The disease can affect any breed...

In the second part of our series on grass sickness, Fran Nunn, a scientist researching the links between the disease and Clostridium botulinum, updates the-racehorse.co.uk on her latest findings.

A relationship between C. botulinum and grass sickness was first proposed in the early 1900s. In the next few decades, research investigated plants, insects, viruses and fungi (mycotoxins) and it wasn't until the early 1990s that the botulinum theory was revisited.

The hypothesis is this - a (probably dietary) trigger causes an upset in the gastrointestinal bacterial flora. This results in C. botulinum type C being able to reproduce and produce the neurotoxin that causes grass sickness.

Initially, it was not known if the gut stasis was a cause or an effect of the disease, but evidence gained by the Medical Microbiology Group at Edinburgh University suggests that it is caused by the neurotoxin. Research also shows us that C. botulinum is present in many healthy horses' guts and therefore only causes a problem when conditions in the gut enable it to reproduce and produce toxins and/or the immune response of the horse to the toxins is insufficient.

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Clover link unlikely

The dietary trigger is unknown. For a while it was thought that clover may be to blame, but that now seems not to be the case. Weather conditions seem to play an important part in the incidence of the disease with outbreaks often following on from a period of dry, cool (often frosty) weather. One idea is that although the grass photosynthesises during this sort of weather, it can't grow efficiently which leads to higher levels of sugar accumulation in the leaves. A sufficient uptake of this sugar may be sufficient to upset bacterial gut flora and lead to C. botulinum growth.

Coupled with susceptibility in certain horses, i.e. stress, age, all of these factors may lead to grass sickness. As such, this is a multifactorial disease that makes research difficult and problematic. However, if it is C. botulinum causing the pathology of the disease, then it is that which could be targeted in treatment or prevention (vaccination) studies.

Vaccine needs backing

At present, the outlook for the treatment of the disease is much the same as it has been for the last few years.

Some chronic cases do go on to make a full recovery and certain horses even return to competition. Recovery though, can take as long as two to three years. Prevention would seem to be the best bet and there have been talks of a vaccine.

Any vaccine would have to be safety tested in horses and then tested in a double-blind clinical trial (whereby neither the owner nor the vet knows if they are giving a placebo). The numbers required for the study would run into thousands and it would require several staff working for a couple of years for follow-up analysis.

All of this could only be undertaken if a vaccine manufacturer could be persuaded to do it. At best, the vaccine would only be desirable in what a manufacturer would see as a niche market. Also, my colleagues and I are not convinced that a vaccine consisting of just the neurotoxin would be efficient - certainly our work indicates that a more complex vaccine, consisting of both neurotoxin and bacterial cell wall would be the most effective, but also the most difficult to licence and produce.