1915 The Lancet  
1138 bactericidal agent being a filterable and dialysable substance inactivated at a temperature of 97° C. It is in connexion with its power to check the growth of the cholera vibrio, however, that this coccus has chiefly claimed attention. Metchnikoff 4 has long entertained the idea that individuals who escape cholera, when that disease is rife in a community, may owe their protection to the presence in the intestinal canal of these air-borne cocci o of other organisms, like bacillus
more » ... bacillus pyocyaneus, antagonistic to the development of the vibrios. This suggestion was recently taken up by Choukevitch,' who infected with cholera vibrios several rabbits which had previously ingested large numbers of the " anti-cholera cocci with their food. Although the rabbits developed cholera and died like the control animals no inference could be drawn from the experiment, since postmortem examinations did not indicate that the "anti-cholera" cocci had been able to survive in large numbers and maintain a vigorous growth in the intestinal canal. Whether or not the future will establish this conception with regard to cholera it would seem probable that the principle of bacterial antagonism will be found to have other, and perhaps therapeutically useful, applications in the wide field of microbic infections. Two examples readily suggest themselves in connexion with meningococcus infections. First, it may well be that the presence of meningococcus inhibiting pneumococci or streptococci on the nasal and pharyngeal mucous membranes will determine the fate of a small number of meningococci deposited there from the inspired air. And secondly, the observations recorded in the first paragraph of this paper suggest that the operation of antagonism may sometimes effect the " cure " of meningococcus carriers. From this the question arose whether one could bring about a similar " curative " procedure. at will. The application of a filtrate of pneumococcus culture, however strongly bactericidal to meningococcus, could not be expected to give any better success than the use of antiseptics, which apparently fail of their object because they do not gain access to all the meningococci. It therefore seemed necessary to implant a living culture of the inhibitory microbes upon the naso-pharynx, in the hope that these would be able to establish themselves and spread over all the area invaded by the meningococci. The pneumococcus culture with which most of the inhibition experiments had been performed had come from a healthy ex-meningococcus carrier, with no history of pneumonia, and had, since its isolation, been passed through 20 or 30 generations on artificial media. These considerations, and the fact that the pneumococcus is usually present in the normal respiratory passages, led me to regard its use as quite devoid of danger. Broth cultures of it were sprayed first on the naso-pharynx of my fellow worker, Dr. Harold Tanner, whose help in this part of the inquiry I wish here to acknowledge, and subsequently on five carriers, with and without preliminary sterilisation of the naso-pharyngeal surface by silver iodide. To our surprise we found that the pneumococci were apparently unable to establish themselves in the naso-pharynx of these carriers, for although implanted in very large numbers they could not be recovered in any quantity from swabs taken after a few hours or on the following day. In the case of another carrier we implanted 4 Metchnikoff: Annales de l'Institut Pasteur, 1894. 5 Chonkevitch : Ibid., 1911. streptococci grown from his own saliva, but these also seemed unable to gain any hold in the naso-pharynx. Apart from their "taking root" and multiplying in the naso-pharynx, it was not to be expected that the pneumococci or streptococci introduced would have any inhibitory effect upon the meningococcus established there, and in five of the six carriers no evidence of such an effect was noticed. In the sixth case the pneumococci probably gained a slight hold at first, for the meningococci almost disappeared from swabs for nearly two days,. but after that time regained their earlier pre.. dominance. This last partial success seems, at any rate, to suggest that, with more knowledge of theprecise conditions which enable the inhibitory organisms to establish themselves, the method might prove of some value. My thanks are due to Captain S. R. THE following, which is a report to the principal medical officer of British East Africa on my findings. and treatment in blackwater, may be of interest. The patient, an intelligent European aged 53, had blackwater some four or five months ago, for which I attended him. For the last four months he had been living in a malarial district and had been having a lot of fever. On Sept. 12th he took 20 grains of quinine hydrochloride ; this. brought on blackwater in a few hours. With it came vomiting, diarrhoea, and jaundice. He knew in a common-sense way how to treat himself before my seeing him. He was brought into Nairobi on the morning of Sept. 14th, some 40 miles in a motor-car. He brought in with him his urine of the 13th. The urine of the 13th and the 14th contained, both oxy-and met-hsemoglobin. I had been noticing for the last year that all blackwater urines are excessively acid. This man's urine of the l3tlh and the 14th contained an enormous quantity of acetone,. and showed the aceto-acetic acid reaction very markedly. These samples were highly acid by litmus paper. His. kidneys are quite sound. At midday on the 14th, as soon as I found the acetone, 1' began giving potassium bicarbonate 3 i. every hour in heaps of water; he was able to keep down six doses. I then lessened the dose and gave sodium bicarbonate, with the result that he passed urine very freely, and next morning his urine was strongly alkaline, with not a trace of haemoglobin, but still with a small quantity of acetone. He was feeling much better, his jaundice was clearing, he was passing largequantities of urine, his spleen was less tender, and hisdiarrhoea was almost gone (this went jJO/I'i passu with the acetone). On the 16th there was no haemoglobin and noacetone ; he was much better and was hungry. The urinewas decidedly alkaline. (Note that the haemoglobin disappeared 24 hours before the last trace of acetonuria.) It will be seen that I gave CaC], as a set-off to potassium and sodium-they all three are blood alkalinisers. As soon as acetone was gone I put him on increasing doses of quinine. When last I treated this man for an attack of blackwater fever CaCI2 (which is an alkaliniser, but not nearly so strong as potassium) apparently prevented hsemoglobinuria from recurring. His history was as follows : I found him suffering from fever and very ill (he had been having fever for months). I gave him an injection of quinine gr. xx. at 10 A.M. and told him to drink plenty of water. At 5 P.M. he was passing urine as black as ink and was very ill indeed. I gave him CaCl2 i., which he kept down. Next morning the blackwater was gone. I then gave an injection of quinine gr. xxv., and he took CaCl2 gr. xx. every two hours for four times. He drank large quantities of water, tea, and coffee. With. this larger dose of quinine he showed no sign of blackwater.
doi:10.1016/s0140-6736(01)56058-4 fatcat:nzgytwqpunfz5c7lveznpfyvem