Viral Diseases I Flashcards

1
Q

What are 4 ways that viruses can overcome the skin barrier?

A
  • Trauma/ abrasions
  • Arthropods (insects)
  • Animal bites
  • or Iatrogenic (caused by the vet)
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2
Q

How could you classify a pappilomavirus?

A
  • Small
  • Non-Enveloped
  • not easily disinfected by organic detergents
  • can survive low pH and high temperatures
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3
Q

What is the consequence of papillomavirus having double stranded DNA?

A

genome is infectious (they can replicate straight away)

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4
Q

What is the negative of the papillomavirus replication strategy?

A

It requires actively dividing cells
It onky has 8 genes so it requires hsot enzymes

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5
Q

At what part of the skin is the virus shed?

A

at the top (where skin is shed)

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6
Q

What do viruses induce in the skin?

A

Hyperplasia, Causing the skin cells to be produced more rapidly so the virus can move its way through the skin

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7
Q

What do papillomaviruses cause?

A

warts (benign neoplasms that usually regress spontaneously as the immune system recognises them as foreign)

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8
Q

What is the meaning of the DNA being episomal?

A

it replicates autonomously and is not integrated inti the host genome

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9
Q

What occurs when the papillomavirus progresses into malignancy?

A

Virus genome is then integrated into the host DNA
* thus the host cell is transformed (also known as malignant transformation)
* site of integration is random

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10
Q

In what species are papilloma warts most common?

A

Most common in cattle compared to any other species

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11
Q

What do pure papillomas (bovine papilloma) infect?

A

Only infect epithelial cells (keratinocytes)- squamous papillomas

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12
Q

What do fibropapillomas infect?

A

they infect keratinocytes, but also sometimes the underlying layers to cause fibropapillomas

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13
Q

What are the clinical signs of Bovine Papillomavirus?

A

Hyperplasia and hyperkeratinisation 4-6 wks after exposure
Then leading to- raised plaques, proliferating epidermis, pedunculated masses

these usually regress after 1-6 months

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14
Q

What are the clinical features of equine papillomavirus?

A

Warts/ sarcoids do occur and they are commonly associated with BPV-1 and BPV- 2
Sarcoid is the most common skin tumour of horses
(most common in horses less than 4 years old)

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15
Q

What are the most common papillomas in dogs?

A

The most common are oral papillomas in young dogs
they typically regress spontaneously in 8 weeks
they can very rarely progress to squamous cell carcinomas

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16
Q

What can you use to diagnose papillomavirus?

A
  • PCR
  • Immunohistochemistry
  • Histopathology
17
Q

What is the definition of a papilloma?

A

small benign growth that originates in squamous cells

18
Q

What are ‘warts’?

A

Common name given to skin papillomas

19
Q
A
20
Q

What are sarcoids?

A

equid specific, papillomas but go on to ulcerate and are defined as fibroblastic skin tumours

21
Q

What are fibropapillomas?

A

like sarcoids in other animals, they usually involve dermal fibroblasts

22
Q

What is the disadvantage of the papillomavirus replication strategy?

A

Requires actively dividing cells

23
Q

How many recognised types of Bovine Papillomavirus are there?

A

at least 10

24
Q

What type of papillomas only infect epithelial cells?

A

(3,4 and 6 Xipapillomavirus) also known as pure **papillomas **

25
Q

What type of papillomavirus infects keratinocytes and the underlying layers (1 and 2
Deltapapillomavirus)

A

Fibropapillomas

26
Q

What do bovine papillomas look like 4-6 weeks after exposure?

A
  • Raised plaques
  • Proliferating Epidermis
  • Pedunculated masses
27
Q

When do bovine papillomas usually regress?

A

Usually regress spontaneously within 1-6 months but can then go on to ocassionally cause cancer

28
Q

Where are sarcoids in horses usually found?

A
  • Head
  • Ventral abdomen
  • Limbs
29
Q

What can you use to confirm the presence of the virus within lesions?

A

Immunohistochemistry

30
Q

What can you use to diagnose and stage tumours?

A

Histopathology

31
Q

Why do papillomavirus’s not usually turn malignant?

A

DNA is episomal, replicates autonomously, and is not integrated into the host genome

tumour supressing genes are activated