Equine neurology, toxicology, myopathy Flashcards
Which viruses have a primary neurotropism in horses? Which arbo viruses are associated with CNS disease in horses? Which cause neuropathy by damaging BBB?
Viruses with primary neurotropism: - Rabies - Borna virus Arbo viruses: - Eastern, Western and Venezuelan equine encephalitis - Japanese encephalitis - West Nile virus Damage BBB: - EHV-1, 4 - Equine Infectious Anaemia (EIA)
How are neurological viral diseases diagnosed in horses? Normal findings?
History:
- geographical location
- recent travel
- onset and duration
- other horses
- vaccination history
Clinical examination:
- fever
- normally symmetrical, multifocal or diffuse lesions
CSF analysis and serology:
- most commonly mononuclear pleocytosis and increased protein concentration
- culture, PCR, ELISA, IFAT to identify Ag or Ab
Medical imaging and functional testing:
- CT/MRI: usually non specific intracranial oedema
PM examination:
- Histopath: usually immunohistochemistry and/or PCT amplification necessary
Treatment for neurological viral diseases in horses?
Isolate (because fever + neurological signs = infectious unless proven otherwise!)
Quiet, dark stable with deep bedding and padded walls
Turn recumbent horses every 4-6 hours
Sling?
NSAIDs
Corticosteroids?
Antiviral therapy: acyclovir, valacyclovir
Ag-specific therapy: WNV
Vitamin E, thiamine
What do the different Equine Herpes viruses cause?
EHV-1: respiratory, abortion, myeloencephalopathy EHV-2: keratitis EHV-3: coital exanthema EHV-4: respiratory EHV-5: multi nodular pulmonary fibrosis EHV-6 to 8: donkeys
EHV-1: features of the virus?
Alpha herpes virus Specific to horses Enveloped capsid containing DNA genome Latent infections Humoral immunity is very short lived Naturally low Ab level May occur sporadically or as outbreaks
EHV-1 pathogenesis? Neurological signs?
Vasculitis and thrombosis of arterioles in brain and spinal cord (viral endotheliotropism)
May or may not show prior respiratory signs or fever
May be recent history of respiratory disease or abortion in the premises
Sudden onset and early stabilisation of signs
Signs:
- ataxia in hindlimb or all 4, or recumbent
- cauda equina signs: atony of bladder, flaccid tail and anus, perineal hypoalgesia
- occasionally show cranial nerve involvement
Diagnosis of EHV-1?
Virus isolation/PCR: - Nasal swab - Buffy coat - CSF Serology: - Complement fixation, ELISA - 4 fold rise in titre or >1:80 CSF: xanthochromia
Management of neurological EHV-1? Prevention?
Isolate
Prognosis reasonable with good nursing care
- better if nor recumbent
- recovery days-weeks (up to 1 year)
- poor prognosis if recumbent >24h
Recurrence of neurological signs not reported
Vasculitis: NSAIDs, corticosteroids, aspirin (anti-thrombotic)
Prevention: vaccination for EHV-1 and 4 (but ineffective against neurological form and possibly worsens case if given during neurological outbreak)
Rabies: Type of virus? Transmission? Pathogenesis?
Lyssavirus
Rhabdovirus family
Neurotrophic
Transmitted by saliva contaminated bite wounds
Uncommon in horses
Pathogenesis:
- Local inoculation at wound site
- Access to peripheral nerve
- Gradual movement centrally
- Replication in spinal/dorsal root ganglia
- Rapid spread in CNS (cord, brain, sympathetic trunk)
- Centrifugal spread down nerves (salivary glands)
- Incubation period very variable: 9 days - 1 year (depends on strain, host species, inoculum, proximity of inoculation to CNS)
Signs of rabies in horses?
No pathognomonic signs
From mild hindlimb lameness to sudden death
Signs depend on euro-anatomic location of pathology
Forms: Spinal -> paralytic form: - most common - localised hyperaesthesia: self mutilation of extremity/site of inoculation - progressive ascending: ataxia, weakness, lameness - recumbent 3-5 days Brain stem -> dumb form: - unusual in horses - depression - anorexia - head tilt, circling - ataxia - dementia/blindness - salivation/dysphagia - tail/penis/bladder paralysis - self-mutilation Cerebrum -> furious form: - unusual in horses - photophobia/hydrophobia - aggression/bizarre behaviout - hyperaesthesia - tenesmus - muscle tremors - seizures Forms can co-exist or progress
Rabies PM exam in horses?
Histology: eusinophilic inclusion bodies (Negri bodies) within neurones
Fluorescent Ab
Arbovirus groups A, B and C?
Arbovirus Group A: Togaviridae: - EEE, WEE, VEE Arbovirus Group B: Flaviviridae: - WNV: Hapanese encephalitis Arbovirus Group C: Bunyaviridae: - limited reports of infection in horses
Limitations to a neuro exam in horses?
Size
Behaviour/danger
Recumbency
Neuro exam in a horse?
From a distance: - Mentation - Behaviour - Posture Cranial nerves Observe and palpate neck and back: - muscle atrophy, asymmetry, sweating - range of movement - cervicofacial reflex - cutaneous trunci (panniculus) reflex) Tail: voluntary movement, tone Perineal reflex, tail clamp, anal tone Males: external genitalia Rectal exam: assess lumbar, sacral or coccygeal vertebrae, bladder volume and tone
What is cranial nerve I? What is its function? What is seen with dysfunction? How can you evaluate it in horses?
Olfactory nerve
Function: olfaction
Dysfunction: reduced or absent smell
Evaluation: difficult and subjective
What is cranial nerve II? What is its function? What is seen with dysfunction? How can you evaluate it in horses?
Optic nerve Function: vision Dysfunction: partial or complete blindness (dilated, unresponsive pupils) Evaluation: - vision (obstacles) - menace response (>2wks) - PLR - visual placing
What is cranial nerve III? What is its function? What is seen with dysfunction? How can you evaluate it in horses?
Oculomotor nerve Function: - pupil size - eyelid movement (ispilateral dorsal, ventral and medial recti, ventral oblique, elevator palpebrae) Dysfunction: - ventrolateral strabismus - inability to rotate eye dorsally, ventrally and medially - dilated unresponsive pupil - ptosis of upper lid Evaluation: - PLR - physiological nystagmus - eye position at rest
What is cranial nerve IV? What is its function? What is seen with dysfunction? How can you evaluate it in horses?
Trochlear nerve
Function: contralateral dorsal oblique muscle
Dysfunction: dorsolateral strabismus (fundic examination)
Evaluation:
- physiological nystagmus
- eye position at rest
What is cranial nerve V? What is its function? What is seen with dysfunction? How can you evaluate it in horses?
Trigeminal nerve
Function:
- sensory innervation of face
- motor innervation to masticatory muscles
Dysfunction:
- masticatory muscle atrophy and jaw weakness (dropped jaw if bilateral)
- facial hypo/anaesthesia
- neurotropic keratitis
Evaluation:
- size and symmetry of masticatory muscles
- sensory function (corneal, palpebral, nasal)
What is cranial nerve VI? What is its function? What is seen with dysfunction? How can you evaluate it in horses?
Abducens nerve Function: ipsilateral lateral rectus and retractor bulbi muscles Dysfunction: - medial strabismus - inability to move eye laterally and to retract eyeball Evaluation: - physiological nystagmus - eye position at rest - corneal reflex
What is cranial nerve VII? What is its function? What is seen with dysfunction? How can you evaluate it in horses?
Facial nerve Function: - motor to facial muscles - taste for rostral 2/3 of tongue - lacrimal gland Dysfunction: - drooping - inability to move ear and lip - absent blink - KCC Evaluation: - facial symmetry - palpebral reflex - menace response - corneal reflex - STT
What is cranial nerve VIII? What is its function? What is seen with dysfunction? How can you evaluate it in horses?
Vestibulocochlear nerve Function: - hearing - vestibular function Dysfunction: - partial or complete deafness - signs of vestibular disease Evaluation: - BAER - signs of vestibular disease: head posture, physiological nystagmus, gait, blindfold
What is cranial nerve IX? What is its function? What is seen with dysfunction? How can you evaluate it in horses?
Glossopharyngeal nerve Function: - motor to pharynx and palate? - sensory to caudal 1/3 of tongue and pharynx - salivary glands Dysfunction: - dysphagia - absent gag Evaluation: - gag
What is cranial nerve X? What is its function? What is seen with dysfunction? How can you evaluate it in horses?
Vagus nerve Function: - larynx, pharynx and oesophagus - all thoracic and abdominal viscera Dysfunction: - dysphagia - inspiratory dyspnoea - dysphonia - regurgitation - absent gag Evaluation: - gag - oculocardiac
What is cranial nerve XI? What is its function? What is seen with dysfunction?
Accessory nerve Function: - trapezius - part of sternocephalicus Dysfunction: trapezius atrophy
What is cranial nerve XII? What is its function? What is seen with dysfunction? Evaluation?
Hypoglossus nerve Function: motor to tongue Dysfunction: - tongue deviation/atrophy - problems with prehension Evaluation: - tongue size, tone and symmetry
Possible causes of an abnormal posture in horses?
Orthopaedic problem
Neurological:
1. Loss of spatial awareness - conscious proprioceptive deficits at rest, abnormal posture when stop/not correcting (don’t manipulate limb)
2. inability to move limb
Define ataxia? What to look for?
Subconscious proprioceptive deficits seen as irregular and unpredictable movement
Lood for poor coordination, swaying, limb moving excessively during swing phase (weaving, abduction, adduction, crossing limbs, stepping on self)
Exaggerated by tight circles, sudden stopping, backing, hills, raising head
Types of ataxia in horses?
Cerebellar: - no weakness - hypermetric ataxia - other signs of cerebellar disease e.g. tremor, lack of menace response Vestibular: - loss of balance - hypometric ataxia - wide based - other vestibular signs e.g. head tilt, nystagmus Spinal (most common in uk): - dysmetric ataxia - +/- weakness
Classification of ataxia severity?
Subtle: deficits barely detected at normal gait, occur during backing, stopping, turning, swaying, neck extension etc
Mild: detected at normal gait, exaggerated by above manoeuvres
Moderate: prominent at normal gait, tend to buckle and fall with above manoeuvres
Severe: tripping and falling spontaneously at normal gait to complete paralysis
What neurological problem causes weakness in horses?
Interruption to general somatic efferent pathways (motor pathways) Extensor weakness: - sinking/buckling - weak when pulling tail Flexor weakness: - toe drag/delay in picking up - swinging movement
Motor tract lesion (UMN): tail pull during movement Motor neuron (LMN): tail pull at rest
West Nile Virus: Epidemiology? Pathogenesis? Signs?
Epidemiology:
- replicates in birds = reservoir
- mosquitoes (Culex) transfer virus from birds to a number of species (horses and humans)
- human and horses are terminal hosts
Pathogenesis:
1. Initial virus replication at site of inoculation
2. Viraemia -> signs of uncomplicated infection (fever, depression, anorexia)
3. In some horses virus enters CNS:
- diffuse or multifocal encephalomyelitis
- involvement of spinal cord common (unlike EEE / WEE)
Neurological signs:
- muscle fasciculations over entire body (particularly head and neck)
- weakness, ataxia, dysmetria
- cranial nerves may be affected
- mentation may be affected (indirectly due to
intracranial oedema)
- sudden death in some horses
Treatment:
- hyperimmune plasma specific to WNV available in USA
- supportive care
- NSAIDs
- DMSO? Mannitol? to reduce oedema
- corticosteroids?
Prognosis:
- few cases gradually resolve -> long term neurological deficits
What plants are poisonous to horses?
Wild: - Ragwort - Giant hogweed - Water hemlock - Foxglove (Digitalis) - Deadly nightshade - Bracken fern - Oak/acorn - Rhododendron - Houndstongue Garden: - Sorghum - Oleander - Lantana Fungal/toxin elaboration: - Endophytes e.g. ryegrass, fescue toxicoses - Contamination e.g. mouldy corn
Which poisonous plants are hepatotoxins? What are the toxins?
Ragwort - pyrollizidine alkaloid
Houndstongue - pyrollizidine alkaloid
Lantana - triterpene acids, lantadene A, lantadene B
Ragwort: Name? Which stages toxic? Pattern of growth? When ingested? Toxicology?
= Senecio jacobaea
Toxic at all stages of growth and when dried
Biennial:
- spring: Small rosettes (commonly ingested)
- summer: up to 1.5m tall with distinctive yellow flowers and ragged leaves (rarely ingested except in preserved forage)
Unpalatable when fresh -
usually ingested in preserved state
Toxicology:
- hepatotoxic pyrrolizidine alkaloids or triterpene acids cause liver failure
- pyrrolizidine alkaloids alkalate DNA, stop hepatocyte cell division, causing megalocytosis and liver failure
Clinical signs of liver failure from ragwort?
Weight loss Jaundice Dullness and depression Muscle tremors and weakness Frequent yawning Inappetance and difficulty swallowing Respiratory noise/laryngeal paralysis Compulsive walking/incoordination/head pressing Photosensitisation Colic Encephalopathic signs: classic signs are quiet, dull, head press
Diagnosis of ragwort poisoning?
Examine hay for ragwort leaves Clinical signs Test blod: - non specific signs of liver damage - specific alkaloid detection (definitive) PM
Methods of control of ragwort?
Spraying herbicide (blanket or spot):
- cannot use land for grazing for weeks to months
- leaves bare patches where ragwort can easily re-establish
Uprooting and burning (manual or mechanical):
- labour intensive
- wear gloves to prevent skin irritation
Cutting:
- less effective as roots remain and can re-establish
- only done when field not in use to prevent flowering, seeding and spreading
- ensure cuttings removed
?Grazing land with sheep which may be resistant to toxicity before turning horses out:
- controversial
Which poisonous plants are myotoxins an enterotoxins? What are the toxins?
Myotoxins:
- sycamore: hypoglycin A
Enterotoxins:
- oak/acorns: tannins
Sycamore poisoning: Toxicology? Clinical signs? PM?
Toxicology:
- hypoglycin A?
- acquired multiple Acyl-CoA dehydrogenase deficiency
- causes atypical myopathy
Clinical signs:
- weakness, fasciculations
- recumbency
- red urine (myoglobinuria)
- marked elevations in serum muscle enzymes (CK, AST)
PM: widespread myonecrosis (skeletal and cardiac)
Spring and autumn - sudden weather change? - horses at pasture
Acorn/oak poisoning: Toxicology? When ingested? Pathology? Clinical signs? Diagnosis? Treatment? Control?
Toxicology:
- oak leaves and acorns contain tannins
- highest tannin content of sap in spring
Acorns Sept-Oct
Pathology:
- gastroenteritis
- haemorrhages in abdominal cavity over GIT and beneath endo and epicardium
- subcutaneous oedema over pelvic limbs and along ventral body wall
Clinical signs:
- parachute/acute/sudden death
- colic
- tenesmus
- haemorrhagic diarrhoea
But poisoning rare in horses - some unaffected
Diagnosis:
- acorn husks/shells in faeces
- urinary phenolic content to differentiate from other colics
Treatment:
- as medical colic (IVFT, analgesia, oral laxatives, diuresis, acid/base balance, serum calcium levels)
Control:
- fence off oak trees in autumn when acorns are abundant
- pick up acorns from pasture
What poisonous plants are cardio-respiratory toxins? Toxin?
Oleander
Rhododendron
Fox glove
Contain cardenolides or cardiac glycosides which interfere with electrical conductivity of the heart -> arrhythmias/sudden death
Oleander: Which parts toxic? Toxin? Signs? Necropsy?
All parts very toxin Cardiac glycosides Signs: - Diarrhoea/melaena - Disruptive cardiac arrythmias - Death often within minutes Necropsy: - Nil findings - Plant?
Which poisonous plants are dermotoxins?
St John’s Wort
Giant Hogweed
St John’s Wort: Where found? Growth? What does it cause?
Hedgerows and gardens
Slow expansion, perennial
Primary photosensitisation
Hypericin - therapeutic agent?
Giant Hogweed: What does it cause?
No specific signs
Oral irritation/ulcers
Which poisonous plants are neurotoxins?
Deadly nightshade Yew Hemlock Sorghum Flatweed Singletary Pea Ryegrass Mouldy corn
Sorghum: What is it? Toxin? What does it cause?
‘Milo’/’Sudan’ grass
Chronic cyanide poisoning? - cyanogenic glycosides
Bladder paralysis
Flatweed: Where found? What does it cause?
Common wild plant in stable yards and poorly maintained pastures (dandelions) Widespread Ingested in low amounts normally Stringhalt (but not really in UK) Persistent neurologic deficits
Deadly nightshade: Signs of poisoning? Treatment?
Atropine related signs (parasympatholytic): - mydriasis - shivering/muscle spasms - tachycardia - dry mucous membranes - colic (ileus/obstipation) Treatment: - neostigmine? (but may be worse than the poisoning!) - activated charcoal - fluids etc
Bracken fern: How bad/common? Toxicology? Clinical signs? Diagnosis? Treatment? Prognosis?
Overstated effects - heavy/persistent ingestion?
Not very common
Contains thiaminase -> vitamin B1 (thiamine) deficiency
Carcinogenic?
Clinical signs (bracken staggers):
- anorexia
- cardiac dysrhythmia
- crouched stance, arched neck, feet wide apart
- incoordination
- convulsions
- clonic spasms and opisthotonus then death
Diagnosis:
- low blood thiamine (not pathognomonic)
- elevated pyruvate
- bracken on pasture or in hay
- known ingestion
Treatment:
- thiamine every 12h IM or slow IV for up to 7 days
- avoid IV if possible (anaphylactic reaction)
Prognosis:
- therapy usually highly effective if early
Mare’s tails poisoning: Pathogenesis? Signs? Treatment?
Thiaminase
CNS signs predominate
Treatment: thiamine
Hemlock and water hemlock: What do the plants look like? Toxicology? Which parts of plant toxic? When? Clinical signs? Treatment?
Flowers/leaves similar to cow parsley
Distinct irregular purple blotches on stem
Hemlock flowers and fruits contain most toxic alkaloid
Water hemlock roots and leaves
Especially poisonous in dry, hot summers
Toxicology:
- hemlock: alkaloid coiine (nicotine like action)
- water hemlock: cicutoxin and cicutol
- first stimulating and then depressing autonomic ganglia
- curare-like effect
- paralysing skeletal muscle motor nerve endings
Clinical signs:
- agitation, nervousness
- twitching
- seizures
- excess salivation
- dilated pupils
- skeletal muscle weakness
- cardiac abnormalities
- difficulty breathing
- death from respiratory paralysis
May develop following ingestion of only small quantities
Treatment: activated charcoal and/or lavage
Yew: Where found? Toxicology? Which parts poisonous? Pathology? Clinical signs?
Evergreen - hedges and gardens Toxicology: - alkaloid taxines - all parts of tree poisonous Pathology: - distended stomach - inflammation if death occurs after several hours - liver, spleen and lungs engorged with dark blood Clinical signs: - trembling - ataxia - bradycardia - hypothermia - weak - dyspnoea - rapid death
What are the main feed-borne mycotoxins that affect horses?
Mouldy corn toxicity
Rye grass staggers
Fescue toxicosis
Mouldy corn poisoning: Toxin? Pathology? Signs?
Mycotoxin = fumonisin B1 Infected corn/commercial foods Can be fatal to horses Pathology: liquefactive necrosis of brain Signs 2-4 weeks after ingestion: - anorexia - blindness - ataxia - head pressing - circling - hyperexcitability - seizures - recumbency/death
Ergot/rye grass staggers: Toxin? Signs? Treatment?
Associated with endophyte infected plant - produces toxin Lolitrem B
Signs:
- trembling, unsteadiness and poor muscle coordination
- erratic and anxious behaviour
- milder cases may display some trembling of head, neck, shoulders
- signs worsen if exposure increases
Treatment:
- get better quickly if take off pasture
Fescue toxicosis: Features of plant?Toxicology? Which horses affected? Clinical signs?
Perennial tufted grass, related to ryegrass 10cm - 2m tall Toxicology: - toxicity due to endophyte Acremonium coenophialum - most significant alkaloid substance produced is the ergo peptide ergovaline Affects pregnant mares and unborn foals Clinical signs: poor reproductive function: - prolonged gestation - abortion - premature separation of chorion - dystocia - thickened and retained placenta - lack of milk let down - reduced pregnancy rates - immature foals born - poor foal immunity
Aflatoxins: Which plants? Which toxins? Where? Clinical signs? Treatment? Management?
Aspergillus 5 major toxins: - B1, B2, G1, G2, M1 - B1 most important Mostly stored feeds Poorly recognised clinically Clinical signs: 1. Sudden death: - no premonitory signs 2. Neurotoxic syndrome: - incoordination, aimless walking - lethargy -> mania, convulsions - delirium - sweating - death 3. Hepatotoxic syndrome: - head swelling, jaundice - depression, signs of liver failure - coma -> death No effective treatment Management: - remove contaminated feed - supportive therapy - high dose vitamin B - vitamin B1? - sedation if required - mannitol/DMSO - laxatives/activated charcoal?
Blue-green algae: Where? Toxicology?
Natural water courses - looks like algae but isn’t
Cyanobacteria
Highly toxic
Bran disease: Cause? What does it cause?
Ca/Po4 imbalance
Secondary nutritional hyperparathyroidism
Lead poisoning: Clinical signs?
Peripheral nerve dysfunction: - motor nerves worse -> weakness - minimal sensory loss Depression Weight loss Laryngeal/pharyngeal paralysis -> dysphagia, aspiration pneumonia Facial paralysis Anal/bladder paralysis Colic Diarrhoea Hepatic failure Blindness Seizures Coma -> death Lead crosses placenta: - premature/weak/still born foals
(can look like rabies or botulism)
Treatment of lead poisoning in horses?
Remove source Chelation therapy Ca disodium EDTA - binds out bone lead Fluids Nursing support High dietary calcium
Selenium poisoning: How happens? Signs?
Supplement overdose - care with cattle licks as horses need less selenium per day than ruminants Seleniferous plants Signs: - hair loss (mane, tail) - laminitis
Monensin poisoning: When seen? Signs?
Chicken feed often contains monensin (coccidiostat for poultry but highly toxic to horses)
Acute - sudden death, diarrhoea
Chronic - cardiac failure DCM
Glycogen branch enzyme (GBE) deficiency: How does it present? Diagnosis?
Foal dies suddenly
Poor body condition
Muscle biopsy - PAS staining unusually absent
Polysaccharide storage myopathy: Why happens? Presentation? Diagnosis? Treatment?
Pathogenesis:
- accumulation of glycogen = storage disease on exercise
Poor performance
Becomes stiff and reluctant to move after short period of exercise
Raised muscle enzymes
Semimembranosus muscle biopsy – abnormal accumulation of PAS positive material and evidence of cell degeneration/regeneration, amylase resistant inclusion bodies
Treatment: low carb, high fibre diet (oil to replace carbs for energy)
Chronic exertional rhabdomyolysis: How does it present? Diagnosis?
Stress
Intermittent muscle cramping and stiffness
Poor performance
Mild elevation of CK and aspartate aminotransferase
Muscle biopsy – cellular degeneration/regeneration but normal PAS staining
Hyperkalaemic periodic paralysis (HPP): How does it present?
Well muscled (Sire impressive) Periods of sweating and muscle fasciculations over shoulder, flank and neck Lasts 30 minutes and is weak Seems to happen when excited or stressed
Treatment for acute and chronic exertional rhabdomyolysis?
Acute: pain relief, fluids, ACP
Chronic: warm up, avoid stress and high energy feeds
