Equine Dysautonomias Flashcards
(Grass sickness)
Which animals does grass sickness affect?
- horses
- ponies
- donkeys
Most commonly affected ages
- 2-7y/o
What time of year are most cases seen?
- between April and July, with a peak in May
- in some years, a 2nd, smaller peak occurs in the autumn or winter
Risk Factors
▪Causal agent unknown
– Likely associated with toxin
▪Horses on pasture
▪Mechanical droppings removal
▪Presence of domesticated birds on field
▪ Stress
▪Animals in good-fat body condition
▪Cool, dry weather with a temperature between 7 and 11°C
▪Frequent worming
▪History of grass sickness cases on premises
What is equine grass sickness?
- A generalized dysautonomia affecting primarily the enteric nervous system
What signs aid in its diagnosis?
- Non-GI signs
What nervous system does it mainly affect?
- the parasympathetic NS
Acute vs subacute vs chronic survival
▪Acute – die rapidly
▪Sub Acute – survive >2days
▪Chronic – survive >7 days
Clinical diagnosis based on
▪ Decrease in GI motility from mouth to anus with a decrease in GI
secretions
Clinical signs of acute grass sickness
▪Severe gut paralysis leads to signs of acute colic
▪Difficulty swallowing
– Can result in discharge from nose
▪Drooling Saliva
▪Nasogastric reflux
– Due to widespread ileum which results in them backing up with fluid into the stomach
▪Mucous coated, hard droppings
– Evidence of delayed or slowed passage through the GIT
▪Muscle tremors and patchy sweating
▪ Tachycardia
– Typically between 60-80bpm
▪Usually die or are euthanised within 2 days of clinical signs
Clinical signs of sub-acute grass sickness
▪Similar to acute but less severe
▪Difficulty swallowing
– Can result in discharge from nose
▪Mild-moderate colic
▪Sweating, muscle tremors
▪Rapid weight loss
– tucked up appearance
▪May eat small amounts of food
▪May die or be euthanised within 1 week of clinical signs
– Die usually due to further decrease in appetite, continued colic signs and profound weakness
▪ Low head carriage
▪ Standing with legs underneath then
Clinical signs of chronic grass sickness
▪More insidious
▪Mild or intermittent colic
▪Reduced appetite
▪May have some difficulty eating, but salivation, gastric reflux and ileus are not a major feature
▪Rapid and severe weight loss/emaciation
– tucked up appearance
▪Some may recover
Diagnostic Tests
- Ileal biopsy
- Rectal biopsy
Ileal biopsy
▪Best diagnostic test
▪Requires laparotomy (midline or flank)
– Laparotomy decreases survival
– Evidence of neuronal degeneration within enteric ganglia and depletion of ganglia
– Vacuolation
▪Pathology localized to ileum in chronic EGS ▪Generalised intestinal pathology in acute disease
Rectal biopsy
- found to have 871% sensitivity, 100% specificity in a study of 14 horses
- not widely used in equine practice
Histological findings
▪Chromatolysis, vacuolation of cells within
autonomic ganglia
▪also affects other autonomic ganglia
Phenylephrine Test
▪ Horses with EGS develop bilateral ptosis (downward pointing of the eyelashes)
▪ Topical application of 0.5% phenylephrine to one eye
▪ examination 30 minutes later
▪ Positive test = reversal of the ptosis in that eye, increase in angle between the corneal surface and the eyelash.
▪ test useful in supporting of defective smooth muscle activity as an underlying cause of the ptosis
▪ BUT False positives seen - normal horses can show some response to this test
▪ In combination with clinical signs that are compatible with equine grass sickness, a positive result gives reassurance it’s a case of equine grass sickness.
Oesophageal Endoscopy
▪Linear oesophageal ulcers
▪indicative of gastro-
oesophageal reflux
▪In absence of severe ileus and extensive gastric distension
▪suggestive of
lower oesophageal sphincter dysfunction
– It doesn’t prevent gastric contents coming back up into the oesophagus
▪Many EGS horses do
not have oesophageal ulcers
Treatment
▪Nursing care is paramount for a successful outcome
▪Symptomatic therapy for each individual problem
– Analgesia
-> Promotes voluntary feeding – reduces pain associated with swallowing and abdominal pain
-> Oesophageal/gastric ulceration – Acid suppression and sucralfate
Supportive Care
Feeding
▪ Small feeds every 30-60minutes
▪ Hand feeding (don’t leave horse to eat)
▪ Hand grazing
▪ Varied diets
– These horses quickly lose interest in food so changing it can help stimulate appetite
Appetite stimulation
▪ Diazepam 0.02mg/kg IV BID-TID
▪ These drugs don’t often do much
Nursing
▪ Grooming
▪ Access to other horses
▪ Rhinitis – steam, mucolytics
Prokinetics
▪ Cisapride has most data – no longer available
▪ Neostigmine
▪ Used to try and promote GI motility
Prognosis
▪Carried a poor-grave prognosis
▪ Rhinitis has been associated with a poorer prognosis
Case study:
▪Successfully managed cases of chronic equine grass sickness
▪Large variation in time taken to return to normal bodyweight
▪9 +/- 7.5 months
▪Time to return to work 11.8 +/- 6.9months
▪Long term follow up of 16 competition horses
– 81% returned to their original work
– 19% returned to other work
Confirming diagnosis
▪ Cranial cervical ganglion
▪ Cranial mesenteric ganglia
▪ Ganglia is subrenal
▪ Remove spleen
▪ Raise kidney, remove suprarenal connective tissue - contains adrenal
▪ Obtain the cranial mesenteric ganglia
▪ Section extending from mid aorta, cranial pole of kidney to peritoneum
PM
Prevention
▪ Cause not yet known.
▪ In areas where the disease is prevalent, stabling the animals during the spring
and early summer will reduce the likelihood of disease.
▪ Association with weather, some owners living in affected areas now stable their horses when dry weather with a temperature of 7-11°C has persisted for 10 consecutive days.
▪ Stabling new horses that move onto premises where the disease is known to occur.
▪ If certain fields are ‘bad’ for the disease, they can be grazed by other stock, especially in spring and summer.
▪ If a case occurs amongst a group of horses, it is probably best to move the others out of that field provided this does not involve too much stress associated with transportation or mixing with strange horses.
Differences in pathology between acute and chronic cases
Chronic:
- pathology tends to be localised to the ileum
- may explain why they have milder clinical signs and are more likely to recover
- larger proportion of the GIT is still functional
Acute:
- pathology is generalised and tends to affect entire GIT
- so rapid progression of clinical signs and poorer prognosis
