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After the infective nature of acute rheumatism has been accepted, there are still various views on the actual process of the disease. The bacteriological view is that the disease is a specific one produced by a specific organism. On the other hand, Chvostek, Singer, and others consider that rheumatism is not caused by a specific organism, but is merely an attenuated pyæmia, the exciting cause of which may be any one of the pyogenic cocci. Another view is that an unknown virus is the cause of simple uncomplicated rheumatism, and that a secondary infection with pyogenic cocci produces the cardiovascular lesions.

The author, accepting the view that the organism described by Netter, Triboulet, Wassermann, Poynton and Paine, and Ainley Walker is the specific agent of acute rheumatic fever, shows that by the experimental infection of animals with this organism lesions are produced which closely agree with those of the disease as they appear in the human subject.

Wassermann's "Streptococcus aus Chorea." This micrococcus was isolated originally from a child suffering from chorea. The organism grows as a streptococcus and is usually smaller than the streptococcus pyogenes. It will grow well on the ordinary nutrient media, but the author found that it grew best on alkaline beef broth and glycerin blood agar. After incubation on blood agar for twenty-four hours at 37 degrees C., small, discrete, colourless, and transparent colonies make their appearance, which in another twenty-four hours become somewhat flattened out, and after still further incubation grow down into the medium. About the second day the blood agar changes from a bright red colour to a dull brown or even greenish tint. This alteration in colour is due to the action of the micrococcus, as was proved by a control experiment; the change in colour only takes place where the organism is actually growing. It does not occur in cultures of the streptococcus pyogenes

of the streptococcus septicæmia, and is probably due to acid formation and the reduction of the oxyhæmoglobin by the micrococci of rheumatic fever. The micrococcus grows


on peptone agar i per cent. alkaline to phenolphthalein, on glycerin agar, and on peptone gelatin; the last medium is not liquefied. It will also grow in milk and broth, neutral to litmus, and in peptone broth i per cent. alkaline to phenolphthalein. Of the fluid media a growth is best obtained in glycerin veal broth, and is visible as a flocculent mass after twenty-four hours' incubation, which tends to settle at the bottom of the tube. When grown on solid media the micrococci are about 0.5 to 1 m in diameter, and form chains with eight to ten cocci in each chain. The individual cocci in these chains are usually arranged in pairs. After incubation for 48 hours at 37 degrees C., the organisms appear as diplobacilli, each bacillus apparently representing an individual pair of cocci. After longer incubation further involution forms are seen, small bacilli of irregular shape, about 2.5 to 3 p in length, and 0.5 to I in thickness, arranged in short chains. In the fluid media the chains do not consist of more than six cocci, sometimes grouped as diplococci.

These characteristics also apply to the micrococcus sent to the author by Dr. Ainley Walker and by Dr. F. J. Poynton. The organism isolated by Dr. Walker was obtained from the blood and urine of patients suffering from chorea, endocarditis, subcutaneous nodules, and arthritis, i.e., from patients suffering from acute rheumatism. Dr. Poynton's culture was obtained by incubating the valve from the mitral orifice of the heart in a fatal case of acute rheumatism.

In this paper the author describes in detail his own inoculation experiments on twenty-eight rabbits and two monkeys. For these experiments, cultures forty-eight hours old were used, and the life history of the particular cultures is given in

The rabbits were inoculated in various ways, for the injections were made into the veins, joints, and pericardium in different cases; the monkeys were inoculated intravenously.

The result of the innoculations was the production in these animals of all the changes which are found to occur in acute rheumatism. A microscopical examination of the diseased tissue of the infected animals was made in all cases, as well as of the exudations into the joints and pericardium, and in by

each case.

far the larger number of cases the specific micro-organisms were present. In one rabbit a film was made of the exudation from the iris; this showed the micrococci to be present, and cultures were obtained in a pure state from it.

This investigation shows that the three different streptococci isolated by Wassermann, Poynton, and Walker, from cases recognised clinically as undoubted rheumatism, all reproduced fully the stigmata of rheumatism in the rabbit and monkey. In no single case, among a large number of experiments, was there any abscess formation, though infarcts were often found. On the other hand in corresponding experiments with organisms isolated from cases of pyæmia in man, abscesses were found in the experimental animals and cardiac lesions were comparatively rare.

The micro-organisms, obtained in different ways from cases of rheumatic fever, are shown in this investigation to be able to produce arthritis, iritis, pericarditis, myocarditis, endocarditis, and pleurisy, with visceral infarcts, in animals, both rabbits and monkeys. “From this it naturally follows that the particular micro-organism in question, called the micrococcus rheumaticus by Walker, the diplococcus rheumaticus by Poynton, and the streptococcus aus chorea by Wassermann, is the actual infective and causal agent of acute rheumatism. Acute rheumatism is therefore of microbic origin, and the acute causal agent is a micrococcus closely resembling the streptococcus pyogenes in its chief characteristics."




A STUDY OF MESENTERIC OCCLUSION. By ROSWELL PARK, M.D. (Annals of Surgery, April, 1904).

PARK begins an important paper on this subject by relating details of two cases.

The first was that of a man, aged 45, who, while in apparently good health, was suddenly seized with severe abdominal pain. At the end of twenty-four hours the abdomen was rigid and distended, and the patient was collapsed and was vomiting a material, which had a coffeeground appearance; his pain, which had been very severe, was less. Abdominal section was performed, and it was found that the whole small intestine, from stomach to cæcum, was gangrenous; that there was gangrene of a part of the large intestine, and that the parietal peritoneum seemed almost as much involved as the visceral. Death occurred two or three hours after operation.

The second case was that of a woman, aged 33, who was suddenly seized with severe abdominal pain and vomiting. Park saw her at the end of thirty hours, when her abdomen was distended; she had fæcal vomiting and there was no passage of fæces or flatus. The abdomen was opened, and the whole small intestine was found to be gangrenous. The patient died at the end of forty-eight hours. No post mortem examination was allowed in either case.

Mesenteric occlusion was first described by Virchow in 1859. Occlusion of the mesenteric vessels is not easy to explain; but it must be remembered that, while the veins of the mesentery have no valves, the arteries, like those in the brain, are terminal, and collateral circulation is therefore not prompt or complete. After tying the superior mesenteric artery, the blood supply of the intestine is at once cut off. According to Gallavardin, the most frequent cause of mesenteric occlusion is mitral stenosis, the next most common cause being probably arterio-sclerosis. Falk collected records of seventeen cases of embolism of the intestinal arteries, and for purposes of

diagnosis it is important to remember that in every one of them there

was evidence of embolic disturbance elsewhere. Thrombosis of the mesenteric vessels is nearly always an extension of a primary lesion in the veins of the kidney, intestine or pelvis. It occurs after acute appendicitis, pyelophlebitis, intestinal ulceration, &c.; but, curiously, it is rare after typhoid ulceration. In typhoid the veins are often affected, but much more often those of the lower limbs than those of the intestine. It is not necessarily a main mesenteric artery that is occluded. The blockage may occur in a branch, and then results in an annular necrosis of the intestine over a greater or less area. As soon as the artery supplying a particular part of the intestine becomes plugged, there promptly ensues an anæmia of the gut, venous stasis and loss of contractility following. The extent of the gangrene may vary from a slight annular gangrene to a gangrene of a great portion of the bowel, as in the cases which Park describes.

Symptoms :-The first symptom is, as a rule, an absolutely sudden and very severe abdominal pain, sometimes paroxysmal, sometimes continuous. Vomiting occurs early; the vomited matter being bloody and often, after a short time, fæcal. There may be diarrhæa at first, but symptoms of obstruction

more common. The abdominal wall is rigid and meteorism soon makes its appearance. The patient's general condition is one of collapse.

When mesenteric embolism or thrombosis is suspected, one should search over the rest of the body for similar lesions elsewhere, as their discovery would add to the certainty of diagnosis.

Differential diagnosis is difficult or, indeed, almost impossible. A suddenly occurring gangrene of any abdominal viscus gives rise to practically the same symptoms.

As examples may be cited gangrenous appendicitis, acute necrosis of the spleen, acute necrosis of the gall bladder. Perforative lesions, too, as for instance perforation of a gastric ulcer, give rise to much the same symptoms. Hence Roswell Park lays stress on the importalice of obtaining, if possible, an accurate


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