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3. Food Animal 4 > Ruminant Neurology 2 pt 2 > Flashcards

Ruminant Neurology 2 pt 2 Flashcards

1
Q

Bovine Spongiform Encephalopathy
- significance
- similar diseases?
- what is it?

A

 Reportable disease
 “Mad Cow” Disease
<><>
Transmissible Spongiform Encephthalopathies:
 Kuru – Papua New Guinea
 Creutzfeld-Jakob Disease (CJD)
 Gerstmann-Straussler-Scheinker syndrome
<><>
 Slowly progressive, fatal neurodegenerative disease

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2
Q

B. S. E.
- agent?
- pathogenesis

A

 Prion diseases
 Normal prion protein (PrP) – host encoded
membrane protein without nucleic acid
 PrP-BSE → induces a post-translational change in the protein
 Aggregation & accumulation in the brain →
 Progressive neurologic dysfunction

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3
Q

B. S. E.
- incubation
- age of onset
-signs?

A

 Long incubation period
 Age of onset: 4 – 6 years (range 20 mo– 18 years)
 Insidious onset
<><>
 Signs:
 Apprehensive; Fearful of handlers
 Separate from herd; Excitable (extreme)
 Hyperesthesia; Hyperresponsive
 May be extreme!!
<><>
Pytalism
Increased head rubbing
Muscle fasciculation
Vocalization (excessive)
Head tossing
Excessive licking
Yawning
Head butting
Flehmen response
Restlessness
Relative bradycardia
Recumbency

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4
Q

B. S. E.
 Infectivity; tissues affected

A

 Brain
 Spinal cord
 Retinal tissue
 Optic nerve
 Nerve ganglia – cervical, thoracic, trigeminal
 Facial, sciatic nerves
 Distal ileum (GALT)

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5
Q

B. S. E.
- prevention considerations, control
- experimental infection species

A
  • Likely lone entity; possible link to Scrapie ? ?
  • Change in rendering processes resulted in spread.
  • Animal byproducts fed to animals.
    <><>
     Ban feeding of bovine meat, bone products to
    cattle.
     People – new variant CJD
    <><>
     Experimental infection - other animals: mice,
    sheep, goats, pigs, cats, mink, primates
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6
Q

BSE - Diagnosis, PM

A

 No ante-mortem test available
<><>
 Necropsy specimens:
 Histology: neuronal degeneration, intraneuronal vacuolation
 Preceded or concurrent with accumulation of PrP- BSE.
 Obex of the medulla = tissue of choice

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7
Q

BSE – Differential Diagnosis

A

Viral encephalopathies:
 Rabies
 Pseudorabies
 Borna disease
<><>
 Listeriosis
 Polioencephalomalacia
 Lead poisoning
 Parasite migration
 Abscesses
 Tumors
 Vitamin A toxicity
 Hepatoencephalopathy
 Metabolic diseases

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8
Q

BSE
- tx, prognosis
- resistance? sensitivity?

A

 Treatment: None
 Prognosis: Grave
<><>
 Organism resistant to:
- Autoclaving
- Disinfectants
- Rendering
- Long-term storage
- Ultraviolet radiation
- Thawing
- Boiling
- Formalin incubation
<><>
Organism sensitive to alkaline digestion

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9
Q

BSE – Control Canada

A

 1997 – mammalian protein sources eliminated in bovine feeds (except swine, equine sources)
 Some bovine tissues cannot enter human food chain: skull, brain, trigeminal ganglia, eyes, tonsils, spinal cord, dorsal root ganglia of cattle over thirty months of age, distal ileum
 Note: material that cannot enter human food
chain cannot enter into animal feed, pet food,
fertilizer

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10
Q

Scrapie
- what is this?
- who does it affect
- agent
- vs BSE??

A

 Transmissible spongiform encephalopathy
 Sheep, goats
<><>
PrP-Sc
 Distinct from BSE
 Three different types
<><>
 Sheep can be experimentally infected with BSE but not know to occur naturally

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11
Q

Scrapie
- age affected?
- progression
- signs

A

 Age – usually 1-5 years of age
 Slow onset/progression – over several months
 Early behavioral changes, weight loss
> Separate from flock-mates
> Nervous, restless
Pruritus – scratch against objects, with horns & hooves

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12
Q

Scrapie
 Pruritus consequences
- ddx??

A

 Head, withers, flank, tail base, back, rump, lower limbs
 Secondary wool loss, excoriation, dermatitis
 May have ocular & aural lesions
<><>
 “Scratch reflex” – nibbling, lip licking, rhythmic
head movements
 Note: this response may occur w other neurologic or skin diseases (ectoparasites!!)

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13
Q

Scrapie
 Other clinical signs (not pruritus)

A

 Bruxism, pytalism, regurgitation
 Tremors – head, body
 Depressed demeanor
 Exercise intolerance
 Hypermetria
 Ataxia
 Stupor, collapse, convulsions
 Death

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14
Q

Scrapie
 Pathophysiology –
- tissue
- transmission
- timing of signs

A

 Found in nervous tissue and GALT
<><>
Also can be found in:
 Lymphoreticular tissue
 Kidneys
 Placenta
<><>
 Transmission mostly during lambing season
(placenta and fluids)
<><>
 Spread by way of the vagus nerve to the
brainstem brain
<><>
 Neural dysfunction may precede histologic
changes or PrP-Sc accumulation

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15
Q

Scrapie
- Epidemiology, geography
- etiology
- resistance?

A

 Occurs world wide, except Australia & New Zealand
 Genetic basis to susceptibility & resistance
<><>
PrP gene:
 3 important codons (171, 136, 154)
- Site 171 alleles:
 QQ – susceptible
 QR - resistant
 RR – resistant
<><>
Resistance selection: pedigree, phenotypic
expression of disease, genetic testing for resistance

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16
Q

Scrapie
- treatment
- prognosis
- dx
- PM

A

 Treatment – none
 Prognosis – grave
<><>
Diagnosis:
 ? Lymphoid tissue – Immunohistochemistry (PrP-
Sc)
 ? Retropharyngeal, tonsils, nictitans, rectoanal
junction
<><>
 Post mortem examination – brain & spinal
cord; brainstem (obex), tonsilar tissue, medial
retropharyngeal lymph nodes
 PrP-Sc: IHC, Western blot, ELISA

17
Q

Scrapie
 Differential diagnosis:

A

Similar to BSE in cattle
 Also pregnancy toxemia
 Maedi-Visna

18
Q

Scrapie
- control?
- human risk?

A

 Control – reportable disease
 Zoonoses ??? – no known link between classic
Scrapie & CJD

19
Q

Pseudorabies
- other names?
- disease?
- pathogen?
- other animals?

A

 Aujesky Disease, Mad Itch, Bulbar Paralysis
 Acute, severe, usually fatal encephalitis
 Suid herpesvirus – type 1 (Su-HV1)
 Family: Herpesvirus, Subfamily: alphaherpes virus
<><>
 Swine – domestic & feral (may develop latent inf)
 Almost any mammal except primates
> Cattle, sheep, goats, cats, dogs (horses – rarely)
> Wildlife – raccoons, opossums, skunks, rodents

20
Q

Pseudorabies - geography

A

 USA – eradicated from domestic pigs
<><>
 Not identified in:
 Canada
 Greenland
 Australia
 African Countries

21
Q

Pseudorabies
- clinical signs in ruminants

A

 Incubation 2 – 7 days
 Illness – 8 hrs to 3 days, may be found dead
<><>
Ruminants – paresthesia; acute severe pruritus (self trauma, abrasions, swelling, alopecia)
 Fever, bellowing, bloat, feet stamping, excess
salivation, twitching, tongue chewing, ataxia, circling, nystagmus, strabismus
 Aggression or depression
 Progressive neurologic signs; usually fatal

22
Q

Pseudorabies
- tissue localization
- vs other herpes?
- transmission
- spread in body

A

 Virus can be cultured from neural tissue
 Mostly distinct from other herpes viruses
 Shares some antigens with IBR (may confound
some serologic tests)
 Transmission – oral, intranasal, intradermal,
subcutaneous (present in nasal mucosa, saliva,
secretions)
 Axonal transport

23
Q

Pseudorabies
 Epidemiology, causes of infection
- hosts
- environmental survival
- susceptibility

A

 Usually spill over from swine to ruminants & other species; latent infection in swine is important.
 Nasal, inhaled, oral, fecal-oral, venereal
 “Dead end” hosts may transmit but usually die
within a few days
 May persist in environment for 4 days (straw)
 Virus susceptible to drying, UV radiation,
temperature >37°C, disinfectants

24
Q

Pseudorabies
 Necropsy

A

 Non-suppurative encephalitis
 Neuronal degeneration
 Eosinophilic intranuclear inclusion bodies
> Cowdry type A

25
Q

Pseudorabies - treatment and control

A

 Treatment – none
 Control - management

26
Q

Spastic Syndrome
- what is this?
- who is affected? age?
- cause?
- pathogenesis?
- vs Elso Heel?

A

 Inherited Periodic Spasticity, Stretches
 Progressive spasticity & stiffness of hind legs when stand up; leg held in backwards extension
 Holstein & Guernsey cattle
 Age: 3-7
 Thought to be inherited, autosomal dominant with incomplete penetrance.
 Pain may precipitate an episode; ambulate normally in between episodes
 Pathology & pathophysiology – remain obscure
 Elso Heel – calves; age 1 week to 1 year (similar signs, unknown if same disease

27
Q

Peripheral Nerve Damage - front body!
- which nerves are commonly damaged?
- syndromes?

A

 Facial nerve
<><>
 Suprascapular n – infra- & supraspinatus mm;
“Sweeney”
<><>
 Brachial plexus (many nn.) – trauma, wound, infection, neoplasia
<><>
 Radial nerve – lateral aspect of elbow, (elbow flexion, extensors of lower limb); dropped elbow, knuckling
<><>

28
Q

Peripheral Nerve Damage - back body!
- which nerves are commonly damaged?
- syndromes?

A

 Femoral nerve – distributed to the quadriceps femoris m., over extension of hip or stifle; cannot extend stifle, stay apparatus non-functional
<><>
 Sciatic nerve – hip extensors, stifle flexors, most muscles of the hind limbs; trauma, calving injuries, injections
<><>
 Peroneal nerve - damage → hyperextension of the hock, flexion of the lower limb
<><>
 Tibial nerve
<><>
 Obturator nerve

3. Food Animal 4 (16 decks)

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