Equine dysautonomia Flashcards
Discuss equine grass sickness?
Equine Grass sickness is an important sporadic disease of the horse at pasture, causing a generalised dysautomia. It affects the enteric nervous system resulting in decreased intestinal motility and decreased GI secretions. This can result in gastro-intestinal ileus and/or large colon impactions leading to ileus. In addition to the enteric changes, there are changes in the sympathetic and parasympathetic nervous systems that lead to a range of complex clinical signs, including sweating, muscle fasciculations, ptosis and tachycardia (beyond what is expected for the degree of pain / hypovolaemia). This can aid in the diagnosis of the condition.
Define dysautonomia?
Dysautonomia or autonomic dysfunction is a condition in which the autonomic nervous system (ANS) does not work properly. This may affect the functioning of the heart, bladder, intestines, sweat glands, pupils, and blood vessels. Dysautonomia has many causes, not all of which may be classified as neuropathic.
Formulate a differential list for dysphagia in the horse. Include exotic infectious agents?
- Equine Grass Sickness
- Small intestinal strangulated lesion (can cause dysphagia from pain)
- Choke
- Botulism
- Hypocalcaemia
- Equine motor neurone disease
- West Nile Virus
- Eastern/ Western Equine myeloencephalitis
- Guttural pouch tympany
- Empyema
- Guttural pouch mycosis
- Lead poisoning
- Tetanus
- Equine protozoal myeloencephalitis
Review the epidemiological studies to highlight important factors that may lead to cases of equine grass sickness J.L. Wood, E.M. Milne, D.L. Doxey A case-control study of grass sickness (equine dysautonomia) in the United Kingdom Vet J, 156 (1) (1998), pp. 7–14?
List the important risk factors:
- Continuous grazing
- Younger animals
- Grazing in areas where the disease has been before- HIGH RISK
- Recent changes in pasture
- Season (April to June)
- Dry cold weather
Describe what measures you would undertake in order to limit further cases on a farm / livery yard?
- Don’t graze animals on pastures where there have been cases of equine grass sickness previously
- Co-grazing with ruminants is a protective factor
- Regular poo picking
- Increase access to forage
- Reduce changes between pastures, particularly if the animal has never grazed the area before. (Such as a recent livery change)
- Limit grazing of younger at risk animals at peak risk periods (Dry cold weather in April for example)
Tabulate the clinic signs that can occur with ACUTE, SUBACUTE and CHRONIC grass sickness. Indicate the prognosis for each form of disease and how you will manage them?
Review key primary research regarding the role of Clostridium botulinum in the aetiopathogenesis of equine grass sickness?
There is evidence of the involvement of botulinum type C in the aetiopathogenesis of equine grass sickness due to the presence of botulinum C antibodies in cases confirmed with Equine Grass Sickness.
Found in 48% of ilium samples in horses with grass sickness, suggests there may be some involvement but nothing has been confirmed yet.
There is a theory that the botulism type C is reducing the immunity to equine grass sickness, this means there is a risk of horses that have been exposed to botulism C having an increased risk of developing Equine grass sickness.
Further discuss the link between Clostridium botulinum in the aetiopathogenesis of equine grass sickness?
The aetiology of equine grass sickness (EGS) is still unknown. There is increasing evidence that toxicoinfection with Clostridium botulinum type C is involved. Epidemiological evidence shows that resistance to EGS can occur in older horses and those that have been on a particular pasture for longer or have been in prior contact with the disease. This resistance may be in the form of an immune response to the aetiological agent. Levels of systemic antibodies to the surface antigens of C. botulinum type C (using the closely related and safe C. novyi type A as a phenotypic marker) and to the botulinum type C neurotoxin (BoNT/C) were investigated in horses with and without EGS.
Horses with grass sickness were found to have significantly lower levels of systemic IgG to both surface antigens and BoNT/C. Horses with low levels of systemic immunity to these antigens may be more susceptible to developing EGS. There were no significant differences in antibody levels between the different categories of EGS, suggesting systemic immunity to C. botulinum type C does not play a significant role in influencing the severity of the disease. However, horses that had been in contact with EGS or that were grazing land where it had occurred frequently in the past had significantly higher antibody levels to these antigens. These horses may have been exposed to subclinical doses of C. botulinum type C and BoNT/C, resulting in the production of a protective immune response against the putative aetiological agent. This finding is of potential significance for the prospect of prevention of EGS by vaccination against C. botulinumtype C.
