Dr. Einhorn further describes a series of test experiments mad upon healthy persons, with the result that, in each case, after the application of direct faradism there was a marked increase i acidity. The conclusion that the faradic currents increase th production of the gastric juice seems to be justifiable.

As regards clinical experience, the most marked results hav been obtained in cases of dilatation, and also in chronic gastri catarrh; the improvement in the latter cases being demonstrabl by chemical analysis. Two cases especially are to be noted c very aggravated chronic gastric catarrh in which free HCl coul never be found after the test meals; the same could be easil detected after the stomach had been faradised internally for te minutes. Dr. Einhorn also mentions two cases of pure gastralgi which derived benefit from the internal application of the galvani

current.

I cannot pretend to have offered to you in this paper anythin original, or even anything particularly novel; but I was desirous bringing before the Section, however imperfectly, a subject which in the course of some reading and a little observation, had been c particular interest to myself.

ART. VI.-Some Recent Modifications in our Views of Enter Fever and its Treatment." By M. A. BOYD, M.D., F.R.C.S.I M.R.C.P.I.; Physician, Mater Misericordiæ Hospital, Dublin. SINCE Murchison wrote his classic treatise on Enteric Feve we have added almost nothing clinically to the accurate an scientific description he gave of the disease. He covered in tha description almost the entire ground in connection with the diseas and its history, and in the closeness of his reasoning as to it ætiology he foreshadowed all that bacteriology has since discovere regarding it. In fact, it is only in its bacteriological aspect tha any additions have been made to the subject, and it is from thi side alone that any additional knowledge is likely to come whic can finally determine the mode of its origin. The additiona bacteriological data, however, we now possess have considerabl narrowed the issues, and enabled us to regard the disease from th standpoint of being an acute infective disease which heretofor

Read before the Section .of Medicine in the Royal Academy of Medicine Ireland, on Friday, December 18, 1891.

it was not considered, in which, like phthisis and pneumonia, a special bacillus plays the important part.

Since that bacillus was discovered by Koch and Eberth, and its peculiarities and mode of growth were studied, more especially by the latter observer, our views as to the etiology of the disease have considerably changed, and the time has, I think, now come when, taking advantage of the experiments of various other bacteriologists, in addition, we may form more definite ideas as to its mode of propagation, to its prevalence at particular seasons, and the causation of the symptoms present in its various stages, as well as to suggest some rational means for treating it.

I shall first refer to the typhoid bacillus and its discovery. In 1880 Koch and Eberth almost simultaneously discovered in the intestines, the mesenteric glands and lymphatics, and especially in the spleen of patients dying of enteric fever, a bacillus, which, though frequently found in the intestines as the common Bacterium termo, assumed at particular seasons, or owing to some alteration in the normal vital resistance of the individual, an acutely infective process, infiltrating the adenoid tissue and lymphatics of the intestine, accompanied by the chain of febrile phenomena we designate typhoid or enteric fever. Owing to the difficulty of finding a suitable nutrient medium on which to grow it outside of the body, this bacillus could not be differentiated from other bacteria inhabiting the alimentary canal until Koch succeeded in isolating and growing it on dry gelatine plates; since then all pathologists are familiar with its appearance and mode of growth. So far all experiments have failed in producing the disease from these cultivations by inoculation; but bearing in mind it grows both as an aerophyte and as an anaerophyte, it may be innocuous in the former condition and infectious in the latter when in the alimentary canal, when the vital resistance of the tissues in that situation may be from some reason altered. What may produce these alterations I shall allude to presently. Gaffky, in his observations on this bacillus, has given us some valuable information as to its situation and growth. It is one of the few bacilli found to develop freely in water, and it grows abundantly in milk. He also found it in the soil through which water percolates, and it grew freely in all albuminous media. He also found it more abundant in all these media in the autumnal season more than any other—a fact of considerable importance. If, however, this bacillus is found so frequently in the food we eat, the water we drink, and in our

I

intestines, how, we may ask, is it that it does not infect the intes tinal glands when present and produce enteric fever in every case For we must all take it in at some time or other if it is not alread present in our intestines. With this question I may link tw others why is it we do not suffer from pneumonia constantl when we always carry about with us the germs of the disease i Fränkel's diplococci; or why not frequently suffer from circum scribed or diffuse suppurations when the micrococci that produc them are frequently present in our blood or tissues?

Why we do not, recent investigations in bacteriology have mad clear. Bacilli or micrococci are in themselves harmless either i the blood or tissues until the vital resistance of some tissue i lowered, from either functional alteration or injury, when the readily find a suitable soil in it on which to grow and multiply It is by this growth and the chemical products generated during i that the mischief is produced, and the poisoning of the tissue around that are most susceptible to its action afford a further fiel for the growth of these micro-organisms.

Let me take, first, the experiments of a distinguished physiolo gist, and, secondly, the course of a fatal disease, with which, clini cally, we are only lately becoming familiar, to illustrate my meaning Professor Kocher, of Berne, in making experiments on animals b destructive injury to tissues, down even to the marrow of bone: with a hot iron, could not produce septic inflammation as long a the animal experimented on was healthy, but if he lowered th vitality of it by feeding it on putrid matters, permitting thereb septic micrococci to enter its blood, a septic inflammation was a once produced. The other disease I have alluded to in illustra tion-namely, septic or suppurative endocarditis-we know arise from either the staphylococcus or streptococcus when present i the blood from any accidental cause, finding a nidus in an inflame endocardium or damaged valve, and the chemical product of it growth is then wafted in the blood current to set up mischief i other situations, where, from anatomical causes or lowered vita resistance, the blood and tissues cannot overcome its invasion The germs of typhoid fever, like all other septic germs, are no regarded as in themselves harmless as long as the tissues wit which they are in contact are healthy, else how can we explain th immunity from the disease that exists in healthy individuals wh constantly either receive them through food or drink into th alimentary canal, or have them as a normal and constant resident

This brings me to the vexed question of the etiology of the disease. If we take it for granted that the bacillus of Eberth is, by its infiltration of the glandular tissue of the intestine, the cause of all the mischief (and, apart from the absence of the inoculation evidence, most pathologists are agreed that this is so), what are the conditions that favour or produce its acute infection of those glands?

We have, first, the evidence that this bacillus is found growing most luxuriantly, and, we must presume, consequently that it is more virulent and more capable of making a vigorous battle for its existence, in the autumn. But it must find the tissues with which it comes in contact in a weakened condition to get the upper hand in the struggle.

Are the intestines at this period of the year in a more weakly condition than at any other, and, if so, from what cause? I think we can answer that question in the affirmative.

How

Most of us are familiar with the gastro-intestinal troubles that are characteristic of the early autumn months, the gastrointestinal catarrh especially; the catarrhal or autumnal diarrhoea; and the frequency of so-called bilious attacks at this season. these catarrhs are produced we have a ready explanation in the rapid fall of temperature in the evenings, after, perhaps, a warm mid-day, when the action of the skin is suddenly checked, and no additional precautions as to clothing are adopted. All hospital physicians are familiar with the sudden onset of bronchial catarrhs at this season also, from the same cause, and the rapid filling of hospital wards with cases of asthma, emphysema, and fresh bronchopneumonia in cases the subjects of phthisis during the previous summer and spring. Now, let us see if this gastro-enteric catarrh is a usual precursor of enteric fever. Murchison, with that acute power of observation which was characteristic of him, mentions it as a most usual symptom preceding and accompanying the fever in its early stages; and he further adds that catarrhal diarrhoea was frequently present preceding the fever, and that it was often difficult to say whether the disease would remain catarrhal diarrhoea or end in enteric fever. Now, it seems to me that this catarrh, in addition to being brought about by atmospheric changes or by food, may be produced also from the absorption of the chemical products of the typhoid bacilli growing on the intestinal contents, when present in large numbers in either food or drink containing them; and that this ptomaïn or toxin was only the weapon they used-as

Professor Burdon Saunderson expresses it-in their struggle for existence to weaken the vital resistance of the tissues with which they were in contact, and make it fall an easy prey. Why, however, should the glandular tissue be the first overcome in this struggle? The reason seems to me obvious, looking at it from a pathological point of view. Adenoid tissue is endowed with a very poor vitality, and very little power of resistance or of repair, when infiltrated or choked from any cause. We see this when it is attacked by a similar bacillus, the tubercular one, whose life-history and the readiness with which it infiltrates and destroys glandular structures, are somewhat similar to the typhoid one in many ways. The epithelial shedding and proliferation of the mucous membrane which takes place must also weaken the defences against the bacillary invasion. The bacilli find the glandular tissue in a condition of derangement from the effects of this catarrh, and i becomes the centre of their habitation.

That this invasion is sudden, and followed by rapid changes in the glands, there can be no doubt. Murchison, for example, found infiltration and swelling of the glands in the case of a patien dying on the second day of the disease, and other observers bea similar testimony.

The entire process in connection with the gland, so far as th typhoid bacillus is concerned, from the time of invasion to death o disablement of the gland, is over in fourteen days-the normal tim of enteric fever from a pathological point of view. After this period however, a new set of enemies appear on the scene in the shape o the suppurative micrococci, which, forming colonies on the injure or necrotic tissues around the glands, begin to generate their pecu liar toxins, producing the hectic character of the symptoms an temperature with which we are all familiar after the first fortnigh of the disease, so that we must regard enteric fever as the resul of the growth in the intestines of two sets of micrococci-th so-called typhoid bacilli producing the symptoms during the fir fortnight, and the suppurative micrococci producing the chara teristic symptoms of its further stages. That other micrococci, well as these latter, occasionally infect the patient from the inte tinal canal, there can be no doubt; and I have at present und my care in the Mater Misericordiæ Hospital a patient with a wel marked attack of erysipelas of the face, in the fourth week of b enteric fever.

If recent bacteriological work has enabled us to grasp these fac