Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

VETM 422: Virology > small ruminant viral diseases - Tesse > Flashcards

small ruminant viral diseases - Tesse Flashcards

sorry if this deck is rough. This was the lecture that we had no wifi for and the slides weren't posted in time :/

1
Q

What is virus induced transformation

A

the ability for a virus to change a cell from normal to a tumor cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

tumors result in genetic changes in:

A

cell proliferation
cell differentiation
apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the two groups of tumor genes that viruses can act on

A

proto-oncogenes (promote growth)

tumor suppressor genes (control protooncogenes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

changes in either protooncogenes and tumor suppressor genes or both results in

A

uncontrolled cell growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

viruses that are able to transform normal cells into tumor cells are referred to as

A

oncogenic viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

oncogenic DNA viruses encode inhibitors of _______

A

tumor suppressor genes between M and G1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

oncogenic RNA viruses (retro and flavi) encode homologs of ____

A

oncoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ovine Pulmonary adenocarcinoma (OPA)/Ovine pulmonary adenomatosis/ovine pulmonary carcinoma/ Jaagsiekte/ Sheep pulmonary adenomatosis are all the same disease, and are caused by:

A

Jaagsiekte sheep retrovirus (JSRV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

JSRV etiology

A

betaretrovirus that carries an oncogene in its envelop protein genome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

JSRV target cells

A

epithelial cells of bronchioli and alveoli (type II pneumocytes), lymphocytes and myeloid cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

JSRV geographic distribution

A

most sheep rearing countries (north america, south america, south africa, russia, most of europe, asia)

NOT found in Australia or new zealand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

JSRV epidemiology

A

most cases in sheep over 2 years, peak at 3-4 year olds. rarely in sheep under 9 mo. Once clinical signs appear its always fatal, though the incidence of infection is much higher than the morbidity rate, as most sheep in an infected flock do not develop tumors during their commerical lifespan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

mortality in flocks recently infected with JRSV

A

30-80% of flock dying of tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

mortality when JSRV has been present in the flock longer

A

1-5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why is mortality from JRSV higher in recently infected flocks

A

no idea, I’ll update this when he responds to my email lol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Transmission of JSRV

A

respiratory route (aerosols or droplets), shed by clinical and subclinically infected animals. close contact increases transmission. vertical transmission via milk and colostrum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

T/f JSRV infected animals are carriers for life

A

true. this is a retrovirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pathogenesis of JSRV/OPA

A

inhalation of virus -> infection of lung epithelial cells -> viral expression -> env-mediated transformation -> additional oncogenic events (eg TERT activation) -> tumor growth and metastasis to lymph nodes -> large tumors and necrosis in lungs AND increase of lung fluid production that increases transmission ->secondary lung infections ->death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

incubation of JSRV

A

6-36 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

rank the following neoplastic cell types seen with JSRV from highest contribution to lowest contribution to the tumors:

  1. clara cells
  2. type 2 alveolar epithelial cells
  3. undifferentiated cells
A

Type 2 alveolar epithelial cells (82%), undifferentiated cells (11%), clara cells (7%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

JSRV gross pathology

A

frothy fluid filling trachea and nares

lungs enlarged, FAIL TO COLLAPSE, edematous

focal to diffuse bulky tumours

enlarged bronchial and mediastinal lymph nodes, with 10% containing metastases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

JSRV clinical signs

A

fever, cough, dyspnea, frothy mucoid discharge from nostrils, progressive weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is the wheelbarrow test and what is it used to detect

A

raising the hindlegs of an animal to check for excess fluid in the lungs. it can be used to detect JSRV in sheep, though it doesnt detect all sheep with tumors, nor does it differentiate early cases from other respiratory diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

JSRV diagnosis

A

clinical diagnosis is hard due to secondary bacterial infections.

RT-PCR in bronchoalveolar lavage cells is only option, as antibodies to this virus have not been detected in serum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Treatment of JSRV

A

no therapy, no vaccine. Culling is only real option (dang.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

why is there no immune response to JSRV

A

tolerance due to endogenous retrovirus elements.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

prevention of JSRV

A

no reliable test for subclinical animals. Quaruntine possible, but unfeasible due to long incubation period.

Maintain single age flocks. Buy from OPA-free flocks. remove lambs at birth and feed with colostrum substitutes and milk replacers to reduce vertical transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

how was JSRV eradicated from Iceland

A

slaughtering all sheep in affected areas. to save genetic potential from all these euthanized flocks, embryo transfer may be used.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Maedi-Visna: Ovine progressive pneumonia (OPP) etiology

A

disease of sheep and occasionally goats. Lentivirus (a retrovirus)

31
Q

Ovine progressive pneumonia infective agent

A

maedi-visna virus

32
Q

Maedi-Visna/ OPP target cells

A

monocytes/macrophages
dendritic cells

33
Q

T/F: all animals infected with Maedi-Visna develop fatal, progressive, untreatable disease syndromes

A

false. most infections are subclinical, only a small portion of animals develop the fatal syndromes

34
Q

What is the “maedi” part of Maedi-visna

A

dyspnea

35
Q

what is the “visna” part of maedi-visna

A

neurologic signs

36
Q

transmission of Maedi-visna

A

respiratory/colostrum/sexual contact

37
Q

T/f Maedi-visna can cause poor milk production

A

true. This is due to indurative mastitis

38
Q

Maedi-visna gross findings

A

lungs fail to deflate, contain coalescing multifocal gray-white nodules/plaques (proliferative pneumocytes) with adjacent atelectatic depressed parenchyma.

Thick mucosa in the trachea, swollen and heavy lung with no deflation.

Cigar sized enlargement of the mediastinal lymph node.

39
Q

Histological findings of maedi-visna

A

interstitial pneumonia

40
Q

visna form of MVV

A

rare. Brain and spinal cord are infected, leading to neurological signs (ataxia, hind limb weakness, incoordination, tremor, paresis and paralysis). Eventually fatal

41
Q

maedi form of MVV: non lung signs, fatal why

A

in addition to respiratory involvement, can lead to arthritis and mastitis. Fatal due to secondary bacterial infections

42
Q

Maedi-visna diagnosis

A

AGID, western blotting, RT-PCR

43
Q

Maedi-visna control

A

remove lambs prior to feeding of colostrum (though this doesn’t stop transplacental infection)

44
Q

Caprine arthritis and encephalitis (CAE) etiology

A

lentivirus (a retrovirus) than infects sheep and goats

45
Q

what are the four progressive and untreatable disease syndromes caused by CAE?

A

polyarthritis in adults

Encephalomyelitis in kids and adults

indurative mastitis

chronic interstitial pneumonia

46
Q

transmission of CAE

A

colostrum, milk

47
Q

CAE target cells

A

macrophages, DCs, synovial membrane cells

48
Q

what percentage of animals infected with CAE develop the untreatable disease syndromes?

A

20%

49
Q

What are the four pathological manifestations of CAE

A
  1. CNS: invades white matter, destroys myelin and causes perivascular accumulation of mononuclear cells.
  2. Joints: invades synovial membrane cells and results in multinucleated syncytia
  3. chronic interstitial pneumonia
  4. hard udder (indurative mastitis) due to infiltration of lymphocytes
50
Q

what are the gross CNS signs due to CAE

A

focal discolouration in spinal cord and brain.

Meningitis

51
Q

what are the gross JOINT signs of CAE

A

edematous thickening of joints with villous atrophy. Fibrosis, mineralization, and necrosis of synovial membranes

52
Q

diagnosis of CAE

A

Clinical picture, pathology, and laboratory diagnosis on blood

53
Q

Clinical pathology of CAE

A

lymphopenia, marked pleocytosis in CSF, red tinged synovial fluid with high mononuclear cell count and low viscosity

54
Q

laboratory diagnosis of CAE

A

AGID test
Elisa, western blot, radioimmunoassay, virus isolation, RT-PCR, IHC on blood samples

55
Q

control of CAE

A

no cure, no vaccines. prevent vertical transmission via milk and colostrum.

56
Q

An animal is considered CAEV free when:

A

it has two negative AGID tests 6 months apart

57
Q

Contagious ecthyma/orf/sore mouth/ scabby mouth are all the same disease caused by:

A

orf virus, which belongs to poxviridae.

58
Q

T/F: Orf only affects small ruminants

A

false. it can infect sheep, goats, alpacas, muskoxen, dogs, humans

59
Q

geographical distribution of orf

A

worldwide, wherever sheep and otgher small ruminants are raised

60
Q

Orf transmission

A

direct contact or fomites. very resistant to the environment despite being enveloped. Orf infection occurs through breaks in the skin

61
Q

T/f orf has a low morbidity but a high mortality

A

false. high morbidity, low mortality

62
Q

incubation period of orf

A

2-3 days

63
Q

target organs of Orf

A

skin and oral mucosa. commonly near mouth, nose, ears, eyelids, feet, udder and perineum

64
Q

target cells of orf

A

epitheliotropic, infects epidermal keratinocytes

65
Q

clinical signs of Orf in animals

A

initial papules, pustules, vesicles that progress to thick brown scabs over areas of inflammation and ulceration

66
Q

clinical signs of orf in humans

A

single papule/pustule on exposed part of body. may come with a low grade fever or mild lymphoadenopathy

67
Q

Orf histologically

A

epithelial hyperplasia, intracytoplasmic inclusions, ballooning degeneration

68
Q

Give some reasons why the Orf vaccine is “one of the worse vaccines ever made”

A
  • vx’d animals develop classical lesions of the disease
  • vaccinated animals shed the virus
  • vaccines can infect humans
  • vaccine doesnt produce long lasting immunity
69
Q

Bluetongue etiology

A

reoviridae, orbivirius. Transmitted by biting midges of the genus culicoides

70
Q

what species does blue tongue affect

A

sheep, cattle, deer, goats, and camelids

71
Q

blue tongue distribution in cAnada

A

most of canada is free of disease, but climatic change and vector habitat shift may change this. Has been found in BC and Ontario in the past

72
Q

Blue tongue clinical signs in sheep

A

high rectal temp
eye and nasal discharges
drooling from mouth ulcerations
swelling of mouth, head and neck
lameness and inflammation at coronary band
difficulty breathing
abortion and developmental abnormalities

73
Q

blue tongue virus (serotype 8)

A

causes cerebellar aplasia which may become permanent when cell types that dod not regenerate (like brain tissue) are affected

74
Q

How does species variation affect the clinical signs of blue tongue?

A

serious illness and death in sheep, deer and other wildlife.

Cattle, goats, and elk get mild infection.

Cattle that are persistently infected with one strain of bluetongue will not show signs until infected with another strain

VETM 422: Virology (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions