Equine Grass Sickness AKA Equine Dysautonomia

Note: Grass Sickness Vaccine Trial Pilot Study Announced "The Equine Grass Sickness Fund, The Animal Health Trust and the Royal (Dick) School of Veterinary Studies, University of Edinburgh are delighted to announce that a small pilot trial of a vaccine to protect against grass sickness has been approved by the Veterinary Medicines Directorate. A total of 100 horses and ponies have been enrolled for this pilot study, with thanks to the participating owners for their support.

This pilot study is in preparation for a full vaccine trial, which is likely to commence in 2013-2014 subject to securing sufficient funding, which will involve at least 1000 horses and ponies. We have great hopes that these vaccine trials will mark an enormous breakthrough in the prevention of this devastating disease. ..."

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Equine Grass Sickness is a rare but predominantly fatal illness in horses. Grass sickness affects all types of horses, ponies and donkeys and has affected some well known horses including the thoroughbred stallion Dubai Millennium.

History

The first cases of grass sickness were recorded in eastern Scotland in 1907.

Grass sickness is a polyneuropathy affecting the central, peripheral and enteric nervous systems. The majority of visible clinical signs are related to paralysis within the digestive tract although nerve damage occurs throughout the body. There are three forms of grass sickness:

1. Acute Grass Sickness (AGS) - Horses display signs of colic and require euthanasia or die within 48 hours.
2. Subacute Grass Sickness (SAGS) - Horses display clinical signs similar to AGS but with less severity and may survive up to 7 days.
3. Chronic Grass Sickness (CGS) - Horses present with severe and rapid weight loss and a selected portion of these cases may survive.

Clinical signs common to all subsets include: depression, anorexia, colic (moderate with AGS/SAGS and mild with CGS), excess salivation, constipation, nasogastric fluid secretion, patchy sweating, muscle tremors and eyelid drooping.

Diagnosis of grass sickness in the live animal requires a thorough clinical examination including a rectal examination. Definitive diagnosis can only be made at surgery (where biopsies of the gut are taken) or at post-mortem (where biopsies from the nerves are taken). Differential diagnoses for grass sickness are varied and include: any other cause of colic and weight loss, tying-up, laminitis, botulism, choke and dental problems.

There is no treatment for grass sickness. All cases of AGS and SAGS should be euthanised upon diagnosis as the condition is fatal. A proportion of CGS cases can survive following periods of intensive nursing. Overall the mortality rate of equine grass sickness is considered to be over 95%.

The cause remains unknown, however present research suggests that toxin production from the bacterium Clostridium botulinum type C is involved. Clostridium botulinum is a soil-borne bacterium, which may be better known for producing clinical signs of botulism. Research has suggested that Clostridium botulinum may cause grass sickness when the spores of C. botulinum type C are ingested and produce their toxin locally within the intestine.

The main risk factor for grass sickness, as the name may suggest, is grass. The disease is almost always seen in grazing animals, although there are isolated reports of the condition occurring in stabled horses. Grass sickness is most frequently seen in young horses aged between two and seven, and is particularly prevalent during April, May and June, and later in the autumn, after a spurt of grass growth.

Research has identified a number of other risk factors which may increase the likelihood of a horse developing grass sickness including: soil disturbance, worming with Ivermectin based dewormers, movement to new pasture, stress, grazing on a field which has previously produced a case of grass sickness.

Current research in equine grass sickness includes development of a nationwide surveillance scheme for grass sickness in Great Britain. This scheme hopes to identify all cases of grass sickness which occur from 2000 onwards. This scheme is run by the Animal Health Trust, in collaboration with the Equine Grass Sickness Fund, the University of Edinburgh and the University of Liverpool, following funding from The Horse Trust. More information on this scheme can be found at the dedicated website Equine Grass Sickness Fund.

The Equine Grass Sickness Fund is a dedicated charity raising funds to tackle the disease. Their website contains useful information regarding all aspects of grass sickness including management of chronic grass sickness cases.

Clostridium botulinum; Case-control Study

Reasons for performing study: Equine grass sickness is a high mortality disease which, despite many years of investigation, is of unknown aetiology. Recent findings indicating that the disease is associated with Clostridium botulinum require support from an epidemiological study that recognises and controls for potential confounders, e.g., age, time of year and premises.

Hypothesis: EGS is associated with low antibody levels to C. botulinum antigens.

Methods: A matched case-control study was conducted. Data were collected from 66 histologically confirmed cases of EGS and 132 premises-matched control horses. The probability of EGS in horses was modelled using conditional logistic regression.

Results: EGS was significantly associated (age-adjusted P<0.005) with low antibody levels to each of 3 clostridial antigens; C. botulinum type C and C. novyi type A surface antigens and a C. botulinum type C toxin complex toxoid. These serological risk factors for EGS remained highly significant when entered into multivariable models. This study also identified new horse-level risk factors for EGS; feeding hay or haylage was associated with a decreased risk of disease, change of feed type or quantity during the 14 days prior to disease was associated with increased risk, and the use of an ivermectin anthelmintic at both the ultimate and penultimate treatments was also associated with a significantly increased risk of EGS.

Conclusions: This study provides strong support for the role of C. botulinum in the aetiology of EGS and identifies managemental risk factors for the disease.

Potential relevance: Increasing anticlostridial antibody levels by vaccination and appropriate managemental interventions may decrease the risk of EGS occurring.

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