The suppression of tuberculosis /

by Emil von Behring

I cannot fail to express my conviction of the general diffusion of tuberculosis in densely crowded populations, and of the consequent futility of all attempts to suppress the disease by means of isolation and segregation. What would be the outcome if we were to adopt the suggestion seriously put forth, to send all the tubercularly infected soldiers to hospitals, later discharging them as unfit for service? We should not have more than 5% left for active service, and even this small number would probably after the lapse of a few years be declared tuberculous. At the most I can assent only to the separation of the coughing consumptive from the apparently healthy individual; and these should be sent, not to sanitaria [Heilstätten], but to homestead colonies [Heimstätten] such as we formerly maintained for lepers.

We need not, however, idly fold our hands and become fatalists who see the inevitable destruction of the human race by tuberculosis. Tubercular infection does not by any means signify tubercular consumption. It is just this enormous diffusion of tubercular infection which demonstrates, better than anything else, the curability of many tubercular diseases, their liability to spontaneous cure; for I must admit that I have little faith in the curative action of any of the numerous methods of treating tuberculosis. Here also the maxim formerly applied to diphtheria holds true, “mild cases go on to recovery, severe infections are fatal”; and here as in diphtheria I was confronted by the question whether there are ways and means to prevent severe infections with bad prognoses, or to convert severe infections into mild ones with favorable prognoses. You will be able to answer this question yourself if I now give you the results of my experimental investigations on the occurrence and prevention of tubercular consumption. I shall begin by discussing the requirements necessary for the development of tubercular consumption in man.

But first of all I must say that according to my ideas there has not yet been a single well-authenticated case in which pulmonary consumption has originated in adult persons as the result of a tubercular infection developing epidemiologically, i.e., under essential conditions for infection occurring in nature. Even counting those cases in which mortuary assistants, butchers, and laboratory workers have been severely infected through the subcutaneous tissues, I still fail to find any proof that a traumatic infection has caused pulmonary consumption in an individual not yet infected with tubercle bacilli.

I am well acquainted with the argument by which it is sought to prove that pulmonary consumption may develop as a result of inspiration of particles of dust or moisture containing tubercle bacilli. The facts on which this argument is based are the greater occurrence of tuberculosis and a higher mortality rate from that disease among nurses, occupants of houses in which there are pronounced cases of phthisis, among the inmates of prisons, etc. But, considering the figures previously given, showing the enormous diffusion of tuberculosis, the objection is surely justified that the persons thus dying of consumption already had a tubercular focus in the lungs and that this pulmonary disease, under a mode of life favorable to tuberculosis, was converted into florid phthisis.

In order not to be misunderstood, I wish to emphasize here that I do not at all deny that infection can be caused in adults by inoculation with tubercular virus. In fact, I assume that few of us in advanced life escape such infection. But that this infection leads to cavity formation in the lungs, is, I believe, fully as unproved as the assertion that bovine tubercular virus has caused human pulmonary consumption in even a single instance. Koch has very properly pointed out the entire absence of proof for this last statement. I can go still further in my concessions to the prevalent view that consumption results from the inhalation of particles of dust or moisture laden with tubercle bacilli. I concede not only the possibility but the actual occurrence of pulmonary tuberculosis going on to consumption, as a result of infection of an adult person. I concede this in the sense that on the basis of an infantile infection a pulmonary tuberculosis has developed which becomes manifest only through the agency of the additional infection. However, the opportunity for infection with tubercle bacilli cannot by itself be a deciding factor in the development of pulmonary consumption. I can here cite the experience of Dr. Moritz Schmidt of Frankfurt a. M., who has examined a great number of cases of tubercular laryngitis. In his experience of over forty years he has certainly been exposed, more than others, to tubercular infection. But neither he nor any of his numerous assistants has ever become consumptive.

My experiments on animals have shown me that the lesions characteristic of human pulmonary consumption are developed only after there have been extensive and long-continued disturbances of the vital functions of the organism. Our ancestors introduced the term “dyscrasia” and “diseased constitution” to express this idea. I have succeeded, especially in goats, but also in other animals, in producing a clinical picture exactly similar to that of human pulmonary consumption. In these animals I first produced a moderate degree of immunity against tuberculosis by a lengthy course of treatment, and then I injected a strong tubercular virus into the circulation. I regard the lesions in pulmonary consumption as being produced in similar fashion. They are the expression of an infection in an individual who, owing to a very early previous infection with tubercle bacilli, is less susceptible to the new infection. These late infections may in isolated cases be referable to the inhalation of tubercle bacilli. They may, however, be due to already existing tubercular lesions, and so be regarded as auto-infections or metastases. Were we to inject into the tissue juices of a person not yet partially immunized against tuberculosis an amount of tubercle bacilli equal to that usually found in the lungs of consumptives, the person would die of an acute miliary tuberculosis, but he would never develop pulmonary consumption.

There is another argument against the common assumption that primary infection by way of the respiratory organs is the cause of consumption, and this is furnished by an analysis of the anatomical findings. If we allow an individual, entirely free from tuberculosis, to breathe tubercle bacilli, the opportunity for an intestinal[4] infection is surely presented; on the other hand, that any bacilli whatever reach the lungs directly cannot be positively affirmed. Infection of the organs of the pharynx and larynx in these cases always corresponds to disease of the lymph-vessels and glands in the neck, and gives the individual the scrofulous habitus. Now let us recall the neck of consumptives. It appears almost as if, at the time when an individual may be designated as being a candidate for consumption, the organs of the neck were already quite immune against a vulgar tubercular infection.

I could multiply the arguments in favor of my assertion that, in order to have pulmonary consumption follow infection with inspired tubercle bacilli, it is necessary to have constitutional changes in the organism due to an early previous infection. I hope, however, to have sufficiently established my reasons for rejecting the current theory of the origin of consumption, a theory due mainly to the valuable and detailed researches of Cornet.

I must decline to accept another wide-spread view, namely, that hereditary influences are deciding factors. Theoretically an intra-uterine infection with tuberculosis is certainly possible, and in a few cases such an infection has actually been proven. But neither the parental nor the pre-parental transmission of tubercle bacilli, nor the hypothetical transmission of a body predisposition to tuberculosis, is of any practical importance. Nevertheless, according to my researches, the view prevalent among the laity regarding the important influence of parents, grandparents, and other near relatives, in the etiology of consumption, is entirely justified and proper. I, too, am of the opinion that one can properly speak of the bad prognosis in cases of family tuberculosis. If, in taking the history of a patient, I should elicit the fact that several near relatives had died of consumption, and if, then, by means of the tuberculin reaction or of inoscopy, I made the clinical diagnosis of a tubercular infection, I should be very pessimistic in my prognosis, even though the infection were not otherwise manifest.

I may very properly be asked how I can deny hereditary transmission and yet place so high a rating on the influence of the ancestors, cognates, and house-fellows, in the production of pulmonary consumption. A little explanation regarding the meaning of certain terms will make my ideas perfectly clear.