and it is only by following patients for years both clinically and, especially, microscopically that the true value of emetine as a specific can be determined. Half of my own cases relapse within six months to a year after treatment, but of the 12 cases treated and re-treated by me in 1912 and 1913 not one relapsed during 1914. Cases treated by Lyons, by Walker, and by Baermann and Heinemann have been followed for several years and have never relapsed, although still carrying entamœbæ. Brem's 38 standard, eradication of the entamœbæ to cure the patient, may have to be modified; some of these entamœbæ may have lost their pathogenic properties toward their present host. On the other hand, Seguin believes that unless both entamœbæ and cysts disappear permanently, relapse is inevitable. In cases relapsing within short intervals after treatment the infection may have been kept active by trophozoites, some of which have escaped destruction; but in cases relapsing months after treatment it has been found that during the symptom-free interval the stools contained only cysts. As shown by Baermann and Heinemann, Walker, Vedder, and others, many cases of dysentery, after the use of emetine, become chronic carriers of cysts. Where these amabæ lie which escape destruction is not known. Baermann and Heinemann suggest that in locations with a poor blood supply emetine fails to reach them. They also suggest that some amabæ may be only damaged, and that after their recovery a local or general tissue immunity may cause them to encyst. Vedder suggests that it is only the entamabæ in the lumen of the bowel which survive, and that carriers be irrigated with quinine or silver nitrate. Walker 39 has worked out this point of latency in balantidial dysentery in the monkey, and finds it due to three factors: First, the organisms may fail to penetrate the healthy gut and are living for the time being as commensals in its lumen; second, the chronicity of the ulcerative process may account for the lack of symptoms; and, third, there may be extensive colitis and ulceration without any dysenteric symptoms. He undertook to repeat this work with entamœbæ, but, unfortunately, none of his animals became infected. He considers it probable, however, that the latency of entamoebic dysentery is due to similar causes. It is to be hoped that this will be definitely worked out in animals, as evidence from autopsies on human carriers will take a great while to accumulate. Very little progress has been made as yet on the problem of the control of carriers, although it is gradually becoming evident that they are the chief source of infection, either through direct contact 40 or through flies.41 Mathis 42 classifies carriers as either convalescents who still discharge amabæ or as healthy carriers. Working in Tonkin, he found that 8 per cent. of the natives he examined were carriers of dysentery. In Manila, Willets 43 found in a routine examination that 37.5 per cent. of 900 natives and 100 Americans were carrying entamœbæ, and states that a careful examination would probably raise this figure to 55 per cent. In a differential diagnosis of the encysted forms from 76 individuals he found entamoeba histolytica present in 64.5 per cent. Thus from 20 per cent. to 30 per cent. of the population of Manila are seen to harbor the pathogenic entamoeba. In North Carolina I have reported entamœbæ present in 40.8 per cent. of 551 routine examinations, but no differentiation of species was made.** Christie 45 reports from Borneo that 30 per cent. to 40 per cent. of the entire population are amoebic dysentery carriers. VIII. ACTION OF EMETINE AND ENCYSTMENT OF AMEBÆ In fresh specimens the action of emetine on entamœbæ is, to all appearances, like that of quinine. Locomotion ceases, the organism becomes circular in outline, the ectoplasm bulges, and the entamoeba bursts or fades and disintegrates. In stained specimens James has shown that emetine causes a granular degeneration of the nucleus with a fibrillar disintegration of the cytoplasm, resembling the changes produced in the malarial organism after the administration of quinine. Concerning the chemistry of the destruction of entamœbæ by emetine, nothing is known. The constant finding of cysts in the stools of carriers suggests that somewhere up the line there is a focus of active trophozoites, because only the vegetative stage is constantly productive. This vulnerable focus, whether in the lumen or gut wall, must engage our search in studying the carrier problem. That the entamabæ are encysted in the stools shows that they have passed through an unfavorable environment. It is true that rapid asexual division through a number of generations will so tire out protoplasm that it will enter the sexual phase to rest and recuperate, but, if this were the only cause of intermissions in dysentery, the stools between attacks would show nothing, for cysts do not produce cysts; so that, while the entamæbæ may continue to thrive in some limited or sheltered region, on their way to the outside they are passing through hostile territory. The subject of unfavorable environment and the encystment of amœbæ has recently been investigated by Cropper and Drew.46 They have demonstrated that in cultural ambæ neither drying, starvation, acid, nor alkali will produce encystment, but that soluble bacterial products, such as choline, are necessary. They show that amabæ encyst first where bacteria are densest, and I have recently seen this confirmed for both amabæ and paramecia on solid media in Dr. H. P. Barret's laboratory. These observers have shown further that choline in dilute solution stimulates the reproduction of amœbæ, that 1 per cent. choline applied to amabæ kills them instantly; and that if the strength of the choline solution be gradually increased it invariably causes encystment. (Their statement that encystment is not a part of the life-cycle of amoeba does not hold for the parasitic entamœbæ.) Cropper and Drew have demonstrated that simply the removal of this hostile environment will not produce excystation, but that soluble ferments, either from bacteria or tissues, are necessary. It would be very interesting to know whether very dilute solutions. of emetine would produce encystment in cultural amœbæ, and whether the carrier stage is more likely to follow the use of emetine than the use of quinine or arsenic. Increased knowledge of the action of emetine on amabæ awaits further development of the experimental work of James and of Cropper and Drew, and the gaps in our knowledge of the action of emetine on the pathogenic entamoeba causing dysentery, we hope, will soon be filled in by experimental work on the cat. REFERENCES 1U. S. Dispensatory, 19th ed., p. 673. 3 "BROWN, W. C.: 1911, "Amoebic Dysentery,” p. 232 (Wm. Wood & Co.). Encyclopædia Britannica. DOUGLAS, S. R.: 1913, Brit. Med. Jour., ii, p. 2683. ' WALSH, TULL: 1891, Ind. Med. Gazette, September. • VEDDER, E. B.: 1911, Bull. Manila Med. Soc., March. ROGERS, L.: 1912, Brit. Med. Jour., June 22, No. 2686, p. 1404, and August 24, No. 2695, p. 405. WALKER, E. L.: 1911, Philippine Jr. Sc., vi, 4, p. 259. 'Low, G. C.: 1914, Abs. in Jour. Trop. Med. and Hyg., June 15, xvii, 12, 183. 10 LYONS, R.: 1913, New Orleans Med. and Surg. Jour., lxvi, 4, 278. " PAUL and CROWNLEY: See U. S. Dispensatory references. 12 MERCK & Co.: 1914, Adv. in Ind. Med. Gazette, March, p. 126. 18 ROGERS, L.: 1913, "Dysenteries," p. 128 (Oxford Med. Pub.). 14 BAERMANN, G., and HEINEMANN, H.: 1913, M. m. W., xl, Nos. 21 and 22. 15 'ROGERS, L.: 1914, Ind. Med. Gazette, March, xlix, 3, 85–88. 16 KENG, L. B.: 1914, Jour. Trop. Med and Hyg., xvii, No. 15. 17 SEAL, C. B.: 1914, Ind. Med. Gaz., xlix, 3, 106. 18 LE BLANC, B. O.: 1913, New Orleans Med. and Surg. Jour., 66, 5, 398. 10 BIZARD: 1913, Ann. Hyg. et Med. Col., xvi, 4, p. 564. 20 GUILLEMAT: 1913, Ann. Hyg. et Med. Col., xvi, 4, pp. 1115–1118. 21 SEGUIN: 1913, Ann. Hyg. et Med. Col., xvi, 4, p. 1155. *ORTICONI: 1913, Bull. Soc. Path. Exot., vi, p. 609. 23 MAURRAS and HERVIER: 1913, Ibid. 24 ALLAN, W.: 1914, Amer. J. Trop. Dis. and Prev. Med., vol. i, No. 8, pp. 565-672. 25 CARTER, R. M.: 1914, Ind. Med. Gaz., xlix, 3, p. 109. 26 ARCHIBALD, R. G.: 1914, J. Trop. Med. and Hyg., xvii, 11, p. 161. " JAMES, W. M.: 1913, Amer. J. Trop. Dis. and Prev. Med., vol. i, No. 6, pp. 431-446. WHERRY, W. B.: 1912, Jour. Inf. Dis., x, 2, pp. 162-165. " VEDDER, E. B.: 1914, Jour. A. M. A., lxii, pp. 501-506. 30 LYONS, R.: 1914, Southern Med. Asso., Richmond, Va., November. NOGUE: 1913, Ann Hyg. et Med. Col., xvi, 4, p. 1122. 2 BRAU: 1913, Ibid. 85 BARLOW, N.: 1914, Amer. J. Trop. Dis. and Prev. Med., i, 12, 864. ** WALKER, E. L., and SELLARDS, A. W.: 1913, Philippine Jour. Sc., viii, 4. PHILLIPS, L.: 1913, Rev. Med. d'Egypte, October, 1913, No. 10. "WILLETS, D. G.: 1914, Philippine Jour. Sc., ix, No. 1, p. 93. 37 GAIDE, J., and Mouzels, P.: 1913, Ann. Hyg. et Med. Col., xvi, 4, 1150. ss BREM, W. V., and ZEILER, A. H.: 1910, Amer. Jour. Med. Sc., cxl, 11, p. 669. " WALKER, E. L.: 1913, Philippine Jour. Sc., viii, 5, 333. 40 ALLAN, W.: 1910, Medical Record, January 8. "STILES, C. W., and KEISTER, W. S.: 1913, U. S. Pub. Health Reports, November 28. MATHIS, C.: 1913, Abs. in Trop. Dis. Bull., iii, 9, 448. 43 WILLETS, D. G.: 1914, Philippine Jour. Sc., ix, 1, p. 79. “a CROPPER, J. W., and DREW, A. H.: 1914, “Researches into Induced Cell Reproduction in Amoeba" (John Murray, London). VOL. I. Ser. 25-2 AN INFORMAL CONSIDERATION OF THE CLINICAL VALUE OF GRAPHIC METHODS IN THE STUDY OF HEART-DISEASE BY WILLIAM N. BERKELEY, A.B., Ph.B., M.D. Attending Physician at the Good Samaritan Dispensary, New York City THIS paper is not addressed to specialists, but to the physician at the bedside. He it is who must finally decide the clinical value of any new method of precision in diagnosis and treatment, and his hard practical sense may in the long run be implicitly relied on to prove all things clinical and hold fast only that which is good. If he decide finally that polygraphs are only a laboratory toy, in the laboratory they will remain. But he appears to be already deciding that the polygraph is a valuable instrument, giving not only diagnostic and prognostic information of the first importance, but also many useful indications for treatment as well. It is in the hope of reinforcing this decision that the present paper has been written. Let me first give the objections that present themselves to the use of the polygraph; then, supposing these disposed of, I will append a brief mention of the various apparatus now in use, concluding with an elementary consideration of tracings as an aid to diagnosis, prognosis, and treatment, with some easy illustrative examples of normal and pathological records. First among the objections is the amount of trouble and time required in learning to use the instrument and read the tracings. One medical friend of mine, to whom I recently showed some of my records, sighed deeply and said: "Well, I have my opinion of a man who can seriously spend his time on such a complicated and useless business as that!" And among my post-graduate students some come bravely forward and say at once, when I begin to talk of tracings: "Doctor Berkeley, if you don't mind, please let us take that up when we come to New York again next winter!" Yet I still maintain that the subject is not so difficult as it at first 18 |