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How are neurological viral diseases diagnosed
History
Clinical exam
CSF analysis and serology
Medical imaging and functional testing
Post mortem examination
What history should be asked
Information about the geographical location of the horse and recent ravel history
Determine the onset and duration of clinical signs in the affected horse
Information on health status of other horses in the vicinity of the affected animal
Vaccination history
What would be seen in a clinical exam
Normally fever
Neurological signs depend on neuroanatomical location
What causes fever
Replication of virus at entry site
Specific organ infection
Viraemia
What CSF changes are most common in viral encephalitis
Mononuclear pleocytosis
Increased protein concentration
What diagnostic methods can identify the pathogen or antibodies in CSF
Culture
PCR
Antibody detection test
What medical imaging tests use used for CNS disease
CT
MRI
EEG
What is the availability and anatomical reach of CT/MRI in vet patients
Very limited typically only in the head to mid-cervical region
What do CT/MRI usually show in encephalitis
Often non specific intracranial oedema
What post mortem methods are used to diagnose
Histopathology
Immunohistochemistry
PCR
What are the general recommendations for treatment
Isolate
Quiet, dark stable
Deep bedding
Padded walls
How often should recumbent horses be turned
Every 4-6 hours
What drugs can be given as general treatment
NSAIDs
Antiviral therapy
Ag-specific therapy
Vitamin E
Thiamine
How can disease be prevented
Vacccination
Minimise exposure to vector or reservoir
What are the main disease syndromes caused by EHV-1
Respiratory disease
Abortion
Myeloencephalopathy
What condition is associated with EHV-2
Keratitis
What condition is associated with EHV-3
Coital exanthema
What disease is linked to EHV-4
Respiratory disease
What condition is associated with EHV-5
Multinodular pulmonary fibrosis
Which equids are affected by EHV-6 to EHV-8
Donkeys
What type of virus is EHV-1 and what are its key structural features
Alpha herpes virus specific to horses
Enveloped capsid containing a DNA genome
What are the key features of EHV-1 immunity and infection persistence
Establishes latent infections
Humoral immunity is very short lived
Horses naturally have low antibody levels
How does EHV-1 occur
Sporadically or as outbreaks
Outbreaks of myeloencephalopathy
What causes the neurological clinical signs seen in EHV-1 infection
Vasculitis and thrombosis of arterioles in the brain and spinal cord due to endotheliotrophism
What preceding clinical history may be present in horses with EHV-1 neurological disease
They may or may nit show prior respiratory signs or fever
There way be a recent history of respiratory disease or abortion on the premises
What are the early stabilisation signs of EHV-1
Ataxia in hind limbs or all 4 up to recumbency
Atony of bladder
Flaccid tail and anus
Perineal hypoalgesia
Cranial nerve involvement
How is EHV-1 diagnosed
Virus isolation - nasal swab, buffy coat, CSF
Serology - complement fixation, 4 fold rise in titre
CSF - xanthochromia
What two sources can lead to EHV-1 neurological disease
A new infection from a respiratory outbreak
Reactivation of latent virus
What factors can reactivate latent EHV-1, even though this is less likely in the neurological form
Stress
Illness
Overcrowding
What are the key management principles and prognosis indicators for EHV-1 neurological cases
Isolate affected horses
Prognosis is reasonable with good nursing care
Better if not recumbent
Recovery can take days to weeks
Poor prognosis if recumbent for more than 24 hours
Which treatments are used to address vasculitis in EHV-1 neurological disease
NSAIDs
Costicosteroids
Aspirin
What EHVs are there vaccinations for
1 and 4 but ineffective against neurological form
What type of virus causes rabies and how is it transmitted
Lyssavirus
Single stranded enveloped RNA virus
Transmitted via saliva contaminated bite wounds
What is the tissue tropism of the rabies virus
It is neurotrophic targeting nervous tissue
Where is rabies most commonly found
Africa
Middle and Far East
South and North America
How common is rabies in horses, and why is it significant
It is uncommon in horses but is an important zoonotic disease
How is rabies typically transmitted to horses
Via saliva droplets
Canid or carnivore bites on the limbs
Describe the early pathogenesis of rabies from inoculation to CNS entry
Virus locally incoluated at the wound
Enters peripheral nerves
Moves centrally via slow centripetal axoplasmic flow
Replicates in spinal and dorsal root ganglia
How does rabies spread after reaching the CNS
Spreads rapidly through CNS
Moves centrifugally down nerves to tissues including salivary glands
What factors influence the variable incubation period of rabies (9 days–1 year)
Virus strain
Host species
Amount of inoculum
Proximity of the inoculation site to CNS
Why does proximity of inoculation to the CNS affect rabies incubation time
Shorted distance to nerves and CNS allows faster centripetal neural spread reducing incubation duration
How do clinical signs of rabies vary and why are there no pathognomonic signs
Signs range from mild hindlimb lameness to sudden death
Varies because they depend entirely on neuro-anatomic location of pathology
What clinical forms of rabies occur based on lesion location and how do they present
Spinal cord - paralytic form
Brainstem - dumb form
Cerebrum - furious form
What are the early signs of the spinal/paralytic form of rabies and where do they occur
Localised hyperaesthesia
Often with self mutilation
Typically at the extremity or inoculation site
How does the spinal/paralytic form of rabies progress clinically
It shows progressive ascending ataxia, weakness, lameness leading to recumbency within 3-5 days
Is the dumb strain common in horses
No it is unusual
What are the signs of the dumb form
Depression
ANorexia
Head tilt
Ataxia
Dementia
Blindness
Salvation and dysohagia
Tail, penis and bladder paralysis
Self mutilation
What are the signs of the furious form
Photo and hydrophobia
Agression
Hyperaesthesia
Tenesmus
Muscle tremors
Seizures
Why is diagnosing rabies difficult in live animals, and what clinical suspicion is used in endemic areas
Signs are vague and non specific
In endemic areas rapidly progressive neurological signs are assumed to be rabies
How is rabies confirmed post-mortem
By histology showing oesinophilic Negri bodies within neurons
By flourescent antibody testing
How does rabies effect humans
Almost always fatal
Vaccinated humans receiving post exposure boosters will survive
How does rabies effect horses
100% fatal
Best to kill on suspicion
Limit human contact
Early diagnosis essential
How do you control and prevent rabies
Vaccination very effective
Horses rarely infect other animals
International controls
Where is West Nile Virus found
Africa
Along Nile river
Middle east
Appearance in North America
Occasional outbreaks in Europe
What is the main reservoir for West Nile Virus and how is it transmitted to other species
Birds act as a reservoir
Mosquitoes transfer the virus from birds to other hosts
Why are humans and horses considered terminal hosts for West Nile Virus
Because they do not develop sufficient viraemia to transmit the virus further
What are the early events in West Nile Virus pathogenesis after inoculation
Initial viral replication at the inoculation site
Followed by viraemia causing fever, depression and anorexia
What happens when West Nile Virus enters the CNS in horses
It causes diffuse or multifocal encephalomyelitis commonly involving the spinal cord
What are the neurological signs of the West Nile Virus
Muscle fasciculations over entire body
Weakness, ataxia and dysmetria
Cranial nerves may be affected
Mentation may be affected
Sudden death in some horses
How is West Nile Virus treated
hyperimmune plasma specific to WNV available in USA
NSAIDs
Mannitol to decrease oedema
Corticosteroids
How is West Nile Virus daignosed
Ag specific testing
Virus culture of brain material post mortem
Immunohistochemistry post ortem
What is the prognosis of West Nile Virus
Few cases gradually resolve leaving long term neurological deficits
How is West Nile Virus prevented
Reduce vector contact
Vaccination