Ladies and Gentlemen,—I thank you unaffectedly for the great, and, I feel, undeserved honour that you have done me in making choice of your President for the coming year.

In spite of attempts at classification, most observers will agree that the disease known as neurasthenia has no definite boundary line. However strict an attempt is made to define its limitations, everyone who has to do with these cases must admit that the symptoms frequently merge into those associated with other conditions, such as those known as psychasthenia, melancholia, hypochondriasis, anxiety neuroses, obsessions and others. Even hysteria in its less pronounced forms is not always easy to separate from neurasthenia, and in not a few instances some of the salient features of both diseases may be present at the same time, and that this close association is recognised is shown by arguments that have occasionally been put forward for placing the disease known as traumatic neurasthenia into the category of traumatic hysteria. All classification is artificial and provisional, but useful and necessary as it is for studying the general group aspects of disease, there is the danger of over-estimating its importance, and of being tempted to feel the necessity of labelling a disease and then treating it according to such rules as are applicable to the label which has been placed upon it.

The occurrence of micro-organisms in the urine is well known to be associated with a variety of pathological conditions, among which mental diseases have been included. A definite connection between urinary bacteria and insanity, however, does not seem to have been made out, the subject being even more obscure than the relation of the intestinal flora to mental disease, which has been much more frequently investigated.

Except in asylums, dysentery in this country is a rare disease to-day. Yet it was once far otherwise, and to our ancestors the “bloody flux” was a household word. It was endemic here from the earliest times, and as we follow it down we find that it always presents the same characteristics of bursting out in an epidemic form at fairly regular intervals, then dying down to isolated cases for a longer period until the cycle was complete for the next outbreak. It was only in the latter half of the nineteenth century that it vanished from our midst, and so complete has been its departure that it has also disappeared from our memories, and to-day we have forgotten what a virulent pestilence it once was.

Since 1901, when Kruse first isolated his so-called “pseudo-dysenteric” bacilli from an institution outbreak of dysentery in Westphalia, much research on the subject has been carried out in Germany and in the United States, and the bacteriology has been well established. In this country, however, comparatively few outbreaks have been investigated, and of these only a few can be considered satisfactory. As a matter of fact, most of the early work is valueless, as non-selective media alone were used for isolating the supposed organism. Thus in 1898 Dr. Goodliffe investigated an epidemic in the Lancaster County Asylum, and came to the conclusion that it was due to a bacillus resembling B. coli, which he styled “the bacillus of ulcerative colitis.” A similar view was held by Dr. Gemmell in his monograph on the disease. Campbell, working at Rainhill in 1899, cultivated from the fæces of eight dysentery patients an organism which was almost certainly of the coli group, and regarded by him as a very likely cause of the disease. Although conversant with the writings of Chantemesse and Widal, who were the precursors of Shiga and were then actually working on B. dysenteriæ, he apparently failed to realise the significance of their investigations. In 1899 also, an outbreak at Mickleover Asylum was the subject of research by the Medical Superintendent, Dr. Legge, and Dr. Barwise, M.O.H. for Derbyshire. What was termed a “virulent” form of B. enteritidis sporogenes was here regarded as the cause of the disease, having been isolated from eight cases; but a “non-virulent” form was also found in the stools of healthy patients. All these observers, so far as I can gather, employed agar only for primary cultivation, and none of them carried out any satisfactory agglutination tests. In the first volume of Mott's Archives of Neurology, Durham published the results of some work emanating from the Claybury laboratory. He claimed that from the blood, bile and certain abdominal viscera of seven out of eight patients who had died from dysentery he had cultivated a coccus so minute that it was able to pass through the pores of a Berkefeld filter. Cultures were never made from the fæces; subcultivation in a series of generations was found impossible; and the results of agglutination and animal experiments were negative. Dr. Eyre, of Guy's Hospital, was certainly the first in Britain to show asylum researchers the way to a sounder bacteriological knowledge of the disease. Using the Conradi-Drigalski medium, in 1904 he recovered Shiga's bacillus from the fæces of four out of five Claybury patients suffering from the acute form of the disease, and post-mortem from two out of four additional cases, agglutination being obtained with the organisms, and an anti-dysenteric serum in a dilution of 1–200. As the result of further investigation, he found the bacillus of Flexner also present in several of the series, and in a private communication stated that he had detected it altogether in six out of nine acute, and fifteen out of thirty-five chronic cases, none of the latter yielding Shiga's bacillus. Hewlett (1904) tested the sera of two asylum dysentery patients with B. dysenteriæ (obtained from Flexner), and obtained a positive result in 1–50 in one case and 1–100 in the other. In a paper read before the Royal Academy of Medicine in 1905, McWeeny described a bacillus of the mannite-fermenting dysentery group which had been isolated from a severe (subsequently fatal) case in Clonmel Asylum. This organism was noteworthy, inasmuch as it produced no indol, and caused the death of several rabbits while an attempt was being made to immunise them. In the following year Candler, of Claybury, investigated the fæces of six cases suspected to be suffering from acute dysentery. “In five of them an organism resembling the Flexner type was isolated and submitted to the usual tests. The sixth was subsequently proved to have intestinal tuberculosis.” As the result of an examination of five cases occurring in one of the Sussex county asylums in 1908, Bushnell, using Conradi plates, found no dysentery bacilli present, but his report is short and incomplete. An important research was made by Aveline, Boycott and Macdonald of the Lister Institute in 1909. They obtained specimens of dysenteric fæces from Cotford Asylum, and from seventeen out of nineteen Flexner's bacillus was recovered. The spleen and mesenteric gland of a fatal case yielded it also. MacConkey's bile-salt-lactose-neutral-red agar was employed for separation of the organisms by these investigators for the first time in this work. Agglutination was obtained with patients' serum and organisms up to 1–200 and 500, and a multivalent dysentery horse-serum was shown to agglutinate in a dilution of 1–1,000, and when tested to 1–10,000, time allowed being two hours.

Few authorities on mental disease are agreed as to the part played by syphilis in causing mental deficiency. Similarly, the cause of epilepsy, although it is one of the oldest known diseases, has remained undetermined by the methods of investigation hitherto employed.