It is impossible to say with certainty that the outbreak of illness in Manchester was due to ergot, but the evidence available strongly supports the view that ergot was the cause. The train of symptoms and pathological changes, though not necessarily peculiar to ergot poisoning, are strongly suggestive of this origin and this conclusion is reinforced by the fact that all the sufferers consumed rye bread made from rye which contained a significant proportion of ergot. The ergot isolated from this rye, after being kept for many months under conditions which were unfavourable for the preservation of its toxic properties, was found at the expiration of this period to contain some toxin and the amount found was consistent with the ergot having been highly active when fresh and therefore quite capable of causing the outbreak of illness which developed at a period shortly after the harvest when the toxic properties of ergot are greatest.

As a result of my inquiry the following facts of interest have emerged:

1. A considerable quantity of rye is grown in England and Wales and more than half of it is allowed to ripen. The districts in which most of it is grown are Yorkshire, Lancashire, Cheshire, Monmouth and Essex. Rye in this country is seldom, if ever, free from ergot and the degree of infection varies from year to year in each district according to the season, weather, seed and other conditions.

2. Rye bread is eaten to a large extent (in Liverpool and Manchester at any rate) by Jews, and rye for these towns is obtained almost exclusively from Lancashire and Yorkshire.

3. The rye grain is usually not treated in any way before milling, that is to say, no attempt is made to remove any ergot which may be present; it is ground into meal in the condition in which it comes from the threshing machine.

4. On the assumption that some of the rye consumed in Manchester contained 1 per cent. of ergot, a half-pound loaf of bread of which this rye is a constituent would contain 4 to 5 grains of ergot. Although this is a relatively small dose, it is possible that if consumed over lengthy periods, especially if the ergot were in an actively toxic state, pathological conditions might ensue.

5. The samples of rye actually examined by the Public Analyst were not found to be toxic. This may possibly be accounted for on the ground that the method employed for extracting the toxin was not satisfactory, or to the fact that the ergot examined was at least six months old, by which time it would normally have lost most if not all of its toxicity.

6. Damp weather favours the growth of ergot and the climatic conditions of the summer of 1927 were just those most suited to the development of ergot. It is probable therefore that the rye crop was heavily infected and the ergot rich in toxins.

The clinical characters of the outbreak, so far as they have been recorded, strongly support the view that ergot was responsible; all the necessary factors and conditions for the production of illness were present and it is not surprising that it occurred.

In view of the potential danger the obvious preventive measures to which I have already referred should be put into operation. Rye crops should be grown with such precautions as to reduce the risk of ergot infection to a minimum. Millers of rye for human consumption should install the necessary machinery to remove, so far as possible, any small proportion of ergot which the rye may contain.