originates from poor stock transmits a diathesis and develops types of tissue that pre-dispose to disease. The burden of proof seems to show that tuberculosis is transmitted in rare instances from the mother through the area vasculosa or the placenta to the child; that in rarer instances it John Brown of old, it is "still marching on.” During the past few years it has been my privilege to supervise the selection of a large number of selected lives, and this question, what is a tubercular type? from a medico-insurance point of view is a vital one, for it is presumed and accepted as a fact that where there are sub is conveyed from the father through the sperma-jective or objective conditions or symptoms this tozoids, and that, in the vast majority of cases, it is due to direct infection and not to inherit ance. In this paper I have attempted to give facts as closely as possible, and I must leave you to draw your own conclusions. The question of heredity in either aspect, through predisposition or disease, has not been settled by the eminent scientists quoted in this article, and I fear that it is beyond the province of the Hennepin County Medical Society to arrive at any safe conclusions. WHAT IS A TRUE TUBERCULAR By C. A. McCollom, M. D., Head Physician M. W. of A.; Supreme Med. Director Royal Fraternity; Chairman Med. Section N. F. Cong.; Prof. Preventive, Legal and Insurance Med., Med. Dept., Hamline University. Minneapolis. For years we have labored under the notion that every case of tuberculosis was an heirloom, which could not, under any circumstances, be avoided; that this condition was entailed and must be endured. The "white plague" walked through the world wherever cultured man resided, and followed his wake into barbaric lands, to the cost of these poor people of their lives. The movement of this curse is highly instructive, and its study has lead to the immortal discovery by Koch of its cause, the bacillus tuberculosis. This etiological factor in the spread of this infectious disease has proven that a culture ground is required for its propagation, While vast numbers are subjects of its inroads, nevertheless it is one of the most preventive of diseases, but practically and clinically it is like *Annual Address of the Vice President of the Hennepin County Medical Society, December 6, 1897. class can be eliminated, but where one finds that one in seven die of tuberculosis which entered with a clear bill of health, one can not but believe that there is a condition outside of the pure heredity. Having examined death proof after death proof with this in view, one can not but help arriving at this conclusionthere is a predisposition to contract this contagion, which is pronounced in a certain class. It is the province of nature to repeat herself in form and individual peculiarities, but the vital resistance of that individual is his own, which can be moulded and kneaded by circumstances into an ideal creation or a weakling. The “survival of the fittest" is true. Man's environments change constantly. Today he is in the height of felicity, tomorrow in the depths of despair. This constant change tells upon his cellular makeup. Food, drink, occupation, habitation and social life are prime factors in determining this condition. Immunity alone means health. It is a hard fact to own, when the A No. I risk dies within three years from tuberculosis whose personal, moral and family history was clear, that there is something wrong in the methods of examination, something has escaped us, some factor has not been brought out. All men are exposed to this contagion. The germ is omnipotent. All health records of our cities show this. Over 20,000 have been reported in the city of New York alone, and this does not cover the cases; where one is reported, scores escape record. The animal man is peculiar; he is always willing some stranger should walk the plank, but objects to being marooned himself. Public health can accomplish much when public thought acts as a willing helper: until then we must confront the question: will the case in point contract tuberculosis? Post-mortem records tell us that all cases which contract this contagion do not proceed to a final and fatal result, but that the condition is stopped, burned out, as it were, thus emphasizing the statement that some are immune, that this soil is not the kind upon which this germ will grow; the culture medium is not proper. We can ascertain an individual's make up, note his cellular tissue, whether lean as Cassius or fat as Falstaff, swarthy as an Indian or blond as Mund of old; they remind us only of family or race peculiarities, and nothing of his health or vital resistance, unless we can bring something else with it. This something else is a combination of all these factors, complexion and temperament, stature and idiosyncrasys,-his diathesis. Heredity in itself is not the only cause of this predisposition. It is an important one, but is often defeated. Exposure to contagion, by this class, is almost certain, sooner or later, to end in the contraction of the disease, but another type is required, where heredity is clean, and direct exposure results in contraction, while others similarly exposed escape. The same might be said of exposure to all contagion, but the percentage of "takes" is smaller in the tubercular exposure than in any other infection. It there was no difference in this respect we could not reasonably argue that a certain class was immune and a certain class susceptible, but experience forces us to this conclusion. While as said before, certain factors combined make the diathesis, this does not make the tubercular type alone. Still other conditions are required. With only these we could not yet bring in a verdict of guilty, but we must still search for more. Tone is a condition much overlooked in making a prognosis. It is a certain state or quality of the nervous system which determines the vital resistance. It is part of the business of the nervous system to somewhat control the function of nutrition. Should this be low with deficient nutrition, the diathesis would be intensified, while any condition, circumstance, occupation or environment, which depresses this tone, correspondingly reduces the vital resistence and intensifies the predisposition, and if there is no inherited taint, causes an artificial condition which, should the party be exposed, will find a culture ground in which the germ will thrive and reproduce its kind, thus fulfilling its mission. Predisposition is often inherited in this particular, that the offspring has a different stature and cellular composition which are not sturdy and vigorous. This is often acquired by certain environments. Where there is an inherited predisposition, improper food will render the same pronounced, so will occupation. But this class give us due notice, either by family history, or subjective or objective evidence, but the acquired predisposition, often the result of some other condition, accidental in itself, is the type we wish to determine, and the one who seemingly is sturdy and has a reserve store of vitality, but who contracts this contagion. By what factors can we discover his predisposition? This question is a vital one, and has not been fully solved. Habits of life, active or sedentary; mode of living, particularly excess in eating and drinking and use of narcotics; exposure to extremes of heat and cold, owing to the occupation whose environments tend to deteriorate; history of frequent, slight catarrh; recent pneumonia, pleurisy or bronchitis; tendency to light weight, and where we find a tendency to continual slight rise in temperature. In fact every condition which will, in itself, interfere with proper nutrition will predispose to this condition. The number of persons who will acquire this predisposition is then only limited by their being within the lines of normal physiological health. A continual deflection toward an enfeebled state of nutrition already predisposed, and this condition is the true tubercular type. The loosely built, coarse skinned individual whose connective tissue is not finely knit, is void of vital resistance, and is quite prone to be culture ground, giving good foothold for the bacillus tuberculosis. Recent pleurisies, that is, within three years, have proved a favorite culture ground, and the sequence of the cases is too often tubercular. Pneumonia, especially if recurrent, predisposes. Referring again to heredity. It is presumed that direct lines are observed, and not side issues. Father, mother, brother, sister, grandparent, if we take in the aunts, uncles and even going back to great-grandparents, heredity would prove all conditions and none would be exempt. Taking, then, the direct line, the inherited want of vital resistance is seen in the children; this, combined with unsanitary surroundings is an element of predisposition to any predisposing cause, and particularly prone to the various manifestations of tuberculosis, disclosing in a large number of cases tubercle history. As the child grows this natural element of selection gradually weeds out the weakling until we reach man's estate, when the young man or woman is thrown on his or her own resources, and the tendency to defeat heredity, which has been gradually increasing, is now, by this change of condition, checked, and the predisposition exerts itself. This tendency to de feat heredity can be fostered, and is proof positive of the benefit of preventive and therapeutic measures. It is in the adult who has no family or personal history of tubercle or depressing cause that we wish to find some sign post whose finger will guide us to determine this hidden. flaw in an otherwise splendid expectancy. The life work of the physician is to discover some marked degeneration which has, by its subjective condition, required the victim, from personal discomfort to consult us. He opens his very soul to our vision, and we have a ready and persistent helper in our effort to diagnose his condition, which has now become pathognomonic. But when we pass upon the individual who is sans ailment and wants a policy or benefit for his dependents, the conditions are reversed. We have no helper; minor subjective conditions are denied, and unless there are marked objective conditions, we too often miss the game. As a result rigid laws, governing selection are in force, built upon heredity. Late experiments tell us that this condition is at fault. While this governs one class, the other still escapes. The trained observer is always impressed with the case. Outside of his mere physical examination, the personel, so to speak, of the party, impressed one with a particular notion of his vital resistance. This faculty should be cultivated, as this lack of vital resistance is the predisposition. which renders contagion liable. In the light of modern pathological investigation we must admit that tuberculosis is an infectious disease. This has been proved beyond a shadow of a doubt, and that it is endemic, we might say epidemic, and possibly pandemic, as its mortality is of the pandemic character.. With this condition universal we must admit that there is a certain immunity. Now this is natural to all, as before stated. Natural immunity is a condition of physiological health, but this condition can end at any time. Heredity predisposes, but the most robust, if exposed to intense infection, will become tubercular. The doctrine of immunity teaches us that the serum of the nutrient fluids of the body carry constituents which are antidotal to the materies morbi of infection. While this, in the prime condition, is pronounced, this may, by reason of constitutional weakness, be lessened, so that this inherited tendency will determine upon slight infection. When the parents are nonphthisical, among the adults the males particularly being exposed by reason of occupation or wedlock, become consumptive. Among the children the females, by reason of constant exposure at home, show the larger mortality, the outdoor life of boys prolonging their lives, as their natural immunity is not destroyed by the intense infection of home exposure. While in the case of the female by reason of being constitutionally without normal vital resistance and constant home exposure, they contract the specific infection, which, in this case, is tuberculosis. In the report of the Brompton Consumption Hospital, we find the following: One thousand cases of tuberculosis. One or both of the parents were tubercular in 272 cases. This was from the poor class. One thousand cases of those whose environments were better gave 120 Or that heredity affects less than ten per cent of the offspring. These figures are those of children. During the past two years I have noted in nearly 1,600 deaths, 254 from tuberculosis, 65 of them gave a tubercular history outside of parents, 42 gave a history of some depressing cause; 157 under standard weight, 19 were passed as first-class, while the infected condition was overlooked by the local examiner; 123 were perfect in all respects. Nearly one-half contracting their contagion who gave no sign, and less than one-quarter gave a tubercular history. The moral: What is a tubercular type? We are upon the footstool of an unknown quantity. Let X represent the same. 408 Masonic Temple. THE EARLY DIAGNOSIS OF PULMONARY TUBERCULOSIS.* By Geo. Douglas Head, B. S., M. D., Instructor in Pathology in the University of Minnesota, Minneapolis. The post-mortem records of Heitler, Osler, Harris and other observers, prove beyond doubt that nature unaided cures many cases of pulmonary tuberculosis. If the disease could be recognized in its earliest beginnings, when only a lymph node, or an alveolus of the lung was involved, the cellular forces of the body, stimulated to increased activity by a generous supply of pure air and nutritious food could probably effect a cure in a large per cent of cases. Knowing as we do that medicine possesses no drug which can stay the progress of this disease, and recognizing the curative value of nature's forces in dealing with its initial stages, it behooves us to concentrate our energy in a search for the most adequate means of detecting the very beginnings of the infection. *Read before the Hennepin County Medical Society. December 6, 1897. In order that we may stand upon common ground in the consideration of this subject, we must agree as to what shall constitute an early diagnosis of pulmonary tuberculosis. In other words, how soon after the infection takes place would it be necessary to recognize the disease in order to say that we had made a diagnosis in the early stage of pulmonary tuberculosis. The answer to this question must depend upon knowledge furnished by the pathologist, not the clinician. All clinicians would agree that the examiner who detected a tubercular area 2 c. c. square in a patient's lung would have early located the tuberculous process, and have made an early diagnosis. And yet the pathologist might say that such a lesion was in fact a late manifestation of the disease. To make an early diagnosis we must detect early lesions, and only by outlining the initial pathological lesions of the infection are we able to say what is and what is not an early diagnosis. Tubercle bacilli carried in the inspired air may fall upon any part of the mucous membrane of the respiratory tract from which an entrance into the body may be effected. If the locality selected be the tonsils, pharynx, larynx or upper trachea, the bacilli rarely reach the lung, and the consideration of such lesions falls without the scope of this paper. More commonly the epithelia covering the bronchi or the bifurcation of the trachea serve as gateways of infection, and the bacilli carried through the mucous membrane of these structures fall into the lymph stream and are floated away to the bronchial lymph nodes, ten or twelve of which drain this region. In the interstices of these glands they lodge, multiply and create an area of tubercular tissue, or kept in abeyance by the developing cells around them, postpone an active invasion until the stagnant or retrograde cellular changes of mature years offer a more favorable period for their development and the manufacture of the toxine. It is here in these bronchial lymph nodes that one of the earliest lesions of pulmonary tuberculosis is to be found. They are the primary sources from which a secondary infection of the lung proper may arise. If we are prepared to make an early diagnosis of pulmonary tuberculosis, we should be able to detect a tubercular lesion in these glands. Most often the bacilli gain entrance to the deeper portions of the lung and fall upon the epithelial lining of the terminal bronchioles or the alveoli themselves. Here they multiply, establish an inflammatory center, and produce the tubercular nodule or the tubercle. The formation of these small tubercles in the terminal bronchioles and alveoli of the lungs is an early lesion of pulmonary tuberculosis, and the diagnosis of the disease at this stage would be an early diagnosis. Any tuberculous lesion which has passed on to the process of caseation is not pathologically an early lesion, nor would the diagnosis of the disease at such a stage be an early diagnosis. In the history of the tubercle we recognize the inflammatory or formative stage, the stage of caseation and the stage of excavation or sclerosis. Only when the disease has been detected in the first or formative stage, can it be said that an early diagnosis has been made. But the objection might be raised: A diagnosis in this stage of the disease would be many times impessible with our present diagnostic methods. This is just the point I wish to make, that from a pathological standpoint, with our present well recognized means of diagnosis, medical men are rarely able to make a diagnosis in the initial stage of pulmonary tuberculosis. Let us turn to a consideration of the agencies at our command for the detection of an infection of the lung by tubercle bacilli... In ascertaining whether a patient has or has not pulmonary tuberculosis, we depend upon: First, a study of the clinical symptoms; second, a study of the physical signs; third, the examination of the sputum for bacilli; fourth, the use of tuberculin injections. The last mentioned method is not generally well recognized and does not at present have the sanction of the profession. When the bronchial lymph nodes are involved the clinical symptoms are ill defined and inconstant. Among those described by the various authors are pain of an aching character referred to the root of the neck, fever, cough dry obstructive and excited or deep inspiration; dyspnoea of a spasmodic character; dysphagia and change in the sounds of the voice. None of these symptoms are, however, diagnostic, for the glands may grow to large masses in the mediastinum without a single one of the above symptoms being complained of. Of the physical signs, dullness cannot with certainty be detected on account of the intervening sternum. Râles and feeble or obstructed breath sounds over the compressed bronchus may be heard. But these are likewise inconstant, and do not with certainty determine a tubercular process. In the main, the physical signs are as uncertain as the clinical symptoms. and the knowledge obtained from a study of both may be suggestive but is never absolutely diagnostic. Neither are we aided by an examination of the sputum, since the bacilli appear in the exudate only when the infected tissue ulcerates through into a bronchus, which is late in the history of the disease. With these the only well recognized means for detecting tuberculosis of the bronchial lymph glands considered, we must admit that we are unable to diagnose with certainty a tubercular infection of these structures, the existence of which is a source of secondary infection for the lungs proper, or the means by which a general tuberculosis may be disseminated. The only possible means by which such a lesion could be early detected would be by the injection into the body of some substance, which, acting upon this tubercular tissue would manifest some symptom of diagnostic value. This I believe we have in tuberculin. The rise in temperature following its injection into the body is pathognomic for tuberculosis, and is the most valuable means at our command for determining the presence of such a lesion. Turning to tuberculosis of the terminal bronchioles and alveoli of the lung, of what value are the present diagnostic methods for early detecting the presence of the tubercles? Of the clinical symptoms cough and a constant temperature are the most often manifested, yet these only suggest the possibility of the disease, and we examine the lungs and search the sputum to confirm or deny our suspicion. Ziegler, the pathologist, speaking from the standpoint of experimental tuberculosis, says: "The onset of a tuberculous infection can not be determined in human beings, since the symptoms of the disease only show themselves after the process is extended to some degree." The physical signs produced by freshly deposited tubercles are negative; a full sized mature tubercle is the size of a millet seed. Such bodies are too small to cause appreciable dullness, and too minute to appreciably obstruct breath sounds, or delay the onflow of mucus. An interesting question here arises: How large an area of infected lung can exist before its presence can be detected by physical signs? Pepper, in his "Textbook of Medicine," recites a case in point: He diagnosed a tuberculous lesion in the right infraclavicular region in a young man who presented himself for examination. Increased vocal resonance, abnormal broncho-vesicular breathing and increased bronchial whispering were the physical signs detected. The patient was killed soon after in an accident, and a tuberculous area the size of a filbert was found post mortem. The area Pepper detected was large enough to include one hundred alveoli of the lung. Fresh formed tubercles are not larger than one alveolus of the lung. When we consider the skill of Pepper in physical diagnosis, we can readily see that even the most proficient diagnostician is not in a position to detect the earliest lesion of a tubercular lung infection, and in the great majority of cases the disease has been sometime in existence before the most careful examiner is able to detect physical signs. in the lungs. The detection of tubercle bacilli in the sputum is the most certain means at our command for establishing the presence of pulmonary tuberculosis. Many times bacilli are present before any pronounced physical signs can be detected, and yet bacilli are not given off in the sputum until the cellular disorganization has begun, and then we are dealing with a later stage of the disease, when the body rarely overcomes the infection. It is in the formative stage of tuberculosis, when the clinical symptoms are uncertain, the physical signs negative and bacilli absent from the sputum, the bronchitis of the clinician, that some means more delicate than any at present employed would be of greatest value in arriving at a correct diagnosis. Such a diagnostic aid is tuberculin. Injected into the body of tuberculous individuals it causes a temperature reaction so characteristic and constant as to be of the greatest value in establishing the character of the pathological lesion. The profession in general will not accept this means of detecting pulmonary tuberculosis, because it is believed that its use tends to either augment the process already existing or open new channels. for a farther infection of the patient. To the consideration of these objections I wish to call your attention. Tuberculin injected into tuberculous individuals causes a definite and characteristic rise of temperature. Injected into the non-tuberculous person it causes no rise in temperature, nor other abnormal symptoms. The reason why a rise in temperature results from its injection into the tubercular individual is. that the tuberculin acting upon the tissue in the involved area causes an inflammation in the surrounding tissues. In this inflammatory process an increased flow of blood is supplied to the tubercular area. This additional blood supply sweeps out from the tissue an increased quantity of tuberculin, and this, with the tuberculin injected, causes a rise in temperature. Three questions now arise for consideration: First, does this inflammation in the tissue around and about the tubercle augment the tubercular process? Second, does it offer new avenues for bacilli to gain an entrance to other parts of the body? Third, does it cause a necrosis, or breaking down of the tissues of the tubercle? The histological researches of Riehl, Jacobi, Rindfleisch, Schimmelbusch and Kromayer agree in demonstrating that tuberculin does not |