Equine Grass sickness

Equine Grass Sickness

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• Legenda: Equine grass sickness (dysautonomia)- neurological disease. Degeneration of neurons in autonomic nervous system, somatic nervous system involvement also reported. Affects all Equidae, fatal, 1% incidence in some parts of the UK.

Equine Grass Sickness

• Aetiology
• Remains unknown
• Several infectious/ toxic agents- plants, fungi, insects, viruses, bacteria and toxic compounds- implicated since disease first reported 100 yrs ago
• Current leading hypothesis- result of Clostridium botulinum types C and D. Toxin produced locally in horse's GIT by resident bacteria
• PME- acute toxaemia of bacterial origin- characteristic of C. botulinum
• Aetiological hypothesis supported by 2 successful vaccination trials in 1922 and 1923. Soon discarded..
• Recent interest- C. botulinum and type C and one neurotoxins produced by organism (BoNT/C)- identified in ileum and faeces of horses with grass sickness vs control horses.
• Cases- lower serum concentrations of antibody against C. botulinum C and BoNT/C. Increased mucosal IgA against BoNT/C and BoNT/D (neurotoxin from type D)- small intestine of acute cases.
• Epidermiology
• First described in Scotland in early 1900s.
• Since seen in many Northern European countries
• A clinically and pathologically identical disease, mal seco, (dry sickness), recognised in South America
• Causal agent not confirmed- number of risk factors fo development of disease are well recognised. They have 4 groups.
• Horse related risk factors
• Season/ climate related risk factors
• Premises related risk factors
• Management related risk factors

Epidemiology- related factors

• Horse- related Risk factors
• Age- young horses (2-7yrs old). Rare in older horses (immunity/ tolerance). Rare in foals- protected through maternal antibodies, failure to ingest large quantities of grass also responsible.
• Body condition- good/fat body condition- more likely to develop condition.
• Immunological status- low antibody levels to C. botulinum C surface antigen and BoNT/C, increased risk of developing disease.
• Season/ climate related risk factors
• Seasonal incidence- occur throughout the year. Peak incidence in Northern Hemisphere in the spring/ early summer
• Weather patterns- outbreaks of grass sickness associate with cooler temperatures (7-11oC) and drier weather with irregular ground frost in two weeks before outbreak.

Epidemiology- related factors

• Premises related
• Types of establishment- higher numbers and presence of young horses on premises- associated with increased risk of recurrence of grass sickness. Stud farms/ livery/ riding stables- higher recurrence rate than other premises, reflect large numbers/ young age of horses.
• Soil type- sand and loam soils- increased risk of recurrence. Chalk soils -decrease risk of recurrence. Reason- unclear, reflect difference in soil types or greater likelihood of pasture disturbance in field containing sand/ loam soil
• Soil nitrogen content- increased soil nitrogen= risk factor for grass sickness. Associated with increased growth of pasture herbage- analogous to dietary change (risk factor)
• Previous occurence of grass sickness- more likely to recur on premise with previous cases of disease has occurred.
• Management related
• Grazing- development associated with grass access. Cograzing with ruminants- protection from condition, not clear if due to grazing practices there are smaller numbers of horses. Or cograzing- removal of aetiological agent from pasture
• Dietary change- change in quantity and type of food available are risk factors. Changes in gastrointestinal flora- promote multiplication of aetiological bacterial agent within intestine, toxin production and absorption.
• Movement/ stress- increased risk. Immunological naivety to agent and/or alteration in gastrointestinal flora
• Pasture disturbance- construction, mole activity= increased risk. Facilitate transfer of soilborne organism onto the pasture surface- available for ingestion.
• Anthelmintic use- high frequency use is a risk factor. Specific ivermectin based product. Altered flora/ local immunity.
• Droppings removal- mechanical removal, increased risk.
• Grass cutting- reduce rate of recurrence. Reduced grazing

Clinical signs

• Subdivided into 3 catergories- acute, subacute and chronic. Reflect duration of illness, reflect severity of neuronal loss (enteric nervous system).
• Clinical signs- dysfunction of the autonomic (includes enteric) nervous system. One exception- muscle fasciculations observed over triceps and quadriceps
• Acute
• Animals usually die/ euthanased on humane grounds an/or due to hopeless prognosis for survival within 48hrs of onset
• Subacute
• Similar to acute form, often less severe. Difference reflect a difference in the severity of neuronal loss/ dysfunction- large volume reflux of gastric fluid following nasogastric intubation and small intestinal distension appreciated during transrectal palpation/ ultrasonographic examination of acute cases seldom occur in subacute cases.
• Very firm 'pseudo-impactions' of caecum and large colon detected during transrectal palpation.
• Hopeless prognosis for survival. Euthansia within 2-7 days of onset of clinical signs.
• Chronic
• Insidious onset, affected animals survive >7 days. Many make a recovery with intensive nursing care.
• Develop a 'tucked up' abdominal silhouette, base-narrow stance- term ' elephant on a tub' appearance.

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• Legenda: Part 1

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• Legenda: part 2

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Diagnosis

• No definitive non-invasive antemortem diagnostic test.
• Majority of causes- recognising clinical signs, analysing findings of rectal examination (firm secondary large colon and/or caecal impaction), eliminate disease with similar signs.
• Consider signalment and epidemiological charateristics of the case.
• Repeat examinations- necessary before diagnosis made.
• Haematology, biochemistry, peritoneal fluid and urinalysis results- non specific
• Oesophageal endoscopy and barium swallow procedures- defective oesophageal motility
• Additional endoscopic findings (acute)- oesophageal ulceration- reflux oesophagitis.
• Topical phenylephrine eye drops (dilute to 0.5%) in one eye, exam in 30 minutes- reversal of ptosis in ipsilateral eye, increase angle between corneal surface and eyelash.
• Definitive diagnosis- identify characteristic histopatholgical changes in autonomic/ enteric ganglia at PME, or after collection of an ileal biopsy obtained at exploratory laparotomy.
• PME- full circumferential section of ileum, submit for histopathology, with sample of autonomic ganglion
• Variety of ganglia affected- submitted for histopathology (cranial cervical ganglion is simplest to locate)
• Ex-lap--> some suspected cases of acute/subacute grass sickness to R/O existence of surgical condition affecting GIT. Adverse effects on prognosis. Chronic cases- diagnosis on clinical signs only

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• Legenda: DDx for equine grass sickness- comparing historical and clinical differences

Pathology

• Postmortem confirmation- attempted in cases diagnosed clinically.
• Important- potential association between the disease and the premises on which the horse was grazing- any association/ future risk avoidance strategies are based on factual diagnostic confirmation
• Certain gross pathological findings- suggestive of grass sickness, elimination of other disease processes - beneficial in supporting clinical diagnosis
• Absolute diagnostic confirmation- reliant on identification of characteristic chromatolytic neuronal changes (loss of Nissl substance, neuronal swelling/ vacuolation, intracytoplasmic eosinophilic spheroids, eccentric and pyknotic nuclei) identified during histopathological examination of autonomic ganglia/ enteric neural plexuses.
• Acute cases- neuronal degeneration in enteric plexues is widespread.
• Chronic cases- ileum may only be severely affected area of GIT
• Acute grass sickness findings
• Oesophageal erosions- reflux oesophagitis
• Gastric and small intestinal distension with fluid
• Subacute grass sickness
• Impaction of the large colon with dry ingesta
• Black coating over firm ingesta (adherent to colonic mucosa)
• Chronic grass sickness
• Lack of ingesta, apparent shrinkage of GIT
• Emaciation of the carcase in long standing cases

Treatment

• Acute/ Subacute cases
• IV fluids
• Analgesics
• Regular gastric decompression
• All above initiated until a clinical diagnosis becomes more definitive- marked degeneration and loss of enteric intramural plexues is irreversible--> euthansia should be recommended once a diagnosis is reached.
• Chronic cases- considered for treatment if they are willing to drink/ swallow feed. Retain some ability to drink/ swallow feed. Have no continuous moderate/severe signs of colic
• Tx- intensive nursing care.
• Variety of highly palatable foods should be available. High energy, high protein feeds- ideal; mixed with molasses, biscuits and succulents (apples and carrots) to improve palatability. Wet and dry food should be available.
• Some may need to be hand fed.
• Housed, regular in-hand walking,, allow access to grass.
• Kept warm, weighed regularly during tx--> objective assessment of their response to nursing care
• Mild to moderate post prandial colic- often noticed. Manage with phenylbutazone (2.2-4.4mg/kg BID), or flunixin (0.5-1,1mg/kg BID) and omeprazole (4mg/kg SID).
• Signs due to delayed gastric emptying; varying degrees of intestinal dysmolity. Motility enhancers/ appetite stimulants been used- disappointing results

Prevention

• Risk avoidance strategies
• Prevention strategies- reduction/ avoidance of premises/ management related risk factors and implementation of protective factors (esp for high risk horses- young/ newly introduced animals during spring/ summer or climatic conditions)
• Premises
• Avoid- previously affected premises; soil exposure
• Managment
• Minimise- grazing; movement to new premises; change of feed; pasture disturbance; frequent use of ivermectin-based products; mechanical removal of droppings
• Protective factors
• Cograzing with ruminants; regular grass cutting; hand removal of droppings; provision of supplementary forage feeding
• Vaccination
• No vaccine currently available for prophylactic use.
• 1920's vaccination trial and recent epidemiological and serological evidence supports a role for C. botulinum type C in aetiopathogenesis of grass sickness.
• Work is being undertaken to evaluate the safety and immunogenicity of recombinant protein-based vaccine against C. botulinum toxins; commercially available vaccine in horses.
• Results of trials are favourable , appropriate licenses are approved (providing obtained funding), randomised controlled field trial will be carried out in the near future on high risk premises.

Long term prognosis

• ~80% of selected cases of chronic quine grass sickness survive
• There are no accurate indicators in chronic cases at initial presentation- used to predict the duration of supportive care required/ success of the outcome.
• One study- the degree of dysphagia (closely associated with appetite) and severity of rhinitis= best predictors of survival.
• Principal problems encountered in first 2 months following discharge- mild colic, poor appetite, dysphagia, sweating, coat changes (piloerection affecting anatomical sites previously affected by patchy sweating)
• Successfully managed cases of chronic grass sickness- large variation time in the time taken to return to normal bodyweight (mean 9months; standard deviation 7.5months); to return to work (mean 11.8months; standard deviation 6.9months); long term follow up of 16 competitive horses revealed 81% of them returned to their original work, 19% returned to other work. Most are regarded to be working well/ very well by owners.