LAST April, the colt Mister Baileys set a new record time for winning the 2000 Guineas 鈥� one of the five classic events in the English horse racing calendar. The three-year-old proved itself a top sprinter over the one-mile course at Newmarket. More unusually, Mister Baileys went on to finish fourth in the longer and more arduous Epsom Derby. This horse was at the top.
Mister Baileys鈥檚 performance was so impressive, in fact, that by the end of the flat racing season last autumn he was worth more off the track than on it. The owners retired Mister Baileys to the National Stud in Newmarket where a top-quality stallion can earn 拢6500 for 鈥渃overing鈥� a single mare. But a mere ten weeks after Mister Baileys鈥檚 arrival, disaster struck. The record-breaking stallion turned into a sickly bag of bones. Mister Baileys went down with a potentially deadly disease known as grass sickness.
Even though grass sickness was first identified at the turn of the century, its cause is still baffling veterinary scientists. In Britain alone, grass sickness kills at least 600 horses a year and debilitates an unknown number elsewhere. It is not discriminating and a child鈥檚 pet pony is as likely to suffer as a valuable racehorse. Toxins, produced by fungi living among the grass which horses eat, are the most probable cause. Currently the betting is on fungi of the group Fusarium as the culprits. But researchers must wait until they have more detailed data using tissue culture techniques borrowed from molecular biology before they can rule out other possibilities, such as the grasses themselves producing toxic alkaloids.
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Whatever the source of the toxin, its effect is devastating. It affects the nervous system, damaging the functioning of the autonomic ganglia. As a result, the illness paralyses the muscles in the horse鈥檚 intestines, making swallowing difficult and preventing the normal action of the gut. For horses with the acute form of the disease there is little hope of recovery, the stomach sometimes swells so much that it bursts and death usually follows mere days after diagnosis. Horses with a less severe form of the disease can survive if given the right drugs, intravenous feeding and a great deal of care and attention.
Northern exposure
The disease is common in Scotland, northern England and Scandinavia with a few cases each year being reported in Belgium, the Netherlands and France. There has also been one reported case in Australia, and in 1992 researchers in Argentina realised that mal seco, a condition that affected horses in Patagonia was most probably grass sickness.
The pattern of distribution provided the early clues to the cause of the disease. While no obvious environmental factor links all the places where grass sickness occurs, there does seem to be some connection between location and disease. Vets have diagnosed grass sickness in several horses grazing the same field, but only rarely in horses housed in stables. Affected animals may not have been on the land at the same time and the incidents may occur several years apart. The number of cases also varies at different times of year, with most occurring in early summer, and another, smaller peak in autumn. These clues suggested the cause would be found in something on the pasture land.
James Wood, a researcher with the Animal Health Trust in Newmarket, has searched hard for clues from the environment. He has just completed the first national survey of the factors accompanying grass sickness cases in horses. One of his key findings is that horses often come down with the disease after being treated against gut worms. But Wood doubts if there is a direct link between the worming procedure and the disease. Instead, he believes that the horses which are wormed more often are those that live on heavily grazed fields where they are more likely to pick up worm eggs shed by other horses. On these fields, where the grass is very closely cropped, horses might also be swallowing more soil containing the unknown agent.
Not surprisingly, researchers have first turned their attention to fungi, as they are well known to contain toxins and clostridial bacteria, which are known to produce poisonous chemicals. Studies of the autonomic ganglia bear this out. Although the ganglia are damaged, the cells within them show no signs of inflammation. This suggests that the paralysis is not the result of a bacterial or viral infection of the horse鈥檚 body, but that it is caused by a chemical poison that does not elicit an immune response.
The hard question is which one, and where does it come from. David Doxey at the Veterinary School at Edinburgh University has compared the fungi found in the guts of horses with grass sickness cases with those found in the guts of normal horses. No fungal species was unique to the affected animals. He thinks that the culprit is a common fungus requiring specific conditions to produce a toxin or that the affected animals are sensitive to a chemical produced by a particular strain of fungus.
The latest research suggests that Fusarium might be to blame. Thanks to a grant from the European Commission, teams from the Argentinean National Institute of Agricultural Technology and from Scotland were able to get together and compare data. The fact that Scotland and Patagonia are so far apart provides a good opportunity to rule out many factors, such as the fungi and bacteria that are known to be exclusive to one or other of these areas.
Jean Robb, formerly a microbiologist at the Scottish Agricultural College, and now a 鈥渞etired鈥� freelance scientist working from Tweedsmuir, has been to Patagonia and collected samples of soil and foliage from both countries. In both sets of samples she found similar strains of Fusarium, which is known to produce toxins under certain circumstances.
Testing whether Fusarium is to blame would be a nightmare, if all the experiments had to be conducted with live horses. Fortunately, Huw John, a cell biologist researching grass sickness at the Moredun Research Institute near Edinburgh, has come to the rescue. He has developed a culture of equine nerve cells that can be used in the hunt for the toxin.
Nerve cells are notoriously difficult to grow in culture, and they often die before researchers can run their tests. But John has immortalised them by introducing growth-promoting genes into fetal horse cells using a retrovirus. The retrovirus invades the cell and inserts its package of genetic material into the DNA of horse nerve cells. The particular gene he has introduced is temperature sensitive. That makes it possible for him to put cultured fetal cells into a dish at the temperature at which the growth promoting gene is active and keep them growing continuously. He can then take some of these immortalised cells and raise the temperature to switch off the gene he has introduced. The cells stop dividing and differentiate into nerve cells. By this clever technique, John can provide a constant supply of horse nerve cells for use in experiments.
The great advantage of John鈥檚 technique, which is new to veterinary researchers, is that it makes it possible to carry out simultaneous tests in the laboratory on a whole range of potential toxins. Already. he has done the obvious thing and tested Fusarium extract. The result: it has a lethal effect on the nerve culture. Does that mean that the cause of grass sickness can be announced? Unfortunately not, explains John. The next step will be to identify the actual toxin in Fusarium extract that kills the nerve cultures, then researchers will look to see if this toxin is in the autonomic ganglia of horses that have died from grass disease. Only then can he be fairly sure of the cause.
It is possible that although Fusarium extract kills nerve cells in culture, it never reaches a damaging concentration in the live horse. Although horses eat huge amounts of grass in a day, it is far from proven that enough Fusaria grows among grass for it to be dangerous. It could turn out, says John, that they must look elsewhere for the cause of grass sickness. The build up of alkaloids from plants, including grasses, could be a possibility and another collaborator, Robert Nash at the Institute of Grassland and Environmental Research in Aberystwyth, is using gas chromatography and mass spectroscopy to search for alkaloids in the ganglia of horses that died from grass sickness.
Extra clues are coming from Katherine Whitwell, a veterinary pathologist and a former colleague of Wood at the Animal Health Trust, who has taken a slightly different approach in her bid to identify the cause and reduce the incidence of grass sickness. She has identified a disease in hares which has the same pathology as grass disease and which often occurs in the same places.
This research may be directly helpful as an early warning system, alerting horse owners to the existence of the agent that causes grass sickness. But Whitwell also believes that it should be easier to find the culprit in a small animal like a hare than in a large one like the horse. Already, John has found that blood serum from hares affected by the disease kills his cultured horse nerve cells. Analysing the serum should thus provide extra information about the nature of the toxin.
For now, Mister Baileys appears to be winning his battle against grass sickness. Fed by a stomach tube on a diet including guinness and cottage cheese, he is gradually regaining his strength. And although his racing days are certainly over, his vets are confident that a more sedentary, but no less important career in the Newmarket stud, could still be on the cards.