Week 4- Equine Infectious Neurological Diseases Flashcards
What is West Nile Virus?
Vector borne Flavivirus
» Causes West Nile Encephalitis
» Zoonotic notifiable
* ‘Testing for Exclusion’ Scheme (APHA)
* Not in the UK, but likely to come – we have the vector (Culex pipiens)
* Seen in horses travelling from endemic countries (2019, 2022)
* Important to know clinical signs and what to do if suspect a case
Report to DEFRA rural services hotline
* Europe, N. & S. America, Asia, Africa…
What are the Clinical signs of West Nile Virus?
Dull/lethargic/somnolence
* Fever
* Facial paralysis, dysphagia
* Muscle fasciculations
* Para or tetra-paresis
* Ataxia
* Recumbency
How would you diagnose West Nile Virus?
IgM capture ELISA, (Ab detection cELISA) on serum or CSF
* CSF analysis: Pleocytosis (lymphocytosis), elevated protein levels
* Postmortem: PCR from tissue sample
How would you treat West Nile Virus?
No specific treatment
* ICU nursing care and monitoring, NSAIDs, recumbent horse care
How would you vaccinate against West Nile Virus?
Inactivated vaccine
* May complicate testing
* Core vaccine in North America
* Risk basis in the UK (horses travelling to endemic countries)
What three things does EHV-1 cause?
- Respiratory disease in young animals
- Abortion or Neonatal Death
- Equine Herpesvirus myeloencephalopathy
What is the pathology of equine herpesvirus?
Following respiratory tract infection (And/or reactivation of latently infected horses)
some virulent strains of EHV-1 demonstrate endotheliotropism
Endothelial cell replication and infection
Vasculitis and thromboischaemia of small arterioles
What two areas does EHV-1 affect?
Nervous System
» Ischaemic neuronal death
» Multifocal
» Myeloencephalopathy
**AND **
Uterus
Placental disease
Abortion/stillbirth
Foetal Infection
What are the signs of equine herpesvirus myeloencephalitis?
Pyrexia, dull, inappetent – viraemic phase
* Sudden onset neurological signs
* Ataxia & paresis: hindlimbs > forelimbs
* Caudal spinal cord segments (Cauda equina signs)
* Bladder distension and urinary incontinence
* Faecal retention
* Penile protrusion in males
* Flaccid tail & anus
How might you Diagnose Equine Herpesvirus?
Nasal or nasopharyngeal swab PCR
* Serology (paired serology)
* Virus isolation
* CSF: Xanthochromic (yellow)
How might CSF analysis be useful?
Useful in diagnosis of CNS disorders
» Viral/bacterial encephalitis, meningitis, abscess, haemorrhage, neoplastic disease
» Cytologic analysis may help in treatment plan
How would you take different CSF taps?
Atlanto-occipital (AO) tap: requires short anaesthesia but relatively straightforward technique
» Lumbosacral tap: Standing sedation
» Standing cervical centesis: Ultrasound guided centesis of C1-C2
How might you treat Equine Herpes Virus?
Symptomatic
* NSAIDs, nursing, palatable feed, IVFT
* Anti-viral medication
* Valacyclovir
What is the prognosis for EHM?
Prognosis variable
* Better chance of full recovery if not recumbent
* If recumbent >24h: Grave prognosis
What is the difference between tetanus and botulism?
Clostridial neurotoxins inhibit neurotransmitter release
* The location at which they do this results in different clinical signs
* Tetanus: tetanic/spastic paralysis
* Botulism: flaccid paralysis
What is clostridium tetani?
Gram positive, obligate anaerobe
* Spore forming bacteria
* Ubiquitous in soil/faeces
* Forms three toxins: tetanospasmin and tetanolysin most important
* Antibodies to tetanospasmin are protective (vaccination)
What do tetanus wounds look like?
Especially if deep, necrotic/reduced blood supply
* Penetrating wound, injection site abscess, metritis, castration,
foot abscesses…
* Routine prophylaxis (vaccination) is important
* Cases may have no visible wounds
What are the clinical signs of tetanus?
Localized stiffness – muscles around the original infection * Jaw, (Lock jaw), Neck, hind limbs * Third eyelid protrusion, nostril flaring, raised tailhead * Progresses to generalised stiffness (saw-horse stance) * Dysphagia * Hyperaesthesia (spasms to touch and sound) * Recumbency, paralysis or respiratory muscles * Autonomic signs * Tachy/bradydysrhythmias * Miosis
What are the treatment goals for tetanus?
Eliminate C. tetani organism
* Penicillin or metronidazole
* Clean and debride wound
* Neutralise toxin
* Antitoxin: does not neutralise toxin that is already in nerve
* Give antitoxin BEFORE wound debridement
* Give tetanus vaccine (toxoid) to stimulate active immunity
How might you treat tetanus?
Control muscle spasm
* Drugs like methocarbamol and diazepam can be used
* ACP (not hugely effective), alpha 2 agonists
» Nursing
* Padded stable ideal
* Or anaesthetic induction box
* May need slinging
* Minimise stimulation
* Cotton wool in ears
* Low light
* Low traffic
* Nutritional support and hydration
* Sling if recumbent
What is the tetanus vaccination?
Tetanus toxoid
* Start at 6mo of age
» Two vaccines four weeks apart
* 1st booster 6-24 months (depends on product)
* Boosters usually every 2 years
» Vaccinate mares in last trimester to confer immunity via colostrum
What is the tetanus antitoxin?
Used to provide protection during risk period
* Any unvaccinated horse with wound/castration/abscess
* Combination of toxoid and antitoxin often given to at-risk/naïve horses
* Often given to foals at 1 day old?
* Comes in big bottles, expensive…in theory shouldn’t be used after
broached for >24h!
What are the three routes of entry for botulism?
- Ingestion of pre-formed toxin ‘forage poisoning’
* 2. Ingestion of spores, production of toxin in GIT,
* 3. C. Botulinum infection via wound
What are the clinical signs of botulism?
Weakness, poor muscle tone, flaccidity
* Ptyalism, loss of tongue tone
* Cranial nerve dysfunction – dysphagia, ptosis
* Trembling, sweating, laboured breathing
* Reduced parasympathetic activity → decreased GIT motility
* Progress to recumbency
* Death may occur due to paralysis of respiratory muscles
How might you diagnose botulism?
History spoiled feed
* Clinical signs
* Laboratory tests challenging/unreliable
* Mouse bioassay
How might you treat botulism?
- Nursing: palatable soft feed
- Sling if needed
- Ventilator in young foals
- Supportive/symptomatic treatment
- Hyperimmune plasma
- Botulinum antitoxin – need to know the correct serotype
- Significant association with survival
What is the prognosis for botulism?
48% survival
What is Equine Grass Sickness?
Neuronal degenerative condition affecting the neurons of the autonomic nervous system
* Parasympathetic, Sympathetic & Enteric nervous system
» Also affects somatic efferent lower motor neurons
» Polyneuropathy/multisystem disease
» Most significant and profound dysfunction is in the enteric nervous system
* Intestinal dysmotility
What does equine grass sickness evidence suggest?
Evidence suggests ingestion of a neurotoxin involved
* Likely pasture derived
* Individual pastures with high incidence
* Some geographic areas worse affected than others
What are the three main presentations of equine grass sickness?
Acute
* Fatal (<48hrs)
Sub-acute
* Fatal (<7 days)
Chronic → some survive
* Reports vary, approx. 1/3 fatality rate
What are the main clinical signs of EGS?
Dullness
* Anorexia & Dysphagia
* Ptosis
* Patchy Sweating
* Tachycardia (to some extent)
* Muscle fasciculations
* Dry mucous-covered faeces
* GIT ulceration
* Oesophageal, gastric
What are the clinical signs of acute and subacute EGS?
Gastric distension and reflux (acute)
* Complete absence of GIT borborygmi
* Small intestinal distension (acute)
* Colon Impactions (subacute)
* Colic Signs
* Severe Tachycardia
* Sweating
What are the clinical signs of chronic EGS?
Weight Loss
* Cachexia
* Weakness
* Base Narrow Stance
* Weight Shifting
* Dry, mucous covered faeces in rectum
* Rhinitis sicca
What is the main treatment for chronic EGS?
- NURSING IS KEY
- Manual faecal evacuation
- Nutritional support
- Feed little and often, often need tempting. TPN/PPN?
- May require enteral feeding tubes
- Monitor hydration status
- Analgesia
- Often uncomfortable after eating
- Care RE masking impactions → monitor faecal output
- Treat secondary problems
- Aspiration pneumonia
- Some on liquid feed develop diarrhoea
- Address rhinitis sicca (emollients)
- Tire quickly: careful hand walking and slow return to exercise
What is the prognosis for chronic EGS?
Stop if continuous weight loss, no recovery of appetite
* Prediction curves based on rate/severity of weight loss
How does a Phenylephrine eye test help diagnose EGS?
Sympathomimetic
* 0.5% phenylephrine applied topically > transient reversal of
ptosis 20 to 30 minutes later
* Not sensitive (false positives and negatives)
What does the EGS Histopathology look like?
Ileum best to sample
* Neuronal chromatolysis
* Loss of Nissl substance
* Eccentricity or pyknosis of nuclei
* Neuronal swelling and vacuolation
* Accumulation of intracytoplasmic eosinophilic spheroids
* Axonal dystrophy
