Grass Sickness in Horses
Dr. E. Milne, BVM&S, PhD, MRCVS
INTRODUCTION
Grass sickness is a disease of horses, ponies and donkeys in
which there is damage to parts of the nervous system which
control involuntary functions, producing the main symptom of gut
paralysis. The cause is unknown but the nature of the damage to
the nervous system suggests that a type of toxin is involved. The
disease occurs almost exclusively in horses with access to grass.
The disease was first recognized about 1907 following an outbreak
in army remount horses near Dundee. The incidence increased
markedly and at least in Scotland, hundreds of horses, mainly
draught animals, died annually from grass sickness in the 1920s.
It is said that the losses were so severe that the introduction
of tractors was artificially accelerated as a result. In the
1990s, grass sickness continues to kill horses of all breeds and
it has been estimated that approximately I in 200 die annually
from the disease in Scotland. Grass sickness has been a research
interest of the Moredun Foundation for many decades and an active
Grass Sickness Research Team involving collaboration between the
Moredun and the Royal (Dick) School of Veterinary Studies
(R(D)SVS) has been in existence since 1986.
DISTRIBUTION
Great Britain has the highest incidence of grass sickness in the
world but the disease is well recognized in northern Europe,
especially Sweden, Denmark and Germany, with fewer cases in
France, Belgium, Italy, Holland, Norway and Switzerland. The
disease has not been authentically reported from Africa,
Australia, Asia or North America but a condition
indistinguishable from grass sickness called mal seco (dry
sickness), has now been recognized in Argentina, the Falklands
and Chile. Within Great Britain and Ireland, there is a pattern
of distribution. The highest incidence is in eastern Scotland,
particularly Perthshire and Angus with many fewer cases in the
west. It is often erroneously stated that grass sickness is a
Scottish disease but it occurs in most parts of England and
Wales, albeit less frequently. As in Scotland, eastern England
has more cases and grass sickness is a significant problem in
many areas including Northumberland, Yorkshire, Co. Durham and
East Anglia. It does not seem to occur in Ireland.
SPECIES, BREED AND GENDER
Grass sickness affects horses, ponies and donkeys, and there have
even been cases in a captive zebra and a Przewalski's horse. It
used to be thought that Clydesdales were more susceptible and
that Shetland ponies and thoroughbreds were resistant but this
has been disproved and the incidence in different breeds reflects
their numbers in the general population in the worst affected
areas of the country. Mares may be at slightly less risk than
stallions and geldings but this is still under investigation.
ln the early 1990s, a disease almost identical to grass sickness
was discovered in hares, some of which occurred on pastures where
there had been recent cases of the equine disease. However, there
is no evidence that hares and horses can pass the disease to each
other.
AGE
Grass sickness occurs in all ages from 4 months to over 20 years
but the greatest number of cases occurs in 2 to 7 year olds with
a peak at 3 to 4 years. The reason for the age distribution is
uncertain although young foals presumably are not affected
because they are not consuming sufficient herbage with which the
disease is associated. The lower incidence in older horses
suggests that animals exposed to the causative agent may develop
a degree of resistance to the disease.
SEASON
Cases occur in every month of the year but most are seen between
April and July with a peak in May. In some years, a second,
smaller peak occurs in the autumn or winter. At least in
Scotland, the lowest incidence is in August which may be a
weather-associated effect (see below).
FEEDING
Grass sickness, as its name suggests, is strongly associated with
grazing but there have been a few cases in animals with no access
to pasture. In these rare cases, hay has been implicated as the
source of the causal agent. Although most cases have been at
grass full-time or during the day, the disease can affect horses
which have only a few minutes' access to grass daily. There is no
association with type of pasture (new ley, permanent pasture,
hill grazing, clean or 'horse-sick' pasture) nor with
fertilization. Giving supplementary feeding in the form of
concentrates or hay does not have a protective effect.
PREMISES
It is well recognized that certain premises, or even fields
within single premises are associated with the occurrence of
grass sickness cases. The reason for this is unknown and much
effort has gone into comparing 'good' and 'bad' fields especially
with respect to the plant and fungal species present (see below).
Animals which have been on an affected premises for less than 2
months are more likely to develop the disease. Commonly, only one
animal is affected at a time but 'outbreaks' of the disease with
several cases in a period of a few weeks are not infrequent.
PREDISPOSING FACTORS
Stress appears to be a factor in predisposing to the disease and
a significant number of animals have a history of recent stress
including recent purchase, mixing with strange horses, traveling
a long distance, breaking and castration. Animals in good to fat
condition also appear to be predisposed.
Many horse owners have firm opinions about the type of weather
prevailing when grass sickness cases occur. In a survey of
weather conditions in the two weeks preceding multiple-case
outbreaks, it was found that cool, dry weather with a temperature
between 7 and 11oC was recorded in a statistically significant
number of instances. This may partly explain the higher incidence
of the disease in the eastern side of Britain where such
conditions are more prevalent and the low incidence in August,
the wettest month of the year in Scotland.
Preliminary results of a recent survey suggest that the risk of
developing grass sickness is slightly higher in horses which are
wormed more frequently. However, it should be emphasized that the
consequences of not worming can be very serious or even fatal and
it is not suggested that owners should decrease their use of
wormers. There is also no indication that wormers themselves
contain the toxin that causes grass sickness.
CAUSAL AGENT
The cause of grass sickness is unknown despite almost 90 years of
investigation. Many potential causes have been examined over the
years including poisonous plants, chemicals, bacteria, viruses,
insects and metabolic upsets but none has survived scrutiny. A
common suggestion by horse owners is that mineral or vitamin
deficiencies may be the cause but studies have not shown any link
with the disease. It does not appear to be contagious and the
type of damage to the nervous system suggests that a toxic
substance rather than an infectious agent is likely to be
involved. Circumstantial evidence is accumulating, including the
weather conditions associated with the disease, to suggest that a
fungal toxin is a likely candidate.
Currently, the Grass Sickness Research Team is investigating the
distribution of microscopic fungi growing on the herbage in
affected pastures. Early results suggest that a fungus called
Fusarium is always present on pastures where grass sickness has
recently occurred but it is too early to
state whether it has a direct relationship with the disease.
Fusarium species can also be found on pastures in Argentina.
Studies are also underway to determine whether these and other
pasture fungi produce toxins capable of damaging isolated horse
nerve cells grown as a culture in the laboratory. However, other
possible causes have not been discounted and the involvement of
clostridial bacteria is also being investigated.
CLINICAL SIGNS
Grass sickness occurs in three main forms, acute, subacute and
chronic, but there is considerable overlap in the symptoms seen
in the three forms. The major symptoms relate to partial or
complete paralysis of the digestive tract from the oesophagus
(gullet) downwards. In acute grass sickness, the symptoms are
severe, appear suddenly and the horse will die or require to be
put down within two days of the onset. Severe gut paralysis leads
to signs of colic including rolling, pawing at the ground and
looking at the flanks, difficulty in swallowing and drooling of
saliva. The stomach may become grossly distended with
foul-smelling fluid which may start to pour down the nose.
Further down the gut, constipation occurs. If any dung is passed,
the pellets are small, hard and may show a 'cheesy' coating of
mucus. Fine muscle tremors and patchy sweating may occur. In this
form, the disease is fatal and the horse should be put down once
the diagnosis is made.
In subacute grass sickness, the symptoms are similar to those of
the acute disease but are less severe. Accumulation of fluid in
the stomach may not occur but the horse is likely to show
difficulty swallowing, mild to moderate colic, sweating, muscle
tremors and rapid weight loss. Small amounts of food may still be
consumed. Such cases may die or require to be put down within a
week, or may progress to the chronic stage.
In chronic grass sickness, the symptoms come on more slowly and
only some cases show mild, intermittent colic. The appetite is
likely to be reduced and there will be varying degrees of
difficulty in swallowing but salivation, accumulation of fluid in
the stomach and severe constipation are not a feature. One of the
major symptoms is rapid and severe weight loss which may lead to
emaciation. Previously, it was thought that nearly all such cases
died and that the few which survived made only a partial recovery
and were subsequently useless for work. This is now known to be
incorrect (see section on treatment).
DIAGNOSIS
The symptoms described above may seem quite clear-cut but
unfortunately not all affected animals show all these signs and
it can be sometimes be very difficult for the veterinary surgeon
to distinguish grass sickness from other causes of colic,
difficulty in swallowing and weight loss. This is compounded by
the fact that there is no non-invasive test for diagnosing the
disease in the live animal although certain blood tests
(haptoglobin, cortisol and catecholamines) and examination of
peritoneal fluid can be helpful, when considered together with
the symptoms. A definite diagnosis can be made only by
microscopic examination of nerve ganglia after death or by
surgical removal of a piece of small intestine by opening the
abdomen. Characteristic degenerative changes in the nerve cells
can then be demonstrated in the tissues.
TREATMENT
As previously stated, treatment should not be considered in acute
and many subacute cases. However, in chronic cases, if the
animals are not in much pain, can still cat at least a small
amount and are still interested in life, treatment of chronic
cases can be attempted. The correct selection of potentially
treatable cases using these criteria requires experience but is
essential.
Not all chronic cases are treatable. The management of
selected cases has been the subject of study by the Grass
Sickness Research 'ream since 1989 and the results have
challenged the view that chronic cases either die or at best only
partly recover. Treatment of chronic cases involves provision of
palatable, easily swallowed food e.g. chopped vegetables, grass
and high energy concentrates soaked in molasses. It is essential
that high energy foods are consumed as chronic cases fed
roughages and succulents alone will invariably die.
Nursing is also vital and provides the mainstay of management.
The patients require constant stimulation by human contact,
frequent grooming to prevent them becoming scurfy and sticky
with sweat and, in some cases, rugging which has been found to
reduce sweating and prevent hypothermia.
A trial using cisapride, a drug which is
used to increase gut activity in man, has been completed
recently. The results indicate that when given by mouth to horses
with chronic grass sickness, cisapride increases the activity of
the partially paralysed gut. Although cisapride does not cure
grass sickness it is a valuable part of the management of chronic
cases. Unfortunately, it is of no help in acute and subacute
disease. By careful attention to the management regime we have
developed, the recovery rate for carefully selected cases in the
R(D)SVS Large Animal Hospital is now approximately 70% and
veterinary practitioners in the field are now reporting success
when following the same regime. Contrary to commonly held views,
a follow-up study has shown that 41% of these recovered cases
were back to work including hunting, racing, eventing, 33% were
being hacked, preparing for competitive work or being used for
breeding and the other 26% (the more recent cases) were still
gaining weight and recovering at the time of the survey. None of
the survivors were described as being of no use. This represents
a major improvement in the prognosis for such cases compared with
the situation before the late 1980s.
PREVENTION
Until the cause is known, it is difficult to give sound advice
regarding prevention. In areas where the disease is prevalent,
stabling the animals during the spring and early summer will
reduce the likelihood of disease. Following the discovery of an
association with weather, some owners living in affected areas
now stable their horses when dry weather with a temperature of
7-11 oC has persisted for 10 consecutive days. Stabling is
particularly advisable for a new horse which has been moved onto
a 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.
CURRENT RESEARCH
The Grass Sickness Research Team is currently undertaking several
lines of investigation. (1) The development by Dr. Huw John at
the Moredun Research Institute, of a laboratory culture of the
type of nerve cells damaged in grass sickness opens up the
possibility for testing many potential causal agents simply and
cheaply. The initial stages of the work were supported by the
Grass Sickness Fund and the project is now funded by the
Horserace Betting Levy Board. (ii) The pattern of damage to the
nerve cells in different parts of the gut is being mapped out
which should help to elucidate how the causal agent spreads round
the body. (iii) The work on the management of chronic cases is
continuing and a nurse is employed full-time to look after these
animals. These studies are generously supported by the
International League for the Protection of Horses and the Grass
Sickness Fund. (iv) A study of the fungal species on grass
sickness affected and non-affected pastures in the U.K. and
Argentina is being made and the toxins they produce are being
tested on cultured nerve cells. (v) The possible involvement of
bacterial toxins in grass sickness is being evaluated and is
funded by the Horserace Betting Levy Board.
