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THE 
 
 INTESTINAL PUTREFACTIONS 
 
 CLINICAL STUDIES 
 
 OF 
 
 ENTEROCOLITIS 
 
 BY 
 
 CHARLES FENNER PECKHAM, M. D. 
 PROVIDENCE, RHODE ISLAND 
 
 Snow & Farnham Co., Printers 
 1916 
 
Copyright, 1916 
 By CHARLES FENNER PECKHAM 
 
 All rights reserved 
 
CONTENTS 
 
 CHAPTER I. 
 Enterocolitis. 
 
 The stages of enterocolitis; the primary stage; the secondary 
 stage; the tertiary stage; the three diagnoses — anatomical, 
 chemical, bacteriological; absence of sense of pain in intestinal 
 mucosa; symptoms — local, general; the tertiary stage. 
 
 CHAPTER II. 
 
 The Micro-organisms of the Intestinal Canal. 
 
 Difficulties in their study; deductions from fecal and urinary 
 findings ; classification ; effects of their growth ; structural changes in 
 the organs; intestinal putrefactions; antisepticus intestinalis; putre- 
 faction never present in normal individuals; conditions favoring 
 the putrefactive process; rate of absorption in the intestines; 
 bacteria — list of species; molds; cultural experiments; list of 
 intestinal molds; yeasts. 
 
 CHAPTER III. 
 
 The Examination of Feces. 
 
 Chemistry; microscopy; methods. 
 
 CHAPTER IV. 
 
 The Examination of Urine. 
 
 The indices of putrefaction; chemical examination and methods; 
 microscopy; apparatus; Ehrlich's aldehyde. 
 
 CHAPTER V. 
 
 The Indolic Type of Intestinal Putrefaction. 
 
 The primary stage; in childhood; sources of infection; ascending 
 infections; symptoms; the secondary stage; dyspepsia, indigestion, 
 nervous indigestion; local disturbances of function; the special- 
 ized organs; the gastric contents; the urine; the feces; the ter- 
 tiary stage. 
 
 CHAPTER VI. 
 
 The Saccharobutyric Type of Intestinal Putrefaction. 
 
 Definition; the primary stage; symptoms; the abdominal organs; 
 the function of the liver; the gastric contents; the feces; the urine. 
 
iv CONTENTS 
 
 CHAPTER VII. 
 
 The Acetic Type of Intestinal Putrefaction. 
 
 Definition; beta-oxybutyric acid; diacetic acid; acetone; the 
 primary stage; absence of alarming symptoms; the secondary 
 stage; acetone production without serious symptoms; diacetic 
 acid and the liver function; chemistry; the pancreas; diabetes; 
 glycogen; sugars and starches; surgical lesions; the nervous sys- 
 tem; the feces; the urine; the tertiary stage. 
 
 CHAPTER VIII. 
 
 The Oxalic Type of Intestinal Putrefaction. 
 
 The primary stage; the secondary stage; symptoms; chronic 
 rheumatism; the intermittent type; the feces; the urine; types 
 of molds found in the feces; the tertiary stage; moniliasis. 
 
 CHAPTER IX. 
 
 The Oleic Type of Intestinal Putrefaction. 
 
 Intolerance of certain fats; the primary stage; psychoses; the second- 
 ary stage; the blood; the feces; torulae; the urine; lipase and 
 the higher fatty acids. 
 
 CHAPTER X. 
 
 The Ammoniacal Type of Intestinal Putrefaction. 
 
 The primary stage; the secondary stage; duration and symptoms; 
 the urinary system; ammonia in the urine; calculus formation; 
 the urine; the feces; the liver; in combination with saccharo- 
 butyric type. 
 
 CHAPTER XI. 
 The Uric Acid Type of Intestinal Putrefaction. 
 Importance of intestinal condition. 
 
 CHAPTER XII. 
 Malaria, Syphilis and Tuberculosis. 
 
 Possibility of malarial infection in enterocolitis; general consid- 
 eration of malaria in New England; the blood; classification; 
 sensitization; anti-anaphylaxis; the course of malarial infections; 
 the four stages of chronic malaria; life history of the Plasmodium; 
 the transmission without the agency of the mosquito; absence 
 of secondary stage; syphilis; tuberculosis. 
 
CONTENTS V 
 
 CHAPTER XIII. 
 
 The Protein Poison. 
 
 Sensitization; individual peculiarities and susceptibilities; in 
 the primary stage of enterocolitis; acute indigestion; permeabil- 
 ity in certain mucosae; particulate proteins; the three stages. 
 
 CHAPTER XIV. 
 
 The Treatment of Enterocolitis. 
 
 In general; the primary stage; intestinal antiseptics; the second- 
 ary stage; the mixed infections; the indolic type; the saccharo- 
 butyric type; the oleic type; constipation. 
 
 CHAPTER XV. 
 
 General Consideration of Enterocolitis. 
 
PREFACE 
 
 In the year 1906, Professor Herter published his epoch- 
 making work on the Common Bacterial Infections of the 
 Digestive Tract. Before this, other medical thinkers had 
 pointed out the way; Schmidt and Strasburger had published 
 their monumental work on the human feces and Metchni- 
 kof¥ had noted the connection between intestinal putrefac- 
 tion and the duration of human life. It remained for Herter, 
 however, to give the impulse that led to the application of 
 these discoveries in clinical practice. It was through his 
 classic teaching that physicians learned to use the three 
 great weapons: chemistry, bacteriology and biology, in the 
 fight. Various phenomena such as hyper- and hypochlorhydria, 
 indicanuria and autointoxication, so called, fitted themselves 
 into the clinical pictures ; diseases that at first sight seemed to 
 be intimately connected with faulty metabolism in the hu- 
 man tissues were proven to arise not through any parenteral 
 biochemical process but in spite of it. Organic lesions were 
 given the prominent position that they deserve, while the 
 various types of intestinal putrefaction were used as avenues 
 of information through which a knowledge of the nature 
 and mode of attack of the enemy might be gained. 
 
 In the preparation of this book, that great enemy of the 
 arts, fleeting time, has, of necessity, placed certain limita- 
 tions upon the task. Its preparation has been a labor of 
 great satisfaction. By far the greatest satisfaction, however, 
 rests in the fact that what was formerly a matter of conjecture, 
 can through laboratory methods be brought to a point of 
 
viii PREFACE 
 
 absolute certainty. This should give the physician, through 
 
 the directness of his therapeutic attack, greater power in 
 
 the battle with disease, and should he, through the methods 
 
 set forth in the following pages, win the fight, prolong the 
 
 useful life or even alleviate the suffering of some unfortunate 
 
 human being, the writer will feel that his labors have been 
 
 well repaid. 
 
 The Author. 
 
 Six Thomas Street, 
 Providence. 
 
CHAPTER 1 
 
 ENTEROCOLITIS 
 
 The course of this disease may be divided into three stages, 
 and these for convenience in clinical study may be termed 
 primary, secondary and tertiary. In the primary stage a 
 sudden onset accompanied by more or less acute symptoms 
 is the rule. The secondary stage is marked by a period of 
 increasing gastrointestinal disturbance, either continuous or 
 intermittent, extending over a considerable length of time. 
 The tertiary stage begins with the advent of low-grade in- 
 flammatory changes involving the stroma and parenchyma 
 of some organ or group of organs of the body. 
 
 The duration of the primary stage is a matter of days, 
 that of the secondary stage may be reckoned in years or 
 decades, while that of the tertiary stage depends upon the 
 vitality of the organs involved. The primary stage may 
 begin in early infancy, in childhood, in adolescence or at any 
 time during the life of the patient. Many of the obscure 
 febrile disturbances of infancy and childhood, while not 
 recognized at the time as the beginning of a disease that may 
 lead to inefficiency and premature old age, mark the begin- 
 ning of a chronic enterocolitis. 
 
 Certain families seem especially liable to the ravages of 
 this disease and upon questioning these patients, it will be 
 found that their ancestors for many generations have died of 
 diseases traceable to intestinal putrefaction, such as arterio- 
 sclerosis, cirrhosis of the liver and other low-grade inflam- 
 matory disturbances in various specialized organs, at ages 
 well below sixty. 
 
 Errors in diet, constipation, overindulgence in animal food 
 are not of such importance in the etiology of enterocolitis 
 
2 INTESTINAL PUTREFACTIONS 
 
 as is the reduction of vitality incident to the stress and com- 
 petition of modern life and the lack of nourishing food and 
 fresh air. 
 
 As the most prominent predisposing cause, the habitual 
 use of purgatives and cathartics, especially the salines, 
 may be given a prominent position. The irritation of the 
 intestines, through the daily use of sodium phosphate, sodium 
 sulphate, magnesium sulphate and potassium bitartrate so 
 lowers the resistance of the intestinal mucous membrane as 
 to encourage the invasion of the infecting micro-organisms. 
 Cathartics of less irritating character may also be a very 
 prominent factor in the development of this condition. 
 
 To the results of emotional excitement, grief, disappoint- 
 ment and other depressants of the resisting power, may be 
 added the exposure to strains of bacteria with which the 
 patients were not accustomed to deal. 
 
 Before beginning the treatment of these patients, three 
 diagnoses should be made: 
 
 First: The anatomical diagnosis, dealing with the nature 
 and extent of the alimentary catarrhal process, the position 
 of the abdominal viscera and the condition of the liver, heart, 
 kidneys and other internal organs. 
 
 Second: A chemical diagnosis directed to estimating the 
 patient's capacity for oxidizing acids and toxins and to deter- 
 mine the nature of the intoxication. 
 
 Third: A biological diagnosis covering the character of 
 the intestinal fauna, and the presence of parasites in the 
 tissues of the body. 
 
 Primary Stage. 
 
 In the primary stage the clinical picture is one of acute 
 infection. There may be a rise in temperature preceded by 
 a chill, anorexia and vomiting. The local symptoms may 
 not be pronounced but pains in various portions of the ab- 
 domen are prominent if the colon is markedly involved. 
 These pains are generally referred to some of the flexures 
 
ENTEROCOLITIS 3 
 
 of the large intestine. If, however, parts of the alimentary 
 canal higher up are affected the pain is referred to the epi- 
 gastrium. Often mucous stools, stained saffron yellow, will 
 be noted. This disturbance may vary in severity from one 
 so slight as to pass unnoticed to toxemia so overwhelming 
 as to cause sudden death. Other subsequent attacks do 
 not generally equal the first in severity. There may be 
 constipation or diarrhoea. 
 
 Secondary Stage. 
 
 Convalescence from the primary stage of this disease may 
 appear to the patient to be complete. A chemical or micro- 
 scopical examination of the patient's feces, urine and blood, 
 however, will show that a marked change has taken place. 
 That a condition has developed that if allowed to go on, will 
 eventually impair the usefulness of the victim, or lead to a 
 premature decay of some or all of the functions of his body. 
 Unlike the primary stage, this is of long duration, running 
 a course of years or even decades. It is a stage when changes 
 generally take place gradually, when like the mills of the 
 gods the grinding process is slow but the grist exceeding fine. 
 Ten, twenty or even thirty years may pass before a vital 
 organ begins to suffer changes, but these changes are as sure 
 to come as the changes of the seasons. 
 
 This stage is characterized by dyspeptic symptoms, de- 
 scribed by the patient as severe or slight, as the suscepti- 
 bility or resistance of the individual may vary. These com- 
 plaints may be transitory or continuous. 
 
 It is unfortunate that the gastro-enteric mucosa is not 
 more liberally endowed with the sense of pain and that very 
 few intestinal lesions give this symptom in a marked degree 
 until the disease has progressed far enough to involve the 
 muscular or peritoneal coat. The intestinal mucosa often 
 suffers such damage that the nutrition of the individual is 
 irreparably undermined, with no other alarming symptom, 
 perhaps, than a more rapid loss of flesh than a dyspepsia 
 might cause. 
 
4 INTESTINAL PUTREFACTIONS 
 
 The symptoms and physical signs of this stage may be 
 classified as general and local. The general symptoms arise 
 from the attack of toxins upon the patient's tissues, causing 
 irritation and depression of vitality in various organs, or 
 groups of organs. Bearing this in mind, the various clinical 
 pictures met with in this stage, can be easily composed and 
 their great variety fully explained. 
 
 From the patient's standpoint the course of the disease is 
 not continuous. At the time of the acute attacks he is in 
 misery: during the periods of remission, he enjoys compara- 
 tive comfort. Each attack, however, leaves a certain amount 
 of damage behind it, varying in amount with the natural 
 resistance of the affected organ. 
 
 Locally, a train of symptoms and physical signs presents 
 itself that has its origin in the direct irritation of the intes- 
 tinal mucosa. Spasms, which may reach the point of pro- 
 ducing intense pain, referred to the pylorus, the stomach 
 or the intestines are common. The pylorus is the most 
 frequent site of this disturbance, apparently arising from the 
 effort of the intestine to protect itself from the irritation of 
 the acid stomach contents. This may become so persistent 
 as to lead to continuous nausea or prolonged vomiting. 
 Spasms of the colon are next most frequently encountered, 
 and often lead to spastic constipation with triangular, rib- 
 bon-like or scybalous stools of small calibre, and consider- 
 able pain and tenesmus. 
 
 While the symptoms in this Secondary Stage may be so 
 mild as to escape ordinary notice, yet a patient in this con- 
 dition of comparative comfort, may be in even greater danger 
 than one showing the most pronounced symptoms. How 
 often have we noted a change in physical condition gradually 
 develop in certain people. They do not consider themselves 
 ill, they manage to perform their daily tasks with satisfaction 
 to themselves and to their employer, and complain, if they 
 complain at all, only of a slight lack of their former endur- 
 ance; yet they do not appear to be in perfect health. To 
 the practiced eye, their illness may be diagnosed offhand as 
 
ENTEROCOLITIS 5 
 
 progressive anemia of obscure origin, and eventually they die 
 suddenly of cardiac, renal or hepatic diseases which are as- 
 cribed, perhaps, to overwork. The long-standing intestinal 
 putrefaction, which was the direct cause of their untimely end, 
 is usually overlooked. 
 
 Tertiary Stage. 
 
 When organic lesions of any organ can be demonstrated 
 clinically, the Tertiary Stage may be said to begin. For 
 some time before this, however, organic changes, though not 
 apparent upon physical examination, have been slowly 
 advancing. 
 
 The onset of this stage may be either gradual or extremely 
 sudden. In the latter case, a diagnosis of acute inflammation 
 is often erroneously made. If of sudden onset, the symp- 
 toms may be very violent and often so severe as to cause 
 death. The fact should be borne in mind, however, that 
 the lesions in the kidney, heart, blood vessels or other special- 
 ized organs have not arisen de novo, but as the result of a 
 long-standing toxemia. 
 
 If the onset of this stage is gradual very few symptoms 
 will at first be given. More often, however, the presence 
 of some physical signs discovered in the course of the exam- 
 ination of the urine, feces or blood, or in the physical exam- 
 ination of the patient will disclose the fact that the fight is 
 lost. In other individuals the sudden cessation of improve- 
 ment or a rapid loss of strength and endurance show only 
 too plainly the beginning of some organic changes. 
 
 In the case of individual organs, the importance of these 
 to life may have a great bearing upon the subsequent course 
 of the disease. Lesions is such organs as are intimately 
 connected with digestion, metabolism and excretion naturally 
 have a most deleterious effect upon intestinal catarrhs and 
 putrefactions. Failure of the organs of circulation may 
 bring on passive congestions or anemias that preclude the 
 possibility of any improvement in intestinal conditions. 
 The function of the nervous mechanism of the viscera may 
 
6 INTESTINAL PUTREFACTIONS 
 
 be so damaged as to upset the balance of the various abdom- 
 inal organs and to impair their vitality. 
 
 Death may result from the failure of some organ necessary 
 to life or the result of some intercurrent disease to which 
 the patient's weakened condition opens the way. 
 
CHAPTER II 
 
 THE MICRO-ORGANISMS OF THE 
 INTESTINAL CANAL 
 
 The micro-organisms that are the causative agents in 
 chronic catarrhal processes affecting the gastro-intestinal 
 canal and the various passages connecting therewith, offer 
 a field for study, that up to the present time, has been very 
 lightly cultivated. Limited as is the field in most cases to 
 the study of the feces, the fauna of the higher parts of the 
 intestinal lumen, in the human subject at least, is extremely 
 difficult to investigate. As these diseases are rarely, per se, 
 fatal, the patient's death being the result of the secondary 
 changes taking place in some distant organ, we must of neces- 
 sity rely upon specimens taken at the time of operation upon 
 the upper intestinal canal or upon the gall ducts for our 
 information. Deductions from the chemical findings in both 
 feces and urine have been found of great assistance in throw- 
 ing light upon the character of the infective process. For 
 example, the presence of a very strong reaction to Ehrlich's 
 aldehyde in the feces leads us to suspect a luxuriant growth 
 of the short, plump bacillus, which in pure culture gives a 
 remarkably sharp response to this test, in the duodenum 
 and jejunum, even if these bacilli have disappeared by the time 
 the fecal specimen reaches the laboratory for examination. 
 
 From the clinical standpoint the vegetable parasites of the 
 intestinal canal and the passages directly connected with it, 
 may be divided into three classes: 
 
 1. Those which, gaining access to the intestine, invade 
 the tissues of the host. 
 
 2. Those which feed upon the epithelium of the mucus 
 membrane of the intestine and rarely penetrate more 
 deeply into the tissues. 
 
8 THE MICRO-ORGANISMS 
 
 3. Those which grow in the contents and the mucus 
 covering the surface of the intestinal canal and do not 
 directly attack the mucous membrane. 
 
 The group of intestinal infections herein described belong 
 to parasitism of the third class and include the bacteria, 
 hyphomycetes and saccharomycetes. 
 
 The effect of the growth of micro-organisms may be clas- 
 sified as follows : 
 
 1. The direct parasitic effect: diversion of food supply, 
 chemical changes in the chyle, rendering it unfit for absorp- 
 tion. 
 
 2. The production of toxic by-products, such as acids 
 and acid salts, aromatic bodies, protein bodies, ethereal 
 sulphates, ammonia. 
 
 3. The effect upon the organs directly concerned in 
 internal metabolism, including overwork in oxidizing 
 acids, ethereal sulphates, etc., and the direct toxic effect, 
 leading to structural changes in distant organs. 
 
 Changes in these organs may be classified as follows: 
 
 In the parenchyma: hyperplastic and increased function, 
 atrophic and diminished function. 
 
 In the stroma: hypertrophy, fibrosis, degeneration, con- 
 traction, cirrhosis, calcification. 
 
 These changes may involve cardiac, arterial, hepatic, renal, 
 gastro-intestinal, nervous, muscular, articular, ovarian, pan- 
 creatic or any of the various forms of animal tissue, with a 
 syndrome corresponding to the special type of degeneration. 
 
 The animal parasites of the intestinal canal are without the 
 matter under discussion and will only be mentioned when 
 their presence has some bearing upon the subject at hand. 
 
 As the putrefactive processes of the alimentary canal are 
 studied clinically and in the laboratory, the questions often 
 arise. Why do the contents of the normal human intestine 
 remain so nearly sterile ? Why, in normal stools, do we 
 find so few micro-organisms of the putrefactive type and 
 such a luxuriant growth of the bacillus communis coli ? 
 
OF THE INTESTINAL CANAL 9 
 
 We find also that feces kept in an incubator for days do not 
 undergo a great change in their bacterial fauna; that outside 
 of an increase in the number of the special types present 
 when that stool was passed, even after the specimen has been 
 exposed to contamination in the laboratory, very few new 
 types of micro-organisms develop. 
 
 The feces of infants may be kept in a temperature of 98.6°F. 
 for a week or more without change and even the addition of 
 such feces to culture media will check the growth of certain 
 micro-organisms. * 
 
 There seems to be some antiseptic present in normal feces 
 that has a specific or selective action against the "wild" 
 strains of bacteria. This body is probably secreted by the 
 liver and pancreas and by the intestinal mucosa and in health 
 keeps all bacteria in check, except the colon bacillus peculiar 
 to the genus homo. The strength or power of this antiseptic 
 varies inversely with the age of the individual and by gauging 
 its strength an accurate estimate of the relative age can be 
 made. 
 
 An intestinal catarrh gives very little trouble until this 
 antiseptic begins to be diminished in amount or in strength, 
 and in no case can recovery be considered complete until 
 repeated examinations of the feces show that this function 
 has been regained to an extent commensurate with the age of 
 the individual. If the antiseptic body could be produced 
 synthetically or by extraction, it could be truly said that one 
 of the springs of life had at last been found. 
 
 Putrefaction is never present in the intestinal canals of 
 normal animals and when found is always an evidence of 
 disease. When present, we may assume an impairment of 
 the antisepticus intestinalis in the chyle and feces. This 
 antiseptic, as we said before, is selective for every type of 
 bacteria with which the organism habitually comes in contact, 
 except the colon bacillus. 
 
 There are several conditions that may weaken or depress 
 the secretion of this antiseptic — 
 
 *Herter, Com. Bac, Inf. Digestive Tract, p. 13. 
 
10 THE MICRO-ORGANISMS 
 
 (a) The general reduction of vitality through grief, 
 pain and misfortune. 
 
 (b) The attack of toxins, such as those produced in 
 the growth of B. tuberculosis, treponema pallida, Plasmodium 
 malariae and other micro-organisms. 
 
 (c) The direct effect of catarrhal processes upon the 
 mucosa. 
 
 To thoroughly comprehend the process, the intestinal 
 canal must be regarded as a hollow organ continuous with 
 other external epithelial surfaces of the body. The contents 
 of the intestine are, in consequence, as much outside the 
 body as the water in which we wash our hands. There is a 
 marked difference, however, between the mucous membrane 
 and the skin and this is in the rate of absorption. While 
 this for many chemical bodies is fairly active on cutaneous 
 surfaces, on the intestinal surface it is of extreme activity. 
 This fact is taken advantage of by the bacteria of intestinal 
 putrefaction, which by their toxins and aggressins still fur- 
 ther reduce the vitality of the body tissues. 
 
 The vegetable parasites may be considered under the follow- 
 ing heads: (1) Bacteria, (2) Hyphomycetes or molds, (3) 
 Saccharomycetes or yeasts. While this classification may 
 not be strictly and scientifically accurate, still it answers all 
 the requirements of clinical study. 
 
 The following list of bacteria, according to the classifica- 
 tion of Chester will be found of great service in the study 
 of this subject in the laboratory. This list gives most of 
 the bacteria encountered in this class of work and for con- 
 venience of reference the number given in Chester's valuable 
 work is prefixed. 
 
 1. BACTERIA: 
 
 A . Streptococcus : 
 
 2. Str. enteritis Hirsch. 
 7. Str. enteritidis Escherich. 
 10. Str. canis. 
 
OF THE INTESTINAL CANAL 11 
 
 11. Str. coli. 
 15. Str. lactis. 
 
 B. Micrococus: 
 
 6. M. pyogenes albus. 
 20. M. aerogenes Miller. 
 22. M. alvi. 
 
 27. M. Mendozae. 
 
 34. M. cumulatus v. Besser. 
 
 35. M. salivarius Biondi. 
 
 43. M. ovalis Escherich. 
 
 44. M. lactis. 
 
 45. M. candicans. 
 
 61. M. subflavus V. Besser. 
 64. M. pyogenes aureus. 
 
 C. Sarcina : 
 
 1. Sarc. pulmonum. 
 
 4. Sarc. flava. 
 
 5. Sarc. lactis. 
 
 7. Sarc. lutescens Stubenrath. 
 9. Sarc. lutea. 
 
 11. Sarc. cervina Stubenrath. 
 
 12. Sarc. fusca Gruber. 
 
 D. Planococcus: 
 
 E. Planosarcina : 
 
 3. P. Sarc. Samesii. 
 
 F. Bacterium: 
 10. Bact. aceti. 
 
 17. Bact. acetigenum. 
 
 18. Bact. aceticum. 
 
 20. Bact. aerogenes. 
 
 21. Bact. capsulatum. 
 57. Bact. Bienstockii. 
 
 62. Bact. dysenteriae. 
 71. Bact. lactis. 
 
 166. Bact. Welchii. 
 
12 THE MICRO-ORGANISMS 
 
 166. 
 
 Bact. aerogenes capsulatus. 
 
 171. 
 
 Bact. thermophilum. 
 
 210. 
 
 Bact. subtiliforme. 
 
 211. 
 
 Bact. simile. 
 
 
 Bact. Mellanby & Twort.* 
 
 G. Bacillus: 
 
 2. 
 
 B. coli. 
 
 5. 
 
 B. enteritidis. 
 
 21. 
 
 B. typhosus. 
 
 Zd>. 
 
 B. alcaligenes. 
 
 37. 
 
 B. Friedbergensis. 
 
 39. 
 
 B. Schafferi. 
 
 65. 
 
 B. Shigae. 
 
 75. 
 
 B. bucalis. 
 
 84. 
 
 B. tachyctonus. 
 
 113. 
 
 B. dysenteriae. Kruse. 
 
 116. 
 
 B. Wesenbergii. 
 
 142. 
 
 B. prodigiosus. 
 
 155. 
 
 B. Lesagei. 
 
 194. 
 
 B. subtilis. 
 
 238. 
 
 B. putrificus. 
 
 243. 
 
 B. car is. 
 
 245. 
 
 B. solidus. 
 
 250. 
 
 B. botulinus. 
 
 251. 
 
 B. butyricus Botkin. 
 
 252. 
 
 B. amylobacter — Clostridium butyn 
 
 254. 
 
 B. Kedrowskii. 
 
 256. 
 
 B. sporogenes. 
 
 
 B. bifidus (vide Herter p. 41). 
 
 
 B. acidophilus. 
 
 
 B. acidolacticus. 
 
 
 B. anthracis symptomatic!. 
 
 
 B. cloacae. 
 
 
 B. entericus. 
 
 
 B. liquefaciens ilei. 
 
 *Protein'Split Products, Vaughn, 1913, p. 294. 
 Journal Physiol. 1912, XLV, 53. 
 
: , OF THE INTESTINAL CANAL 13 
 
 B. mascerans. 
 B. violarius acetonicus. 
 B. oedematis maligni. 
 B. paraputrificus. 
 B. proteus vulgaris. 
 
 H. Pseudomonas: 
 
 2. Ps. monadiformis. 
 29. Ps. capsulata. 
 
 /. Microspira: 
 6. Msp. comma. 
 
 10. Msp. protea. 
 
 /. Spirillum: 
 
 2. Sp. Massauah. 
 
 K. Spirochaeta: 
 L. Mycobacterium: 
 
 3. Mycobact. influenzae. 
 9. Mycobact. diphtheriae. 
 
 13. Mycobact. tuberculosis. 
 
 M. Streptothrix: 
 
 1. Streptothr. bo vis. 
 
 11. Streptothr. chromogena. 
 
 14. Streptothr. farcinica. 
 
 N. Leptothrix: 
 M. Cladothrix: 
 
 6. C. intestinalis. 
 
 N. Thiothrix: 
 0. Beggiatoa: 
 
 2. HYPHOMYCETES OR MOLDS. In the more severe 
 types of enterocolitis the fecal fields regularly show the 
 presence of this class of micro-organisms. A great deal of 
 work remains to be done among the members of the fungi 
 of this group that are parasitic in the intestinal canal. 
 
14 THE MICRO-ORGANISMS 
 
 Cultural experiments have shown the great importance 
 of these fungi in the pathology of this disease. Their 
 biological processes are usually rapid and intense and 
 the resulting chemical bodies at times extremely toxic both 
 to the mucosa of the intestinal canal and to the general body 
 parenchyma. The enzymes that they use in gaining their 
 livelihood are of great activity, are very diffusible and are 
 so constructed as to act extracellularly. These ferments 
 attack starches, sugars, cellulose, proteins, oils and fats with 
 vigor. The waste products of the growth of these micro- 
 organisms are also important and generally extremely irri- 
 tating. Their enzymes, under certain conditions, are capable 
 of doing great damage to the tissues of the body that have a 
 fatty structure, especially the nervous system. In other 
 catarrhs their damage arises not so much through toxic 
 action as through mechanical obstruction of the absorbing 
 surfaces of the intestinal mucosa. They very generally 
 may be classed as Fungi Imperfecta 
 
 (a) Trichothecium : 
 
 Septate, never forms sporangia, conidiophores not united 
 into definite bodies; conidia and hyphae never pigmented. 
 Conidia double celled, solitary, not in chains; both cells 
 smooth; conidiophores not branched; conidia at tip, never 
 on sides of conidiophores; conidia spherical or pear shaped, 
 two cells often unequal in size; conidiophores long. 
 (Buchanan.) 
 
 In sprue in Gram stained fecal preparations the hyphae 
 are positive, deeply stained, unless degeneration has set in, 
 when they are positive and negative in sections or areas. 
 They are septate, the septa being spaced about 5 microns. 
 The stroma stains granularly with here and there punctate 
 nuclear matter. Branching is not noted. The hyphae shows 
 a tendency to bend at the septa in more or less obtuse angles. 
 They occur in felted masses or in twisted strands, strongly 
 resembling silk floss. The length of the hyphae is usually 
 30-40 microns, the diameter 1.5 to 2.0 microns. 
 
 The conidia are double celled, solitary, never in chains. 
 
OF THE INTESTINAL CANAL 15 
 
 Both cells are smooth, conidiophores not branched, conidia 
 borne on the tip, never on sides of conidiophores. The cells 
 are pear shaped and are unequal in size; the conidiophores 
 are long, with constrictions spaced about eight times their 
 breadth; the dimensions average 3.6x1.5 microns. 
 
 This apparently is a member of the family Mucedinaceae, 
 genus Trichothecium. 
 
 (b) Monilia: 
 
 Conidia never borne in sporangia; mycelium septate; 
 conidiophores never united into definite bodies; hyphae 
 and conidia never colored or smoky; conidia one celled, never 
 multi-celled; conidiophores never sharply differentiated from 
 mycelia, sometimes lacking. Conidia develop by breaking 
 up of hyphae. Conidia develop on definite branches; myce- 
 lium well developed and compact. — (Buchanan.) 
 
 In the fecal fields, this mold occurs as a rod about 6x1 
 microns with square ends. The ends are usually Gram pos- 
 itive. The body of the micro-organism is Gram negative 
 with one streak of Gram positive matter along the side. The 
 conidia are cuboidal in form, and are capsulated with une- 
 venly stained protoplasm. Their dimensions are approxi- 
 mately 1x2 microns. 
 
 The monilia grow luxuriantly on glucose nutrient agar 
 media. The mycelia are compact, branching, positive or 
 negative to Gram stain, according to their age. They are 
 cuboidal in shape, with dark. Gram positive lines across the 
 ends of the hyphae and many of the hyphae have on the 
 side a Gram positive line, as in the types found in the feces. 
 The hyphae are 4 microns in diameter, septate and branch- 
 ing. Smaller aerial hyphae, the tips breaking into square- 
 end oidia, 4x7 microns in diameter, will be noted. The 
 cuboidal structure of the mold is very characteristic. The 
 hyphae and conidia are coated with mucus. Grown under 
 anaerobic conditions, the hyphae and conidia are smaller 
 and approach more nearly to the type found in feces. Con- 
 siderable gas is produced in growth under these conditions. 
 
16 THE MICRO-ORGANISMS 
 
 (c) Torula: 
 
 Family Dematiaceae : conidia never borne in sporangia; 
 septate mycelia; hyphae and conidia are both dark or 
 smoky; conidia never spiral or radiate; mycelium little devel- 
 oped, breaking into oidia, or on short lateral hyphae; conidia 
 in chains easily broken apart into free conidia. If the co- 
 nidial chains are not easily broken apart, genus Hormiscium. 
 — (Buchanan.) 
 
 In the fecal fields torulae when young are strongly Gram 
 positive and take the form of hyphae of medium size, 1.50 to 
 2.00 X 10 to 30 microns. As they develop, slight indenta- 
 tions appear along the edges. In the shorter ones, con- 
 sisting of two elements, this gives the micro-organisms a 
 "dumbbell" form. As the chains grow older, the bodies of 
 the conidia become negative with Gram positive dots at 
 either pole. Often a constriction is noted in the middle 
 portion of the conidia, giving a dumbbell form, with nega- 
 tively staining body and two polar Gram positive bodies. 
 The conidial chain may contain as many as twenty conidia. 
 Occasionally the hyphae of these torulae, in which conidial 
 division has not occurred, may be observed. These are 
 septate, usually Gram negative or delicately positive, with 
 a small positive dot in the central zone of each section. 
 
 In glucose media the growth of these torulae is very luxuri- 
 ant. At the end of four or five days, at room temperature, 
 a fuzzy, slimy growth starts out from the line of feces with 
 which the media is sown. Under the microscope a few hyphae 
 will be observed. These measure 2x4 microns to 3 x 50 
 microns, are usually broader at one end than the other and 
 take a delicate blue tint with Gram stain. Many of the 
 hyphae will be seen dividing into conidia. They are usually 
 found in mycelia, consisting of two or three elements, rarely 
 more. The conidia are fusiform, one celled; capsulated, 
 1.9 to 2.5x3.5 to 7.5 microns, many showing Gram positive 
 polar dots and areas. Neither the conidia nor the hyphae 
 have a mucous coating. With iodine they stain yellow with 
 clear areas. 
 
OF THE INTESTINAL CANAL 17 
 
 In certain putrefactions where the presence of fatty acid 
 crystals in the stools is especially marked, this micro-organism 
 is very abundant in the fecal fields and seems to vary in num- 
 ber with the severity of the intestinal condition. The reader 
 is referred to the chapter on Oleic Putrefaction for further 
 information, 
 
 (d) Sporotrichum. 
 Septate, never forming sporangia, conidiophores never 
 united into definite bodies; conidia and hyphae never 
 pigmented; conidia single celled, conidiophores sharply 
 differentiated from the mycelium, conidiophores branched 
 or unbranched, but conidia never forming a terminal head, 
 hyphae never whorled, branched and conidia produced 
 irregularly on lateral conidiophores, never from minute teeth ; 
 conidiophores are never upright. — (Buchanan.) 
 
 3. SACCHAROMYCETES OR YEASTS: 
 
 A host of yeasts gain their livelihood in the contents of the 
 intestinal canal. Whether their presence in the intestines 
 is harmful, or whether they may be regarded as benign, is 
 an open question. We observe, however, that the greater 
 their abundance, the more severe the sickness and also that 
 the predominance of the round-cell type is an unfavorable sign. 
 There has been a great deal of work done with these micro- 
 organisms in connection with the brewing and wine industry, 
 but at present our knowledge of the pathogenic varieties, 
 with the exception of those invading the tissues, is fragmentary. 
 
 The position that they may occupy in certain symbiologi- 
 cal putrefactions is important. In this connection their 
 presence in many feces from individuals showing a marked 
 increase in acetone production, is interesting. 
 
 Many strains are known to produce bodies of extremely 
 disagreeable taste and odor and as materials repulsive to the 
 olfactory system of humanity are not generally well born, 
 either enterally or parenterally, an abundant growth of 
 Saccharomycetes in the intestinal canal is always viewed 
 with suspicion. 
 
CHAPTER III 
 THE EXAMINATION OF FECES 
 
 Laboratory workers very generally regard the examination 
 of fecal matter as disgusting in the extreme. When, however, 
 this subject is approached in a true scientific spirit, these 
 investigations lose their repulsiveness and are no more dis- 
 agreeable than many other things that must be done in the 
 pursuit of science. 
 
 The best container for fecal specimens is a wide-mouthed 
 preserve jar, fitted with the ordinary cover and rubber ring. 
 
 For the safety and convenience of the laboratory force, 
 jars with insecure covers, jelly glasses and specimens mixed 
 with water, toilet paper and urine should be refused. It 
 is customary after finishing the examination of a specimen 
 to sterilize with formaldehyde solution. The contents of 
 the jars are then thrown into the watercloset and the jar 
 thoroughly washed. The jars are then broken to avoid the 
 possibility of further use and to save storage space, packed 
 away in barrels to be removed by the ash man at his next visit. 
 
 The result of the examination is carefully recorded and 
 the stained microscopical preparations are preserved for 
 future reference in ordinary slide boxes. 
 
 Upon the receipt of a specimen the name and date are 
 immediately recorded in the laboratory register and given 
 a number which is pasted upon the container. This number 
 is recorded in the history of the patient, affixed to the speci- 
 mens taken for preservation and carried in the record of all 
 cultures. The result of the examination is recorded on the 
 history card of the patient under the following heads: 
 
 1. Macroscopic. 
 
 2. Chemical. 
 
THE EXAMINATION OF FECES 19 
 
 3. Microscopic. 
 
 (a) In water. 
 
 (b) With Lugol's solution. 
 
 (c) With Gram's stain. 
 
 (d) With carbol-thionine stain. 
 
 (e) With iodine stain (full strength Lugol's solu- 
 
 tion). 
 
 (f) With carbol-fucine stain. 
 
 4. The Diagnosis. 
 
 Under the heading macroscopic examination, the follow- 
 ing facts are recorded: 
 
 (a) The form: sausage-shaped; scybalous; soft; soft with 
 scybalae; broken; fibrous; spongy; fermenting; creamy; 
 creamy solidifying upon cooling; liquid; liquid with solid 
 portions or scybala; granular; serous; watery; bloody. 
 
 (b) The color: brown; reddish brown; brownish yellow; 
 yellow-brown; yellow; grayish yellow; gray; light gray or 
 clay color ; black ; green ; olive. 
 
 (c) Mucus : Khs,enc&; presence; amount; jelly-like; glairy; 
 mucopurulent; tapioca-like; masses free or intimately mixed; 
 bloody; bile-stained. 
 
 (d) Gross .particles: presence or absence; soap masses; 
 enteroliths, intestinal sand. 
 
 (e) Parasites: presence or absence; kind; condition. 
 
 (f ) The odor : aromatic ; stinking ; butyric ; acetic ; musty ; 
 ammoniacal; ether-like. 
 
 Chemical examination : 
 
 This includes as a routine measure the tests for blood, 
 for acidity and the estimation of the reaction to Ehrlich's 
 aldehyde. 
 
 For occult blood the benzidin, acetic acid, hydrogen perox- 
 ide test is usually employed as the most convenient. The 
 aloin or guiac test may be used, if preferred. 
 
 All of these tests are valueless unless that patient has been 
 
20 THE EXAMINATION OF FECES 
 
 on an iron free diet for several days. Therefore all kinds 
 of meat, green vegetables and medicines containing iron 
 should be excluded from the dietary for at least forty-eight 
 hours before taking the specimen. 
 
 This test may be performed in a test tube. It is more 
 convenient, however, to use a shallow glass vessel, such as a 
 Petri dish, as in the case of very delicate reactions it is con- 
 venient to examine with the microscope for particles positive 
 to benzidin. 
 
 The benzidin should be fresh and the acetic acid pure. 
 Contamination with any vessels stained with any prepara- 
 tion of iron should be carefully avoided. A small piece of 
 the feces under examination is placed in a Petri dish, a little 
 to one side of the centre. This is mixed with an equal amount 
 of hydrogen peroxide. A small amount of benzidin is 
 placed on the opposite side of the dish and mixed with two 
 or three drops of concentrated acetic acid. Then with a 
 clean glass rod the two mixtures are brought in contact. If 
 blood is present in any amount the customary green tint 
 will be observed at the juncture of the feces, hydrogen perox- 
 ide mixture and the benzidin acetic acid solution. If no 
 color is apparent to the naked eye, the specimen may be 
 examined with the microscope for the presence of green- 
 colored particles, denoting the presence of blood in minute 
 amounts. 
 
 The reaction to litmus is then recorded. For the estima- 
 tion of total acidity or for total alkalinity, one gramme of 
 the feces is emulsified with 9 c.c. of distilled water. The 
 reaction of this is estimated by either ^ HCl or ^ NaOH, as 
 the case may require, using phenolphthalein as an indicator. 
 
 The estimation of the value of the response to Ehr- 
 lich's aldehyde is of great importance. A comparison of 
 the strength of this reaction in the feces with that of the urine 
 gives an absolute value for the efficiency of the liver. The 
 following is the process: A clean beaker is first weighed and 
 the weight recorded. A mass of the fecal matter under 
 examination is spread out in a thin layer over the bottom 
 of the beaker, evaporated to dryness on the hot-plate and 
 
THE EXAMINATION OF FECES 21 
 
 the beaker and contents weighed while still warm. The 
 weight of the beaker and dried contents, less the weight of 
 the beaker alone, is then multiplied by 100 and cubic centi- 
 metres of water added to equal this amount. The mixture 
 is then heated and stirred until solution takes place, drawn 
 into the 1 c.c. roller pipette and the aldehyde solution No. 2 
 titrated, as is described in the chapter on the Urine. 
 
 For example : 
 
 Weight of beaker and dried feces less 
 
 weight of beaker 0.45 grammes. 
 
 Times 100, equals 45 c.c. of H2O added. 
 
 Under titration 0.16 c.c. of this solution causes 5 c.c. alde- 
 hyde solution No. 2 to show a pink fluorescence. Multiply 
 by two for value of 10 c.c. of aldehyde solution. Result 
 0.32 c.c. is the aldehyde value of the feces. 
 
 The proteolytic and amylolytic activity of the feces may 
 be estimated with Mett's tubes, egg albumen and starch 
 paste. Exhaustive investigations upon the enzymes present 
 in the feces conducted in my laboratory have shown very 
 little of practical value. 
 
 Extensive chemical process for the quantitative estimation 
 of mucus, mucine, fats, proteins, carbohydrates; oleic, butyric, 
 acetic, diacetic, formic, propionic, oxalic and other acids and 
 their salts; indol, phenol, skatol and various complex pro- 
 ducts of bacterial growth and biological activity may be 
 followed out, if time permits. 
 
 The specimen is then prepared for examination with the 
 microscope. 
 
 A thin emulsion of feces and plain water or decinormal 
 salt solution is made, mounted on several slides, and care- 
 fully searched for the eggs, oncospherae or embryos of the 
 intestinal parasites. This is a very important procedure 
 and its omission may lead to very embarrassing situations. 
 
 One to six slides are prepared with weak Lugol's solution 
 as a staining fluid and examined wet. 
 
22 THE EXAMINATION OF FECES 
 
 Formula: Dilute Lugol's Solution. 
 
 Water 50 c.c. 
 
 KI 0.5 grammes. 
 
 Lugol's Sol. 5 c.c. 
 A very speedy and convenient method is the following, as 
 it avoids the use of beakers or other containers. A drop or 
 two of dilute Lugol's solution is placed on a clean glass slide 
 and mixed with a small particle of the feces under examina- 
 tion with the aid of a small wood applicator. This can be 
 burned when the operation is completed. Care must be 
 taken not to have too strong a mixture of feces and solution, 
 yet is it convenient to have one portion of the specimen 
 rather thick to aid in the search for fat needles and fat sheaves. 
 The mixture had better be spread out in a long, narrow 
 strip over the slide, so that the cover glass will not become 
 wet on the upper surface and soil the objective of the micro- 
 scope. 
 
 The preparation is first examined for free starch and, if 
 present, the appearance and kind, whether potato, wheat, 
 oat, etc., recorded. Starch granules are stained blue. A 
 search is next made for muscle fasciculi. These will be with 
 or without striae and in either case the fact should be noted- 
 Crystals should next be searched for. These may be fatty, 
 triple phosphate, oxalate of lime, Charcot-Leyden, iron, 
 bismuth or the residue of some drug administered to the 
 patient. The yeasts are next examined and their character, 
 whether oval or round, and the relative abundance, recorded. 
 The vegetable detritus is examined and its description re- 
 corded. Finally a search for amoebae is made. 
 
 Four cover glass preparations are then made, two thin 
 and two thick. One of the thin preparations is stained after 
 the method of Gram, the other is stained with carbol-thionine. 
 One thick one is stained with full strength Lugol's solution, 
 the other with carbol-fuchsine. 
 
 Gram's Method. 
 Three drops of aniline oil are shaken with 10 c.c. of water 
 and filtered. Five drops of a saturated alcoholic solution 
 
THE EXAMINATION OF FECES 23 
 
 of gentian violet is added to the aniline water. The speci- 
 men is stained with this solution for three minutes. The 
 stain is poured ofif and without washing is flooded with Lu- 
 gol's solution, which is allowed to act for two minutes, decol- 
 orized with absolute alcohol, counter-stained with Bismarck 
 brown, dried and mounted in Canada balsam. 
 
 The Carbolic Thionine Blue (Nicolle) is prepared as follows: 
 Formula: Thionine blue 1.0 gramme 
 
 Carbolic acid 2.5 grammes 
 
 Distilled water 100 c.c. 
 
 Filter. 
 
 Before using, dilute with equal quantity of distilled water 
 and again filter. 
 
 Stain the specimen fifteen minutes with the above, wash 
 thoroughly and soak in tap water for one half hour. 
 
 In this preparation the alkali forming organisms will be 
 stained dark blue, the acid producing violet. 
 
 The thick film is then stained for fifteen minutes with 
 Lugol's solution, carefully washed to avoid the presence of 
 potassium iodide crystals in the finished preparation and 
 mounted in Canada balsam. The other is stained with hot 
 carbol-fuchsine, decolorized with ten per cent nitric acid 
 alcohol and counter-stained with methyl blue. Carbol- 
 fuchsine solution does not keep well and we find it a 
 great convenience in our laboratory to keep phenol solution 
 and the fuchsine solution separate. The method of staining 
 is as follows: 
 
 Upon one corner of the smear, a small drop of concentrated 
 phenol solution (liquefied crystals) is placed. One drop of 
 alcohol is then added to complete the solution of the phenol. 
 Six drops of water and one drop of a saturated alcoholic 
 solution of fuchsine are placed on the smear. This is heated 
 until the liquid begins to steam, allowed to stand for ten 
 minutes, decolorized with nitric acid alcohol, counter-stained 
 with methyl blue, dried and mounted in Canada balsam. 
 
 Micro-organisms are never named in the history card 
 unless a full identification through cultural methods has been 
 
24 THE EXAMINATION OF FECES 
 
 carried out. The record of the description and not of the 
 name has been found of the greatest convenience. As our 
 knowledge of the micro-organisms that are parasitical in the 
 intestinal contents grows, records and specimens can be 
 gone over again and very useful information acquired from 
 the study. 
 
 The description of the various types, however, is recorded 
 very fully and covers the following points: 
 
 (a) The groups: streptococcus, micrococcus, sarcina, 
 planococcus, planosarcina, bacterium, bacillus, pseudomona, 
 microspira, spirillum, mycobacterium, streptothrix, lepto- 
 thrix, cladothrix, thiothrix, beggiatoa, molds, yeasts. 
 
 (b) Characteristics of form: long, short, straight, 
 curved, dimensions in microns, square or round ends, oval, 
 diplococci-like, dumbbell-like, clavate, cuneate, capsulated, 
 non-capsulated, growing in chains, growing in masses, fila- 
 mentous, hyphae-like, septate or non-septate. 
 
 (c) Sporulation: equatorial, polar, bipolar, chlamydo- 
 spore type, conidia-like, stained or unstained, round or 
 oval, discrete or in masses, the size of the spores in microns. 
 
 (d) Staining: Gram positive or negative, lightly or 
 intensely, evenly, granularly, punctately, irregularly, sec- 
 tionally. 
 
 (e) The growth : luxuriant or scanty. 
 
 To avoid illness among the laboratory assistants, the usual 
 safeguards against infection should be thoroughly enforced, 
 as many feces contain organisms that are pathogenic in a 
 greater or less degree. Bichloride or carbolic solutions 
 should be constantly at hand and great care in the use of 
 laboratory towels and utensils should be taken. In the case 
 of the incubator, a ventilating tube leading to the chimney 
 is a great convenience, especially if the laboratory is in imme- 
 diate connection with other rooms, and should be supplied 
 when possible. 
 
CHAPTER IV 
 
 THE EXAMINATION OF URINE 
 
 The study of the urine in enterocoHtis gives much valu- 
 able information. When properly and carefully performed 
 a diagnosis can be made in many instances by this means 
 alone, but much better results will be obtained if the urinalyses 
 and the fecal examinations are compared and the findings 
 in each carefully verified. 
 
 The customary routine examination of the urine is first 
 completed and recorded in the patient's history. This 
 investigation includes the color, the odor, the cloudiness, 
 the specific gravity, the amount of albumen or its absence, 
 a quantitative estimation of the reduction of Fehling's solu- 
 tion, the amount of chlorides and phosphates, the reaction 
 to litmus and microscopically, a thorough search for casts, 
 epithelium, pus and crystals. 
 
 The chemical bodies that will be hereafter referred to as 
 the indices of intestinal putrefaction are next taken up in 
 order. At the present writing they are classed as follows: 
 
 Indican blue, 
 Indican red. 
 Acetone, 
 Diacetic acid. 
 Oxalic acid, 
 Uric acid, 
 Ammonia, 
 
 The body responding to dimethylaminobenzalde- 
 hyde. 
 
 The following test for indoxyl has proven the most con- 
 venient and reliable. The reagents required are chem- 
 ically pure strong hydrochloric acid, a 0.5 per cent solution 
 of potassium permanganate and chloroform. The appa- 
 
26 THE EXAMINATION OF URINE 
 
 ratus required is very simple — a 25 c.c. glass-stoppered grad- 
 uated cylinder and a 1 c.c. pipette. The cylinder is first 
 filled to the 5 c.c. mark with urine, then to the 10 c.c. mark 
 with hydrochloric acid and Ic.c. of chloroform added by 
 means of the pipette. The potassium permanganate should 
 be added a drop at a time and the tube well shaken between 
 each addition, until upon standing the chloroform ceases 
 to grow darker in shade. The two most frequent errors to 
 be guarded against are the too rapid addition of the 
 reducing agent, i.e., the permanganate solution, and insuffi- 
 cient shaking. The depth of the blue or red color of the 
 chloroform is compared with that of the color-scale and the 
 result recorded. In urines showing the mixed types the 
 proportions of blue and red are estimated in comparison 
 with the scales. 
 
 For the sake of the accuracy of this test, as well as in the 
 case of any other of the tests for the putrefactive indices, all 
 administration of medicinal agents should be suspended for 
 at least twenty-four hours before the urine is taken. 
 
 The presence of acetone is determined by Lieben's or by 
 Gunning's test. If the patient has not taken alcohol the 
 former is preferred. The urine should be as fresh as possible 
 and the amount taken for testing is 50 c.c. An Erlenmeyer 
 flask, fitted with a rubber cork and a bent glass tube of proper 
 length to reach within a centimetre or so of the bottom of 
 a test tube surrounded by cold water, is used for distillation. 
 The process must not be carried on too rapidly. The dis- 
 tillate is then treated with a drop or so of Lugol's solution 
 and decinormal sodium hydrate solution added until the 
 color of the iodine has been discharged. The strength of 
 the reaction is expressed in plus marks, thus: + 0000 repre- 
 sents a trace or a slight odor of iodoform upon heating the 
 mixture, ->-+ 000 an abundance of crystals when examined 
 microscopically yet not visible to the naked eye, + + + 00 a 
 visible precipitate, ++ + + a considerable precipitate, 
 and finally + + + + + a reaction so strong as to produce 
 an immediate cloudiness upon adding the sodium hydrate 
 solution. 
 
THE EXAMINATION OF URINE 27 
 
 If greater accuracy is desired, by slow distillation, using 
 ice water in the condenser, collecting the iodoform on a fil- 
 ter, washing first with very dilute hydrochloric acid and 
 then with distilled water, and finally weighing with the ana- 
 lytical balance, the results may be expressed in milligrammes 
 of iodoform per lOOc.c.of urine, and this figure used in judg- 
 ing the progress of the illness. 
 
 If Gunning's test is used the tube should never be heated 
 until the black precipitate of nitrogen iodide has entirely 
 disappeared. 
 
 The Gerhardt's or Bordeau red reaction is used in test- 
 ing for diacetic acid. It is absolutely necessary that the 
 urine be perfectly fresh. In moderately cool weather, if 
 the morning urine can be examined before noon of the same 
 day, the test may be depended upon for accuracy, but during 
 the summer months it is much safer to have the patient pass 
 urine in the office and the examination made immediately. 
 All medicines should be omitted for twenty-four hours before 
 the urine to be tested is taken. The strength of the reac- 
 tion is recorded in plus marks, with a statement of the char- 
 acter of the reaction. If the test is negative the symbol 00000 
 is used; if a light brown shade is obtained Bn + 0000; darker 
 shades of brown are expressed by extra plus marks as in the 
 case of the test for acetone. If the test gives absolutely no 
 red shade, the symbol By 00000 is added, while extra plus 
 symbols are added to express reactions of increasing inten- 
 sity until the deepest Burgundy reactions are recorded as 
 By + + + + +. An admixture of the two colors may also 
 be recorded by these fomulae if desired; for example, Bn + + 
 000 By +0000 would mean a moderately light brown reaction 
 showing a faint red tint. If the precipitate of ferric phos- 
 phate obscures the test it may be removed by filtration. 
 
 The brown shades, outside of the question of the presence 
 of diacetic acid, are also valuable in the estimation of the 
 amount of organic acids and acid salts excreted by the kid- 
 neys. 
 
 Oxalic acid always occurs as calcium oxalate when present 
 in the urine. After centrifuging and examining under the 
 
28 ' THE EXAMINATION OF URINE 
 
 microscope, the number of crystals of this compound may 
 be expressed as few, numerous, abundant or extremely abun- 
 dant, as the case may be. 
 
 Their abundance, however, may be much better expressed in 
 the number per cubic millimetre of urine times the average 
 diameter in microns of the bases of the crystals. 
 
 The presence of uric acid crystals is always noted in the 
 record of the urinalysis, but as a general thing the quantita- 
 tive estimation of the amount of this acid is not carried out. 
 
 The presence of ammonium-magnesium phosphate crys- 
 tals in any abundance usually means that a putrefactive 
 process with the production of ammonia is present in the 
 intestinal canal. The source of this ammonia should 
 always be confirmed by comparison with the fecal analysis. 
 If the latter shows the reaction for free ammonia or the pres- 
 ence of triple phosphate crystals, the ammoniacal type of 
 putrefaction may be diagnosed. 
 
 The test with dimethylaminobenzaldehyde is of great 
 value. There are two methods of recording this test — by 
 the use of the color scale, and by titration. In both methods 
 the following formula is used: 
 
 Ehrllch's Aldehyde Solution, No. 1. 
 Para-dimethylaminobenzaldehyde 15 grammes. 
 
 10% Solution sulphuric acid 300 c.c. 
 
 This gives a clear, amber-colored solution, which upon stand- 
 ing takes on a greenish tint and upon boiling has an aromatic 
 odor reminding one of new-mown hay. This solution im- 
 proves with age. 
 
 To perform the test, five cubic centimetres of the urine 
 are brought to the boiling point and the solution added drop 
 by drop until no further deepening of the red tint can be 
 obtained. While the mixture is still hot, the shade is com- 
 pared with the color scale and the result recorded. A mod- 
 ification of the ordinary hemoglobinometer may also be used. 
 In either case the strength of the reaction will be expressed in 
 a percentage based upon the color scale used in estimation 
 of the hemoglobin in the blood. The depth of the color may 
 
THE EXAMINATION OF URINE 29 
 
 also be recorded in plus marks, 00000 representing an ab- 
 sence of any reaction, + + + + + the deepest red tints and 
 the intermediate shades by combinations of the two symbols. 
 
 The use of color scales in the laboratory is hedged about 
 with inaccuracy, and it has been found that the titration 
 method, especially in instances where this test has been used 
 in checking the dietary of the patient, gives much more 
 uniform results. 
 
 The apparatus required for the proper performance of 
 this operation consists of a one cubic centimetre pipette 
 graduated in 0.01 c.c, a roller pinch-cock with rubber tubing, 
 a 10 c.c. graduated cylinder, test tubes and Bunsen burner. 
 There is nothing especially novel about this apparatus except- 
 ing the roller pinch-cock, and upon the smoothness of the 
 operation of the latter the success or failure of the test will 
 in a great measure depend. This consists of two metal 
 rollers and the containing frame. The rollers are 1.5 centi- 
 metres in diameter and 2 centimetres on the face. The sur- 
 face of the first roller is scored parallel to its axis' with a hack- 
 saw, in order that the rubber tubing that is to pass between 
 them may not slip. The scorings have a depth of 0.5 milli- 
 metres and are spaced 1 millimetre from edge to edge. A 
 knurled wheel is fitted to the shaft of this roller and the outer 
 edge of this wheel is supplied with a small crank handle. The 
 second roller is left smooth and revolves on a shaft constructed 
 to engage the yoke mentioned below. The frame is con- 
 structed of 2 millimetre flat stock, enough length being allowed 
 for securing the apparatus firmly to its support, bored and 
 slotted so that the scored roller and knurled head has a good 
 running fit, and the smooth roller may be brought towards or 
 away from its companion as may be required in the adjustment 
 of the apparatus. A yoke and adjustment screw is then fitted 
 to impart motion to the shaft of the smooth roller in such a 
 manner that the surfaces of both rollers will always remain 
 parallel. With rubber tubing of proper length any pipette 
 may be operated with this device and it has been found 
 very convenient in measuring infected solutions. 
 
30 THE EXAMINATION OF URINE 
 
 The following formula is used in making this determination: 
 
 Ehrlich's Aldehyde Solution No. 2. 
 Aldehyde solution No. 1 10 c.c. 
 
 Distilled water 90 c.c. 
 
 Five cubic centimetres of this solution are raised to boiling 
 temperature in a test tube. When the surface of this solu- 
 tion is observed at an angle of 45°, the base of the tube rest- 
 ing on a white surface, a delicate green color will be noted. 
 If this color is not present, or if a red tint is noted before the 
 addition of the urine, some of the utensils are not clean and 
 the operation should be repeated with fresh solution. The 
 pipette is then filled to the zero line with the urine under 
 examination and any excess of urine removed from its tip 
 with blotting paper. The solution is kept at the boiling 
 point during the titration and urine added drop by drop until 
 the surface of the mixture when observed at an angle af 45° 
 assumes a delicate pink shade. The amount of urine used 
 multiplied by two is the value usually used in expressing the 
 strength of the reaction. This figure, of course, is inversely 
 proportionate. 
 
 The matter of the dimethylaminobenzaldehyde reaction 
 in both urine and feces has been under discussion for the past 
 fourteen years without arriving at any definite conclusions. 
 Skatol, urobilogen and glycosamin have by various authori- 
 ties been mentioned as the bodies responsible for this reaction. 
 Professor Herter first noted that the urines from individuals 
 suffering from the most excessive intestinal putrefactions 
 were especially liable to give the most pronounced reactions. 
 Among my own patients I have learned to associate this 
 reaction with severe constitutional symptoms and to regard 
 a lessening of its strength a most favorable sign, an increase, 
 as foreboding disaster. 
 
 The color of the urine has little influence upon the strength 
 of this reaction. As many dark urines give a very delicate 
 reaction, while in others of a pale straw tint it is very well 
 marked, apparently the urinary pigments cannot be held 
 responsible. 
 
THE EXAMINATION OF URINE 31 
 
 Urines that gave a reaction of 0.10 and that were kept in 
 the light and shaken frequently did not give any increase in 
 its strength. Others were extracted with ether to remove 
 urobilogen and both the ether and the residual urine tested. 
 The aldehyde value of the urine remained unchanged. The 
 ethereal extract, evaporated to dryness and dissolved in 
 alcohol, was negative. 
 
 The question of the protein split products was taken up 
 as a possible source of this reaction. Egg white was pre- 
 cipitated by 95% alcohol, filtered, the filter washed thor- 
 oughly with ether, dried and powdered. This was digested 
 in two per cent sodium hydrate absolute alcohol, after the 
 method of Vaughn, and both the alcohol and the solid remain- 
 ing portion tested with aldehyde. The alcoholic extract was 
 positive. The solid portion took on a pink shade when exam- 
 ined by light reflected from the surface of the particles, while 
 by transmitted light they were a delicate gray. Specimens 
 of the untreated egg white were negative to aldehyde. 
 
 In the case of dessicated thyroid gland the soluble portion 
 was negative, the insoluble portion gave a dark red reaction. 
 
 The sugars were uniformly negative. 
 
 Cultures of mixed fecal bacteria were positive. Broths 
 when freshly prepared were negative. When putrefaction 
 had begun they showed a marked reaction to aldehyde. 
 
 Witt's peptone was positive, as well as other beef prepara- 
 tions, advertised as "predigested." Blood was negative, 
 the scales from psoriasis were negative. Specimens of Witt's 
 peptone were extracted with absolute alcohol, filtered and 
 dried. The filter was positive, the filtrate was negative to 
 aldehyde. Typhoid bacterins were negative. 
 
 Fluid extract of ergot was positive. Vaughn has called 
 attention to the presence of certain protein split products in 
 claviceps purpurea, so this reaction was not surprising. 
 
 Ergo toxin, a trade name given to an ergot derivative, gave 
 a positive time reaction. Upon first adding the aldehyde 
 solution no change in color was noted upon boiling. After 
 standing a few minutes the mixture changed to a pronounced 
 purple color, which deepened with further boiling. 
 
32 THE EXAMINATION OF URINE 
 
 A specimen of ernutin, another ergot derivative, gave the 
 same reaction as ergo toxin. 
 
 When ernutin was treated with boiling ten per cent H2SO4 
 and allowed to stand twenty-four hours the reaction with 
 aldehyde in the hot was very sharp and distinct. 
 
 Specimens of ergamin, said to be Beta-iminazolylethylamin, 
 were negative. When digested with ten per cent HaSO'* for 
 several days this drug was still negative. 
 
 Specimens of pancreatic gland substance, combined with 
 bile salts were slightly positive. 
 
 Fel bovis was negative. 
 
 Various preparations containing bile salts were negative. 
 
 It was noted that during the titration of the aldehyde 
 solution that at the instant the change in color took place, 
 there was also an ebullition of some gas, probably hydrogen. 
 
 Noting the fact that this reaction depended upon a change 
 in color of the reagent from green to red, and that this appar- 
 ently took place through an increase in the size of the mole- 
 cule of the aldehyde, the question of oxidation came to mind. 
 The aldehyde solution was consequently tested for response 
 to oxidizing compounds. Hydrogen peroxide even in very 
 weak solutions gave a marked positive reaction. Magnesium 
 peroxide also gave a very strong positive reaction. Potas- 
 sium chlorate, potassium permanganate, nitric acid, bismuth 
 subnitrate and zinc oxide were negative. Fuming nitric 
 acid (nitrous acid) in the cold produced a yellow reaction 
 with the escape of gas; upon heating, the mixture 
 grew darker and finally assumed a reddish brown color. 
 
 Two forms of fecal fields are regularly found in patients 
 whose urine and feces give a marked reaction to aldehyde. 
 The first shows a very luxuriant growth of short, plump, 
 round end. Gram negative rods, which are probably the 
 bacillus of Mellanby and Twort. In the second these bacilli 
 are absent and in their place hyphae and conidia are found 
 in abundnace. The bacilli probably produce in their growth 
 a near chemical neighbor of beta-iminazolylethylamin that 
 is responsible for this reaction; and cultures from such feces 
 are also strongly positive to aldehyde. In the case of the 
 
THE EXAMINATION OF URINE 33 
 
 molds the evidence pointing to the production of fi-i is not 
 so clear. In view of the fact that the response of aldehyde 
 to oxidizing agents, even in minute amounts, is especially 
 prompt, the presence of an oxidase, the result of the bio- 
 logical activity of intestinal molds, may possibly account 
 for this reaction in case the bacilli are absent from the fecal 
 fields. 
 
 If the liver is efficient this body will not appear in the urine 
 in an amount proportionate to its abundance in the feces. 
 It will be reduced in its passage through that organ to such 
 an extent as to no longer respond to aldehyde. 
 
 Judging from urinalyses in subjects undergoing typhoid 
 immunization, this reaction does not appear in the urine 
 during the course of parenteral protein digestion, at least in 
 normal individuals. 
 
 In the urine of sufferers from epilepsy the response to 
 aldehyde is remarkably strong and more especially so when 
 an attack is imminent. The presence of a value as low as 
 0.05 is generally followed by a convulsion within twenty-four 
 hours. 
 
 The test for urobilin is useful in estimating the amount 
 of the destruction of erythrocytes that is taking place. Schles- 
 inger's method will be found the most convenient. The 
 following reagents are required: 
 
 1. Zinc Acetate Alcohol. 
 Absolute alcohol 100 c.c. 
 Zinc acetate to saturation. 
 
 2. Lugol's Solution. 
 
 To the unfiltered urine an equal amount of the zinc acetate 
 alcohol is added. This is shaken and a few drops of Lugol's 
 solution added. The mixture is then filtered and the degree 
 of fluorescence of the filtrate recorded in plus marks. 
 
CHAPTER V 
 
 THE INDOLIC TYPE OF INTESTINAL 
 PUTREFACTION 
 
 In this type, the onset of the primary stage may be very 
 acute with a diagnosis varying frqm enteric grippe to para- 
 typhoid fever. 
 
 In children, we often meet with attacks of fever lasting 
 from a few days to several weeks, in which the urine gives 
 a very strong reaction for indican. The sera of these children 
 do not agglutinate the typhoid bacillus. This is usually 
 the beginning of an enterocolitis with this type of intestinal 
 putrefaction and the gravity of this condition is not given 
 the attention it deserves. This type often develops in the 
 course of a chronic enterocolitis, which in the beginning 
 showed another type of putrefaction. 
 
 Infection in these cases may take place in two ways: 
 by way of the mouth through the agency of those vegetables 
 which are grown in intimate contact with the soil, such as 
 radishes, lettuce and celery, by contact, either direct or 
 indirect, with sources of infection in street dust, water closets, 
 door handles and car straps; or by infections extending up- 
 ward from the colon. In the latter form of infection, which 
 may be called the ascending form, insufficiency of the intes- 
 tinal valves, certain ptoses of the intestines or a weakness 
 of peristalsis, facilitating the progress of bacteria from 
 one portion of the intestine to another, may be assumed. 
 
 Certain families seem to have a special lack of resistance 
 of the intestines against this form of bacterial invasion. 
 
 The symptoms of this condition may be considered, accord- 
 ing to the various stages, viz. the primary stage, if such 
 exists; the secondary stage and the tertiary stage. 
 
 The symptoms in the primary stage may range in severity 
 
THE INDOLIC TYPE 35 
 
 from those causing little trouble, such as suddenly develop- 
 ing headaches and mild abdominal symptoms, to severe 
 febrile attacks, confining the patient to bed with high temper- 
 ature. These symptoms may last from three days to two 
 weeks, often giving a clinical picture which strongly resembles 
 a mild typhoid infection. The true nature of these symp- 
 toms is apt to be overlooked, but an examination of the urine 
 will show the presence of indican in greater or less amounts. 
 
 In the secondary stage, the symptoms are not generally 
 constant. Attacks of dyspepsia, so-called indigestion, 
 epigastric pressure or distress, lasting for a fortnight per- 
 haps with a remission of about a month and then a return of 
 symptoms, is a suspicious syndrome. In this stage the 
 symptoms are confined to the abdominal organs and are 
 described as distress or discomfort, burning, pyrosis, with 
 or without constipation or diarrhoea. These are laid at the 
 door of indigestion or dyspepsia, nervous being a most 
 favorite prefix. As a collateral diagnosis, the patient may 
 add chronic appendicitis, chronic cholecystitis and intes- 
 tinal indigestion to the list of his complaints. Obscure dis- 
 turbances of nutrition and metabolism are at times prominent. 
 
 The tongue is very generally coated, especially in the 
 morning, and the breath has a fecal odor. For the relief 
 of this the patients resort to habitual catharsis very early 
 in this stage. While cathartics give a marked temporary 
 relief in this type, no permanent improvement is ever noted 
 from their use. 
 
 The circulatory system shows functional disturbances very 
 early in this stage and in many instances the patient believes 
 that he is the victim of some severe and fatal cardiac dis- 
 order. Palpitation, tachycardia, fainting spells and dysp- 
 noea are frequent complaints. 
 
 The nervous system is also the seat of many functional 
 disturbances and such disorders as headache, either fre- 
 quent or habitual, insomnia, vertigo, neurasthenia are very 
 apt to be present. Migraine, however, is rare in this type 
 of putrefaction and its presence always leads one to suspect 
 some of the more severe acid types as its cause. 
 
36 THE INDOLIC TYPE 
 
 The specialized organs, the eye, the ear and the genital 
 system may also show some disturbance of function. Many 
 of these patients complain of impotence or sterility and it is 
 interesting to note that, in common with the other forms of 
 chronic infection, the birth rate among these sufferers is low 
 and the offspring of poor vitality. 
 
 These patients usually pass the secondary stage in an 
 anemic condition. Their strength is poor and even if there 
 is no complaint of its loss, still their endurance is very unsatis- 
 factory, both for physical and mental work. 
 
 In this stage the physical examination shows little of mo- 
 ment. The liver is neither larger nor smaller than normal ; the 
 stomach is normal to palpation. The colon may be dis- 
 tended but not tender. The position of the abdominal 
 viscera will correspond to the patient's habitus. Physical 
 signs of disease in other organs will be lacking. These in- 
 dividuals, on the other hand, give the examining physician 
 the impression that they are ill. 
 
 The stomach contents show little of interest. There is 
 usually, however, a hyperchlorhydria but no evidence of 
 organic gastric disease. 
 
 The urine, in the secondary stage, will show no evidence 
 of kidney involvement. The strength of the indoxyl reaction, 
 however, will give very valuable information concerning the 
 severity of the intestinal condition that is slowly but surely 
 undermining the patient's health. 
 
 The gross appearance of the feces is usually fairly normal. 
 They may be formed, soft or liquid, their condition depend- 
 ing upon the kind and amount of cathartics the patient is 
 using. There is little mucus; no gross particles; the color 
 is dark; the odor not abnormal. The reaction is alkaline. 
 With Lugol's solution free starch is absent, muscle fasciculi 
 and crystals are absent, yeast cells are few in number and 
 oval in type. 
 
 It is in the preparations stained according to the method 
 of Gram that we find the most valuable information con- 
 cerning this type of putrefaction. Upon the first glance 
 through the microscope, the great prominence of the blue 
 
OF INTESTINAL PUTREFACTION 37 
 
 or Gram positive organisms will be noted. The largest of 
 these will be a bacillus, capsulated, growing end to end in 
 pairs. This will be recognized as the bacterium Welchii. 
 These are not usually very abundant and their growth, in 
 the milder grades of this type of putrefaction, is not luxuriant. 
 The next most abundant form will be the bacillus bifidus — 
 medium sized, irregularly contoured rods, often of headlet 
 form, at times bifurcated. The bacillus putrificus is absent 
 unless the disease has been in progress for some time. Posi- 
 tive micrococci are very rarely observed, as in the simple 
 indolic type ulcerative processes are rare. An occasional 
 Clostridium may be observed. 
 
 In the negative field the small number of bacilli of the colon 
 type will be noted. In the lighter grades their number may 
 be considerable, but in the more severe putrefactions they 
 will be absent. The severity of the catarrhal process may 
 be estimated by their number — the less abundant they are 
 the more severe the disease. The fine, negative bacilli of 
 the liquefaciens ilei type may be present when the stools are 
 soft in consistency. Short, fat rods without capsules are 
 usually absent. It is rare to find hyphae and spores except 
 in the more severe grades of putrefaction and then only 
 when the disease has been in existence for some years. 
 
 The preparations stained with thionine show the same 
 micro-organisms mentioned above. 
 
 The iodine field is generally negative. In some speci- 
 mens, however, a few Clostridia may be noted. 
 
 The blood shows little of moment in the average patient. 
 In the latter part of the secondary stage, the Hb. value begins 
 to diminish and in some instances the number of red cells 
 are reduced. An anemia of the pernicious type places the 
 individual in the tertiary stage of the disease. The fact 
 must be borne in mind, that the blood may be the point of 
 attack of this toxinwithout other organs showing organic lesions. 
 
 The secondary stage may continue for fifteen to thirty 
 years without greatly impairing the patient's capacity for 
 work. The sufferers are much more likely to regard them- 
 selves as more uncomfortable than sick. 
 
38 THE INDOLIC TYPE 
 
 In the tertiary stage abdominal symptoms, per se, form 
 a very unimportant part of the dinical picture. Consti- 
 pation may be present or often an intermittent diarrhoea 
 The symptoms referred to the intestinal canal are not so 
 impressive as those that arise from organic disease of the 
 heart, kidneys, liver or other organs that have begun to find 
 their burden too great. 
 
 Various forms of muscle and joint lesions are common 
 in the tertiary stage, such as myositis, osteoarthritis and 
 rheumatoid arthritis and the finger joints usually are the 
 seat of calcareous deposits. 
 
 In the nervous system organic lesions are met with of various 
 grades of severity, leading to psychoses, neuralgia, low grades 
 of paralysis and disturbances of function. 
 
 In certain sufferers from this tpye of putrefaction a con- 
 dition develops that may best be described by the term pre- 
 senility. Outside of a low grade anemia, great depression 
 and loss of strength and endurance they show very few 
 symptoms. The physical examination is usually negative, 
 the blood pressure normal or below normal, but besides a 
 marked indicanuria little can be found. They become a 
 burden to themselves and their family and usually die from 
 some intercurrent disease. 
 
CHAPTER VI 
 
 THE SACCHAROBUTYRIC TYPE OF 
 INTESTINAL PUTREFACTION 
 
 "This form of intestinal derangement is characterized by 
 a chronic putrefactive process (having its seat mainly in the 
 large intestine and lower ilium) and due to the action of very 
 large numbers of strictly anerobic butyric-acid producing 
 bacteria, capable of multiplying by means of spore forma- 
 tion."— (Herter.) 
 
 The onset of the primary stage of this type of putrefaction 
 is more generally gradual than sudden. There are patients, 
 however, who date their trouble from some acute illness, 
 although the presence of a true saccharobutyric type at 
 that time cannot, of course, be determined. 
 
 The secondary stage is of long duration. There is not 
 usually a very marked departure from a condition of fair 
 health, but the patient's most frequent complaint is one of 
 indigestion, dyspepsia or of other symptoms due to the 
 irritation resulting from the presence of ammonium butyrate 
 in the intestinal canal. Constipation is usually the rule, 
 but often a diarrhoea may be present, which in some instances 
 may prove refractory to treatment. Considerable burning 
 accompanies this acute disturbance. The constipation 
 will follow the usual course, beginning as the atonic 
 type, passing into the spastic stage, but rarely, in 
 uncomplicated cases, reaching the point of stercoraceous 
 diarrhoea. Often the amount of flatus is greatly increased, 
 the composition of which will be found upon analysis to be 
 hydrogen and nitrogen. The flatus is usually of very little 
 odor, the aromatic character of normal human feces and 
 flatus will be absent. Occasionally a mild odor of old cheese 
 may be noted. 
 
40 THE SACCHAROBUTYRIC TYPE 
 
 The mouth is frequently sore and the tongue, from the 
 tendency of the superficial epithelial layer to exfoliate rap- 
 idly, is usually bright red. The tongue may be glazed and 
 its surface is often cracked. In very severe conditions the 
 skin may also be extremely irritable, especially sensitive to 
 light and wind, and in many of these people the exposed sur- 
 faces of the body are in a constant state of inflammation 
 during the summer months. In some people the subcutane- 
 ous and the submucous tissue is liable to attacks of oedema 
 of very severe grade, the so-called Quincke's oedema, and 
 the possibility of this swelling involving the glottis must 
 always be borne in mind. The muscular system is often the 
 seat of rheumatic pains of greater or less severity. 
 
 In the nervous system, outside of some vertigo or head- 
 ache, nothing very alarming is present. 
 
 In the circulatory systems very few disturbances are found 
 excepting slight irregularities in the heart's action and pal- 
 pitation. 
 
 If the liver is still equal to its task, very little trouble will 
 be noted outside of the intestines. When the patient's diet 
 has been of such nature as to encourage this type of putre- 
 faction, acute disturbances will result with an increased 
 production of butyric acid. The liver is then found swollen 
 and often tender to pressure. 
 
 A mild grade of anemia is very common. 
 
 The patients often complain of a moderate loss of strength, 
 often progressive, and their endurance is generally so poor 
 that the completion of the day's work becomes extremely 
 burdensome. 
 
 The onset of the tertiary stage is not violent, gradually 
 the signs and symptoms of degeneration in few or many 
 organs make their appearance and the patient slowly sinks 
 under the burden that the wreck of some specialized organ 
 imposes. 
 
 Examination of the gastric contents usually shows very 
 little of a pathogenic nature. 
 
 It is in the examination of feces, however, that the most 
 valuable information is found. 
 
OF INTESTINAL PUTREFACTION 41 
 
 Macroscopically the stools may be of large or small calibre, 
 the color varying from deep brown to reddish brown, except 
 at times of diarrhoea, when they approach a light yellow tint- 
 They often contain mucus. 
 
 Stained with dilute Lugol's solution, free starch is occasion- 
 ally found, but muscle fasciculi with striae are uniformly 
 absent. Clostridia may be abundant. With Gram's stain 
 the abundance of positive diplobacilli and biscuit-shaped 
 bacilli with strongly refracting capsules will be noted. The 
 smaller bacilli, often headlet in type, will be very numerous 
 and the large and small filaments will be absent. Large, 
 lemon-shaped Clostridia will be seen, growing in groups and 
 sporulating. In the negative field the presence or absence of 
 the colon bacillus and, if present, their numbers will give very 
 valuable information as to the severity of the infection and 
 the length of its standing. The greater the number of bac- 
 teria of the colon type found in the fecal fields, the lighter 
 and more amenable to treatment will be this condition. 
 The presence of streptococci, staphylococci is always a bad 
 sign and denotes the presence of ulcerative processes in the 
 small intestine or in the colon. With thionine stain most 
 of the micro-organisms will take a violet shade, especially 
 the B. Welchii. Very few will take a blue shade in this type 
 of putrefaction. The iodine fields will generally show an 
 abundance of the Clostridia of Prazmowsky, sporulating and 
 of very luxuriant growth. The field will be mildly Gram 
 positive to absolutely positive according to the severity of the 
 condition. 
 
 The urine will be acid and usually of high specific gravity. 
 Blue indican is never present in simple cases, although in- 
 dican red will be found in small amounts. Diacetic acid and 
 acetone are uniformly absent. The test with Ehrlich's alde- 
 hyde is usually negative. In the tertiary stage albumen 
 and casts often make their appearnace; in the primary and 
 secondary stages, the urine is microscopically negative. 
 
 This is the most common type of intestinal putrefaction 
 as well as the least fatal. The duration of many cases must 
 be measured in decades, not in years. In many individuals 
 
42 THE SACCHAROBUTYRIC TYPE 
 
 with the milder grades little inconvenience is suffered. They 
 may realize that they have a liver, that certain articles 
 of food are better left uneaten. Their general health, how- 
 ever, is not markedly impaired and they often attain a ripe 
 old age and die from some intercurrent disease without ever 
 entering the tertiary stage of enterocolitis with the sac- 
 charobutyric type of intestinal putrefaction. 
 
 The liver is the organ most liable to attack. Through 
 years of overwork in oxidizing the acid products of the dis- 
 ease a cirrhosis finally develops. This in turn, through the 
 pressure of the contracting fibrous tissue, further damages 
 the stroma until finally the patient ends his days on a milk 
 diet. This type is especially common in individuals who 
 have overindulged in severe physical exercise, such as the 
 professional football player, the heavy weight lifter, the iron 
 bar bender, and others who earn their living by feats of 
 strength and have thereby injured the oxidizing power of 
 their liver. In such individuals the probability of a complete 
 recovery is very remote. 
 
CHAPTER VII 
 
 THE ACETIC TYPE OF INTESTINAL 
 PUTREFACTION 
 
 This type is characterized by the production of ^-oxy- 
 butyric acid, diacetic acid and acetone, either singly or in 
 combination, in the intestinal canal. 
 
 The primary stage is not usually marked by symptoms 
 severe enough to confine the patient to bed, and is passed 
 with the diagnosis of overwork, in need of a tonic, or some 
 of the terms so often used in slipshod diagnosis is applied to 
 it. At this period the tongue is usually coated, some abdom- 
 inal distress may be present and occasionally constipation or 
 diarrhoea of mild grade. In other words, the patient sud- 
 denly finds his vitality reduced from some obscure cause. Re- 
 covery in this stage may be spontaneous and complete. 
 
 If this condition advances to the secondary stage, the 
 patient begins to notice an increasing loss of strength and 
 vigor. With this he begins to develop a pallid complexion, 
 notices that his tongue is habitually coated, finds great re- 
 lief from the more or less constant use of cathartics, but 
 rarely does he report any great diminution of his appetite. 
 As he advances in this stage he complains more and more of 
 intense thirst. The abdominal symptoms in uncomplicated 
 cases are usually of little moment. This stage may run on 
 for several years or even decades. 
 
 The tertiary stage may come like a thief in the night and 
 the individual suddenly awakens to the fact that his days are 
 numbered. On the other hand, the most intense abdominal 
 symptoms of very alarming character may be present. Oc- 
 casionally the nervous system bears the brunt of the attack, 
 and convulsive seizures or a comatose condition will develop 
 without warning. There is always the possibility that, in 
 
44 THE ACETIC TYPE 
 
 the latter instance, the individual may die without regaining 
 consciousness. 
 
 Acetone production is a common occurrence in persons who 
 consider themselves in fair bodily health. In this case, 
 however, we may assume the presence of a mild intestinal 
 catarrh that has so reduced the strength of intestinal anti- 
 septic as to render putrefaction possible, without being of 
 sufficient severity to cause any local symptoms. This ace- 
 tone production may be either continuous or intermittent, 
 varying in severity as the person's intestinal resistance may 
 vary from day to day, or with the character and condition 
 of the food ingested. 
 
 The anemias accompanying this type of putrefaction with 
 the production of acetone alone are often severe and the 
 destruction of erythrocytes very marked. 
 
 In many instances acetone may be present in the circu- 
 lation in such amounts as to impart a pronounced odor to 
 the breath without any marked departure from fair health. 
 
 In diacetic acid, however, we have to deal with a much 
 more potent poison. Rarely is this body found in the urine 
 without toxic symptoms referred to various organs of the 
 body occupying a very prominent position in the syndrome. 
 The liver is very generally the first to feel the attack of this 
 poison and is found swollen, the edge round and firm and 
 usually sensitive to pressure. The liver may be regarded 
 as a filter placed between the circulation through the intes- 
 tinal wall and the general blood stream. One of its most 
 important functions is to promptly remove any acids or toxic 
 bodies from the blood that passes through it and to hydrolyse 
 them into simpler and less irritating chemical bodies. These 
 poisonous bodies, unless they are of such stable composi- 
 tion as to be incapable of oxidation in the animal cells, are, 
 in the case of most of the toxins absorbed from the intestinal 
 contents, reduced to carbon dioxide and water. This chem- 
 ical process is similar to that which takes place when sarco- 
 lactic acid is washed out of the muscular system and brought 
 to the liver for disposal. Therefore, when a severe acid putre- 
 faction is present in the intestinal canal, an increased excre- 
 
OF INTESTINAL PUTREFACTION 45 
 
 tion of carbon dioxid is present, provided a requisite amount 
 of oxygen is supplied to the liver cells. While the liver is 
 equal to the task, the constitutional symptoms are few in 
 number and of little moment. When, however, that great 
 biochemical apparatus begins to find the task too heavy, 
 when the members of the fatty acid series begin to appear 
 in the general circulation and the burden of oxidation is 
 thrown upon the parenteral and parhepatic cells, then the 
 patient first realizes that there is a marked departure from 
 normal conditions. Strange to say, he rarely complains of 
 symptoms referred to the seat of trouble; on the contrary, 
 it is the heart, the nervous system, the kidneys, or a general 
 feeling of weakness that first attracts his attention. 
 
 ^-oxybutyric acid is never found in the urine unless the 
 function of the liver is impaired or exhausted. The complete 
 reduction of one molecule of /9-oxybutyric acid requires nine 
 atoms of oxygen. Thus: 
 
 CH3-CHOH-CH2-COOH + 9 O = 4 CO2 + 4 H2O, 
 in the case of acetone eight are required: 
 
 CH3-CO-CH3 + 8 O = 3 CO2 + 3 H2O, 
 while with diacetic acid eight also are required: 
 
 CH3-CO-CH2-COOH + 8 O = 4 CO2 + 3 H2O. 
 
 The molecule of /9-oxybutyric acid contains four carbon atoms, 
 that of diacetic acid four, while that of acetone contains but 
 three. The hydrogen content is eight, six and six in order. 
 The difference between the two acid bodies lies in the absence 
 of two hydrogen atoms in the group CHOH. As would be 
 expected the greater toxicity of the /3-oxybutyric acid is the 
 result of the presence of the two extra hydrogen atoms that 
 it contains. It does not seem probable that the liver would 
 waste much effort in reducing diacetic acid to acetone : 
 
 CH3-CO-CH2-COOH = CH3-CO-CH3 + CO2. 
 diacetic acid acetone 
 
 On the contrary, the following chemical equation would seem 
 much more probable: 
 
 CH3-CO-CH2-COOH + 80 = 4CO2 + 3H2O. 
 
46 THE ACETIC TYPE 
 
 Most specimens of feces from subjects showing acetone in 
 the urine have a marked odor of this chemical and also show 
 an abundance of bacteria and molds that are known to pro- 
 duce acetone freely in their growth. Careful study of the 
 stools in diabetes leads to the conclusion that the source of 
 /?-oxybutyric acid, diacetic acid and acetone is not the 
 metabolic activity of any human organ, but, on the contrary, 
 that they are the direct result of a chronic intestinal putre- 
 factive process. 
 
 These three poisons have a strongly selective action upon 
 the islands of Langerhans of the pancreas and the tissue in 
 their immediate neighborhood. From the observation of 
 individuals suffering from diabetes mellitus, acetonemia and 
 kindred diseases the conclusion seems logical that acetone 
 and diacetic acid were formed within the intestinal canal for 
 years before the glycosuria developed; that the pancreas 
 never felt the effects of these toxins until the liver became 
 incapable of guarding the general body parenchyma; and 
 that, through inflammation or destruction of the tissue of 
 the islands of Langerhans the production of pancreatic sucrase 
 was finally so reduced as to render the individual unable to 
 utilize his own glycogen. This, of course, in diabetes of the 
 pancreatic type. 
 
 In most sufferers from diabetic conditions it is a compara- 
 tively easy matter to check the production of diacetic acid 
 and acetone in the intestines for a time at least, and the improve- 
 ment shown by these patients is often remarkable. The reduc- 
 tion of the amount of sugar excreted, however, is a different 
 problem. Unfortunately no one has as yet been able to 
 obtain pancreatic sucrase either synthetically or by extraction. 
 Until this is done, our efforts to make diabetic patients util- 
 ize the glycogen that every day is returned to nature, a waste 
 product of faulty metabolism, are not likely to meet with 
 much success. To some of these individuals, however, a 
 ray of hope may be extended. There is the possibility 
 that some pancreatic tissue, handicapped by toxemia or by 
 surrounding inflammatory disturbances, may, when its bur- 
 den is lifted, regain its function. In this instance sucrase 
 
OF INTESTINAL PUTREFACTION 47 
 
 may be elaborated in such amounts as to enable the individ- 
 ual to assimilate carbohydrates in sufficient quantity to sus- 
 tain nutrition. 
 
 In consequence, the amount of sugar found in the urine is 
 not of so great importance is are the strength of the putre- 
 factive indices. These individuals are better nourished and 
 have much greater strength and endurance if considerable 
 amounts of carbohydrates are allowed. When a wound or 
 an abrasion becomes accidentally infected in the course of the 
 disease, a strict starch and sugar-free diet may be put in force. 
 It has often appeared from the study of surgical lesions in 
 diabetes, that too strict a diet had so reduced the resistance 
 of the patient as to court rather than to prevent infection. 
 
 This type of putrefaction often precedes severe degenera- 
 tive processes in the nervous system. Individuals suffering 
 from various psychoses, epilepsy and retinitis pigmentosa, 
 often show this type in a marked degree. 
 
 The feces, when acetone alone is present, may be either 
 scybalous, soft or liquid. They are usually dark in color* 
 varying from brown to blackish brown. Mucus is usually 
 normal in amount, but at times may be abundant. The odor 
 is aromatic, often intensely so, and in some specimens vinegar- 
 like. The reaction to litmus may be acid or alkaline, and the 
 blue paper moistened with water and suspended in the con- 
 taining vessel will often show the presence of volatile acid. 
 
 Microscopically, when stained with dilute Lugol's solution, 
 free starch is generally present in considerable amounts, 
 especially if potatoes are a staple article of diet. Striated 
 muscle fasciculi are uniformly absent. 
 
 Gram stained preparations show an abundance of large 
 bacilli, measuring six by one microns or thereabout, with 
 rounded ends, capsulated and growing singly, never in 
 chains, always positive unless degeneration has taken 
 place, and never unevenly stained nor granular. Spore 
 formation has never been noted in feces. The next 
 most abundant positive micro-organism is the bacillus 
 bifidus — 3 to 5 by 0.2 to 0.4 microns, irregular in form, 
 unevenly stained at times, sometimes bifurcated or of 
 
48 THE ACETIC TYPE 
 
 headlet form. This bacillus bifidus is always found when 
 acetic acid is present in the intestinal contents. Unless the 
 cell body is undergoing degeneration it is always Gram posi- 
 tive, although some bacilli may have negative sections, giv- 
 ing them a mottled appearance. Other bacteria, positive 
 to this stain, such as the capsulatus and the Clostridia may be 
 present, but never in great numbers, nor of luxuriant growth. 
 Among the Gram negative forms, the bacillus coli will be 
 found in abundance in the milder types, less and less numer- 
 ous as the severity of the putrefactive process increases, 
 finally being absent in the most severe grades. 
 
 In preparations stained with thionine blue, outside of a 
 few hyphae and conidia, little of moment will be noted. 
 
 In the thick films when strong Lugol's solution is used as 
 stain, a few organisms positive to iodine may be found. 
 
 When in addition to acetone, diacetic and /3-oxybutyric 
 acid are present, the evidences of disease in the stools are 
 much more marked. 
 
 Macroscopically they may still be scybalous, soft or liquid, 
 but mucus, either membranous, glairy or blood stained is 
 generally a prominent feature. Unless there is a marked 
 ammoniacal putrefaction present as a complicating condi- 
 tion, the feces are extremely acid and cause considerable 
 burning in their passage through the rectum. The odor of 
 these stools stands alone as the most disgusting encountered 
 in the laboratory. It may be described as alcoholic, 
 aromatic, butyric, acetic, musty, stinking and sickening, 
 and while examining these stools one wonders how any 
 patient could pass such feces without having his attention 
 very forcibly called to the condition of his intestinal canal. 
 
 Examined with dilute Lugol's solution, free starch is usu- 
 ally very abundant, Clostridia and iodine positive rods of large 
 size numerous and round and oval yeast cells plentiful and of 
 very luxuriant growth. Striated muscle fasciculi may be 
 present if the patient's health has been much affected, if 
 salted meat has been eaten or if cathartics are habitually 
 taken. 
 
 The Gram positive fields are especially rich and 
 
OF INTESTINAL PUTREFACTION 49 
 
 will contain Clostridia, large round-end rods, granularly 
 stained fusiforms, B. bifidi and B. Welchii in great numbers. 
 The B. putrificus is not regularly present. The negative 
 field is also very rich in bacteria. Large, medium and 
 small rods will be abundant and large hyphae-like bodies 
 often containing chlamydospores, or transparent spores occur- 
 ring singly or in masses will be found abundantly. The colon 
 type will be absent or only sparingly represented. 
 
 It is in the smears stained with strong Lugol's solution, 
 however, that the most characteristic pictures of this 
 diacetic-/?-oxy-butyric putrefaction will be found. The rich- 
 ness of these fields in iodine positive fungi of various form is 
 remarkable. Large deeply stained rods often bearing trans- 
 parent subpolar spores and lightly colored conidia with indis- 
 tinct outline, are very abundant. The spores often occur 
 singly or in masses and in either instance their capsules take 
 a delicate purple color. Clostridia are numerous, usually 
 sporulating and of luxuriant growth. Masses of a fusiform 
 bacillus will be found, staining delicately with iodine, growing 
 in chains and containing small transparent spores. These 
 chains are often laid side by side, giving the effect of several 
 strings of sausages arranged in parallel lines and in close con- 
 tact. Smaller bacilli staining delicately and sectionally are 
 numerous. Granular starchy matter and much bacterial 
 detritus staining a light blue will be abundant. 
 
 The yeasts, more especially those taking the round form, 
 are very abundant in all microscopical preparations. They 
 very generally contain deeply stained, iodine positive granules'. 
 
 The carbol-thionine stain may be used to check up the 
 general microscopical findings and in the search for the 
 micrococci of suppuration that may shed some light upon the 
 severity of the local lesion in the intestinal canal. 
 
 The biochemical process going on in the intestinal canal 
 among the micro-organisms gaining a parasitic livelihood 
 at the expense of their host presents a very interesting prob- 
 lem. The sugars and free starches are first hydrolysed by 
 the hyphomycetes (yeasts and molds) partly into acids of 
 the lower carboxyl series and partly into alcohols. The 
 
50 THE ACETIC TYPE 
 
 latter are still further attacked by a class of mirco-organisms 
 with the production of acetic acid and its near chemical neigh- 
 bors. At this point in the process, members of the bifidus 
 group change these acids into ketones, leaving behind those 
 they are unable to hydrolyse. A part of these products of 
 bacterial metabolism is discharged with the feces. Of the 
 part absorbed, the ketones are excreted by the kidneys and 
 the lungs, while the acids are oxidized in the liver. If the 
 latter organ is unequal to the task imposed upon it, while 
 some of the acids may be oxidized by the cells of the general 
 body parenchyma, the major portion leaves the circulation 
 through the kidneys. 
 
 The urine in this type of putrefaction will show a marked 
 reaction for acetone, diacetic acid or /3-oxybutyric acid, 
 either singly or in combination. High specific gravities are 
 the rule, and the reaction is usually strongly acid. If the 
 pancreas has been attacked sugar is usually present. Many 
 of the urines will contain albumen and casts and these often 
 disappear if improvement is gained through treatment. 
 
 The amount of damage this type of putrefaction does to 
 mankind is remarkable. Its onset is insidious and often its 
 presence is never suspected until symptoms arising from the 
 disturbance of the functions of some specialized organ leads 
 to an investigation of the patient's general condition. Un- 
 fortunately this usually comes too late. It is common among 
 people who gain their living through severe mental labor, or 
 who are exposed to great emotional strains. Certain fam- 
 ilies and also certain races are especially susceptible to its 
 ravages. Among individuals who are the misguided vic- 
 tims of vegetarianism, and who find a great financial saving 
 in a meat-free diet, this disease is very prevalent and fatal. 
 
CHAPTER VIU 
 
 THE OXALIC TYPE OF INTESTINAL 
 PUTREFACTION 
 
 There are certain sufferers from enterocolitis who present 
 a most peculiar history. The primary stage usually escapes 
 notice, although it may be severe enough to confine the pa- 
 tient to bed. In the latter case, intense muscular pains re- 
 quiring anodynes for their relief, weakness and disordered 
 defecation, with or without a discharge of mucus per anum, 
 are prominent symptoms. The primary stage may last from 
 a few days to a week, or even longer and the importance of 
 the attack, as the beginning of a long siege of ill health, is 
 not realized at the time. 
 
 The secondary stage is ushered in with a period of fair 
 bodily comfort of some length, but the patient notices that 
 his strength and endurance are less than they were before the 
 primary sickness. Muscular pains, either constant or inter- 
 mittent, begin to increase until the patient is rarely free from 
 suffering. This condition progresses until his nights are 
 spent in futile efforts to find a comfortable position in which 
 he may rest without pain and his days in regaining, through 
 massage and exercise, his muscular functions. The muscles 
 are not swollen but are at times extremely tender and through 
 disuse become flaccid. This flaccidity leads to the develop- 
 ment of acquired enteroptosis, flat foot and other myastheniae, 
 which add their burdens to those the patient already carries. 
 
 The abdominal symptoms are usually of little moment, but 
 in many of the cases, the intense burning and tenesmus at 
 stool and immediately afterward will upset the most calm 
 and phlegmatic disposition. These people resort to cathar- 
 tics very early in the disease as they find that a series of 
 diarrhoeal discharges have a very beneficial effect upon the 
 
52 THE OXALIC TYPE 
 
 severity of the muscular pains. This free catharsis, so far 
 as the intestinal condition is concerned, only adds fuel to the 
 -flame. The mucus is increased remarkably in amount, the 
 stools become more acrid in their nature and a very bad 
 matter is made much worse. 
 
 There are many infallible remedies for this so-called rheu- 
 matism in the market, each accompanied by a guarantee of 
 sure cure. These are tried in turn, the drastic cathartic 
 effect of each adding its quota of damage. Various irregular 
 practitioners will probably have tried their methods upon the 
 case until, thoroughly steeped in their persuasive conversa- 
 tion, the patient cannot tell whether he is suffering from a 
 displacement of the tenth rib pressing on a nerve, or an ex- 
 aggerated condition of sin and fear. There is one fact very 
 patent to him, however, and that is that he is growing more 
 inefficient day by day, while to outward appearance he is 
 enjoying at least fair health. 
 
 In another class of patients the production of oxalic acid 
 and oxalates is intermittent or cyclical. Sudden attacks of 
 very acute pain, referred to the liver, kidneys or muscles, 
 occur periodically. Under the rigid diet the patient enforces 
 in the few weeks following his illness, the periods of remission 
 are passed in comparative comfort. There will be very few 
 days, however, that the signs of this type of putrefaction can- 
 not be found in the urine and feces. As time effaces the 
 memory of the former attack and the patient uses less dis- 
 cretion in the selection of his food, the train is laid for another 
 explosion. This course may continue for many years and as 
 the importance of the lesion dependent upon foreign micro- 
 scopic crystalline structures in the body parenchyma does 
 not make a great impression upon the average patient, treat- 
 ment is very seldom continued. Finally, a trace of albu- 
 men found by some insurance examiner or a hematuria brings 
 the patient to the realization of the seriousness of his illness. 
 
 His appetite may be enormous, with an especial craving 
 for desserts of various kinds. He may proudly tell you, on 
 the other hand, that animal food could not account for his 
 condition, as he had carefully avoided it for some years. 
 
OF INTESTINAL PUTREFACTION 53 
 
 These are the most important symptoms in the picture of 
 this disease. Other organs may begin to show disturbances 
 of function without demonstrable organic lesions. 
 
 The feces may be either formed, soft or liquid, may or may 
 not contain much mucus and are usually of a musty odor. 
 Chemically they may be acid or alkaline, more generally the 
 latter, and show a pronounced reaction with Ehrlich's alde- 
 hyde. Microscopically, free starch may be present in the 
 more severe grades and absent in the lighter types. Muscle 
 fasciculi are generally absent. Among the crystalline struc- 
 tures those of calcium oxalate may be very abundant, but 
 fatty acid crystals will be very few in number. In Gram 
 stained preparations among the positive micro-organisms 
 many rods of large size with square ends having a positive 
 line across each end and one along the side, with a Gram nega- 
 tive cell body will be found in abundance. Also cuboid spores, 
 single-celled, having a length twice their diameter, capsulated 
 and occurring singly will be abundant. A few bacillus of 
 bacterium Welchii and also a few bacilli bifidi will be noted. 
 The Gram negative field in the milder grades will show an 
 abundance of bacillus communis coli. 
 
 Urinalysis will show no evidence of renal disease in the 
 mild cases; in the more severe cases, however, an albumen- 
 uria, which is usually intermittent will often be noted. The 
 indices of intestinal putrefactions of other types will be very 
 weak or lacking, but the amount of oxalate of lime, found 
 in crystalline form in the sediment of the urine will be remark- 
 able. 
 
 In the tertiary stage casts, either hyaline, granular or 
 bloody may be abundant. 
 
 If the feces are sown on glucose agar, at the end of several 
 days at room temperature, a fuzzy, velvety growth will 
 appear. Stained specimens of this growth will regularly 
 show the presence of monilia. 
 
 The tertiary stage may begin without violent symptoms. 
 The lesions of some organ important to metabolism and 
 excretion at the onset may not attract attention. On the 
 other hand, this stage may begin with such violence as to 
 
54 THE OXALIC TYPE 
 
 lead to the diagnosis of an acute lesion. In this connection 
 the estimate that ninety per cent of cases with a diagnosis 
 of acute nephritis are found on microscopical examination 
 to be chronic is especially impressive. 
 
 As the disease advances into the tertiary stage the symp- 
 toms peculiar to the secondary stage are gradually lost as the 
 more alarming syndrome develops. The patient sinks grad- 
 ually and dies with a diagnosis of nephritis, myocarditis or 
 some other condition degenerative in character, affecting some 
 vital organ. 
 
 An enterocolitis with this type of putrefaction may be 
 called the great moniliasis of the temperate zone. Although 
 many authors have described it as a condition of little moment, 
 still the presence of oxalate of lime crystals in the tissues and 
 more especially in the kidneys is capable of causing lesions 
 from which the patient may ultimately be incapacitated or 
 in many cases meet his death. 
 
CHAPTER IX 
 
 THE OLEIC TYPE OF INTESTINAL 
 PUTREFACTION 
 
 There are certain sufferers from enterocolitis who show a 
 decided intolerance of fats and oils, combined with severe 
 disturbances in the nervous system. This latter may vary 
 in severity from pyschoses of very alarming character, often 
 requiring institutional treatment, to mild neuralgias or neu- 
 roses affecting various organs. 
 
 The onset of the trouble may be either sudden or gradual, 
 usually sudden, and, as in many other intestinal infections, 
 the importance of the primary sickness may be overlooked. 
 Rarely, however, will patients be encountered who will not 
 give a history of an acute illness of greater or less severity, 
 from which they date the beginning of their troubles. 
 
 The primary stage may begin with a most intense prostra- 
 tion of both mental and bodily functions; and the attack is 
 often so violent as to cause acute mania, suddenly develop- 
 ing melancholia, insanity or in some cases death. 
 
 The secondary stage is usually prolonged, lasting in some 
 instances several decades. The psychoses that have devel- 
 oped in the primary stage may continue or may disappear 
 spontaneously. Often new disturbances of cerebral functions 
 make their appearance one after another, until the patient 
 is unable to be cared for outisde of some hospital for the in- 
 sane. 
 
 Another class of individuals develop a special clinical pic- 
 ture, in which a progressive bodily weakness, mild paralyses 
 and severe intestinal symptoms play an important part. 
 Many of these patients show an extreme sensitiveness of the 
 cutaneous surface to sunlight. 
 
 The intestinal symptoms in the primary and secondary 
 stages appear of so little moment, in comparison with others 
 of more alarming nature, that they are overlooked or ignored. 
 
56 THE OLEIC TYPE 
 
 Three or four stools a day are not generally regarded as 
 remarkable by the average attendant. These stools are at 
 times accompanied by considerable burning or tenesmus, but 
 the patient is generally in no condition mentally to take much 
 notice of the fact. In the secondary stage, while light yellow 
 diarrhoeal stools are often found, there may be a severe grade 
 of constipation. A very marked increase in the amount of 
 the feces is always present. Mucus may or may not be pres- 
 ent, and, if erosions or ulcerations arise as a complication, 
 blood in greater or less amount may be passed. 
 
 The blood begins to show evidence of toxic damage very 
 early in the disease, the anemia being characterized by a 
 rapid destruction of erythrocytes. It is rare to find any 
 marked leucocytosis, unless the special point of attack of 
 the intoxication is the spleen or lymphatic system. 
 
 From the physical examination of the patient little light 
 will be thrown upon the conditon. The liver may be smaller 
 than is normal, or the colon may show the signs of atonic or 
 spastic colitis. In most cases the abdominal examination 
 will be negative. An examination of the feces, however, will 
 reveal the cause of the trouble. 
 
 Macroscopically, the stools may be soft, hard or of creamy 
 consistency; the color light yellow, yellowish gray, brownish 
 gray or clay colored, the brightness of their color varying 
 with the amount of fat crystals that they may contain; mucus 
 is generally present in considerable amounts, although it 
 may be absent. The reaction of these stools may be acid, 
 neutral or alkaline. They are, as a rule, however, acid to 
 litmus. Emulsified with dilute Lugol's solution and exam- 
 ined under the microscope the number of fat crystals present 
 is usually remarkable. These may appear in the form of 
 needles, crystals or in the form of sheaves. The size of these 
 crystals will vary according to the kind of fat most abundant 
 in the food. As these crystals are examined, one is impressed 
 with the great loss of fat that is going on in the intestine. 
 Soap crystals may also be abundant. Free starch and 
 muscle fasciculi are usually absent. 
 
 In Gram stained preparations, among the positive micro- 
 
OF INTESTINAL PUTREFACTION 57 
 
 organisms, very large dumbbell diplococci with capsules 
 5 X 2.25 microns in dimensions will occupy a very prominent 
 place. These often grow in the form of large streptococci com- 
 posed of the above named dumbbell diplococci. In some 
 specimens the edge of the micro-organism has a wavy outline, 
 putting one strongly in mind of the form taken by a section 
 of inflated colon. In some specimens of feces this micro- 
 organism may be present in almost pure culture. Various 
 other forms such as the biscuit shaped bacterium Welchii, 
 the smaller sausage-shaped rods, the bacillus bifidi, and a few 
 Clostridia are generally present in moderate numbers. Un- 
 less the feces have been retained in the colon until bacterial 
 autolysis has taken place, the dumbbell diplococci will be 
 found abundant and of luxuriant growth. 
 
 Among the Gram negative forms very large hyphae 10 
 to 12 microns in length by 2 microns in width, which often 
 contain large polar or sub-polar transparent spores, will be 
 noted. These rods at times stain positively in areas. Many 
 fine rods closely resembling the bacillus liquefaciens ilei will 
 be abundant, especially in soft or liquid stools. The bacillus 
 coli, when the disease is of mild nature, is uniformly present. 
 In the more severe conditions, however, it is generally absent. 
 
 In preparations stained with carbolic thionine the dumb- 
 bells and large Gram negative bacilli will be stained a dark 
 blue in distinction to the other micro-organisms, which appear 
 violet in tint. Often other large conidia-like bodies, stain- 
 ing diffusely, with transparent areas will be found in these 
 specimens. 
 
 Smears stained with strong Lugol's solution are usually 
 negative. Occasionally, the large transparent spores, men- 
 tioned above, will be shown very plainly, often in masses 
 of seven to ten. The field may be mixed, lightly or abso- 
 lutely positive, but never negative. 
 
 Feces sown on glucose agar media at the end of three days 
 show a slimy, flat growth, spreading over the surface. This 
 growth is white with a yellow tinge with even border and is 
 slightly raised above the surface of the agar. In Gram stained 
 preparations of this growth a few irregularly shaped hyphae 
 
58 THE OLEIC TYPE 
 
 will be noted but no well developed mycelia. The conidia 
 will be fusiformed, capsulated and if sufficiently decolorized 
 with alcohol or nitric acid alcohol will show characteristic 
 Gram positive polar dots. This is a mold of the genus torula. 
 
 Much work remains to be done upon the molds that gain 
 their living in the intestinal contents. It is probable that 
 many disagreeable, if not dangerous or fatal disturbances 
 which are occasionally encountered in clinical work may be 
 attributed to the toxins and enzymes that they produce in 
 their metabolism. 
 
 Judging from the amount of free oleic, palmitic, stearic 
 and other heavy fatty acids that are present in the feces in 
 this condition, there must be an enzyme of remarkable activ- 
 ity produced in the intestinal lumen. Fat needles are often 
 found in feces of individuals who do not show the same severe 
 nervous symptoms that have been described. In this case, 
 however, the fecal fields do not show the presence of the 
 oleic type of putrefaction and when this latter condition per- 
 tains, some pancreatic disease of a functional or organic 
 nature should be suspected. 
 
 While admitting that oleic acid and its near neighbors in 
 the fatty acid series may be toxic, when used subcutaneously, 
 it is difficult to believe that the great damage to the nervous 
 system, encountered in this type of putrefaction, can be 
 accounted for on the theory of oleic acid absorption from the 
 intestines. It seems much better to explain this group of 
 symptoms upon the basis of a lipase intoxication arising from 
 the metabolic activity of micro-organisms in the intestinal 
 contents. Sufferers from this type of enterocolitis, when the 
 excessive fat splitting process is checked, show a most remark- 
 able improvement in their mental and nervous condition. 
 
 The urine is usually negative both microscopically and 
 chemically. 
 
 The tertiary stage in this type of putrefaction is character- 
 ized by marked degenerative changes in the nervous system. 
 The brain is the usual seat of this attack and the more severe 
 pyschoses when present render it absolutely necessary that 
 the patient pass his days in some institution. 
 
CHAPTER X 
 
 THE AMMONIACAL TYPE OF INTESTINAL 
 PUTREFACTION 
 
 There is a type of enterocolitis of a very severe grade, in 
 which ammonium is produced in great quantities in the 
 intestinal canal, accompanied by a persistent diarrhoea, 
 great physical weakness and a very high grade of anemia. 
 
 In the primary stage great and sudden prostration, diag- 
 nosed as neurasthenia, with rarely a rise in temperature, a 
 weak and rapid pulse, vomiting, abdominal pain and tender- 
 ness often so severe as to suggest an acute peritonitis, are all 
 prominent symptoms. Commonly diarrhoeal stools are pres- 
 ent, often containing mucus and blood or bloody mucus. In 
 some instances, however, persistent constipation will be 
 found. The discharges per anum may contain very little, 
 if any fecal matter and may consist solely of mucus or muco- 
 pus. The illness may be so severe as to cause death or con- 
 valescence may be prolonged for months or even years. 
 
 The secondary stage may last for several decades and 
 patients passing through this stage are usually great sufferers. 
 There is rarely impairment of the mental faculties, but neu- 
 ralgia of great severity is a very frequent symptom. Attacks 
 of herpes zoster are very common, often followed by post- 
 perpetic neuralgias, which make the patient's life one of misery. 
 The circulatory systems show a marked weakness of the 
 musculature of the heart and blood vessels, but rarely is 
 there any increase in blood pressure or an arteriosclerosis. 
 
 In the urinary system secondary infections are generally 
 the rule, leading to pyelitis and cystitis with ammoniacal 
 urine. The precipitation of the earthy phosphates of the 
 urine is very common and in patients who have suffered for 
 several years from this type, one or more phosphatic cal- 
 culi are usually present, in the kidneys, ureter or bladder. 
 
60 THE AMMONIACAL TYPE 
 
 The liver may be enlarged, its lower border swollen, rounded 
 and soft. The gall bladder and gall ducts may also be 
 the seat of calculus formation. The colon may be palpable, 
 prolapsed, distended, crepitant or knotty from the presence 
 of scybala. Intense pain may be referred to its location with 
 burning of greater or less degree. Under X-ray examination, 
 portions may be found showing constrictions, which may be 
 either organic or spastic in origin. 
 
 The urine is light in color, cloudy from the presence of pus 
 or earthy phosphates and intensely ammoniacal in odor. The 
 reaction is uniformly alkaline. The specific gravity is as a 
 rule so low as to lead to a suspicion of an incipient inter- 
 stitial nephritis. As recovery takes place, however, the 
 specific gravity usually rises to normal. Albumen may be 
 present in greater or less amount. An indicanuria of high or 
 low grade may be present, but is not, in simple cases, prom- 
 inently so. Diacetic acid may or may not be present and 
 also skatol. 
 
 Upon microscopical examination, the great number of 
 crystals of ammonium magnesium phosphate, together with 
 the abundance of earthy phosphates, will be remarkable. 
 The presence of casts of various types gives the condition a 
 place in the tertiary stage and organic elements are rarely 
 found in the secondary stage. 
 
 The feces may be liquid, watery, formed or scybalous. 
 The color may vary from yellowish gray in diarrhoeal to dark 
 brown in scybalous stools. Mucus may or may not be ex- 
 tremely abundant. The intense ammoniacal odor of these 
 stools is remarkable. The stools are always strongly alkaline. 
 Litmus paper wet with water and held over the mouth of the 
 container will be turned blue. 
 
 Microscopically, with dilute Lugol's solution, free starch 
 is absent, muscular fasciculi are absent, a few fat needles 
 may be noted, yeast cells, usually of the round variety, will 
 be abundant, while of the crystalline bodies, the number of 
 triple phosphates will be a cause for remark. Many soap 
 crystals will also be found. 
 
 In the Gram stained field, among the positive forms, the 
 
OF INTESTINAL PUTREFACTION 61 
 
 presence of streptococci will be especially noticeable. Many 
 of the capsulatus type will be found, as these grow luxuriantly 
 in alkaline feces. If ulceration is present, cocci and staphylo- 
 cocci will be abundant, their number varying with the nature 
 and extent of the suppurative process. Long filamentous 
 forms, apparently belonging to the B. putrificus group, are 
 very abundant. Occasionally, Clostridia will be present, the 
 alkaline intestinal contents furnishing a very favorable 
 medium for the growth of acid producing bacteria. 
 
 In the Gram negative field, many large rod-like micro- 
 organisms will usually be observed. These, apparently, are 
 the hyphae of molds and may have sections taking the posi- 
 tive stain with more or less intensity. 
 
 Various negative forms, such as the B. liquefaciens ilei may 
 be present. The colon bacilli in the more severe types are 
 absent. In their absence or presence, and if present their 
 number, we find a very useful method of estimating the 
 severity of the intestinal condition. 
 
 In the preparations stained with carbol thionine the micro- 
 organisms are generally stained blue. The capsulatus types 
 usually take the violet tint which is characteristic in speci- 
 mens from the various types of putrefaction. 
 
 With the specimens stained with strong Lugol's solution, 
 free starch detritus is very regularly present. Clostridia 
 may or may not be present. Often the micro-organisms in 
 the immediate neighborhood of the free starch granules take 
 the iodine stain in the less serious types of this putrefaction. 
 
 The microscopical field varies from absolutely positive to 
 mixed, concomitantly with the severity of the enteric catarrh. 
 
 There are many patients in whom the severity of this 
 intestinal condition is masked through the coexistence of a 
 putrefaction of an acid type. So long as the production of 
 acids and ammonia is about evenly balanced, these patients 
 enjoy fair health and are able to perform their daily tasks in 
 comparative comfort. At times, either through changes in 
 the character of their diets, or, perhaps, through the acqui- 
 sition of new and more active strains of either acid or alkali- 
 producing bacteria, the balance is upset, and they suffer 
 
62 THE AMMONIACAL TYPE 
 
 attacks attributable to either one effect or the other. The 
 character of this condition can be easily discovered through 
 the methods of examination set forth in the previous chapters. 
 Marked organic lesions do not generally mark the tertiary 
 stage of this type of enterocolitis. The patients are gradually 
 worn down by attack after attack of an acute nature until 
 they lapse into a condition best described by the term, gen- 
 eral debility. A rapidly advancing pernicious anemia or 
 some intercurrent disease, usually ends their life peacefully 
 and with little suffering. 
 
CHAPTER XI 
 
 THE URIC ACID TYPE OF INTESTINAL 
 PUTREFACTION 
 
 There are certain patients, the victims of mild grades of 
 enterocolitis, in whom there seems to be a chronic deficiency 
 of oxidizing power. This may be a matter of heredity, 
 acquired as the result of sedentary habits combined with the 
 habitual ingestion of great quantities of highly nutritious 
 food, or the result of exhaustion of the oxidizing function 
 through the consumption of alcohols, ethers, aldehydes, acids 
 and aromatic bodies found regularly in the products of the 
 vineyard and of the still. In consequence, a very slight in- 
 crease in intestinal putrefaction upsets their metabolic equi- 
 librium, while any sudden increase in the production of acids 
 in the digestive canal brings on an attack of gout of a severity 
 varying concomitantly with the enteric condition. 
 
 The important point in these cases, however, is that there 
 is an intestinal putrefaction of some type present, not only 
 at the time of the paroxysm, but also during the time when 
 gouty symptoms are absent. If this can be checked and a 
 normal condition of the intestinal mucosa brought about, the 
 patient will experience no further difficulty. The intestinal 
 condition may be diagnosed through the methods laid down 
 in this work. 
 
CHAPTER XII 
 MALARIA. SYPHILIS AND TUBERCULOSIS 
 
 In every case of enterocolitis, no matter what the type of 
 putrefaction may be, an investigation of the possibiUty of 
 a malarial, syphilitic or tubercular infection, singly or in 
 combination, should always be conducted. 
 
 Malaria is one of the most common diseases of civilization. 
 The malarial chill occurring every two or three days has, in 
 New England, become a rarity. In its place we find the 
 chronic, deep-seated infections of long standing in which a 
 diagnosis is extremely difficult from an examination of the 
 blood unless the parasites are in the swarming stage. Often 
 two or more types of malarial parasites may be found in the 
 same person. The spread of malaria through the New England 
 states may be laid at the door of immigration. The subter- 
 tian type is the most prevalent. 
 
 In order to get a correct clinical picture of these malarial 
 conditions we must regard them as a chronic parasitic disease 
 of the liver, spleen, pancreas, bone marrow and other organs, 
 and not of the red blood cells alone. The time during which 
 these parasites lie dormant in these organs may be passed in 
 comparative comfort so far as the patient is concerned. At 
 certain seasons of the year when the blood stream is invaded 
 by the sexual forms of the Plasmodium, or their growth be- 
 comes more active, various intestinal symptoms are prom- 
 inent. These may vary from distress, burning, epigastric 
 unrest, diarrhoea or constipation, to pain in the right side 
 of the abdomen so severe as to simulate appendicitis. 
 
 There is usually no rise in temperature at the time of these 
 attacks. Upon physical examination, the liver is usually 
 found swollen and palpable and often tender. An examina- 
 tion of the blood will show a mild leucocytosis. 
 
 Better results will be obtained in the search for plasmodia 
 
MALARIA, SYPHILIS AND TUBERCULOSIS 65 
 
 if the blood is examined after the method of Manson. A 
 glass slide and cover glass are first carefully cleaned with 
 alcohol. It is especially important that these should be abso- 
 lutely free of all grease, before spreading the blood. The 
 lobe of the ear is next punctured with a small lancet or a three- 
 cornered needle, a very small drop of blood placed in the 
 centre of the cover glass, great care being taken that the glass 
 does not touch the skin. The slide is then breathed upon 
 and the cover glass placed blood downward upon it. This 
 process must be done quickly in order that the drop of blood 
 may not dry. When this is properly done, three zones will 
 be noted in the preparation. The central zone should be 
 absolutely transparent and colorless, the middle zone should 
 have a delicate pinkish yellow tint and the outer zone should 
 be blood red. When examined with a twelfth oil immersion 
 lens, in the central or colorless zone the blood will show 
 scattered erythrocytes, resting flat between the two glass 
 surfaces. In the light colored zone the red cells will be over- 
 lapping or rouleated with clear spaces between. The red 
 area will consist of closely packed red cells with here and 
 there a leucocyte. The central transparent area should be 
 carefully searched for plasmodium, either within or upon the 
 red cells. The second area should be examined for active para- 
 sites and for micro- and macrogametes. These will not be found 
 in the transparent area as the pressure of the cover glass upon 
 the glass slide prevents them from freeing themselves from 
 the red cells. These gametes at room temperature are gen- 
 erally extremely active. 
 
 Stained blood smears are usually of less value than fresh 
 preparations. 
 
 The malarial infections met with may be classified as 
 follows : 
 
 The Quartian Type, Plasmodium malariae. 
 
 The Tertian Type, Plasmodium vivax. 
 
 The Pigmented Quotidian Type, Laverania praecox. 
 
 The Unpigmented Quotidian Type, Laverania immacu- 
 lata. 
 
 The Subtertian Type, Laverania malariae. 
 
66 MALARIA, SYPHILIS AND TUBERCULOSIS 
 
 Any organ of the body may become sensitized to the mala- 
 rial protein. The symptoms that the patients show will 
 depend upon which tissues have acquired the power of digest- 
 ing the protein of the plasmodia. The blood cells may have 
 acquired this property and the remainder of the body paren- 
 chyma, not having the same power, may remain intact. In 
 this case a true picture of pernicious anemia will be given. 
 So, also, the epithelium of the mucous glands and follicles of 
 the intestinal canal may become sensitized to this poison and 
 the other organs of the body remain unsensitized. In this 
 case the patient will give a history of subacute attacks or 
 exacerbation of a low grade catarrhal process, limited to the 
 intestinal canal. Having confirmed the diagnosis by a micro- 
 scopical examination of the blood, it is extremely interesting 
 to follow the course of the intestinal symptoms under anti- 
 malarial treatment. Most of these cases are made very much 
 worse by quinine, at least during the first week of treatment. 
 The reason for these untoward symptoms arises from the 
 fact that the tissues of the intestinal canal during this period 
 are called upon to digest the malarial protein arising from 
 the death of the plasmodia through the toxic action of quinine, 
 in far greater amount than before. In about two weeks 
 after the beginning of anti-malarial treatment, it will be uni- 
 versally found that larger doses than those used in the begin- 
 ning may be used without disagreeable symptoms. 
 
 The fact must be borne in mind that in many of these in- 
 dividuals the power of digesting particulate malarial protein 
 bodies has been exhausted. In other words, that the patient 
 has developed a condition often termed anti-anaphylaxis. 
 The blood in this condition will show a marked leucopenia. 
 The scarcity of the white cells and also their lack of vitality 
 will be noted in the fresh blood preparations if the warm stage 
 is used with the microscope. In normal blood preparations 
 the living leucocytes should never take the spherical form at 
 body temperature. The normal leucocyte is always angular 
 or amoeboid in form. Therefore, so far as the leucocytes go, 
 the number of these cells may be used as a guide to the re- 
 sistance of our patients against the infection. 
 
MALARIA, SYPHILIS AND TUBERCULOSIS 67 
 
 The cover glass had better be ringed with vaseline to pre- 
 vent evaporation in the blood film and consequent crenation 
 of the red cells that might simulate plasmodia attached to 
 the cell surface. An abundance of crenated erythrocytes 
 indicates a deficient vitality of the red cells. If any of these 
 cells have a to-and-fro motion, we may assume that a malarial 
 parasite is attached to it. The study of the minute bodies 
 observed in the plasma of the fresh preparation will lead the 
 examiner to conclude that possibly a sexual cycle takes place 
 in the blood stream, as well as in the mosquito. 
 
 The organisms are often pear-shaped, motile and appear 
 to attach themselves to the red cells by their smaller extrem- 
 ity. Often small poikilocytes and microcytes will be seen in 
 motion, traveling across the field, towed by these pear- 
 shaped micro-organisms. When these larger bodies are free- 
 swimming they take the form of a dumbbell. Their motion 
 is very active. Their bodies are highly refractile and the 
 cytoplasm shows evidence of intracellular circulation. Appar- 
 ently this body eventually divides the two pear-shaped bodies. 
 
 Crescents will also be noted attached to withered or cre- 
 nated erythrocytes. This form is not so active as the pear- 
 shaped and dumbbell forms. They are rather hard to dis- 
 tinguish under the microscope as the light transmitted through 
 the red cells gives their bodies the same tint as the colored 
 corpuscles of the blood. 
 
 The course of malarial infection may be divided into four 
 stages. First, the stage of invasion; second, the stage begin- 
 ning with the establishment of sensitization, which may be 
 called the anaphylactic; third, the stage in which the growth 
 of the Plasmodia and the parenteral digestion of the malarial 
 protein is evenly balanced; fourth, the stage in which the 
 power for protein digestion has been exhausted and the pa- 
 tient enters a condition usually described as anti-anaphylaxis. 
 
 The primary stage or the stage of invasion is devoid of 
 serious symptoms. The patient may have certain prodo- 
 mata, such as mild headache, slight loss of appetite, weakness 
 and lack of endurance, but does not consider himself ill. 
 
 The second stage usually begins with a pronounced chill, 
 
68 MALARIA, SYPHILIS AND TUBERCULOSIS 
 
 followed by a rise in temperature, which in turn is followed by 
 profuse perspiration. This corresponds to the time when 
 the patient's sera, leucocytes and tissue cells have acquired 
 the power of digesting the particulate protein of the mala- 
 rial Plasmodia. This stage may last from one day to two 
 weeks, depending upon the strength of the special strain of 
 malarial plasmodia that are invading the body. 
 
 In the third stage, very few symptoms will be shown out- 
 side of a weakness and loss of strength and endurance. 
 
 In the fourth stage, where the resistance against the attack 
 of the Plasmodia has been completely exhausted, the patient's 
 life becomes one of great misery. In this stage, the symp- 
 toms may be referred to any of the specialized organs, either 
 singly or in groups embracing two or more organs. The cen- 
 tral nervous system is very apt to be the seat of attack and 
 certain comatose, paralytic or neuralgic conditions may be 
 encountered. In the tropics these conditions are frequent 
 and fatal, but in the temperate zone, while not so severe, they 
 are far more common than is realized. Conditions diagnosed 
 as serous apoplexy, sudden cerebral congestions, severe neu- 
 ralgias and attacks of herpes zoster, with or without posther- 
 petic neuralgias, may be caused by a chronic malarial infec- 
 tion in the fourth stage. The circulatory system may be the 
 point of attack and various functional cardiac disorders, 
 often accompanied by a rise in blood pressure, irregular heart 
 action and precordial pain will be noted. If the liver is the 
 point of attack, pain referred to the right side of the abdomen, 
 jaundice, swelling of the liver, attacks with fever, often de- 
 scribed in the tropical countries as bilious remittent fever, 
 will occur. The pancreas may also be the seat of attack with 
 glycosuria, pain and fatty stools. The kidneys may also be 
 attacked and syndomata resembling the black water fever 
 of the tropics, but much less severe, may be observed. In- 
 testinal symptoms will often be prominent. These usually 
 show a certain periodicity and may be accompanied by con- 
 stipation or diarrhoea, a great increase in the amount of 
 flatus and an abundance of mucus in the stools. Pain is apt 
 to be a prominent symptom and may be referred to any por- 
 
MALARIA, SYPHILIS AND TUBERCULOSIS 69 
 
 tion of the abdomen. So severe may these pains be as to 
 simulate appendicitis, biliary colic, and many of the opera- 
 tions undertaken for the relief of the two latter conditions 
 in which no lesion of the appendix or the gall bladder are 
 found may be laid at the door of this disease. 
 
 A few words upon the life history of the micro-organism 
 of subtertian malaria may be of interest. Let us begin with 
 the mosquito of the variety anopheles, in which the salivary 
 glands are charged with the microzoon of this disease. Upon 
 biting a human being the germ enters the lymph channels 
 or the capillaries. In a longer or shorter time, depending 
 upon the number of organisms introduced, the body fluids 
 will contain billions of plasmodia. This may or may not be 
 followed by a sensitization of the general parenchyma or of 
 certain organs or groups of organs. The more general the 
 sensitization, the less liable will the patient be to a chronic 
 malarial infection. The entire crop of plasmodia may be de- 
 stroyed at the time of the first chill. On the other hand, sev- 
 eral chills, each one of less severity than its predecessor, may 
 lead on into the third stage of chronic malaria. If this occurs, 
 the Plasmodia penetrate deeper and deeper into the body 
 tissues and are found no longer in the peripheral circulation, 
 finding their abode in the liver, spleen, brain or bone marrow. 
 At certain periods these plasmodia set free a host of micro- 
 and macrogametes, but between times the blood, so far as 
 micro-organisms are concerned, is free of malarial forms. The 
 time of swarming usually corresponds with the period of 
 malarial symptoms in the individual. If blood containing 
 these forms is eaten by the anopheles, the mosquito becomes 
 infected and can transmit the disease. On the other hand, 
 two cycles may take place within the body, an asexual and in all 
 probability a sexual cycle. The latter type of propagation 
 seems very probable, in view of the fact that asexual propa- 
 gations among all protozoa, without the introduction of new 
 individuals in the chain, eventually result in the degenera- 
 tion of that individual colony. Many of the blood pictures 
 seen in the study of chronic malaria lead to the prediction 
 that this will some day be proven. 
 
70 MALARIA, SYPHILIS AND TUBERCULOSIS 
 
 It seems also probable that malaria may be transmitted in 
 other ways than through the agency of anopheles. More 
 especially when we consider the minuteness and motility of 
 the micro- and macrogametes of the subtertian plasmodia. 
 Possibly, as in syphilis, this type may be transmitted by 
 direct contact with abraded surfaces, or upon the ovules or 
 microgametes of human beings. 
 
 Often no second stage will be noted and the patient will 
 become malarialized without having any of the classic symp- 
 toms of an acute malarial infection. This will account for 
 many of the chronic malarias that give no history of any 
 acute attack. 
 
 Three types of syphilis will be met with as complications 
 in enterocolitis. The first type includes ulcerations, gum- 
 mata and other purely local lesions of the intestinal canal. 
 The second type includes syphilitic disease of the liver, pan- 
 creas and spleen. The third type includes diseases of the 
 nervous system, acting reflexly upon the intestinal canal and 
 also lesions of the intestinal mucosa, corresponding in their 
 pathological processes to the tertiary lesions found upon the 
 skin. In the first two types the Wasserman reaction is 
 usually positive for the blood. In the third type the cerebro- 
 spinal fluid will be positive and the blood negative. In the 
 first type the lesions will be caused by the direct attack of 
 the treponema. In the second, the symptoms will be second- 
 ary to syphilitic disease in the organs supplementary to in- 
 testinal digestion. In the third, the symptoms will arise 
 from the disturbance of the correlation of the mechanical and 
 chemical processes of digestion, in the first case, and in the 
 second, from sensitization phenomena without the local pres- 
 ence of the micro-organism of the disease. 
 
 The lungs should always be carefully examined for tuber- 
 cular lesions and the possibility of tubercular foci in other 
 organs should always be considered. Primary tuberculosis 
 of the intestinal mucosa, while rare, is always possible as a 
 complication of an intestinal catarrh. If ulceration is pres- 
 ent, tubercule bacilli and blood will be present in the feces. 
 A search for tubercule bacilli is always important in the 
 examination of feces. 
 
CHAPTER XIII 
 
 THE PROTEIN POISON 
 
 Protein sensitization or anaphylaxis occupies a very prom- 
 inent position in many of the problems of enterocolitis, and 
 the parenteral digestion of foreign protein bodies and the 
 poisonous effect of the split products of this digestion should 
 be kept in mind. These bodies may enter the intestinal 
 canal with the food, in the mucus from the nose and throat or 
 arise as the result of bacterial growth in the intestinal canal, 
 the passages connected therewith or in the mucosa or sub- 
 mucosa that lines them. 
 
 In nearly every individual, the phenomena of sensitization 
 against certain proteins can be found. In some the pro- 
 teins of fish, in others those of eggs, while in others those of 
 certain vegetables and fruits cause disagreeable symptoms 
 or at least are extremely distasteful. Other sufiferers from 
 enterocolitis notice that certain months of the year are es- 
 pecially uncomfortable so far as their intestinal condition is 
 concerned, and so regular is the recurrence of these periods 
 that a direct connection with some of the pollens that cause 
 hay fever sufiferers so much trouble may be suspected. The 
 desquamations of some of the lower animals may also be a 
 cause of trouble. 
 
 In the primary stage of enterocolitis, sensitization phenom- 
 ena are generally very prominent, often alarming in their 
 intensity and may in certain cases be the cause of sudden 
 death. Most of the attacks of acute indigestion are caused 
 by the so-called protein poison, arising from the digestion 
 of the particulate protein of bacteria or of soluble proteins 
 that have escaped the action of the enzymes normally 
 present in the intestinal canal. 
 
 The mucous surfaces of certain individuals seem to be 
 
72 THE PROTEIN POISON 
 
 especially permeable to certain protein bodies. Ulcerated 
 or eroded surfaces and large areas of scar tissue make this 
 absorption especially hard to control. 
 
 In the case of the particulate proteins, namely the micro- 
 organisms, this sensitization gives complete protection against 
 the further attack of the invading parasite so long as this 
 immunity lasts. In the case of the soluble proteins, however, 
 the amount absorbed may be great enough to exhaust the 
 sensitization of the cells of the body and bring on the condi- 
 tion termed anti-anaphylaxis. This condition is present in 
 many cases of enterocolitis. Consequently, the success or 
 failure of our efforts to relieve our patients depends upon 
 our ability to find which proteins are harmful and which are 
 well borne. 
 
 The symptoms in the primary stage may best be grouped 
 under the term acute-anaphylactic or sensitization shock. These 
 are paralysis of the voluntary muscles, a greatly reduced 
 blood pressure, a spasm of the bronchi and death by suffo- 
 cation resulting from this spasm. This train of symptoms 
 is present in every sufferer from acute indigestion. The 
 patient falls, struggles for breath, goes into a state of syncope, 
 respiration ceases, and he dies, so to speak, with his heart 
 still beating. If recovery takes place the respiration first 
 returns, the weakness rapidly disappears and the patient 
 recovers in a remarkably short time. THe prodroma 
 that are noted in animal experimentation are always well 
 marked, namely the itching of the skin or a disturbance 
 of cutaneous sensation. 
 
CHAPTER XIV 
 
 THE TREATMENT OF ENTEROCOLITIS 
 
 The therapy of enterocolitis furnish many problems of 
 great interest. Upon the success or failure of our efforts, the 
 future usefulness, comfort and prosperity of our patients will 
 depend. It is well to realize in the beginning the magnitude 
 of the task, to gain the confidence of the patient and to avoid 
 promising too speedy a recovery. Many of the patients im- 
 prove wonderfully in a few weeks, take false courage and 
 believe that their health has been permanently restored. 
 Such people should be told frankly that their improvement 
 may be temporary and that the fact that it took place does 
 not affect the length and persistence of the therapeutic cam- 
 paign. The average patient expects great things from the 
 physician and is apt to form a poor opinion of any medicine 
 that does not bite as quickly as the ubiquitous cocktail. 
 Procedures that neither physic nor benumb are beyond his 
 comprehension. Quick results are always expected and it is 
 hard to convince him that the physician cannot supply that 
 very important factor in the treatment of his disease, namely 
 time. It is also difficult to protect your patient from the 
 advice of friends, nurses and irregulars, often to be sure, given 
 with the best intentions, but, from a psychological stand- 
 point, very deleterious. 
 
 While realizing that humanity is prone to err and that the 
 physician should be ever ready to forgive any lapses from 
 routine that are confessedly the result of human weakness, 
 still, never allow a patient to argue this question. The mat- 
 ter should be brought at once to the point of obey or find some 
 other physician. The mental process of the patient who has 
 a history and physical examination completed, submits speci- 
 mens of gastric contents, feces and urine, calls once and is 
 never seen again is hard to explain. This very frequently 
 
74 THE TREATMENT OF ENTEROCOLITIS 
 
 happens and always awakens feelings of regret that the time 
 spent in the study of the case has been wasted, and that the 
 laboratory force has been needlessly exposed to danger. 
 
 In the primary stage of chronic enterocolitis more can be 
 accomplished with a little treatment than in any other known 
 disease. The way is open for direct local therapeusis, but it 
 is absolutely necessary that this treatment should be appro- 
 priate for the condition of the mucous membrane and the type 
 of infection. 
 
 The type should be diagnosed through analysis of feces and 
 urine, the anatomical features cleared up by a thorough phys- 
 ical examination and a search for any organic lesions care- 
 fully made. 
 
 The patient had better rest quietly in bed until the acute 
 period is passed and for good measure a few days more, in 
 order that his strength and resisting power may be completely 
 regained. If possible, he should be kept under observation 
 until the urine is negative, so far as the indices of intestinal 
 putrefaction are concerned and the fecal fields Gram-negative. 
 If after a month has elapsed, the chemical and bacteriological 
 findings are still negative, the patient may be discharged as 
 cured. If, on the other hand, at the end of ten days, the 
 chemical and microscopical findings are still positive, the 
 patient may get up and about and gradually resume the duties 
 of life, provided the temperature and pulse are normal and 
 the general condition warrants it. 
 
 Our efforts in this stage should be directed toward the 
 accomplishment of four things: First, the restoration of asep- 
 tic conditions in the gastrointestinal canal; second, the heal- 
 ing of the catarrh; third, the complete digestion of any foreign 
 protein bodies that have found their way into the mucosa or 
 into the body tissues; fourth, the limitation of the amount of 
 damage that may be done to any organ during the course of 
 this stage. 
 
 To accomplish the first result, the administration of intes- 
 tinal antiseptics is the treatment par excellence. To avoid 
 any irritation of the intestinal mucosa, they should be given 
 in small doses. Certain antiseptics have been found especially 
 
THE TREATMENT OF ENTEROCOLITIS 75 
 
 potent against certain types of bacterial invasion and the 
 smallness of the amount required to produce results is often 
 surprising. The amount of the salycilates in the lymph cir- 
 culating through the ligaments in acute articular rheumatism 
 must be very small and yet the results are remarkable. So 
 also the results that we may get from the use of antiseptics 
 in the intestinal canal vary with what we might term the 
 particularity of those we administer. The antiseptic which 
 in the smallest doses and with the least irritation will acccom- 
 plish the greatest good is the one to be preferred. Intestinal 
 antisepsis is still a matter that gives great room for research. 
 The day is not far distant when the enzymes, the keys fitted 
 for unlocking the proteins and toxins of each special type, 
 will be in common use for the benefit of humanity. 
 
 In clinical investigations the following antiseptics have 
 been found the most useful in the acute stages: 
 
 Sodii Salicylas. 
 
 Dose; Gms. 0.064 or 1 grain every two hours. 
 
 Hexamethylenamina. 
 
 Dose: Gms. 0.064 or 1 grain every two hours. 
 
 Oleum Ricini. 
 
 Dose: Gms. 2.0 or 30 minims, every four hours. 
 
 Acidum Nitricum Dilutum. 
 
 Dose: Gms. 0.064 to Gms. 0.128 or Mi to Mii every 
 two hours. 
 
 Bismuthi Subnitratis. 
 
 Dose: Gms. 0.250 or Gr. iv, every two hours. 
 
 Sodii Benzoas. 
 
 Dose: Gms. 0.064 or Gr. i, every two hours. 
 
 Calomel in divided doses. 
 
 The sodii salicylas will be found most useful in the saccharo- 
 butyric, acetic and oleic types of putrefaction. The hexa- 
 methylenamina in the indolic and oxalic types. The oleum 
 ricini, given in the doses mentioned above, is almost a specific 
 in the oleic type and of great value in the oxalic types of putre- 
 
76 THE TREATMENT OF ENTEROCOLITIS 
 
 faction. Bismuthi subnitratis and acidum nitricum dilutum 
 are of especial service in the oxalic types, although the bis- 
 muth may be administered with advantage to most sufferers 
 from enterocolitis in this stage. Occasionally, it acts poorly, 
 irritates and seems to encourage rather than check putre- 
 faction. The benzoate of soda, while of little value by itself , 
 is very useful in combination with hexamethylenamina in 
 certain individuals, who do not seem to cleave the latter. 
 
 Calomel in small doses deserves a firm place among the most 
 valuable remedies in this stage. The smaller the dose, the 
 better its action. To avoid salivation the usual saline cathar- 
 tic should not be forgotten. 
 
 Drugs that act through the liberation of nascent oxygen in 
 the intestinal canal are not generally a success in the pri- 
 mary stage. 
 
 The catarrhal process may best be handled through the 
 diet. The catarrh, however, if the intestinal putrefaction is 
 held in check, usually recovers spontaneously. As a routine 
 treatment the tincture of belladonna in small doses, Gms. 
 0.064 or Mi, every two or three hours, seems to be of benefit. 
 The acidity of the stomach may be lessened or neutralized 
 with sodium bicarbonate and sodium bromide may be used 
 to check disagreeable reflex disturbances. 
 
 Vomiting from reflex irritation of the intestine or of the 
 central nervous system may be so severe as to require the 
 administration of morphine by hypodermic injection for its 
 relief. 
 
 Sensitization phenomena may form a very important part 
 in the clinical picture in this stage and are often very 
 severe in character. Sudden deaths from acute indigestion 
 are usually the result of shock resulting from the production 
 of beta-iminazolylethylamin. This may be formed in the 
 intestinal canal and be subsequently absorbed, or from the 
 parenteral digestion of foreign protein bodies, which have 
 found their way through the intestinal mucosa. These for- 
 eign proteins may be introduced with the food or be the re- 
 sult of bacterial growth. Death is usually the result of 
 bronchial spasm, the heart still beating after respiration 
 
THE TREATMENT OF ENTEROCOLITIS 77 
 
 ceases. The treatment, therefore, should be directed to the 
 relaxation of bronchial spasm and to raising the blood pres- 
 sure. The first can be best and most quickly accomplished 
 by ether inhalation. If the bronchial spasm has reached the 
 point of respiratory suspension, the hypodermic method may 
 be tried or tracheal insufflation of ether vapor attempted. 
 There are numerous drugs that have a vaso constrictive 
 effect and may be administered in appropriate doses. In 
 the laboratory, barium chloride has been found to be a spe- 
 cific for sensitization shock and in no case has death resulted 
 after an injection of solutions of proper strength from the 
 administration of the protein poisons. Its use in human 
 beings has never been investigated, but if its efifect should be 
 found the same as in the lower animals, it would be a great 
 addition to our list of life-saving drugs. 
 
 The amount of damage done to the mucosa may be limited 
 by rest in bed and by the avoidance of a diet which is irritating. 
 It will be of the greatest advantage to our patient if the heal- 
 ing process has been carried as far as possible before allowing 
 him to return to his regular duties; especially so, if the dis- 
 ease does not show signs of spontaneous recovery. 
 
 Drugs given to check diarrhoea or to produce bowel move- 
 ments should be used with extreme caution. Cathartics 
 retard the healing process and through hastening the intestinal 
 current cause the chyle and feces in the lower intestine to 
 become too rich in nutritive material and thus encourage 
 putrefaction. 
 
 The diet in the primary stage must of necessity be bland 
 and unirritating. Milk, preferably cooked in order that it 
 may be sterile and its proteins slightly hydrolysed, makes, in 
 most cases, an ideal diet. Gruels and broths may be used 
 if the milk is not well borne. Often scraped raw beef on 
 toast can be administered with great benefit in the sacchro- 
 butyric, acetic, oxalic and ammoniacal types. 
 
 In the secondary stage a large and varied armamentarium 
 is an absolute necessity in the fight. The power of the 
 various organisms with which we will be called upon to do 
 battle, to adjust themselves to new conditions and to overcome 
 
78 THE TREATMENT OF ENTEROCOLITIS 
 
 the effects of various chemicals which in the beginning were 
 toxic to them, is well known. In the same manner that the 
 Plasmodium of malaria will become quinine fast, so will the 
 intestinal bacteria become salicylate fast or formin fast. 
 
 Where mixed infections are present the solution of the prob- 
 lem presents even greater difficulties. The suppression of 
 one fauna allows another to gain the ascendency, perhaps to 
 the detriment of the patient. This fact, however, at times 
 may be turned to our advantage, always bearing in mind that 
 there is not only a substitution but also a re-substitution with 
 which to reckon. Remedies often lose their effect after a 
 few weeks and others must be tried in their place. Finally, 
 either the enterocolitis is healed, considerable improvement 
 is gained or the onset of the tertiary stage destroys all hope 
 of a complete recovery and forces us to efforts to postpone 
 that fatal day when some vital organ will cease to function- 
 ate. 
 
 Indolic Type. 
 
 Enterocolitis accompanied with the indolic type of putre- 
 faction, in the primary stage at least, usually heals with great 
 promptness under the administration of hexamethylenamina 
 in small doses, combined with a meat and toast diet. 
 
 In the secondary stage the therapeutic course is more pro- 
 longed. In the milder conditions, however, the catarrh 
 usually heals in a few months under the administration of 
 hexamethylenamina, the correction of starchy indigestion and 
 a diet combining high nutritive value and small weight. In 
 a few individuals, however, this course of treatment will have 
 little effect, the indicanuria will persist and the catarrh will 
 still advance. In this case sodium salicylate should next be 
 tried and after a week's treatment omitted for twenty-four 
 hours and the urine tested for indican. Should the urine be 
 still positive for indican, hexamethylenamina and sodium 
 benzoate should next be administered and test again made. 
 Meanwhile the patient must be carefully watched for any 
 signs of intestinal irritation. If these should appear, the use 
 of antiseptic should at once be discontinued. In some in- 
 dividuals it will be found impossible to establish a condition 
 
THE TREATMENT OF ENTEROCOLITIS 79 
 
 of asepsis or even partial asepsis in the intestinal canal and 
 we must be content with the antiseptic which seems to agree 
 with the patient best and continue its use off and on, while 
 we devote ourselves to the treatment of the catarrh. 
 
 In the treatment of the catarrh the following drugs will be 
 found of great service: The wine of ipecac in small doses, 
 the tincture of belladonna, bicarbonate of soda and bromide 
 of soda. The ipecac apparently increases the secretion of 
 the intestinal mucosa, washes out the mucous glands and 
 turns the current towards the lumen of the intestine. The 
 belladonna, while checking secretion to a certain extent, 
 relaxes the spasmodic condition that so often accompanies 
 these catarrhs and relieves many disagreeable symptoms of 
 reflex nature. Sodium bicarbonate lowers the crest of the 
 acid wave originating in the stomach, helps out the pan- 
 creatic juice in its effort to sustain the alkalinity of the in- 
 testinal contents and renders less irritating the organic acids 
 that the liver will be called upon to oxidize. 
 
 All foci of suppuration should be removed, all bridge work 
 should be consigned to the melting pot, all carious teeth 
 extracted and any pyorrhoea cured or failing in this the teeth 
 removed and a plate fitted. 
 
 Fingers should be kept out of the mouth and nose and the 
 teeth should be thoroughly cleaned at least twice daily. 
 
 The need of antiseptics will be much lessened if the food 
 is as sterile as possible. This condition can be obtained 
 through care in handling raw foodstuffs and especially, in the 
 case of vegetables, by the most thorough cooking. Until 
 the succus entericus has regained its bacteriolytic activity 
 all uncooked foods or foods that have stood some time after 
 cooking, should be prohibited. 
 
 In the secondary stage very little headway can be made in 
 the cure of enterocolitis while excessive putrefactive pro- 
 cesses are going on in the intestinal canal. The best plan is 
 first to give the patient a course of intestinal antiseptics and 
 to delay therapeutic measures directed to the cure of the 
 catarrh until the indices of intestinal putrefaction are no 
 longer present in the urine. 
 
80 THE TREATMENT OF ENTEROCOLITIS 
 
 The name of antiseptic drugs is legion and a list of them 
 can easily be compiled from any text-book on therapeutics. 
 It will be found, however, that the best place to begin the 
 sterilizing process is at the vermilion border of the lips. In 
 some instances the outposts may be pushed as far as the gar- 
 den, the market, the ice box, kitchen and eating utensils, 
 with what may seem favorable results. In the fight for asep- 
 sis the nose and its sinuses, the posterior nares, the tonsils 
 and the teeth must not be forgotten and these matters had 
 best be taken in hand by men who have a correct understand- 
 ing of the task at hand. 
 
 Saccharobutyric Type. 
 
 This can best be treated by means of the salicylate of soda 
 given in small doses as this drug is almost specific in its action. 
 Like all other intestinal antiseptics, however, its long con- 
 tinued administration does not give good results. Its first 
 effect will be to diminish greatly the volume of fecal matter 
 discharged per diem, and as this is generally regarded as an 
 alarming condition by the patient, he had better be prepared 
 beforehand for this result. The first course had better last 
 one week and never longer than two weeks, for if longer con- 
 tinued certain butyric acid producers tend to become sali- 
 cylate fast. 
 
 As the first symptoms of this type arise from the fact that 
 the liver is becoming insufficient for the task imposed upon it, 
 and as this is caused primarily by the excess of butyric 
 acid, either free or in loose combination, in the portal circu- 
 lation, it is well to administer the alkaline carbonates well 
 diluted with water. The liver seems to be better able to 
 handle these acids if they are combined with sodium or potas- 
 sium. This fact is shown clinically by a decrease in the sen- 
 sitiveness of the right hypochondrium and a reduction in 
 the size of the liver. Alkaline mineral waters usually have 
 some cathartic action, therefore their general use is not to be 
 recommended. 
 
 It must not be forgotten, however, that our greatest efforts 
 should be directed to the healing of the enterocolitis, the 
 
THE TREATMENT OF ENTEROCOLITIS 81 
 
 ravages of which allow the growth of butyric acid-producing 
 bacteria to proceed unchecked in the patient's intestinal 
 canal. Drugs, such as ipecac, belladonna, hydrastis, that 
 enjoy a reputation in the treatment of the catarrh may be 
 prescribed, but little can be accomplished through their use 
 if the patient persists in following a diet which favors the 
 growth of those bacteria that are always present in this type 
 of putrefaction. 
 
 Diet alone will always benefit this catarrh in the secondary 
 stage and many of the milder cases can be cured by this means 
 alone. For the first few weeks that the patient is under treat- 
 ment, the diet should be that ordinarily given in diabetes with 
 strict orders to omit all uncooked vegetables. If there is a 
 ptosis or a tendency to ptosis of the viscera, solids and liquids 
 should not be allowed to be taken within two hours of each 
 other. Milk is not well borne by these patients and should 
 always be forbidden. 
 
 The micro-organisms of this type are very generally strict 
 or facultative anaerobes, very difficult to cultivate in the lab- 
 oratory without special apparatus. The patient, moreover, 
 spends the whole of his life in an atmosphere of oxygen of 
 just the right dilution for therapeutic use. The use of ene- 
 meta of atmospheric air often produces marvelous results in 
 these sufferers, more especially if diarrhoea is present. This 
 may best be administered with a bulb syringe, the average 
 amount introduced being six ounces. Two bulbsful usually 
 make this amount in the ordinary Davidson syringe. A 
 special hydro-pneumatic apparatus designed for this pro- 
 cedure was found to have no special advantages over the 
 syringe mentioned above. 
 
 Enemeta of water, decinormal salt solution, antiseptics and 
 astringents uniformly seem to do more harm than good. 
 
 Abdominal massage, electricity and hydrotherapy have 
 been found of little use. 
 
 The correction of ptoses by strapping has been of 
 great service where such procedures are indicated. Experi- 
 ence teaches that the simpler the apparatus can be made 
 the better. After trying the various nicely patterned belts 
 
82 THE TREATMENT OF ENTEROCOLITIS 
 
 that have been invented, finally one constructed of a strip 
 of zinc oxid plaster 3i inches wide, applied across the small 
 of the back, brought forward just about the crests of ilium, 
 crossed midway between the umbilicus and the pubes and 
 secured with a pin, was given the preference. The point of 
 this pin is cut ofif and a small piece of plaster applied to pre- 
 vent injury to the clothing. 
 
 As the patient progresses toward recovery first one vege- 
 table and then another is restored to the diet and the effect 
 carefully noted. Finally most patients can be allowed a 
 regular table diet. On the other hand, many individuals 
 will be encountered who are unable and always will be un- 
 able to indulge in salads or other uncooked vegetables. 
 
 The Acetic Type. 
 
 The acetic type of intestinal putrefaction in the secondary 
 stage can best be handled through the diet and many will 
 recover promptly through this means alone. 
 
 The individuals who have an acetonuria alone, may not 
 consider themselves as departing very far from a normal 
 condition, but when the urine shows repeatedly a reaction for 
 this chemical there are sure to be stormy days ahead. Slightly 
 limiting the amount of starchy foods, the administration 
 of a mild intestinal antiseptic, such as sodium salicylate or 
 hexamethylenamina for a few days usually corrects the trouble. 
 
 When diacetic acid, oxybutyric acid or the acetic deriva- 
 tives are present, the therapeutic problem is one of greater 
 difficulty. The so-called antidiabetic diet will be found of 
 great usefulness as a means of treatment. There is one 
 exception, however, that must be carefully enforced and this 
 is the total abstinence from all raw foods, or from any food 
 that has been allowed to stand long after cooking, such as 
 cold meats, cold vegetables, vegetable salads and foods of 
 like nature. In the severe grades of putrefaction even the 
 drinking water should be first boiled before using and the 
 danger of infectious contact should also be guarded against. 
 
 The intestinal antiseptics mentioned before may be tried in 
 
THE TREATMENT OF ENTEROCOLITIS 83 
 
 turn. There appears to be no fixed rule governing the ad- 
 ministration of the class of remedies. In some, the salicyl- 
 ates may be used to great advantage; in others, hexamethyl- 
 enamina either alone or in combination with sodium ben- 
 zoate will cause the urine to become negative; while in others, 
 Fowler's solution or potassium iodide will accomplish the 
 desired results. 
 
 The intestinal catarrh should be attacked after the indices 
 of putrefaction have either been brought to zero or very 
 materially lessened in strength. Ipecac, belladonna, bis- 
 muth subnitrate or subgallate, dilute nitric acid, the alkaline 
 carbonates may be tried and the ones that seem the most 
 useful in this special case administered. 
 
 As in the other forms of putrefaction, cathartics are to be 
 avoided as much as possible, in order that the contents of the 
 lower portion of the intestinal canal may be as deficient in 
 nutritive material as possible. If the patient seems to be 
 worse when constipated castor oil, aloin, cascara sagrada, 
 may be tried with or without podophylin. The rule is, how- 
 ever, unless the patient shows dangerous symptoms or the 
 disease has progressed so far as to be well-nigh hopeless, to 
 fight it out with the aid of enemeta and lubricants. 
 
 As in the saccharobutyric type, enemeta of atmospheric 
 air, especially if diarrhoea is present as a complication, are 
 often of great service. 
 
 Massage, electricity, hydrotherapy and lavage are of very 
 little benefit. A change of scene and climate is of service 
 as it often removes the patient from a source of infection that 
 impedes his recovery. 
 
 The treatment of the tertiary stage is a task for the well 
 trained internist. The means taken to gain time for the 
 patient, of course, varies with the organ or organs that have 
 been affected through the attack of the disease. The prin- 
 ciples of treatment laid down above will be found of great use 
 in combination with those set forth in treatises upon dis- 
 eases of the pancreas, liver, heart, blood vessels, nervous 
 system and other organs of special function. 
 
84 THE TREATMENT OF ENTEROCOLITIS 
 
 Oleic Type. 
 
 In the primary stage of oleic putrefaction, the patients 
 are generally very ill. In consequence, these patients had 
 better be kept in bed until recovery is well advanced. 
 
 Castor oil in small doses frequently repeated is well-nigh a 
 specific in this type of putrefaction. It should be given in 
 half dram doses, once in two hours. It may seem paradoxi- 
 cal that a type of putrefaction where the invading micro- 
 organism attacks oils with vigor should be improved by the 
 administering of another oil. Castor oil seems to contain, 
 some chemical body which is antiseptic in its action. It is 
 well known that oleum ricini very seldom becomes rancid, 
 while the other edible oils spoil in the course of a few days. 
 Other intestinal antiseptics may be of value if the castor oil 
 is poorly borne by the stomach. Hexamethylenamina either 
 alone or in combination with sodium benzoate is an efficient 
 remedy. This may be alternated with sodium salicylate, 
 if the duration of the primary stage is longer than one week. 
 
 The diet should be absolutely fat free. This excludes 
 milk, cream, butter, the fat of meat and oils of all kinds. 
 Broths, when free of fat, may be allowed, soups thickened 
 with cornstarch, arrowroot or flour, dry toast, finely divided 
 meat, cooked or raw or skimmed milk. 
 
 In the secondary stage, the above named antiseptics may be 
 used alternately. In addition to these, the preparations of ar- 
 senic, especially Fowler's solution in small doses will be found of 
 benefit. Occasionally potassium Iodide will prove beneficial. 
 
 The abstinence from fats and oils must be kept up for 
 several months after improvement has taken place. 
 
 In the tertiary stage little can be done. The patient usually 
 needs constant care, either from an attendant or in some 
 institution. 
 
 In the treatment of enterocolitis constipation is a very 
 troublesome symptom. So strongly has the importance of 
 free evacuations of the bowels, and the so-called constipa- 
 tion high up and its deleterious influences upon health and 
 life, been impressed upon the minds of the patrons of the 
 medical profession, that were this doctrine true and appli- 
 
THE TREATMENT OF ENTEROCOLITIS 85 
 
 cable to all members of the animal kingdom who possess in- 
 ternal digestive systems, the surface of the earth would be 
 left as an habitat for protozoa, bacteria, molds, yeasts and 
 other organisms, who gain nutrition through their external 
 surfaces, and to no others. 
 
 Fortunately, constipation is not such a fatal disease as we 
 have been led to believe. It is a difhcult matter to decide 
 what is the normal habit of defecation for various individuals. 
 Some people have normally two stools a day, others, and in 
 truth they may be in the majority, have one per diem. Many 
 others, strange as it may seem, get along extremely well with 
 one or two a week until convinced by some friend that they 
 would be in better health if their stools were more copious and 
 frequent and take measures to accomplish this result. In such 
 cases, trouble is not long in developing. Many instances 
 have been reported in which the normal habit was as infre- 
 quent as once a month without serious consequences, so far 
 as bodily health and comfort were concerned. When a 
 marked putrefaction is present in the intestinal contents, 
 constipation may become a disagreeable, if not a dangerous 
 symptom. He who attempts to cure sufferers from entero- 
 colitis through the use of cathartics, however, will find that 
 the results of treatment will be uniformly unsatisfactory. 
 
 In connection with the subject of constipation, it is found 
 that the contents of the colon are not, in health, very rich in 
 nutritive materials. The colon may be regarded as the 
 reclamation plant of the gastrointestinal canal. Within its 
 cavity, the greater part of the water, mucus, enzymes and 
 hormones are recovered and turned back again into the blood 
 and lymph streams for future use in the digestive process. 
 
 When through catharsis, the contents of the small intes- 
 tine have been moved forward into the colon before the absorp- 
 tion of proteids, carbohydrates and fats has advanced to a 
 proper degree, putrefaction is greatly favored. If this con- 
 dition is present day after day, in a greater or less length of 
 time, through an overabundance of nutritive material favor- 
 ing the growth of putrefactive bacteria, a catarrhal condi- 
 tion will most certainly be established. 
 
86 THE TREATMENT OF ENTEROCOLITIS 
 
 The stools in enterocolitis often, under analysis, show a 
 bacterial content, living, dead and autolysed, of ninety-nine 
 per cent, according to the investigations of Strasburger and 
 Herter. Consequently it may be assumed that the more 
 copious the stools, the greater the putrefaction. Therefore, 
 a patient who is passing one pound of fecal matter a day is 
 losing 0.99 of a pound of nutrition, plus the amount of carbon, 
 hydrogen and nitrogen that is wasted as gaseous bodies in 
 bacterial metabolism. 
 
 The intestinal condition in constipation may be expressed 
 by the following equation: 
 
 (1) 0+C + I + T. 
 
 In which O may represent obstipation; C, a catarrhal pro- 
 cess; I, an infection with the bacteria of putrefaction, and T, 
 the toxemia arising therefrom. 
 
 It is easy to see that in the presence of certain very toxic 
 members of the families Bacterium and Hyphomycetis, this 
 condition may be dangerous to the patient's welfare and more 
 especially to the integrity of some of the more delicate organs 
 of metabolism and excretion. It is difficult to see, however, 
 how any great harm could be done if the intestinal conditions 
 were so simplified that the equation would read as follows: 
 
 (2) + C. 
 
 Or, bearing in mind the fact that the mass of the stool 
 varies with the bacterial activity, what damage could possibly 
 come to the general parenchyma of our patient, even if he 
 should have but one stool a week, if his intestinal condition 
 could be represented by 
 
 (3) O. 
 
 As a corollary, O may be replaced by D, representing 
 diarrhoea, in equations 1, 2 and 3. In this case we have the 
 condition present in many of our patients, who have con- 
 tracted intestinal diseases in tropical climates and to whom 
 the intestinal equation + C + I + T would give a marked 
 degree of comfort, as well as, in comparison, the greatest 
 satisfaction. 
 
THE TREATMENT OF ENTEROCOLITIS 87 
 
 The use of cathartic medicines is not to be recommended 
 and their long-continued administration will make all chronic 
 conditions much worse. Even in conditions of intestinal 
 atony without catarrh the administration of such drugs will 
 eventually cause a colitis or an enterocolitis to develop. 
 
 Under the teaching of Lane, highly purified mineral oils have 
 come much into vogue for the relief of constipation. The 
 study of feces during such treatment, however, leads to the 
 belief that these oils cause an increase of putrefaction in the 
 intestines. 
 
 The various vegetable gums were also tested as intestinal 
 lubricants. Agar agar gave fair results. Finely ground 
 sea moss of the variety chondrus crispus, however, seems to 
 be the best. It has the advantage of being a native product 
 of low cost, is very well borne by the stomach, is soothing to 
 the intestinal mucosa, produces large well formed stools and 
 seems to check rather than encourage putrefaction. 
 
CHAPTER XV 
 
 GENERAL CONSIDERATION OF 
 ENTEROCOLITIS 
 
 Many of the statements made in the Hterature of entero- 
 colitis do not bear the test of laboratory investigation. The 
 two most commonly reiterated doctrines, the importance of 
 overeating as a causative factor and the bad effect of con- 
 suming certain common articles of food in abundance, have 
 been proven to be without foundation. There are, of course, 
 a great many sufferers from this disease who habitually over- 
 eat and who have done so all their lives, but the fact that 
 they have contracted a chronic catarrh of the intestinal tract 
 must be accounted for on other grounds than an overindul- 
 gence in the pleasures of the table. In the majority of patients 
 conditions bordering on starvation are more generally found. 
 
 Through the teaching of our friends, the vegetarians, the 
 opinion has become very general, that animal foods have a 
 certain poisonous effect upon both mind and body, that their 
 use leads to early decay of the blood vessels and that their con- 
 sumption at best is but a relic of barbarism. People are all 
 the more ready to accept this belief, as the price of meat 
 products has risen to an alarming extent in the past twenty 
 years and the cost of living may be materially reduced by 
 following a meat-free diet. Moreover, cheating the stomach 
 seems to be a very popular pastime among a certain class of 
 people and routines directed to the relief of abdominal symp- 
 toms through starvation treatment are coming more and more 
 into vogue. 
 
 Another great cause of intestinal damage is the very prev- 
 alent use of foods that have been cooked several weeks or 
 months previous to consumption. This applies not only to 
 meats and vegetables, but to cereals as well. This condition 
 
GENERAL CONSIDERATION 89 
 
 may be accounted for partly by the well ordered advertising 
 campaigns conducted through the columns of the press by 
 enterprising manufacturers of such products, but in a greater 
 degree through the innate laziness of the average American 
 cook and the widespread ignorance of the art of good cooking. 
 We are rapidly becoming a tin can and carton race, so far as 
 our food supply is concerned. Even in the rural districts, 
 the tin can has become ubiquitous and the number of empty 
 ones found on the premises may be said to vary inversely 
 with the thrift of the family. Truly it is shameful to find tin 
 cans labeled "pork and beans" upon the premises of any self- 
 respecting farmer. On the other hand, in the best hotels in 
 the land the use of canned vegetables is, if not extremely 
 common, the rule. If a vegetable served on these tables is 
 fresh, even when common in the markets at the time, the fact 
 is remarked upon and used as an excuse for an advance in 
 price. One often wonders what may be the age of the canned 
 goods served in the average restaurant. 
 
 Meat is often a cause of trouble. Some of it served in 
 public eating houses, through age or maltreatment, is irri- 
 tating to the intestinal mucosa, to say the least. The methods 
 of the storage of meat, poultry and eggs is often open to 
 criticism. Meat that requires the liberal use of highly aro- 
 matic condiments to disguise the odor and taste of advancing 
 putrefaction is well known to be dangerous, yet it is served 
 every day in every city. 
 
 Another cause for remark is the filthy condition that exists 
 in the ice boxes, kitchens and serving room, and the unclean- 
 liness of the personnel, not only in public eating houses but in 
 many homes as well. It may seem an exaggeration to state 
 that the cook who prepares our food, the waiter who serves 
 it in so polished a manner, or the scullion who cleans the 
 eating utensils, may communicate sickness, but when one 
 bears in mind the great prevalence of fecal matter upon the 
 hands and person of the average individual, the subject 
 takes a different aspect. It must not be forgotten that the 
 chef may have an intestinal fauna to which he is immune, 
 but which on the other hand may lead to a premature death 
 
90 GENERAL CONSIDERATION 
 
 or at least months or years of incapacity to one of the guests 
 he might inadvertently infect. 
 
 New strains of micro-organisms, introduced through the 
 agency of immigration and travel, no doubt are beginning to 
 have a marked influence upon the intestinal condition of our 
 native population. The intestinal fauna in some of our 
 patients who have lived in the Orient is often remarkable and 
 the effect that the bacteria that these people harbor without 
 inconvenience may have upon the health and vitality of the 
 American born, furnishes a very interesting problem and one 
 deserving of careful study. Possibly, the great decrease in 
 the fecundity of our population may be ascribed to various 
 chronic infections against the attack of which the individual 
 has not acquired an immunity. It is a fact that a conquest 
 is going on through the agency of intestinal putrefactions and 
 of plasmodiasis, instead of by force and arms, that will even- 
 tually change the character of the race. 
 
 The change from country to urban life, the lack of fresh 
 air and sunshine, the intimate contact with sources of infec- 
 tion that a city life necessitates, the competitions, worries 
 and anxieties of modern life, all must have their effect. 
 
 The connection between this catarrh and other general 
 chronic infections such as tuberculosis and malaria is very 
 intimate. So important is this fact that tubercular and 
 malarial infections may be said to be the most common com- 
 plications of the secondary stage of enterocolitis. 
 
 The financial and political loss to the nation resulting from 
 intestinal infections presents one of the most serious prob- 
 lems of enterocolitis. Through its attack the length of life 
 and efficiency of its victims are reduced about twenty-five 
 per cent. It is a greater and more far-reaching problem than 
 the hook worm disease or tuberculosis presents today. 
 
 Sufferers from enterocolitis fall an easy prey to habit-form- 
 ing drugs. Especially liable are they to use habitually the 
 insidious coal tar series or the proprietary articles that con- 
 tain them. Morphine claims a good many victims, and, on 
 account of the depression of sexual desire that accompanies 
 many types of putrefaction, the aphrodisiac effect of cocaine 
 
OF ENTEROCOLITIS 91 
 
 is often sought. The persistence of an acetanilid habit is 
 not generally realized. It is so easily obtained in the open 
 market, its use causes so little comment, so many supposedly 
 innocuous proprietary compounds contain it in large pro- 
 portion, that once formed the habit is hard to break. A 
 vast number of popular beverages and nostrums depending 
 upon caffeine for their stimulating effect are also very popular 
 with these patients and these combined with the ubiquitous 
 cocktail and other alcoholic cordials and tipples add their 
 quota to the damage day by day. 
 
 The average American is to-day not only underfed but also 
 underclothed. The thinness of clothing has become a popu- 
 lar fad. As a result the resistance of the body is impaired 
 by overheated homes and offices. 
 
 The prevention of this disease presents a problem in- 
 timately connected with the prolongation of human life. 
 The return to a simpler life, with lessened worry and anxiety; 
 less time and money spent in the pursuit of pleasures, that 
 must be taken in the end from the family food and clothing; 
 plainer and better food, better cooked; a more evenly bal- 
 anced diet; the abstinence from irritating foods and condi- 
 ments; the avoidance of habitual catharsis; and finally more 
 fresh air and sunshine; all suggest themselves as measures 
 that may well be used in the prevention of enterocolitis.