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Year 2 Equine ID > Equine Neurological ID > Flashcards

Equine Neurological ID Flashcards

1
Q

How are equine infectious neurological diseases divided up?

A

Equine infectious neurological diseases can be:

  1. Viral
  2. Protozoal
  3. PArastitic
  4. Clostridia neurotoxins
  5. BActerial
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2
Q

equine infectious neurological diseases: viral diseases

A
  1. Virus with primary neurotropism
  2. Arbo virus associated with CNS disease (not spec neuritropic but can affect)
  3. Viruses that cause neuropathy by damaging the blood brain barrier, in doing so cause neurological signs
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3
Q

Horse presents with neurological signs. What are the following steps taken to diagnose and treat:

A
  1. History
  2. Clinical Exam
  3. CSF analysis
  4. Medical imaging and functional testing
  5. Post-mortem examination
  6. General recommendations for treatment
  7. Prevention
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4
Q

Equine Herpes virus

different types

A 
1-5 affects horses
1.	EHV-1: Infectious viral respiratory, abortion, myeloencephalopathy
2.	EHV-2: keratitis
o	Affects eye, 
3.	EHV-3: coital exanthema
o	Ulceration around genital area
4.	EHV-4: Infectious viral respiratory
5.	EHV-5: multinodular pulmonary fibrosis
6.	EHV-6 to 8: donkeys
•	9 has been discovered.
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5
Q

Equine herpes virus 1
Type of disease
Clinical signs

A

Equine Infectious Neurological Disease AND Infectious viral respiratory

Horse specific virus

respiratory, abortion, myeloencephalopathy (Inflammation of both the spinal cord and the brain)

Clinical signs:
o Progress very quickly in first 24-48 hours
o After they don’t tend to get any worse
- often resp signs e.g. snotty nose
- may cause abortion
o Ataxia in hind limbs or all 4, up to recumbency
o Cauda Equina signs: atony of bladder, flaccid tail (normally if lift tail should try to clamp immediately) and anus (open), perineal hypoalgesia- can’t retract penis, cant poop or peep
Usually - Tail, rectum, perineum, genitalia and bladder affected
o Occasionally show cranial nerve involvement

• Clinical signs as a result of vasculitis and thrombosis of arterioles in brain and spinal cord (viral endotheliotrophism)

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6
Q

EHV-1 virus genome

EHV-1 infection and latency

A

• Enveloped capsid containing DNA genome
- Travels up trigeminal nerve, once infected remains latent in trigeminal ganglia, only reappearing in periods of stress. Like humans
- • Humoral immunity is very short lived
o Horse can develop antibodies but short lived

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7
Q

How are outbreaks? sporadic or outbreaks?

A

Both!

May be jsut one or several

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8
Q

What is interesting about some clinical signs of EHV-1?

A
  1. Can show respiratory signs and abort if pregnant HOWEVER may not.
  2. So if horse ill but neither these signs shouldnt rule EHV-1 out
  3. simialrly if yard there had been resp issues and/ or abortion but this horse not showing this, can’t rule EHV- 1 out

If caudal part of horse affected (tail, rectum, perineum, genitalia, bladder) than be very suspicious of EHV-1
• lifting tail easily, anus open, constantly dripping urine

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9
Q

Diagnosis EHV1

A

• Virus isolation /PCR:
o Nasal swab
o Buffy coat – period where virus spread throughout body in WBC – when spin blood little line with WBC
o CSF
• Serology:
o Complement fixation, ELISA
o 4 fold rise in titre or >1:80
o CSF: xanthochromia (yellow colouring) – not specific to just herpes
o Try detect antibodies – but issue is it takes a while for antibodies to be produced so take a paired sample – want to see antibody count t increasing on second
• Possible neurovirulent form (gene difference)

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10
Q

Management and treatment EHV 1

A

• Isolate animal – stop transmission
• Prognosis reasonable with good nursing care – horse standing must empty bladder and rectum
- Better if not recumbent
• Recumbent horse are very difficult to manage for a long time. Often after a few days don’t do well
• Vasculitis → anti-inflammatories: NSAIDs, corticosteroids, aspirin (anti-thrombotic)

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11
Q

Recovery time for EHV-1

A

days to weeks (up to a yr!)

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12
Q

How to prevent EHV-1 transmission

A

• Vaccination available for EHV-1 and 4 however vaccine doesn’t claim any protection against neurological
o Just respiratory and abortion

• Possibly worsens if given in the face of an outbreak of neurological disease. Isolate.
o Horses that appear healthy might have contracted it so not recommended to vaccinate

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13
Q

Rabies
genome
How is it transmitted?

A

• Single stranded RNA with envelope
• Neurotrophic – once infects body, straight to neurology
• Transmitted by saliva contaminated bite wounds
Bites
UNCOMMON IN HORSE

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14
Q

What to rememebr with rabies

A

ZOOOONOTIC
NO PATHOGNOMONIC SIGNS
o From mild hind-limb lameness to sudden death
o Can loot a little itchy that it.
o BE VERY CAREFUL – you think you’re treating a horse with lameness or skin issues and then boom

• ALWAYS Assumption of rabies in endemic areas

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15
Q

Pathogenesis rabies

A
  • Local inoculation at wound site
  • Access to peripheral nerve
  • Gradual / slow movement centrally

• Replication in spinal / dorsal root ganglia
• Rapid spread in CNS
o Cord, brain, sympathetic trunk
o Horses mostly to spinal chord (other species straight to the brain)
• Centrifugal spread down nerves
o Salivary glands – then makes infectious if bites another

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16
Q

Rabies incubation period

A 
(9 days-1 year); dependent on:
o	Virus strain
o	Host species
o	Inoculum (virus particles)
o	Proximity of inoculation bite is to CNS – neck much quicker than hoof!
17
Q

Different forms of rabies

A

o Spinal form → Paralytic form – mainly for horses but can be others
o Brain stem → Dumb form
o Cerebrum→ Furious form

18
Q

Spinal or paralytic form rabies

  • how common?
  • clinical signs
A 
•	Most common
•	Localised hyperaesthesia
o	Very itchy 
o	Self mutilation
o	Extremity, site of inoculation
•	Progressive ascending to spinal chord resulting in
o	Ataxia
o	Weakness
o	Lameness
o	Recumbent 3-5 days
o	Death
19
Q

Dumb (brain stem) form of rabies
how common?
clinical signs:

A 
•	Unusual in horses
o	Depression
o	Anorexia
o	Head tilt / circling
o	Ataxia
o	Dementia / Blindness
o	Salivation / Dysphagia
o	Tail / Penis / Bladder paralysis
o	Self-mutilation
20
Q

Furious (cerebral) form rabies

A

• Diagnosis difficult as signs are vague
o If in rabies area be super cautions ALWAYS
o Can look super cholicy/ lame that all
• Assumption of rabies in endemic areas
• Rapid progressive neuro signs
• Post mortem examination: only diagnosis for sure
o Beware! – still infectious
o Histology: eosinophilic inclusion bodies (Negri bodies) within neurones which is pathenomic to the disease
o Fluorescent Ab

21
Q

Rabies and humans outcome and then horses

A

• PEOPLE: ALMOST ALWAYS FATAL
• Vaccinated humans receiving post exposure boosters have all lived
Horse
• Hopeless
• 100% fatal
• Best to kill on suspicion and limit human contact
• Early diagnosis essential

22
Q

Control and prevention rabies

A
  • Vaccination very effective (annual in endemic areas)
  • Horses rarely infect other animals (except vets as we go to do a typical clinical exam!)
  • International controls
23
Q

Arbovirus

A

• Not specifically go to nervous system but they CAN

include WEst nile virus

24
Q

Talk about west nile virus

epidemiology

A

WNV in humans and horses
• Replicates in birds → reservoir
• Mosquitoes (Culex) transfer virus from reservoir to a number of species (horses and humans)
• Human and horses are terminal hosts
• Zoonosis but the horse can’t infect you itself, only from mosquito

25
Q

Pathogenesis WNV

A
  1. Initial virus replication at site of inoculation
  2. Viraemia → signs of uncomplicated infection
    • Fever, depression, anorexia for few days and most horses that is it
  3. In some horses (don’t know why) virus enters CNS
    • Diffuse or multifocal encephalomyelitis
    • Involvement of spinal cord common (unlike EEE / WEE)
    • Neurological signs can be anything, not specific
26
Q

Neurological signs WNV

A
  • Muscle fasciculations over entire body (particularly head and neck)
  • Weakness, ataxia, dysmetria
  • Cranial nerves may be affected so affect forebrain
  • Mentation may be affected (indirectly due to intracranial oedema)
  • Sudden death in some horses
27
Q

Treatment WNV

A
  • No specific treatment
  • Anti-inflammatory and steroids to reduce non specific inflammation in nervous system
  • Hyperimmune plasma specific to WNV available in USA, not UK
  • Supportive care
28
Q

Diagnosis WNV

A

• Antigen/ antibody specific testing: ELISA
• Post mortem:
o virus culture of brain material
o Immunohistochemistry

29
Q

Prevention WNV

A
  • Vaccination in US
  • Reduce vector contact:
  • Environment
  • Repellents

Year 2 Equine ID (7 decks)

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