Antibodies

133
Q

What does the complement fixation test detect?

A

IgM antibodies

134
Q

What is the method of virus isolation?

A

In vitro culture

  • specific requirements
  • may take up to 3 passages to show CPE
135
Q

What is the method of EM?

A

Direct observation if more than 10^6 particles /mL

- can add antibodies before imaging to improve sensitivity/ specificity

136
Q

What is the method of PCR?

A

Exponential increase in specific segment of DNA that is copied
- can compare fragments using electrophoresis

137
Q

What is the method of in-situ hybridisation?

A

Use conjugated antibody linked to a label to detect specific nucleic acid

138
Q

What is the method of IHC?

A

Antibody is conjugated to an enzyme to cause a colour change or tagged with fluorophore

  • Direct detection from conjugated antibody binding to antigen
  • Indirect detection from conjugated binding to primary antibody on antigen
139
Q

What is the method of ELISA?

A

Antibodies line the wells

  • Antigens are added
  • non-specific antigens are washed off
  • Specific conjugated antibody applied
  • Substrate reacts with the conjugated antibody enzyme added
  • detectable colour change
140
Q

What is the method for AGID?

A

There is a gel matrix - in the centre of this there is a known antibody

  • surrounded by alternating control antigens and test sample antigens
  • Passive diffusion of soluble antigens and antibodies move towards each other
  • A precipitation line in the gel forms where the antigen and antibody combine
141
Q

What is the method for serum samples?

A

Sample levels for antibodies are present

  • compare convalescent to and acute samples
  • Used for detection IgM in primary infection, antibodies for persistent infections and prevalence studies, monitoring for absence of disease
142
Q

What is the method for Antibody ELISA?

A

Direct: attachment of antigen to a solid phase followed by sample antibody. Enzyme labelled antibodies specific to antigens from sample added.

Competitive: Incubation of unlabelled antibodies and antigens. Labelled antibodies are added and can bind to antigens not already bound to sample antibodies

143
Q

Method for virus neutralisation?

A

Serum with antibodies is plated with the virus and susceptible cells.
The serum antibody is progressively diluted and repeated.
The titre is inverse of the highest dilution at which the serum still completely inhibits a virus-specific effect

144
Q

What is method for haemagglutination?

A

Some viruses cause haemagglutination (RBC lysis) If antibodies present for virus, then haemagglutination inhibited - no spread in added blood

145
Q

What is the method for complement fixation test?

A

Some viruses cause haemagglutination (RBC lysis) If antibodies present for virus, then haemagglutination inhibited - no spread in added blood

146
Q

How do you choose the best test for your purpose?

A

What questions do you want to answer

  • Do you need a titre?
  • Do you want to know whether one animal is affected or 100 animals?
  • Do you need a viable pathogen?
  • What type of samples are you able to collect and how quickly can these be transported to the lab?
  • How quickly do you need the results?
  • How sure do you want to be about your diagnosis?
  • Is the sensitivity or specificity more important?
  • How much money are you/ client prepared to spend?
147
Q

What is stomatitis?

A

Inflammation of the lips and mouth

148
Q

What species do herpesviruses infect?

A

All species of mammals and birds - but each species has a host specific herpesvirus

149
Q

What kind of nucleic acid do herpesviruses have?

A

dsDNA

150
Q

How do herpesviruses spread?

A

By mucosal contact or droplet

151
Q

What are the clinical signs of herpesvirus infected animals?

A
  • Respiratory disease
  • Abortion/ Foetal death
  • Ulcerative skin lesions
  • Nervous system diseases
  • lymphoproliferative diseases e.g. glandular fever
152
Q

Which herpesviruses are of veterinary significance?

A
  • Equine upper herpesviruses
  • Feline herpesvirus
  • Infectious bovine rhinotracheitis
  • Pseudorabies (Aujeszky’s disease)
  • Malignant catarrhal fever (MCF)
  • Bovine Mammilitis virus (BoHV-2)
153
Q

What is latency?

A

When the viral genome is present but only a few (if any) genes are transcribed

  • no production of infectious diseases
  • virus is “invisible” to the immune system
154
Q

Where are the major sites of latency of herpesviruses?

A

Typically lymphoid or neural tissues

155
Q

What is recrudescence?

A

Reactivation of a virus from latency

  • generally associated with stressors e.g. exhaustion, exposure to excessive UV etc.
  • release of millions of progeny viruses
156
Q

Describe herpesvirus vaccines…

A

There are many vaccines against herpesviruses
- they reduce the severity of the disease but don’t prevent infection, stop establishment of latency or provide long-lasting immunity

157
Q

Describe Bovine Herpesvirus…

A
  • Respiratory disease (IBR)
  • Genital disease
  • Keratoconjunctivitis
  • GI disease in calves
  • Fever
  • Depression
  • Inappetence
  • Profuse nasal discharge
  • Gastroenteritis
158
Q

Describe Bovine mammilitis (BoHV-2)…

A
  • Affects teats and udder

- Or generalised lumpyskin disease

159
Q

Describe Suid Herpesvirus / Aujeszky’s disease…

A
  • Primarily a disease of pigs
  • Reproductive, respiratory and CNS signs
  • Abortin etc. of pregnant sows
  • Usually subclinical in adult pigs
  • Can infect other species
160
Q

Describe Gallid Herpesvirus/ Infectious Laryngotracheitis (ILT)…

A
  • Incubation period of 2-8 days
  • Coughing, sneezing
  • Ocular discharge
  • Dyspnoea
  • Gasping
  • 20-100% mortality
  • Spread by Droplet
161
Q

Describe Gallid Herpesvirus 2 / Marek’s Disease…

A
  • Neoplastic disease of chickens
  • Infiltration of various nerve trunks and/ or organs with lymphoid cells
  • Enlargement of peripheral nerves and feather follicles
  • Iris discolouration
  • Blindness
  • Visceral tumours
  • Infection by inhalation
  • Controlled by vaccination of one day old birds and by breeding resistant chickens
162
Q

Describe MCF…

A
  • High fever
  • Enlargement of peripheral lymph nodes
  • Nasal discahrge
  • Photophobia
  • Inflammation
  • Congestion
  • Erosion of mucosal surfaces
  • Corneal Opacity
  • Dermatitis
  • Bloody diarrhoea
  • Infection via oculonasl route
  • Variable incubation period
  • Death in 100%
  • No vaccine
  • Wildebeest and Sheep MCF
163
Q

What is herpesvirus method of persistence?

A
  • Latency
  • Immunodeficiency
  • Interspecies spread from pigs
164
Q

Control and diagnosis of Herpesviruses…

A
  • Isolation
  • Vaccination
  • Breed resistant chickens
165
Q

Describe the lifecycle of Herpesviruses…

A
  • Replication in cell nucleus
  • Latency in lymphoid tissue and ganglia
  • Reactivate
  • Viraemia
166
Q

Herpesvirus Structure…

A
  • Enveloped
167
Q

What is EHV-1 associated with?

A
  • Respiratory Disease
  • – viraemia
  • Abortion/ Neonatal disease
  • Neurologic Disease
  • Sudden onset with rapid progression
  • urinary incontinence
  • Ataxia and paresis
168
Q

What is EHV-4 associated with?

A
  • Respiratory Disease
169
Q

What is EHV-3 associated with?

A
  • Equine coital exanthema (sex rash)
  • venereal skin disease
  • prepuce, penis, vulva and vagina
  • Diagnosed with virus isolation, acute and convalescent serum testing
170
Q

When do horses with EHV usually abort?

A

In the third trimester of pregnancy

- no clinical signs

171
Q

What is the typical vaccine schedule for EHV?

A
  • Young horses can be vaccinated at 6-9 months
  • – 2 doses given 2-4 weeks apart
  • – 6-12 monthly boosters as needed
  • Mares are recommended to have three doses
  • – two 2-4 week apart after mating then last one in 4-5 months
  • – OR three doses during pregnancy
172
Q

What are the limitations of herpesvirus vaccines?

A
  • Immunity is short lived
  • Questionable in preventing abortion
  • No protection against infection
  • No protection from neurological disease
173
Q

How big are poxviruses?

A

250 x 200 x 200 nm

- biggest veterinary viruses

174
Q

Describe the structure of poxviruses…

A
  • Linear genome (130-280kbp)
  • Encodes ~200 proteins
  • Complex Structure
  • Brick/ Oval shaped
  • Enveloped
  • Survive well in environment
175
Q

What is the host range of poxviruses?

A
  • Narrow host range
176
Q

What type of nucleic acid do poxviruses have?

A

linear dsDNA

177
Q

How do poxviruses spread?

A
  • Skin Abrasions
  • Mechanical vectors e.g. lice
  • Respiratory Aerosis
178
Q

What are the clinical signs of poxvirus?

A
  • Generalised skin lesions
  • Localised skin lesions
  • – orf, cow, pseudocow and deer
179
Q

What are the strains of poxviruses?

A
  • Orthopox: smallpox, vaccinia, cowpos, monkeypox
  • Parapox: papular stomatitis, orf, pseudocowpox
  • Sheep, goat, fowl etc etc
180
Q

How are poxviruses diagnosed?

A
  • EM of scabs
  • AGID
  • Cell culture
181
Q

How are poxviruses controlled?

A
  • Vaccine
182
Q

What is the life cycle of poxviruses?

A
  • Replication in the cytoplasm

- exit by budding or lysis

183
Q

What is the duration of immunity for poxviruses?

A
  • Long-lasting for generalised infections

- Shorter term (<1 yr) for localised infections

184
Q

What species does orf virus infect?

A
  • Sheep
  • Goats
  • People (ZOONOSIS)
185
Q

What are the symptoms of orf virus?

A
  • Scabby mouth
  • Contagious ulcerative pus of skin
  • Contagious pustular dermatitis
186
Q

What are the clinical signs of Orf Virus?

A
  • Localised skin lesions on: Muzzle, gums, tongue, lips, eyelids, feet, teats
  • High morbidity
  • Low mortality
  • Failure to eat
187
Q

Describe the pathogenesis of Orf Virus…

A
  • Trauma to epidermis
  • Ballooning of stratum spinosum
  • Coalesce of numerous discrete lesions into masses and scabby ‘warts’
  • Lesions heal in 10days-8 weeks
  • Rarely sexual spread
188
Q

How do you control Orf Disease?

A
  • By administration of a live, fully virulent vaccine
189
Q

Describe Myxomatosis virus…

A
  • Gelatinous subcutaneous nodules develop at the site of infection within 2-3 days
  • Mortality with 48hours and 21 days
  • Transmission by fleas and mosquitoes etc
190
Q

Why are poxviruses used as vaccine vectors?

A

??

191
Q

What is the diameter of picornaviridae?

A

25-30nm

192
Q

What species do picornaviridae infect?

A

All cloven hoof animals

  • Cattle: indicator species
  • Pigs: Amplifier species
  • Sheep: Maintenance species
193
Q

What type of nucleic acid do picornaviruses have?

A

+ve ssRNA

194
Q

Describe the method of spread of picornaviridae…

A
  • High titres in respiratory secretions
  • Aerosol, direct and indirect
  • Viral shedding before clinical signs
  • Can have carriers
195
Q

What are the clinical signs of picornaviridae infection?

A
  • Increased salivation
  • Vesicles on tongue and lips etc
  • Laminitis/ Exungulation
  • Anorexia
  • Abortion and death in young
  • Severe in cattle and pigs
  • Subclinical in sheep
  • Piglets may get myocarditis causing death
196
Q

What is the main advantage of using virus isolation over PCR etc?

A

Virus isolation demonstrates the presence of live virus in the sample

197
Q

Which stage of the viral replication cycle least likely to be targeted by anti-viral drugs?

A

Adsorption

198
Q

What is the relationship between the size of a virus and prions?

A

Smallest viruses are larger than prions

199
Q

What does tamiflu drug target?

A

Virus release from host cell

200
Q

CD4 anti-HIV drug targets what phase of virus replication?

A

Attachment

201
Q

Which is the most widely used method for cultivation of mammalian viruses?

A

Continuous cell lines

202
Q

How long does it take before CPE becomes evident?

A

May take up to 3 weeks

- samples are passaged 2-3 times

Infectious Diseases (3 decks)

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