Equine Infectious Neurology Flashcards

1
Q

West Nile Virus - Background

A

» 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… » UK surveillance to monitor risk

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2
Q

West Nile Virus - Clinical Signs

A
  • Dull/lethargic/somnolence
  • Fever
  • Facialparalysis,dysphagia
  • Musclefasciculations
  • Para or tetra-paresis
  • Ataxia
  • Recumbency
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3
Q

West Nile Virus - Diagnosis

A
  • IgM capture ELISA, (Ab detection cELISA) on serum or CSF
  • CSF analysis: Pleocytosis (lymphocytosis), elevated protein levels
  • Postmortem: PCR from tissue sample
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4
Q

West Nile Virus - Prevention and Tx

A

» Treatment
* No specific treatment
* ICU nursing care and monitoring, NSAIDs, recumbent horse care
» Vaccination
* Inactivated vaccine
* May complicate testing
* Core vaccine in North America
* Risk basis in the UK (horses travelling to endemic countries)

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5
Q

Equine Herpesvirus Myeloencephalopathy

A

» Caused by EHV-1, which is (to some extent) endemic
1. Respiratory disease in young horses (weanlings, yearlings) Outbreaks in overcrowd, stressful environments
* Fever, cough, nasal discharge
* Older horses (subclinical infection) play important role in outbreaks
2. Abortion or neonatal death: ‘Abortion storm’
* Neonatal septicemia, death
3. Equine Herpesvirus myeloencephalopathy (EHM)+/-pyrexia, respiratory signs
* Can occur singly or results in an outbreak

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6
Q

Equine herpesvirus myeloencephalitis

A
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7
Q

Equine herpesvirus myeloencephalitis Signs

A
  • 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
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8
Q

Equine Herpesvirus Myeloencephalitis Diagnosis

A
  • Nasal or nasopharyngeal swab PCR
  • Serology (paired serology)
  • Virus isolation
  • CSF: Xanthochromic (yellow)
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9
Q

CSF Analysis:

A

» Viral/bacterial encephalitis, meningitis, abscess, haemorrhage, neoplastic disease
» Atlanto-occipital (AO) tap: requires short anaesthesia but relatively straightforward technique
» Lumbosacral tap: Standing sedation
» Standing cervical centesis: Ultrasound guided centesis of C1-C2

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10
Q

EHM treatment

A

» Treatment:
* Symptomatic
* NSAIDs, nursing, palatable feed, IVFT
* Anti-viral medication
* Valacyclovir
* Biosecurity essential - Isolate
* Prognosis variable
* Better chance of full recovery if not recumbent
* If recumbent >24h: Grave prognosis

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11
Q

EHM Vaccination:

A

» At-risk basis
» Competition horses that are subject to periods of stress and gather with large #s of horses
» Not usually recommended in the face of an outbreak of EHM

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12
Q

Toxicoinfectious Diseases: Tetanus and botulism

A

» Clostridial neurotoxins inhibit neurotransmitter release
* Tetanus: tetanic/spastic paralysis
* Botulism: flaccid paralysis

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13
Q

Tetanus: Overview

A

» 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)
» Infection with spores→‘tetanus’
* Wounds
* 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

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14
Q

Tetanus Pathogenesis

A

Learn flowchart

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15
Q

Tetanus Clinical Signs

A
  • Localized stiffness–muscles around 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/brady dysrhythmias
  • Miosis
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16
Q

Tetanus Treatment

A
  • 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
    » 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
17
Q

Tetanus Prevention

A

» 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

» 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!

18
Q

Botulism Overview

A

» Rare in the UK
» USA higher prevalence
* Vaccination in high prevalence areas of USA (Kentucky)
» 8 different serotypes based on toxin produced (A to G)
* Geographic
* Affects treatment
» Route of entry
* 1. Ingestion of pre-formed toxin ‘forage poisoning’
* 2. Ingestion of spores, production of toxin in GIT,
* 3. C. Botulinum infection via wound

19
Q

Botulism: Pathogenosis

A

LEARN FLOWCHART

20
Q

Botulism Clinical signs

A
  • 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
21
Q

Botulism Treatment

A
  • Nursing: palatable soft feed
  • Sling if needed
  • Ventilator in young foals
  • Supportive/symptomatic treatment
  • Hyperimmune plasma
  • Botulinum antitoxin – need to know the correct serotype
22
Q

Botulism Diagnosis

A
  • History spoiled feed
  • Clinical signs
  • Lab tests challenging/unreliable
23
Q

Equine Grass sickness (equine dysautonomia) - Background

24
Q

Grass sickness/equine dysautonomia
Risk factors

A

» 2-7yrs old
» Recent movement
» Recent anthelmintic administration » Particular pasture
» Disturbed pasture
» Mechanical poo picking
» Cool, dry weather and irregular frost

25
Equine Grass sickness/equine dysautonomia Presentations
Acute - Fatal(<48hrs) Sub-acute - Fatal(<7days) Chronic → some survive * Reports vary, approx.1/3 fatality rate
26
Grass sickness/equine dysautonomia Clinical Signs
27
EGS Clinical findings – all categories
* Dullness * Anorexia & Dysphagia * Ptosis * Patchy Sweating * Tachycardia (to some extent) * Muscle fasciculations * Dry mucous-covered faeces * GIT ulceration - Oesophageal, gastric
28
Subacute and acute EGS
* Gastric distension and reflux (acute) * Complete absence of GIT borborygmi * Small intestinal distension (acute) * Colon Impactions (subacute) * Colic Signs * Severe Tachycardia * Sweating
29
Chronic EGS Clinical Signs
* Weight Loss * Cachexia * Weakness Base Narrow Stance Weight Shifting * Dry, mucous covered faeces in rectum * Rhinitis sicca
30
Chronic EGS Treatment
NURSING IS KEY * Manual faecal evacuation Nutritional support * Feed little and often, often need tempting. * May require enteral feeding tubes * Monitor hydration status Analgesia * Often uncomfortable after eating * Care RE masking impactions→monitor faecal output Treat 2° problems * Aspiration pneumonia * Some on liquid feed develop diarrhoea * Address rhinitis sicca (emollients) * Tire quickly: careful hand walking and slow return to exercise
31
EGS Diagnosis
* Definitive = histopathology * Enteric neuronal structures * Autonomic ganglion biopsies * Visualisation of rhinitis sicca indicative * Severity generally worse in non-survivors » Differential diagnoses for acute EGS: * Any strangulating or non-strangulating small intestinal obstruction * Anterior enteritis
32
EGS - Histopathology
* Ileum** * Neuronal chromatolysis * Loss of Nissl substance * Eccentricity or pyknosis of nuclei * Neuronal swelling and vacuolation * Accumulation of intracytoplasmic eosinophilic spheroids * Axonal dystrophy