The intestinal putrefactions; clinical studies of enterocolitis

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; putrefaction 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 specialized organs; the gastric contents; the urine; the feces; the tertiary 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 system; the feces; the urine; the tertiary stage.

CHAPTER XII. Malaria, Syphilis and Tuberculosis

Possibility of malarial infection in enterocolitis; general consideration 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

Preface

In the year 1906, Professor Herter published his epochmaking 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 Metchnikof¥ had noted the connection between intestinal putrefaction 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 human 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 limitations 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.

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 inflammatory 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 beginning 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 arteriosclerosis, cirrhosis of the liver and other low-grade inflammatory 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 competition 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, disappointment 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 determine 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 abdomen 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 epigastrium. 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 microscopical 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, described by the patient as severe or slight, as the susceptibility or resistance of the individual may vary. These complaints 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 comparative 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 intestinal mucosa. Spasms, which may reach the point of producing 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, ribbon-like or scybalous stools of small calibre, and considerable pain and tenesmus.

While the symptoms in this Secondary Stage may be so mild as to escape ordinary notice, yet a patient in this condition 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 endurance; 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 ascribed, 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 symptoms 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 specialized 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 examination of the urine, feces or blood, or in the physical examination of the patient will disclose the fact that the fight is lost. In other individuals the sudden cessation of improvement 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 abdominal 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 necessity 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 throwing 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.

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 classified as follows :

1. The direct parasitic effect: diversion of food supply, chemical changes in the chyle, rendering it unfit for absorption.

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, contraction, cirrhosis, calcification.

These changes may involve cardiac, arterial, hepatic, renal, gastro-intestinal, nervous, muscular, articular, ovarian, pancreatic 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 ?

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.

(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 further reduce the vitality of the body tissues.

The vegetable parasites may be considered under the following 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 classification 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 convenience of reference the number given in Chester's valuable work is prefixed.

1. BACTERIA:

A . Streptococcus :

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.

C. Sarcina :

1. Sarc. pulmonum.

4. Sarc. flava.

5. Sarc. lactis.

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.

Bact. aerogenes capsulatus.

Bact. thermophilum.

Bact. subtiliforme.

Bact. simile.

Bact. Mellanby & Twort.*

G. Bacillus:

B. coli.

B. enteritidis.

B. typhosus.

Zd>.

B. alcaligenes.

B. Friedbergensis.

B. Schafferi.

B. Shigae.

B. bucalis.

B. tachyctonus.

B. dysenteriae. Kruse.

B. Wesenbergii.

B. prodigiosus.

B. Lesagei.

B. subtilis.

B. putrificus.

B. car is.

B. solidus.

B. botulinus.

B. butyricus Botkin.

B. Kedrowskii.

B. sporogenes.

B. acidophilus.

B. acidolacticus.

B. anthracis symptomatic!.

B. cloacae.

B. entericus.

B. liquefaciens ilei.

B. mascerans.

B. violarius acetonicus.

B. oedematis maligni.

B. paraputrificus.

B. proteus vulgaris.

H. Pseudomonas:

/. Microspira: 6. Msp. comma.

10. Msp. protea.

/. Spirillum:

2. Sp. Massauah.

3. Mycobact. influenzae. 9. Mycobact. diphtheriae.

13. Mycobact. tuberculosis.

M. Streptothrix:

1. Streptothr. bo vis.

11. Streptothr. chromogena.

14. Streptothr. farcinica.

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.

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 irritating. 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.

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; mycelium 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 positive. 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 unevenly stained protoplasm. Their dimensions are approximately 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 branching. Smaller aerial hyphae, the tips breaking into squareend 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. Considerable gas is produced in growth under these conditions.

(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 developed, breaking into oidia, or on short lateral hyphae; conidia in chains easily broken apart into free conidia. If the conidial 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 indentations appear along the edges. In the shorter ones, consisting 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 negatively 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 luxuriant. 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.

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 number 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 symbiological 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 disagreeable 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.