Equine grass sickness or EGS, also known as equine dysautonomia, affects horses at pasture, both free-roaming or domestic. It occurs especially in spring or at the beginning of summer and primarily affects animals from 2 to 7 years old. It is a degenerative neurological disease, affecting the nervous system and with a fatal outcome in 90 % of the cases. The causes of the disease remain to date largely unknown.
Grass sickness affects both wild horses and domestic horses. As its name implies it is associated to pasture.
The causes of this affliction have not yet been determined.Studies to discover the origin of the disease have been conducted on the following :
Poisonous substances produces by plants (cyanide in white clover) ;
Chemical toxins produced by bacteria, fungii (Botulinum toxin, mycotoxins ((Fusarium)) or of exogenous origin (nitrates).
Epidemiological studies do not enable us to discard a possible origin in telluric bacteria (bacteria in the soil). When there is a lack of selenium in the soil of the fields, there appears to be a higher prevalence of the disease. Some studies show a relationship between high iron, lead or chromium content in the soil, others with high titane content and low zinc/ high titane and low chromium… The disease has been associated to acidic soils with high nitrate levels.
The risk could possibly be higher in some sandy soils and in organically rich soils.
There does not appear to be any sign of the disease being contagious, even if several cases may be seen in the same studs ; these are due to exposure to the same environmental factors.
Animals living at pasture are more often affected than those stabled, or those alternating between field and stable. Animals between 2 to 7 years of age are the most affected. The disease is much less frequent in foals and in older horses. The breed or gender factors do not appear to have any significance.
There is a peak in the appearance of the disease in May (from April to June), which could be due to weather conditions (mild weather, dry with episodes of frost).
Geographical breakdown
First recorded in Scotland at the beginning of the 20ieth century, the disease is currently present in Northern Europe.
There are sporadic cases in France, but on occasion there are series of cases in a same stud or on a same field.
Symptoms
The disease can evolve following three patterns ::
Acute form, over 48 hours, and which has a fatal outcome (due to the stomach wall rupturing, or to a blood circulation shock) :
No temperature;
Violent colic, paralysis of the digestive tract (from the pharynx to the rectum) emission of large amounts of gas, difficulty swallowing (drinking), gastric reflux, hypersalivation (thick saliva around the corners of the mouth), distended small intestine, meteorisation ;
Sweating located on certain parts of the body (flanks, behind the elbow)
Tachycardia (between 80 to 100 beats per minute).
Sub acute form, in two to seven days ::
Rapid loss of weight, diffuse colic, anorexia, despondancy, sweating, dry droppings (with mucus), muscle twitching around the arm, the stifle)
Depression, eyelids dropping.
Chronic form, from more than a week to several months, the outcome is fatal in 90 % of cases :
Extremely thin ;
Listless attitude, with arched back
Purulent rhinitis, hypothermia ;
The rapid and drastic nature of the weight loss is one of the factors of a prognosis. Horses who do survive remain incapable of effort. Their miserable physiological state, (despite suitably supplementing their feed levels) often makes euthanasia being seen as the best solution.
Diagnosis and treatment
Differential diagnosis
In the acute phase, the first thing diagnosed is a typical bout of colic.
A bout of colic is often observed in the month prior to the onset of grass sickness.
In its acute form, grass sickness should be differenciated from rabies, from botulism ; in the chronic form, it should not be confused with a hepatic complaint, or with a high parasitical load.
Clinical diagnosis and additional examinations
A sore sheet based on clinical signs and epidemiological criteria has been established to decide whether a horse can be a good subject for additional diagnosis tests. In fact the tests which would enable a definite diagnosis to be established on a live animal are not very sensitive and are especially difficult to carry out : biopsy of the ileum, the rectum, the tongue, which show the neuronal degenertion in histology tests.
Even after the animal’s death, only a microscopic necroscopic examination (namely histology) of the lesions to certain ganglions, and lesions of the small intestine, can give a definite diagnosis. Diagnosis remains difficult however, due to the problems in taking samples in everyday situations.
In this disease, the presence of a neurotoxin in the serum of an animal with the acute form of the disease has on some occasions been noted. This examination can be requested from the reference laboratory, Clostridies at the Pasteur Institute.
Note : By the means of in vivo tests, it has been demonstrated that ingesting a large amount of the isolated neurotoxin does not lead to characteristic lesions. This shows that it is impossible to be contaminated by absorbing an already developed form of the toxin
Treatment
There is no specific treatmnet, only supportive treatment can be implemented. The horse must be stabled, and the other horses should be removed from the field.
Some medical tests have been carried out (antioxidants, stimulants for the intestinal motricty) but they do not give results which are satisfactory enough to be proposed as systematic treatment
Sometimes laparotomy surgery can be performed to relieve colic and to take ileum samples.
As the causes of the disease are largely unknown, the only advice proferred is based on the results of epidemiologial studies.
Good knowledge of the nature of your soil : some soils present higher risk, especially humus enriched soils or sandy soils ;
Favor the upkeep of animals by alternating between field and stable, and provide some dry fodder (the risk is higher during the first two months of being put out to pasture ;
Keep an eye on the body condition of the animals. The do-gooders and stressed animals are more at risk ;
Limit the number of grazing animals (there would no longer be a choice in selecting the plants to eat), and the frequency with which new animals are introduced ;
Keep poultry and feathered game off the fields ;
The risk appears to be greater near a stream.
A pasture where there has been a case of grass sickness, should be considered « high risk » for the following two years.
The presence of bovines in a field would appear to be a protection against grass sickness.
Medical prophylaxis
There is no medical prophylaxis to date, since, so far, the attempts to isolate an infectious agent have all resulted in failure.
To remember
Grass sickness is a multisystemic neuropathy associated to grazing which remains a challenge for research and for clinicians
Know more about our authors
Translated from french by : Karen DUFFY Translator
