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 :/
What is virus induced transformation
the ability for a virus to change a cell from normal to a tumor cell
tumors result in genetic changes in:
cell proliferation
cell differentiation
apoptosis
what are the two groups of tumor genes that viruses can act on
proto-oncogenes (promote growth)
tumor suppressor genes (control protooncogenes)
changes in either protooncogenes and tumor suppressor genes or both results in
uncontrolled cell growth
viruses that are able to transform normal cells into tumor cells are referred to as
oncogenic viruses
oncogenic DNA viruses encode inhibitors of _______
tumor suppressor genes between M and G1
oncogenic RNA viruses (retro and flavi) encode homologs of ____
oncoproteins
Ovine Pulmonary adenocarcinoma (OPA)/Ovine pulmonary adenomatosis/ovine pulmonary carcinoma/ Jaagsiekte/ Sheep pulmonary adenomatosis are all the same disease, and are caused by:
Jaagsiekte sheep retrovirus (JSRV)
JSRV etiology
betaretrovirus that carries an oncogene in its envelop protein genome
JSRV target cells
epithelial cells of bronchioli and alveoli (type II pneumocytes), lymphocytes and myeloid cells
JSRV geographic distribution
most sheep rearing countries (north america, south america, south africa, russia, most of europe, asia)
NOT found in Australia or new zealand
JSRV epidemiology
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
mortality in flocks recently infected with JRSV
30-80% of flock dying of tumors
mortality when JSRV has been present in the flock longer
1-5%
Why is mortality from JRSV higher in recently infected flocks
no idea, I’ll update this when he responds to my email lol
Transmission of JSRV
respiratory route (aerosols or droplets), shed by clinical and subclinically infected animals. close contact increases transmission. vertical transmission via milk and colostrum.
T/f JSRV infected animals are carriers for life
true. this is a retrovirus
Pathogenesis of JSRV/OPA
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
incubation of JSRV
6-36 months
rank the following neoplastic cell types seen with JSRV from highest contribution to lowest contribution to the tumors:
- clara cells
- type 2 alveolar epithelial cells
- undifferentiated cells
Type 2 alveolar epithelial cells (82%), undifferentiated cells (11%), clara cells (7%)
JSRV gross pathology
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
JSRV clinical signs
fever, cough, dyspnea, frothy mucoid discharge from nostrils, progressive weight loss
what is the wheelbarrow test and what is it used to detect
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
JSRV diagnosis
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
Treatment of JSRV
no therapy, no vaccine. Culling is only real option (dang.)
why is there no immune response to JSRV
tolerance due to endogenous retrovirus elements.
prevention of JSRV
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 was JSRV eradicated from Iceland
slaughtering all sheep in affected areas. to save genetic potential from all these euthanized flocks, embryo transfer may be used.
Maedi-Visna: Ovine progressive pneumonia (OPP) etiology
disease of sheep and occasionally goats. Lentivirus (a retrovirus)
Ovine progressive pneumonia infective agent
maedi-visna virus
Maedi-Visna/ OPP target cells
monocytes/macrophages
dendritic cells
T/F: all animals infected with Maedi-Visna develop fatal, progressive, untreatable disease syndromes
false. most infections are subclinical, only a small portion of animals develop the fatal syndromes
What is the “maedi” part of Maedi-visna
dyspnea
what is the “visna” part of maedi-visna
neurologic signs
transmission of Maedi-visna
respiratory/colostrum/sexual contact
T/f Maedi-visna can cause poor milk production
true. This is due to indurative mastitis
Maedi-visna gross findings
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.
Histological findings of maedi-visna
interstitial pneumonia
visna form of MVV
rare. Brain and spinal cord are infected, leading to neurological signs (ataxia, hind limb weakness, incoordination, tremor, paresis and paralysis). Eventually fatal
maedi form of MVV: non lung signs, fatal why
in addition to respiratory involvement, can lead to arthritis and mastitis. Fatal due to secondary bacterial infections
Maedi-visna diagnosis
AGID, western blotting, RT-PCR
Maedi-visna control
remove lambs prior to feeding of colostrum (though this doesn’t stop transplacental infection)
Caprine arthritis and encephalitis (CAE) etiology
lentivirus (a retrovirus) than infects sheep and goats
what are the four progressive and untreatable disease syndromes caused by CAE?
polyarthritis in adults
Encephalomyelitis in kids and adults
indurative mastitis
chronic interstitial pneumonia
transmission of CAE
colostrum, milk
CAE target cells
macrophages, DCs, synovial membrane cells
what percentage of animals infected with CAE develop the untreatable disease syndromes?
20%
What are the four pathological manifestations of CAE
- CNS: invades white matter, destroys myelin and causes perivascular accumulation of mononuclear cells.
- Joints: invades synovial membrane cells and results in multinucleated syncytia
- chronic interstitial pneumonia
- hard udder (indurative mastitis) due to infiltration of lymphocytes
what are the gross CNS signs due to CAE
focal discolouration in spinal cord and brain.
Meningitis
what are the gross JOINT signs of CAE
edematous thickening of joints with villous atrophy. Fibrosis, mineralization, and necrosis of synovial membranes
diagnosis of CAE
Clinical picture, pathology, and laboratory diagnosis on blood
Clinical pathology of CAE
lymphopenia, marked pleocytosis in CSF, red tinged synovial fluid with high mononuclear cell count and low viscosity
laboratory diagnosis of CAE
AGID test
Elisa, western blot, radioimmunoassay, virus isolation, RT-PCR, IHC on blood samples
control of CAE
no cure, no vaccines. prevent vertical transmission via milk and colostrum.
An animal is considered CAEV free when:
it has two negative AGID tests 6 months apart
Contagious ecthyma/orf/sore mouth/ scabby mouth are all the same disease caused by:
orf virus, which belongs to poxviridae.
T/F: Orf only affects small ruminants
false. it can infect sheep, goats, alpacas, muskoxen, dogs, humans
geographical distribution of orf
worldwide, wherever sheep and otgher small ruminants are raised
Orf transmission
direct contact or fomites. very resistant to the environment despite being enveloped. Orf infection occurs through breaks in the skin
T/f orf has a low morbidity but a high mortality
false. high morbidity, low mortality
incubation period of orf
2-3 days
target organs of Orf
skin and oral mucosa. commonly near mouth, nose, ears, eyelids, feet, udder and perineum
target cells of orf
epitheliotropic, infects epidermal keratinocytes
clinical signs of Orf in animals
initial papules, pustules, vesicles that progress to thick brown scabs over areas of inflammation and ulceration
clinical signs of orf in humans
single papule/pustule on exposed part of body. may come with a low grade fever or mild lymphoadenopathy
Orf histologically
epithelial hyperplasia, intracytoplasmic inclusions, ballooning degeneration
Give some reasons why the Orf vaccine is “one of the worse vaccines ever made”
- vx’d animals develop classical lesions of the disease
- vaccinated animals shed the virus
- vaccines can infect humans
- vaccine doesnt produce long lasting immunity
Bluetongue etiology
reoviridae, orbivirius. Transmitted by biting midges of the genus culicoides
what species does blue tongue affect
sheep, cattle, deer, goats, and camelids
blue tongue distribution in cAnada
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
Blue tongue clinical signs in sheep
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
blue tongue virus (serotype 8)
causes cerebellar aplasia which may become permanent when cell types that dod not regenerate (like brain tissue) are affected
How does species variation affect the clinical signs of blue tongue?
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
