WORKS TRANSLATED BY
DR. CHARLES BOLDUAN
PUBLISHED BY
JOHN WILEY & SONS.
=Immune Sera: Hæmolysins, Cytotoxins, and Precipitins.= By
Prof. A. WASSERMANN, M.D., University of Berlin. Authorized
Translation by CHARLES BOLDUAN, M.D. 12mo, ix + 76 pages.
Cloth, $1.00.
=The Suppression of Tuberculosis.=
Together with Observations concerning Phthisiogenesis in Man
and Animals, and Suggestions concerning the Hygiene of Cow
Stables and the Production of Milk for Infant-Feeding, with
Special Reference to Tuberculosis. By Professor E. VON BEHRING,
University of Marburg. Authorized Translation by CHARLES
BOLDUAN, M.D. 12mo, vi + 85 pages. Cloth, $1.00.
THE
SUPPRESSION OF TUBERCULOSIS
TOGETHER WITH
OBSERVATIONS CONCERNING PHTHISIOGENESIS
IN MAN AND ANIMALS
AND
SUGGESTIONS CONCERNING THE HYGIENE OF COW
STABLES AND THE PRODUCTION OF MILK FOR
INFANT-FEEDING, WITH SPECIAL REFERENCE
TO TUBERCULOSIS
BY
PROFESSOR E. VON BEHRING
_University of Marburg_
_AUTHORIZED TRANSLATION_
BY
CHARLES BOLDUAN, M.D.
_FIRST EDITION_
FIRST THOUSAND
NEW YORK
JOHN WILEY & SONS
LONDON: CHAPMAN & HALL, LIMITED
1904
Copyright, 1904,
BY
CHARLES BOLDUAN
ROBERT DRUMMOND, PRINTER, NEW YORK
TRANSLATOR’S PREFACE.
The suppression of tuberculosis is of universal interest. A disease
which is so wide-spread and which attacks the human race from so many
points can be successfully combated only by the cooperation of many
different agencies. It is therefore of great importance that the origin
of tuberculosis be well understood not only by physicians, but by many
outside the medical profession, such as dairy- and cattle-men, officers
of health boards, sanitary engineers, etc. In order to present to the
English reader in a concise and authentic form von Behring’s views on
the origin and suppression of tuberculosis, the translator has made
selections of von Behring’s articles from several different sources.
The principal article is translated from a lecture delivered in Cassel,
September 25, 1903. In reply to certain criticisms of a statement in
this lecture, von Behring published an explanation in the _Deutsche
medizinische Wochenschrift_, No. 6, 1904. This is reproduced, in part,
in the Appendix. The two articles, “Observations on Phthisiogenesis”
and “Suggestions concerning the Hygiene of Cow Stables” are taken from
_Beiträge zur experimentellen Therapie_, No. 8, 1904.
Each article, with the exception of the one just mentioned, is
reproduced in full and without changes. In a subject of such
controversial nature it is essential to reproduce faithfully the exact
meaning of the original, and this has been done even though at times
it may have led to awkwardness of expression. In a few cases where an
exact equivalent for the German could not be found the translator has
used the nearest English equivalent, followed by the German word in
brackets.
CHARLES BOLDUAN.
BROOKLYN, July, 1904.
CONTENTS.
PAGE
THE SUPPRESSION OF TUBERCULOSIS (THE CASSEL LECTURE) 1
OBSERVATIONS CONCERNING PHTHISIOGENESIS IN MAN AND
ANIMALS 45
SUGGESTIONS CONCERNING THE HYGIENE OF COW-STABLES AND
THE PRODUCTION OF MILK FOR INFANT-FEEDING 60
SYNOPSIS OF THE METHOD OF MAKING PROTECTIVE INOCULATIONS
OF CATTLE IN AGRICULTURAL PRACTICE 69
CONDITIONS CONCERNING THE DISTRIBUTION OF THE PROTECTIVE
VIRUS 75
APPENDIX 81
THE SUPPRESSION OF TUBERCULOSIS.
THE CASSEL LECTURE.[1]
Although in this lecture I have planned to discuss mainly the
suppression of human tuberculosis, my experiences with bovine
tuberculosis cannot be omitted; for not only have I strong reasons
for believing that bovine tuberculosis plays an important rôle in the
etiology of human tuberculosis, but I am also firmly convinced that by
means of the knowledge gained from the study of bovine tuberculosis,
we shall be able to prevent to a great extent human tubercular
consumption, and favorably influence the course of already existing
tubercular diseases.
Both human pulmonary consumption and _perlsucht_ of cattle (which
often leads to consumption) are caused by minute vegetable organisms,
which it is impossible to differentiate either microscopically or
culturally,--the tubercle bacilli of Koch. It is impossible to have
either tubercular pulmonary consumption or _perlsucht_ without the
presence of these tubercle bacilli; and no matter how susceptible to
tuberculosis an individual may be, a tubercular infection cannot take
place if these bacilli be absent.
In order for the disease to develop, three factors must always be
present: first, the susceptible organism; second, the vegetable
parasite; and third, the necessary opportunity to infect. Under the
last I understand all the conditions necessary to bring the virus to
such a part of the living organism as will enable it to enter either
into the circulation or into other body juices.
Every human individual is by nature susceptible to the action of
tubercle bacilli which have entered his body juices. This is true not
only of human but also of bovine tubercle bacilli. I emphasize this now
but shall give my proofs later. But not every tubercular infection of
the tissues leads to consumption. Frequently the tubercular infection
is followed by such slight disturbances of health that it remains
latent throughout an entire lifetime and is only discovered at autopsy.
Whether the entrance of tubercle bacilli into the tissue juices of an
individual shall end disastrously or not, depends on a large number
of factors. _Congenital_ differences in the degree of susceptibility
undoubtedly play a subordinate rôle. A more important factor is the
degree of virulence of the inoculated virus, and this may fluctuate
within wide limits. Of great importance also is the amount of the
virus and whether the inoculation is single, repeated, or almost
continuous for a longer time. Of transcendent importance, however, are
the age of the individual, his physiological or pathological condition
at the time of infection, other previous diseases, mode of feeding,
occupation, hygienic conditions of his surroundings, etc. In short, all
that we understand by the term _acquired susceptibility_, or _acquired
predisposition_. Finally, I must mention the location and character of
the point of entrance of the virus.
We see at once, therefore, that, in the analysis of a tubercular
infection, it is not sufficient to have determined the presence of the
three necessary factors, susceptibility, the tubercular virus, and
the opportunity for infection. If we wish to understand the manifold
variety of the reaction phenomena exhibited by an individual infected
with tubercular virus, we must thoroughly study all the conditions
above mentioned as well as a great variety of accidental conditions.
Nowadays the term tuberculosis is applied to everything which
constitutes a change in the organism excited by the entrance into it of
tubercle bacilli. In statistics, galloping consumption is thus classed
with tubercular local infection of a joint, gland, abdominal organ,
of a little nodule in the skin of the face, etc. Calcified as well as
other remains of previous lesions are classed as tubercular. We have
every reason to praise as a great scientific advance the discovery that
in manifestations so varied in their importance to life and health
the etiological factor is the same. One must not, however, make the
mistake of classing as one and the same thing tubercular infection
and consumption and prognosticate an inevitable and painful end on
making the diagnosis of tubercular infection. How little the facts
justify such a course is seen in the statistics of bovine tuberculosis
and will be seen also when I come to speak of the statistics of human
tuberculosis.
In studying the statistics of bovine tuberculosis of this province, I
have had the hearty support of the government officials as well as of
many county veterinary surgeons. After my colleague, Dr. Römer, had
examined several thousand head of cattle we ceased our labors because
we were confronted by the depressing fact that larger herds of cattle
were rarely ever free from tuberculosis. As a test to discover the
presence of tuberculosis we made use of small infections of Koch’s
tuberculin. We are aware that there are tuberculous animals which do
not react to this test. _On the other hand, if the method of making the
test be faultless, a positive reaction always indicates that the animal
in question is infected with tuberculosis._ Our figures for these cases
are therefore without doubt too low. Despite this, and despite the fact
that young cattle, even though infected with tuberculosis, often do
not react to the usual dose of tuberculin, we found frightfully high
figures for herds of more than twenty animals. We had to admit that
in this respect we were no better off than other countries. I will
cite one of the most experienced of the investigators of tuberculosis,
Prof. Bang of Copenhagen, who says that in Denmark, in stables of
more than fifty head of cattle, an average of 60% of the animals are
tuberculous. Bang says further: “If one is dealing with a large herd
in which tuberculosis has existed for many years, one may as well omit
testing the full-grown animals. _Most of them will react, even though
they appear perfectly healthy._” To this, as a result of many years’
observation, I should like to add, _and though they may apparently
remain perfectly healthy for their entire life_.
As a rule a herd of cattle on a large farm, though infected with
tuberculosis, presents a fine appearance. Nor does their state of
nutrition, milk production, or calf-raising leave anything to be
desired. Now and then a cow coughs, or, despite plentiful food, loses
flesh. This animal is put aside and the herd, as such, resumes its
magnificent appearance. If in a herd reacting to tuberculin things are
allowed to go on in this way for a number of years, especially if the
cattle be barn-fed, then, to be sure, the number of coughing animals
increases, the offspring deteriorate, the milk and meat production
decrease, until finally the scourge of tuberculosis is plainly marked.
Carefully conducted epizootic researches in our province have led me
to the discovery that a single, native, mountain breed of cattle, that
of Vogelsberg, was probably free from tuberculosis as late as twelve
years ago. Through imported cattle the tubercular infection was then
introduced. But even now the percentage of animals responding to the
tuberculin test is about one-quarter that of other breeds. What is
curious, however, in these cattle is, that whereas, according to common
experience in all other breeds, the percentage of reacting animals
increases with their age, in these Vogelsberg cattle the percentage
from the fifth year on even decreases. This may depend on the smaller
number of animals infected five years ago. Some of the exceptions,
however, I must account for by the definite healing of lesions and a
consequent disappearance of the reaction. The favorable termination
of the tuberculosis in these Vogelsberg cattle I ascribe to the
smaller accumulation of the tubercular virus in the still relatively
little-infected stables, or, what amounts to the same thing, _to a
smaller dose of the virus infecting the suckling calves. These, of
course, take up the infecting agent not only from the mother cow, but
also from the other cattle._ One can plainly see how the percentage of
reacting cattle in this Vogelsberg breed increases from year to year,
and I feel certain that ten years hence these cattle will be as badly
off in this respect as other breeds, provided measures are not taken
to check the advancing infection. Such measures we have had at our
command for some time, and their usefulness has been thoroughly proven.
I know of a large number of herds which, by means of Bang’s rules,
have been made free from tuberculosis and kept so. It is, however, an
expensive procedure and requires the constant supervision of an expert,
and even then is usually possible only on large estates where any
reacting animal may immediately be separated from the unaffected herd.
When, therefore, I published a method of protective inoculation against
tuberculosis, one which I had proved in my own stables, I was pleased
with the spirit of hearty cooperation shown by the owners of large
dairies who had already experimented largely with Bang’s procedures.
Through the courtesy of Count Zedlitz I was enabled to make numerous
preventative inoculations on cattle in three counties of Hesse-Nassau;
from there the experiments were extended to the neighboring grand duchy
of Hesse, and to the large dairy of Bolle in Köpenik near Berlin. As
a result of this work I was able in the beginning of this year to
establish the harmlessness of the procedure. Since then I have had
abundant opportunity to inoculate calves under three months on the
immense Hungarian possessions of Prince Ludwig of Bavaria; also on
those of Archduke Frederick of Austria. Under my direction scientific
researches regarding the protection afforded by the inoculations
have been undertaken by Prof. Eber in the veterinary school of the
University of Leipzig and by Prof. Schlegel in that of the University
of Freiburg; further also by Ober-med. Rath Lorenz in Darmstadt and
by Prof. Hutyra in Budapest. In Marburg I myself have made studies on
highly immunized cattle regarding the production of anti-bodies, have
reared calves on cows immune to tuberculosis, and have investigated the
subject of immune milk.
All the details have been carefully recorded. Some of these protocols
have already been printed, and at the close of this year I hope to
commence the publication and working out of the rest of this enormous
mass of material in my “_Beiträge zur experimentellen Therapie_.”
In the mean time, however, the practical application of my immunizing
procedure continues steadily to gain in extent. Austrian as well
as Swedish investigators, sent by their governments to study the
inoculation technique at Marburg, are to make extensive inoculations
in their native countries. The government of the grand duchy of Hesse
has ordered that the counties use part of their police fund to defray
the expense of inoculating all calves free of charge, provided that the
owners bind themselves to allow the county veterinarian to supervise
the inoculated animals. From all sides I receive requests for this
preventative virus.
Until recently I prepared this virus myself and distributed it free
of charge with the help of private funds. I was able to do the entire
scientific, technical, and administrative work with only a few
assistants. But this is no longer possible, for the expenses have
outgrown not only my financial means, but also, even with great zeal
for the work, my bodily strength. I should gladly have postponed any
change in the manufacture and distribution of the virus until the
Prussian government was ready to take charge of the entire matter.
But the daily increasing labor has made it necessary for me to rid
myself of this burden now, and I have therefore provisionally arranged
that the firm of Drs. Seibert & Ziegenbein of Marburg undertake the
manufacture.
That this free distribution of the protective virus for tuberculosis of
cattle has been completely justified is seen by the report of Koch’s
Institute, entitled, “_Ueber Immunisierung gegen Tuberculose_.” To
be sure, this report contains nothing positive that, as a result of
a large number of experiments, I had not already maintained for some
years. And it lacks, what is especially important in the practical
immunization of cattle, namely, proof in the form of protocols.
Possibly these were omitted because they would fail to substantiate
Neufeld’s assertion that Koch, previous to my publication regarding
protective inoculations of cattle with living tubercle bacilli,
had already made use of the same procedure. I cannot refrain from
observing that Neufeld treats this question of priority in rather
unusual fashion, for he now claims for Koch an immunizing procedure
which I had published as long ago as 1901. It would surely have been
more reasonable to have made these claims sooner, before the success
of the method became so generally recognized in agricultural circles.
Finally I must criticise the author for making similar uncalled-for
claims for the English investigator Macfadyan. As the one most
concerned, such claims might have been made by Macfadyan himself,
yet, so far as I know, that investigator has not even suggested such
a thing. In the case of my diphtheria-serum discovery I can entirely
overlook similar baseless and unjust claims for Roux and for Ehrlich.
Such claims have often been made by medical authors, but neither Roux
nor Ehrlich has ever authorized such a perversion of facts.
However, apart from these inaccuracies, the report of Neufeld regarding
Koch’s tubercular immunizing experiments shows an agreement with my
results which extends into the smallest details. This, then, must
demonstrate to the world the absolute reliability of my immunizing
principle. The entire suppression of bovine tuberculosis is now
only a question of conscientious and properly conducted protective
inoculations, and, of course, also a matter of time.
Just now I am studying the important practical point which for a
long time occupied the attention of students of vaccination. We now
know that protection against variola is only then secured when the
vaccination is followed by a typical inflammatory reaction. Are the
requirements the same for bovine tuberculosis? This I cannot yet
definitely answer; and even under the most favorable conditions I shall
be able to answer it only after a lapse of two years. By that time the
calves that were injected only once and that did not, so far as we
could ascertain, react to the inoculation, will have grown to maturity.
Another important problem, one regarding hereditary immunity, is
already nearer solution. I believe I am warranted in saying that, as a
rule, the immunity against tuberculosis is not transmitted by the cow
to her calf during intra-uterine life. One can readily be deceived by
cases of apparent hereditary immunity. For example, in examining the
fourteen-day-old calf of a highly immunized cow, I found the calf to
possess a comparatively high degree of immunity against _perlsucht_
bacilli. Without my previous experience with infantile immunity to
guide me, I might easily have been led into the error of assuming this
to be a case of hereditary immunity. Comparative tests, however, have
made it very probable that the immunity, undoubtedly possessed by this
calf, was derived from the milk of the immune cow with which the calf
was nourished.
It will still be some time before I can present any experimental
evidence to show whether a cow, less highly immunized than the one just
mentioned, also produces a milk which possesses protective immunity,
and if so, how far it is possible to increase this property; whether
such a milk can be used to combat human tuberculosis; and finally,
whether it can be transported long distances without losing this
property. I have, to be sure, every reason to hope that we are on the
right track when we believe that immune milk constitutes a remedy for
tuberculosis with which no other remedy can even remotely compare. You
will, I am sure, believe that I shall leave nothing undone which will
lead to a realization of these hopes.
Right here, perhaps, it is well to say that, for the purpose of making
very careful therapeutic experiments, I am delivering immune milk to
only a few of my medical friends. I cannot, therefore, meet the many
demands for this remedy coming from medical and other sources. They
are so numerous that I cannot even answer them all. When, as a result
of these clinical experiments, the conditions and restrictions are
determined under which immune milk exerts its therapeutic action, I
shall make public all the facts in regard to this remedy, and thus make
it accessible to every one.
In the mean time I believe it will serve a very useful purpose if I
publish in readily comprehensible form the scientific facts on which
my plans for the suppression of tuberculosis rest. With this, of
course, will come a discussion of controversial points in the field of
tuberculosis investigation which have attracted the attention not only
of the medical profession, but also of the laity.
I shall commence with the question as to what relations exist between
human and bovine tubercle bacilli. Two years ago, in London, Koch
said that the excitants of bovine _perlsucht_ have nothing to do
with human consumption. If this be true, then I must at once admit
that my hopes regarding the utility of cattle immunization for human
therapeutic purposes have very little foundation. It is well known that
the protection afforded by immune bodies excited by the injection of
any virus extends only to the same species of virus, not to that of
different species. Nor, in our entire investigations in immunity, do we
possess a single example showing the possibility of protecting animals
or man by means of one infectious agent against the action of another
of a different species. All this is now so well known that I need not
discuss it. When, therefore, the researches at the Koch Institute show
that it is possible to protect goats, donkeys, and cattle against
_perlsucht_ by inoculating them with human tubercle bacilli, does it
not show that in these diseases there is no difference of species?
According to the recently expressed opinion of his co-workers,
Schütz and Neufeld, Koch in his London address did not maintain that
there is a difference in species. He merely maintained that the
virus of human consumption is not identical with the virus of bovine
_perlsucht_, and that, likewise, bovine tuberculosis is not identical
with human tuberculosis. That, to be sure, would be something quite
different from what the rest of the world understood. Human pulmonary
consumption and bovine _perlsucht_ are anatomically so dissimilar that
it required extraordinarily clever researches and keen reasoning to
lead to the discovery of a common etiological factor in these diseases.
But one can easily go further than this. One can maintain without
exaggeration that tubercular lupus, tubercular scrofula, and other
human tuberculosis localized in joints, serous surfaces, etc., are just
as little identical with pulmonary consumption as are the cases of
bovine _perlsucht_. The term _identical_ does not even fit all cases
of consumption. Strictly speaking, a process or thing is identical
only with itself. Certainly not all tubercle bacilli are identical,
nor yet all kinds of tubercle bacilli. Koch’s assertion that there is
an essential difference between human and bovine tubercle bacilli,
and that these differences are not bridged by any connecting links,
provoked the strongest opposition. This assertion has since called
forth observations from all over the world which positively demonstrate
the existence of intermediary stages in the virulence of tubercle
bacilli derived from mammals. Generally, tubercle bacilli derived from
cattle are more virulent for all animal species, thus far examined,
than are human tubercle bacilli. And the opinion is constantly gaining
ground that bovine tubercle bacilli are also more virulent for man.
In the scientific controversy as to whether the virus of consumption
and that of _perlsucht_ belong to the same species or not, various
misunderstandings have prevented an agreement. Very often the terms
“similar species” and “different species” have been used in a different
sense. It is, of course, wholly a matter of individual judgment where
to draw the line limiting the membership of what, in our minds,
constitutes a species. Even if we apply Darwin’s definition and include
under the term “species” only “organisms of similar origin,” the term
is still very elastic. However, in the light of our present biological
knowledge, based on Darwin’s theory of evolution, we are under no
circumstances permitted to take as a criterion for like and unlike
species such an easily influenced factor as the degree of virulence,
i.e., the capacity for giving rise to pathological changes in another
organism. _Nowadays all botanists and zoologists are agreed on this,
that membership in a species is determined by the origin of the
organism._ An anthrax culture, which has been made entirely avirulent
by means of Pasteur’s procedure for reducing virulence, surely belongs
to the same species as does the virulent variety from which it was
derived. And in this case the difference in the degree of virulence
is far greater than it ever is between human and bovine tubercle
bacilli. If we keep in mind all the functional differences that have
experimentally been shown to exist between tubercle bacilli which
have long lived in a human body and those which have long lived in a
bovine body, we shall surely not go wrong when we assume that with a
little patience and expert knowledge we shall be able to make these two
varieties absolutely similar again, even in respect to their virulence.
Passing now to the discussion of the real subject of my lecture I shall
try to give you an idea of the distribution of tuberculosis in the
human species. Although the number of persons dying of consumption is
frightfully large, the number of tubercular, and tubercularly infected,
persons is much larger. Not until recent years have we secured
tolerably reliable data to enable us to judge of the distribution of
tuberculosis in civilized countries.
If we classify as tuberculous every case in which there are
pathological changes due to tubercle bacilli, then surely the
oft-quoted saying of the noted Greifswald physician is true, “We are
all a bit tuberculous.” It has not been easy to demonstrate this fact
scientifically, and it would have been impossible of demonstration
without the two epoch-making discoveries of Robert Koch, that of
tubercle bacilli, and of tuberculin.
Not even a man of the scientific attainments of Virchow was able to
judge what constitutes tuberculosis, although during fifty years he
had endeavored to formulate data for the differential diagnosis of
post-mortem findings. Since we have learned that Koch’s bacillus is
the bond of union between all the various tubercular diseases, we see
that many inflammatory processes which Virchow described as entirely
distinct and different are nothing else than special stages in the
tubercular infection. The anatomical unit of the tubercular process
is the tiny, translucent gray nodule of millet-seed size described by
Laennec and Virchow, the miliary tubercle. But what may develop from
this may take the form of most widely divergent pathological lesions,
and it was not granted to Virchow to puzzle out the endless variety of
things etiologically the same. Yet it is _etiologically_ that the vital
processes must be analyzed if we wish to have a firm basis for our
struggle against preventable diseases. This has more and more become
the opinion of modern physicians. The progress that has been made,
first in surgery and then in internal medicine, progress that only
fifty years ago was declared by the most eminent representatives of
medicine in those days to be impossible, has been possible only through
the etiological investigations developed by Pasteur and by Koch.
The first principle in the etiological investigation of all vital
processes, and therefore of those concerned in infectious diseases
caused by micro-organisms, is thus formulated by Darwin: “That which
is of the same origin belongs to the same species.” Two infectious
agents may resemble each other ever so closely, but if they have
not the same genealogy, i.e., if they are phylogenetically widely
separated, then, biologically, they belong to different species. And
conversely, size, form, and other properties of certain micro-organisms
may be ever so different. If, however, the organisms are of the same
origin, then, biologically, they belong to the same species. The virus
of anthrax occurs in two forms: as bacilli, and as oval spores. The
quotidian malaria parasite has an extraordinarily complicated cycle of
development. Nevertheless we have no hesitancy in speaking of either an
anthrax virus or of a malaria parasite.[2]
The virus of human tuberculosis, the tubercle bacillus of Koch,
possesses narrowly limited morphological characteristics. It is readily
recognized since Koch published his very accurate description of it
in 1882, and especially since Ehrlich, shortly afterward, published
a specific staining procedure. The tubercle bacilli are familiar to
us as rods of varying length, but of fairly constant thickness, which
occasionally show granular degeneration. I believe it is now everywhere
accepted that the presence of these bacilli in a lesion in the human
body indicates the tubercular character of that lesion. Leprous lesions
with somewhat similar bacilli must, of course, be taken into account,
but these, as a rule, can already be differentiated macroscopically.
Recognizing this significance of the presence of Koch’s bacilli
and applying all other known methods for the identification of
tuberculosis, Dr. Naegeli of Zürich, working under the direction of
Prof. Ribbert, was unable to discover at autopsy a single body over
thirty years old in which there were not some signs of the occurrence
of a tubercular infection. Between the ages of 18 and 30 there were
96%; between 14 and 18, 50%; between 5 and 14, 33%; and between 1
and 5 years, 17%, which showed the presence of tubercular lesions.
In the bodies of infants under one year, on the other hand, definite
tubercular signs were invariably absent.
The astonishing results of these careful anatomical investigations have
been verified by reports from pathological anatomists in other cities;
yet at first sight, they seem to contradict all medical and other
experience, for according to these results all of us assembled in this
hall are tuberculous! But the perfected diagnosis of tuberculosis in
the living person leaves no doubt that Naegeli’s figures, at least for
thickly populated centers, possess general applicability. To be sure,
if we count only the patients who come to the physician because of
tubercular or supposedly tubercular symptoms, then our figures do not
agree with Naegeli’s; nor will the statistics of living persons in whom
we can discover tubercle bacilli agree with the autopsy statistics.
The agreement, however, becomes very close if we make use of a
diagnostic method furnished us by the second of Koch’s above-mentioned
discoveries, the tuberculin injection.
Koch’s tuberculin is a water-soluble tubercular toxin, given off
from the bodies of the tubercle bacilli to the culture medium, and
concentrated together with glycerine. Injected either subcutaneously
or intravenously it causes no reaction in persons free from tubercular
infection. On the other hand, it is one of the strongest poisons for
those who are under the influence of such an infection. Even before
the infection has led to clearly recognizable lesions, and long
before there are any symptoms of tubercular disease, and even if the
most careful physical examination fails to discover a suspicion of
tuberculosis during the entire lifetime of the individual, his peculiar
susceptibility to this tuberculin injection shows that somewhere in his
tissues or body fluids tubercle bacilli are producing their peculiar
changes.
The nature of these changes is becoming somewhat clear to us since
there have been discovered in the extra-vascular blood of tubercularly
infected men and animals coagulation and agglutination phenomena
which are entirely absent in the blood of non-infected individuals.
It appears that the activities of the tubercle bacilli in the body
of the host excite the production of a soluble anti-body. When this
anti-body comes into contact with the water-soluble substances derived
from the tubercle bacilli, Koch’s tuberculin, it is transformed
into an insoluble body. According to my own researches I believe it
probable that this anti-body is formed by the smallest arterioles in
the neighborhood of the infected area. The extent of the agglutination
phenomena varies according to the amount of anti-body and of the
tuberculin with which it comes into contact. This manifests itself
clinically, by the degree of fever, and anatomically, by intravascular
coagulations. The latter, in some cases may lead to exudations or to
the escape of blood from the pathologically altered vessels. As a
result of the tubercular poisoning, we would then have, at autopsy, the
typical picture of a tuberculin reaction.
Tuberculin, in its action as a blood poison for an individual infected
with tuberculosis, behaves like many other infectious poisons. Very
small fractions of the amount sufficient to threaten life cause
a distinct reaction. This is manifested by a rise of temperature
preceded by a sharp fall. I know, through personal experience, of a
case of human tuberculosis in which more than a hundred times the
usual diagnostic dose of tuberculin was administered. But aside from
several days of high fever and a considerable feeling of illness, it
had no damaging influence on the patient’s general condition. Koch,
the discoverer of tuberculin, once took a strong dose of tubercular
poison in the form of dead tubercle bacilli and became very ill. In
his case probably a hundredth of the amount would have sufficed to
cause transient temperature changes and thus have demonstrated that
he also had once been infected with tubercle bacilli. Ten years ago I
myself reacted to a dose of 4 mg. with fever and a pronounced feeling
of illness which confined me to my bed for several days in San Remo.
Therefore I have no doubt about the tubercular infection of my body.
The most instructive evidence to confirm the general truth of Naegeli’s
figures is furnished by the results of investigations made by the
Austrian army surgeon, Dr. Franz, on soldiers of two regiments of
infantry. In order to avoid injuring the health of the individuals
tested, Franz used only very small doses of tuberculin, 1 to 3 mg.,
which, in case the injection was repeated, was increased to 5 mg. In
spite of this, and in spite of the fact that the soldiers represented
the healthiest individuals of the population, he found in one regiment
in the first year of service (1901) 61%, and in the second year of
service 68% of tubercularly infected cases. Franz adds to his report,
which at present I have only in manuscript, that when he employed
the dose originally recommended by Koch, namely one centigram, his
percentage for the twenty-first year of life approached Naegeli’s very
closely, 96%!
On the other hand the Hungarian investigator Dr. Nikolaus Berend has
not obtained a single positive tuberculin reaction in ninety-six very
young children, in spite of the fact that among these were some very
feeble individuals, and children of parents manifestly tubercular; and
further, despite doses as high as 1 cg. We see then that herein also
the statistics coincide with Naegeli’s post-mortem statistics.
Another proof that human tuberculosis is much more widely disseminated
than was heretofore believed is furnished us by a diagnostic method
devised by the French clinician André Jousset, namely “inoscopy.” By
means of inoscopy we can examine microscopically, for tubercle bacilli,
coagulable inflammatory exudates and the blood of suspected cases
of tuberculosis, even though only very few bacilli are distributed
in large amounts of fluid. And we examine these fluids directly,
not indirectly by means of cultures. As a result of the coagulation
the bacilli are fixed by the fibrin, from which they are freed by
dissolving the fibrin with an appropriate digesting fluid.[3] The
bacilli are then separated by centrifuge and can be examined directly
in microscopical preparations. With the aid of this very valuable
diagnostic method we are enabled to demonstrate the tubercular origin
of almost all serous pleurisies, of many exudative peritonites,
of accumulations of fluid in the peritoneal cavity of alcoholic
individuals with liver cirrhosis, of joint inflammations, of exudative
meningites, of many cases of heart-disease and of other classes of
symptomatic affections, where formerly most physicians did not think of
the possibility of these affections being tubercular.
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.
The expression _hereditary transmission of tuberculosis_, or rather,
_of tubercle bacilli_, may be construed in several different ways.
It may mean the hereditary transmission from father or mother, or
from grandfather or grandmother, or from ancestors still further
back. If we designate the parental transmission as _congenital
heredity_, transmission from further back as _pregenital heredity_,
then in my view of the origin of pulmonary consumption, generally
neither congenital nor pregenital heredity comes into play. And,
looking at the matter as I do, if one is still desirous of speaking
of the hereditary influences of relatives, one ought to use the
term _postgenital_. It is now almost everywhere conceded that human
tuberculosis as a rule is actually of postgenital origin.
Experience has taught me that if, in scientific investigation, one
wishes to discover something new, one should study the exceptions to
the rule. In actual practice, on the other hand, it is well to keep
to the rule. We may therefore safely ignore the cases of congenital
tuberculosis, but must all the more thoroughly study the circumstances
which in extra-uterine life govern the tubercular infections which lead
to consumption. And here I believe I have discovered a new principle
which may be expressed thus:
“_The milk fed to infants is the chief cause of consumption._”
This assertion will at first sight be surprising, for it has long been
maintained that the suckling infant receives milk free or almost free
from germs. Mother’s or nurse’s milk is taken by the child in this
condition, and the cow’s milk for artificially nourished children is
usually first boiled or scalded. In later life, to be sure, much less
attention is paid to securing a milk as sterile as possible. How,
then, is this to be reconciled with the above statement, that it is
especially the _milk fed to infants_ which constitutes the chief danger
in causing tuberculosis?
And yet this statement is true, not because the milk fed to infants is
at all worse than other milk, but because the human infant, like the
young of all other mammals, is destitute of the protective agencies
in his alimentary system which at a later period of life prevent the
entrance of disease germs into his tissues. It has taken many years of
experimental work to demonstrate this fact conclusively. At present,
however, the chain of evidence is so strong that I have not the least
hesitancy in building on it my entire plan for the suppression of
tuberculosis.
In this lecture I can do no more than summarize the main proofs for my
assertion regarding the ready penetrability of the infantile alimentary
tract for all disease germs, but especially for tubercle bacilli.
I began with a very interesting fact discovered by my fellow-worker,
Dr. Römer. He showed that true albumins penetrate unchanged the
intestinal mucous membrane of new-born foals, calves, and smaller
laboratory animals, and that they produce the same action on the
organism as when they are injected directly into the circulation. In
adult animals of all species, on the contrary, the true albumins must
first be digested into peptones before they can pass through the mucous
membrane. The anti-diphtheria serum and the anti-tetanus serum contain
curative substances in the form of true albumins. If such a serum be
introduced into the stomach of a healthy, full-grown animal or man,
not a trace of these bodies passes into the blood. On introducing
the serum, however, into the stomach of the new-born, the unchanged
antitoxic albumin can almost entirely be demonstrated in the blood.
This discovery indicates that the mucous membrane of adults, acting
as a dialyzing membrane, does not allow the large molecules of true
albumins to pass through unchanged, whereas the mucous membrane of
sucklings behaves more like a very porous filter.
It was but a step from this discovery to the assumption that the
mucous membrane of infants might behave similarly toward bacteria.
For my first experiments I selected anthrax bacilli, which, when free
from spores and given in milk per stomach, do not affect adult guinea
pigs at all. They are quite rapidly thrown off with the excreta,
remaining, however, a little longer in the cæcum. When the same dose
of bacilli was administered in this way to guinea-pigs less than eight
days old, they died just as rapidly of anthrax as by the customary
method of infection. Next I tried anthrax bacilli whose virulence
had been reduced. These are harmless when injected subcutaneously
into guinea-pigs. _After feeding these weakened bacilli to new-born
guinea-pigs, the blood of the animals contained anthrax bacilli,
though the animals did not die. Incidentally, a fact of considerable
theoretical importance was discovered: that the anthrax bacilli
possess a very intimate affinity for the endothelium of the heart and
blood vessels._
Having thus studied the fate of anthrax bacilli introduced into the
stomach of new-born and adult guinea-pigs, I now turned to a similar
study of tubercle bacilli. Together with Dr. Römer I studied the
behavior of guinea-pigs toward a definitely weighed quantity of
tubercle bacilli given in _one single feeding_. And here also, as
in the case of anthrax bacilli, it was found that when the tubercle
bacilli could be demonstrated microscopically nowhere else in the
alimentary tract, they were often present in the cæcum. After a single
feeding of a small quantity of tubercle bacilli, only the new-born or
the few-days-old guinea-pigs became tuberculous. When larger doses were
administered it happened that older animals also became tuberculous. At
the post-mortem examination of the new-born, a few days later, there
were found submiliary thickenings, with tubercle bacilli in the great
and the lesser omentum. There were also little nodules at a point
on the root of the mesentery, not far from the cæcum. Of especial
interest is the further development of this alimentary tuberculosis
in the guinea-pigs which survived. In these animals, even while their
general health remains good, it is always possible to demonstrate a
tuberculosis of the glands of the neck, a type of disease which may be
said to correspond to scrofula in man. Not infrequently there is later
on developed that type of guinea-pig tuberculosis which has heretofore
been regarded as the expression of an inhalation tuberculosis.
In the results of all these investigations I see experimental support
for the view I have for some time maintained, namely, that the origin
of the epidemiological pulmonary tuberculosis in man and that of the
epizootic pulmonary tuberculosis in cattle is a primary intestinal
infection occurring in very early infancy. In this I leave undecided
whether the bacilli gain access to the body through feeding or through
inspiration.
Upon reflection it will at once be seen that from these experimental
data showing the ready penetrability of the infantile mucous membrane,
another logical deduction follows: If even non-virulent anthrax bacilli
introduced per stomach gain ready access to the circulation of the
new-born, then it must be possible for all the bacteria of milk to do
the same, and we may therefore expect that the accidental presence of
pathogenic bacteria in the milk fed to infants will exercise a damaging
influence on the infant organism. In considering their pathogenic
possibilities the amount of the infectious germs which enter the
system must, of course, be a matter of some importance. Under certain
conditions, however, even a few germs may be sufficient to excite
disease, for in the intestines, especially in the cæcum, they find
an excellent place of incubation where they can multiply. A milk
very poor in disease germs may thus lead to a virulent infection. In
breast-fed infants the danger of introducing disease germs, excepting
tubercle bacilli, of which I shall speak later, is not very great,
for it is very unusual for living germs derived from the interior of
the body to appear in the milk. The germs which can be found, even in
perfectly fresh milk, are derived from the surface of the body, or
from the mouths of the lacteals, or possibly even from the glandular
epithelium, as researches conducted by myself, assisted by Mr. Rösler,
have shown.
But in _artificially nourished infants_ the matter is altogether
different. It would be a miracle if, after all the manipulations to
which the milk supplied to our large cities is subjected, it did not
occasionally contain disease germs derived from the milker or from
other persons who have handled the milk.
If, by the time the milk reaches the city, the proliferation of these
pathogenic micro-organisms has already gone on to a considerable
extent, then usually the milk will contain a number of poisonous
substances in addition to the micro-organisms. Some of these germs are
killed by the scalding to which the milk is usually subjected before
feeding, and the virulence of the rest is much diminished, so that
in boiled milk practically no danger is to be apprehended from the
micro-organisms. We are not at all sure, however, that we have made
the toxins innocuous by this boiling, and probably a great many cases
of intestinal catarrh in artificially nourished children are due, not
to a parasitic, but to a toxic infection.
I said it would be a miracle if artificially nourished infants did
not frequently suffer from milk infections, and I can add that this
miracle does not, in fact, occur. One need only glance at the mortality
statistics of artificially nourished infants in order to realize that
my experimental results absolutely agree with the facts. The following
figures are taken from the excellent report, “Gesundheitswesen des
preussischen Staates im Jahre 1901,” which has recently been published
by the Prussian government.
In the city of Stettin, the mortality for the first year of life was
473.52 for every 1000 living children of the same age; whereas in the
period of 10 to 15 years the mortality was 2.94 to each 1000 living
children of that age. In other words, _during the same length of time
161 times as many infants up to one year died as did children over ten
years_.
Berlin, with a mortality of 286.29⁰⁄₀₀ for the first year of life,
stands about midway in the list of Prussian cities having over 100,000
population. Cassel, with 183.54⁰⁄₀₀, shows about the lowest figure, and
even this is inordinately high, for it is not in the nature of things
that this is so. We are not facing a necessity of nature to which we
must submit like fatalists. This can be readily seen by observing
that there are towns and whole regions in which the mortality figures
for the first year are kept within moderate limits. In Ireland and
Scotland, as well as in Norway and Sweden, the mortality for this
period scarcely exceeds 10⁰⁄₀₀, about one-fiftieth the mortality in
Stettin. In Stockholm I visited a foundling asylum with an organization
bound to excite admiration and wonder, in which, as I recollect, the
mortality was still less.
Nowadays the assertion that the character of the milk fed to infants
is responsible for the great differences in the mortality statistics
is nowhere seriously questioned. There are, however, wide differences
of opinion as to what the determining factors are, and how, in places
where the mortality figures are so outrageously high, we can remedy the
evil.
According to my researches into this subject this problem will not be
successfully solved by the efforts now being made to secure the use of
sterilized milk. I am, in fact, in doubt whether milk sterilization as
at present practised can much longer pass as a hygienic measure. For
the present, to be sure, we have nothing better. But the discussion
of this question does not fall within the scope of this lecture. I
have quoted the statistics of the high infant mortality in our large
cities merely in order to advance a further epidemiological argument
for my assertion that the infant alimentary tract is defenseless
against infectious agents whether these are living or not. Even the
infectious toxins pass unchanged through the intestinal mucous membrane
of very young individuals, though not through that of healthy older
ones. A real advance in milk hygiene can, however, be begun even
now if the milk be pasteurized at the dairies and not at the large
receiving-stations in the cities. In the raising of calves, this
procedure has proven of great value.
I have made exhaustive studies to discover why the intestinal mucous
membrane of the young should offer so little resistance to the passage
of corpuscular infectious substances. I shall content myself here
with the statement that the mucous membrane of new-born individuals
possesses no continuous epithelial covering and that the gland-tubes of
the ferment-producing glands are little, if at all, developed at this
time.
By having thus presented to you the results of my experiments and
explained my epidemiological views, I have not really deviated from
the subject of the suppression of tuberculosis. We have seen that the
tubercle bacilli which gain access to the system through the alimentary
tract in infancy constitute the important etiological factor in the
production of the tubercular infection which leads to consumption, and
I believe that the realization of this great fact will supply us with
a rational plan for combating tuberculosis. It will be necessary to
strive more than ever to secure a suitable milk diet for new-born and
very young children, one based on sound experimental investigations.
The as yet unsolved problem, that of a rational milk hygiene in the
suppression of tuberculosis, coincides with the problem of milk-feeding
of infants in general. The mode of infection is everywhere the same,
but the infectious agents are of great variety. Most of them excite
acute diseases which end either fatally or in entire recovery; in the
latter case with a simultaneous development of immunity. The virus of
tuberculosis, however, behaves quite differently, creeping in most
insidiously, all unnoticed, and being in this respect analogous only to
the virus of leprosy, of syphilis, or possibly of malaria in tropical
countries. It may be months, years, or decades before the infection
leads to manifest disease. This depends on the virulence of the virus,
which is generally much greater in the virus of bovine tuberculosis
than in that of human tuberculosis. It also depends on the number of
bacilli introduced per stomach, and whether such introduction is single
or oft repeated. In the human being months and years may elapse before
the infection is followed by any sensitiveness to tuberculin injections
in the usual dose. If, then, at the time of puberty, or after an
exhausting puerperium, after too great a demand on the milk secretion
(especially with insufficient food), after so-called colds and other
unfavorable meteorological conditions, after muscular over-exertion,
under conditions unfavorable to life, such as improper nourishment,
confinement in insufficiently or badly ventilated rooms, etc., if,
after any of these, pulmonary disease develops whose tubercular
nature we cannot doubt, then we are dealing with the _beginning of
consumption_; the _beginning of tubercular lesions_ is much further
back; and the first introduction of the disease germs, in other words,
the _beginning of the infection_, is far back in earliest infancy.
This must be so, for we see many individuals, though subject to the
most unfavorable conditions, for example, those confined in unsanitary
prisons, wholly escape tuberculosis.
The results of all these scientific investigations lead us back to the
old folk belief in family tuberculosis and hereditary consumption,
with this difference, however, that now we believe the germs of
consumption to be transmitted _postgenitally_ from parents, relatives,
or house-companions. If a coughing consumptive lives together with a
new-born child, especially if cleanliness leaves much to be desired, it
is impossible for this child to avoid infection with tubercle bacilli.
They are present in the particles of sputum which are scattered
about everywhere, and they thus gain access to the mouth and nose of
the infant. From there they reach the intestinal mucous membrane,
which they penetrate, and so they invade the body juices. Not alone
infants, but older persons as well, are endangered in the home of
the consumptive. In these, however, there must previously have been
pathological changes in the alimentary tract, or an overwhelming dose
of the infectious agent, in order to effect an intestinal infection.
Pathological changes, accompanied by the shedding of epithelium,
occur especially in the exanthemata, and particularly after measles.
The laity has long noticed this close relation between measles and
tuberculosis. In the infant, the disposition to intestinal tubercular
infection is entirely physiological and normal. The healthiest and
strongest infant is exposed fully as much as the weak, sickly one, and
perhaps more so, for in the latter other parasites are contending for
the cells on which they feed.
I have now given you a general idea of the origin and spread of the
tubercular infections ending disastrously. This brings us at once
to certain practical points in dietetic hygiene which, though never
entirely neglected, are now brought into prominence.
It is unnecessary for me to further emphasize the necessity, in infant
feeding, to insist under all circumstances on milk absolutely free from
tubercle bacilli; nor, what is equally obvious, that it is absolutely
necessary to keep coughing consumptives away from infants. But I
should like to observe that not only infants but also older persons
should be protected against the possibility of infection, if we have
any reason to fear that the alimentary tract is anywhere deficient
in its protective epithelial covering. I have already pointed out
the importance of the exanthemata in this respect, and I need only
remind you of the many other disturbances associated with the shedding
of epithelium, disturbances due to catching cold, to indigestion,
or the after-effects of certain diseases associated with intestinal
ulceration, etc. There is one other condition which I must not fail to
mention, namely, the temporary exacerbations of a tubercular process,
in which one cannot be too careful in ordering the diet. For that large
class of individuals threatened with consumption, I believe we have a
valuable healing agent in the dietetic therapy made prominent during
the past decade, especially by von Leyden and his pupils. In the same
sense we must regard the temporary residence of tuberculous individuals
in sanitaria as most valuable, for even if the lesions do not heal
there, the progressive downward course of the disease is checked
and the patients learn for the rest of their lives to appreciate
what will benefit and what will harm them. In many cases, therefore,
these sanitaria will prove themselves homes for the prevention of
consumption, even if they are not homes for the cure of tuberculosis.
My own efforts in the field of tubercular therapeutics do not, to be
sure, concern themselves with sanitarium treatment. _Their last aim is
to make all homes for the prevention of consumption, all sanitaria,
etc., unnecessary by means of a protective agent similar to that by
which Jenner made smallpox pest-houses unnecessary._ Institutions for
persons bodily wrecked are like those for persons morally wrecked; they
are products of our civilization, but not desirable products. At best
they are necessary evils.
OBSERVATIONS CONCERNING THE STUDY OF PHTHISIOGENESIS IN MAN AND IN
ANIMALS.
1. It is possible in experiments on guinea-pigs to produce pulmonary
phthisis by infecting these animals from the oral cavity in such a
manner that every direct infection of the lungs (alveolar infection
through the trachea = aerogenous infection of the lung) is excluded.
(_a_) Infection through the parenchyma of the tongue.
(_b_) Feeding of tubercle bacilli with milk.
2. Ascribing the pulmonary phthisis which I succeeded in producing
experimentally to a lymphogenous or hæmatogenous infection of the
lung following previous scrofulous disease. Definition of the term
“scrofula”: multiple, caseating areas of disease in lymph-glands and in
other organs, caused by Tb. infection. Concerning the etymology of the
word “scrofula” (Greek = choeraden), see Virchow’s “Geschwülste,” Vol.
II, p. 558.
3. Other varieties of experimental phthisiogenesis;
(_a_) v. Baumgarten’s experimental method of causing pulmonary
phthisis by means of primary infection of the urogenital
apparatus.
(_b_) The experiments of Troje and Tangl with tubercle bacilli
artificially weakened in virulence.
4. Critical analysis of the so-called “Inhalation Tuberculosis” of
guinea-pigs and rabbits.
(_a_) My own experiments, in which the typical picture
heretofore regarded as that of an inhalation tuberculosis, in
the sense of an aerogenous alveolar infection, was produced by
lymphogenous or hæmatogenous introduction of tubercle bacilli,
with the complete exclusion of a primary alveolar or bronchial
infection.
(_b_) The experiments of Weleminsky (Hüppe).
(_c_) Signs distinguishing tubercular pulmonary consumption
from so-called inhalation tuberculosis.
5. Improbability, so far as importance as a phthisiogenetic factor
is concerned, of a primary bronchial, or even primary alveolar Tb.
infection following aerogenous introduction of Tb. into the mouth and
nose, through the inhalation of dust or droplets containing tubercle
bacilli.
6. Proof for my assumptions,
(_a_) That inhaled tubercle bacilli under circumstances
occurring in nature are taken up by the lymphatic receptive
apparatus without exciting, at the point of entry into the
lymph-channels, any tubercular disease.
(_b_) That inhaled tubercle bacilli, after they have entered
the lymph-channels of the throat, take the following courses:
some find lodgment in the submental glands and glands of the
neck; some are transported to the mediastinal (bronchial?)
glands; some gain the circulation and thus cause hæmatogenous
infections, especially at the peripheral (sub-pleural) endings
of the pulmonary artery, from which then the lung parenchyma
can be infected; finally, some are carried through the stomach
to the lowest portions of the intestines, from where they can
reach the mesenteric lymph-glands, the portal vein, and the
peritoneum.
(_c_) That the introduction of Tb. into the lymph-channels is
accomplished primarily by the leucocytic wandering cell, which
takes up the tubercle bacillus.
7. In the herbivora the Tb. are most commonly carried from the cæcum
to the mesenteric lymph-glands. In man, the agminated lymph-follicles
of the small, and the solitary lymph-follicles of the large intestine
also serve as points of entry (cf. Carl Hof, “Ueber primäre
Darmtuberculose,” Kieler Dissert., 1903. Compare also v. Hansemann,
“Ueber Fütterungs Tuberculose,” _Berl. klin. Wochenschr._, 1903, No. 7).
8. Reference to the peculiar features of the stomach of ruminants and
remarks on primary tuberculosis of the stomach (Schottelius).
9. The primary development of localized foci in the lesser omentum
after infection through the stomach in early nursing period.
10. Peculiarities of the infection of nurslings through the alimentary
tract, experimentally and statistically determined.
(_a_) Feeding experiments with anthrax bacilli and other
bacteria.
(_b_) Feeding of spores.
(_c_) Tubercular virus behaves in many ways more like the
resistant form [spore form] of anthrax virus, especially when
the Tb. virus is present in cheesy pus.
(_d_) The observations of Adalbert Czerny and Paul Moser on the
occurrence of bacteria in the blood of living human nurslings
(1894).
(_e_) Carl Weigert’s statements concerning the penetrability,
for Tb. virus, of the intestinal apparatus of very young
children. (From 1883, cited in _Deutsche medizin. Wochenschr._,
1903, No. 41.)
(_f_) Raw’s communication (_British Med. Journ._, 1903)
concerning 300 cases of _tabes mesenterica_, not one of which
was found to have developed in a child nursed exclusively at
the breast, but rather in those who had been nourished for a
considerable time on cow’s milk.
11. It is probable that in thickly populated countries practically
every person is at some time or other infected with tuberculosis. Aside
from the quantity and quality of the Tb. virus, the outcome of the
tubercular infection is dependent to a high degree on the physiological
state of the infected individual and on accidental conditions of
infection. (Intercurrent pathological factors; endogenous and exogenous
conditions of infection.)
12. Not a single unexceptionable case has been brought forward to show
that under the conditions of life usually present in civilized lands,
an adult person has ever contracted pulmonary, bronchial, tracheal, or
laryngeal tuberculosis without having previously been infected and thus
rendered oversensitive to the tubercular poison.
13. Against the action of tubercle bacilli entering the intestinal
apparatus, healthy, full-grown persons apparently possess sufficient
protection in the character of the mucous surfaces and the
anti-bacterial action of the digestive juices. It has, too, still to be
proved that healthy, full-grown persons become ill with tuberculosis as
a result of eating food (milk, butter, meat) derived from tuberculous
cattle.
14. Very probably adult persons frequently acquire intestinal
tuberculosis through food containing tubercle bacilli, if the
epithelial covering of the intestinal mucosa is defective, or if
perhaps there exist ulcers which extend down to the parenchyma of
the wall of the alimentary tract. (Exanthematic diseases, typhoid,
dysentery, carcinoma, etc.)
15. Whether adult persons in whom the conditions are favorable for
an intestinal infection with Tb. will develop primary tubercular
lesions in the intestinal wall, or in the mesenteric glands and the
peritoneum, will depend mainly on the circumstance whether or not,
owing to a previous infection, they have become oversensitive to
tuberculin. _Individuals oversensitive to tuberculin are inclined to
develop lesions at the point of entry of the tubercular virus_, if
opportunity is given for the introduction of the virus by means of
leucocytic wandering cells. This opportunity is lacking in the virile
infecting period at such places where the lymphatic receptive apparatus
is destroyed [verödet]. (Mucous surfaces of the faucial ring of
consumptives?)
16. In order to explain the mode of origin of cheesy pneumonias and
tubercular broncho-pneumonias it is necessary at autopsy to regard most
carefully the possible direct extension of the infection from cheesy
mediastinal and bronchial glands to the bronchi and their branches,
before thinking of aerogenous or hæmatogenous pathogenesis. (Compare
[Ribbert] Sievers, “Marburg Dissertation,” Aug. 14, 1902.)
17. Critical analysis of several statistical statements which seek
to show that alveolar pulmonary tuberculosis is referable directly
to inhaled tubercle bacilli; especially the statement of Knopf (New
York) cited by Mitulescu (_Zeitschrift für Hygiene_, 1903), that in
Lansing, Mich., twenty employés of a library became consumptive through
handling Tb. laden books.[5] Probability of the correctness of my
assumption that Knopf was misled by unscientific communications from
Lansing. Proof that Mitulescu again misunderstood Knopf.
18. It has not yet been proved that persons cutaneously infected with
human or bovine Tb. have as a result of this developed phthisis. (My
own observations on cases of infection on the hand in persons working
with tubercle bacilli of various origins.)
19. Justification of the statement by Virchow in his “Phymatie,
Tuberculose und Granulie,” that “the history of phthisis is concerned
much more with cheesy hepatization than with tubercles” (Virchow’s
“Tuberkel,” Begriff).
20. The analysis of the origin of pulmonary consumption must begin with
the primary attack (primary regionally as well as chronologically) of
the Tb. introduced into the organism.
21. _As a rule we can regard as points of primary infection polynuclear
leucocytes in the blood and lymphatic receptive apparatus; next
in order are the muscular elements in the walls of the smallest
blood-vessels._ Endothelium and epithelium may become carriers of Tb.
through the action of polynuclear leucocytes which have wandered into
these tissues.
22. In studying the results of an infection with tubercular virus,
aside from the degree of virulence, from the dosage, the single or
repeated Tb. inoculation, and the primary point of attack (regional
and cellular), we have particularly to consider the age at which the
primary infection occurs. I distinguish four periods:
(_a_) Infantile period of infection;
(_b_) Puerile ” ” ”
(_c_) Virile ” ” ”
(_d_) Senile ” ” ”
23. It seems to me that in the epidemiological origin of pulmonary
consumption the infantile Tb. infection, followed by latent or manifest
scrofula in the puerile period, is of great significance, so that
we can formulate the following doctrine: “_An infantile tubercular
infection predisposes to tubercular pulmonary consumption_.” Under
“scrofula” I here include the alteration in the muscle of the
blood-vessels, caused by the Tb. infection, which finds its expression
in the increased sensitiveness to tuberculin, and which in general is
equivalent to “scrofulous diathesis” of the older authors.
24. The primary infection from the mouth or nose with tubercular virus
derived from food or even from inhalation, in the small quantities that
under ordinary conditions of life are concerned, is followed after the
bacilli have entered the circulation, by alterations in the walls of
the smallest vessels. These manifest themselves as follows:
(_a_) Microscopically, by a loosening of the vessel wall,
between whose elements, shortly after the infection, tubercle
bacilli can be found. These bacilli, brought here by the
wandering cells, are set free on the destruction of the cells.
(_b_) In primary functional disturbances which can be
recognized by the temperature curve and the heart action.
(_c_) In secondary tuberculin hypersensitiveness.
25. Following mild infections the alterations in the vessel walls may
retrogress with a suppression [Beseitigung] of the tubercle bacilli.
Without exception, however, the hypersensitiveness to tuberculin
remains, varying in degree and length of time according to the
virulence of the infecting Tb. and to their more or less locally
limited action on the vascular system.
26. After a moderately severe infection there is a formation of
transparent, submiliary eruptions (nowadays our “gray miliary
tubercle”), especially about the smallest vessels of serous membranes.
_These eruptions are capable of becoming organized. In fact, when they
have healed they form a tissue entirely identical with the tissue in
which they originated._ (Bichat, Lebert, Empis, and many other older
investigators.) Aufrecht, _Deutsch. Arch. f. klin. Med._, Vol. LXXV.
27. The introduction of a tubercular virus so strong as to cause the
smallest vessels to become occluded, especially Cohnheim’s terminal
arteries of the spleen, lungs, and kidneys, results in the exudation
of a coagulable fluid and in necrobiosis of the extra-vascular
region supplied by those vessels. (Aufrecht, _Arch. f. klin. Med._,
Vol. LXXV.) Into this dead area tubercle bacilli are dragged by the
wandering cells. These bacilli multiply and cause chemical changes
which manifest themselves first in a fatty (steatomatous) and then in
a cheesy metamorphosis. (Cf. Koch, Volume II of the _Mittheilungen aus
dem Kaiserlich. Gesundheitsamt_, p. 21, and Plate IX, Figs. 45 and
46); my own observations; Aufrecht, 1. c.; compare also the critical
reference by Virchow to the works of older authors, such as Vetter,
Gendrin, Lobstein, Cruveilhier, Bayle, Baillie, Laënnec, Rilliet
and Barthez, Vulpian, Craigie, etc., in “Phymatie, Tuberculose und
Granulie,” and in Vol. II of “Die Krankhaften Geschwülste.”
28. We may enumerate as the result of primary tubercular focal disease
(_a_) Anatomically demonstrable residues.
(_b_) Functional alterations.
29. Functional alterations may remain without any anatomically
demonstrable residues of the primary infectious processes. I divide
functional alterations into
(_a_) Alterations which leave behind them an immunity against
living Tb. virus, probably to be sought for in the peculiar
condition of the vessel musculature and, in the beginning at
least, always associated with hypersensitiveness to the soluble
tubercular poisons.
(_b_) Scrofulous diathesis, consisting in such changes in the
vascular system and the lymphatic apparatus that a renewed Tb.
infection very readily causes cheesy tubercular lesions.
30. As scrofulous infectious processes, I regard
(_a_) Lupus, which I interpret as a cutaneous additional effect
of a tubercular infection.
(_b_) Gland scrofula,[6] inclusive of tuberculosis of the
mediastinal, bronchial, and mesenteric glands.
(_c_) Bone scrofula and joint scrofula.
(_d_) Scrofula in the domain of the external body covering, of
the mucous membranes, and of the lymph-channels.
(_e_) Cheesy metamorphosis in internal organs, inclusive of the
organs of sense, and the vessel intima.
31. The acute miliary tuberculosis in man, which can be clinically
diagnosticated, is to be regarded as a provocative secondary infection,
resulting from scrofula of the blood-vessels’ intima when, on the
disintegration of cheesy intima tubercles, a great many tubercle
bacilli are thrown into the circulation at once. (Weigert-Ponfick.)
32. Disease of the lung apices occurring in the virile period of
infection and, because of its important bearing on the origin of
consumption, considered separately, is preceded by the consequences
of an infantile infection. Foremost among these is the secondary
hypoplasia of the smooth muscle tissue (of vessels, bronchi, and
intestinal wall); next in order come wasting [Veröding] of the
lymphatic apparatus (quantitative and qualitative reduction of
the follicular receptive apparatus of the _tubus alimentarius_);
destruction of lymph-glands; and the secondary hypoplasia of other
primary points of attack for Tb. action (in the spleen, bone-marrow
cavities, on serous surfaces of the large body cavities, and of the
joints). The predilection of the thoracic dome for immobilizing
changes can probably be ascribed to its exposure to the Tb. infection
in connection with precedent mediastinal-gland scrofula; while the
predilection of the lung apices for caseating lesions can again be
brought into causal relation with secondary ossifying processes, of
scrofulous origin, in the joint structures of the thoracic dome (cf.
Aufrecht, 1. c.).
33. In my experiments on tubercular cattle I succeeded in producing
eruptions of gray, non-caseating tubercles, running an acute course, by
means of injections of tuberculin. At the same time it was noticed that
not infrequently after the intercurrent exacerbation had subsided, the
old infectious process had been favorably influenced.
34. Even when caseating lesions are present, the simultaneously
developing submiliary transparent eruptions (granulie, of the older
authors) are to be regarded as capable of being organized and
spontaneously cured. They are much more numerous in man than has
heretofore been assumed. This is shown, for example, by the fact that
upon opening the abdominal cavity of such young individuals as showed
no clinically diagnosticated symptoms of a miliary tuberculosis, these
eruptions were by chance demonstrated.
It is of the highest interest to determine the fate of such individuals
with a healed miliary tuberculosis of the peritoneum, that is,
whether in virile period of life the disposition in them to pulmonary
consumption is increased or diminished.
35. The clinical picture of scrofula in the puerile period of infection
is etiologically complicated by other infectious processes, especially
in the domain of the outer body covering. The functional alterations
in the vascular system, due to an infantile Tb. infection, find their
expression not only in the organism’s increased sensitiveness to
tuberculin, but also in a marked instability [labilität] of the dynamic
equilibrium of the circulation (lymphatic constitution). In consequence
of this, eczematous eruptions due to parasitic and toxic agents result
much more readily in these individuals than in those who have not
suffered such an infantile Tb. infection (one incompletely healed).
36. The symptoms of the so-called “inclination to consumption” are
the expression of a defective overcoming of the infantile and puerile
infectious periods. The hindered development and weakness of the
organs made up of smooth muscle fibres (muscles of the blood-vessels,
intestinal wall, and bronchi) are comprehensible when we remember the
great share that the smooth muscle tissue has in the reaction against
the Tb. circulating in the blood. The question whether the weakened
conditions and hindered development in the domain of the striped
muscles are due directly or indirectly to the Tb. infection cannot be
answered without further investigations. Similarly, we do not yet know
the mechanism of the origin of the chest anomalies seen in candidates
for consumption. A partial impoverishment of the intestinal lymphatic
receptive apparatus is presumably accountable for the fact that even a
plentiful supply of food is unable to increase the accumulation of fat.
37. The possibility must also be considered that in the course of the
puerile period of infection the development of a caseating tubercle may
proceed in the joint tissues between costal cartilage and breast-bone,
and that such a scrofulous thoracic affection is clinically much
less readily diagnosed than a similar affection in bones of the
extremities. Further, that such a lesion in the lower extremity is much
more readily recognized than one in the upper extremity, since even
slight alterations in the bony tissues of the lower extremity, because
of functional disturbances in walking and running, make themselves
manifest.
38. For a detailed analysis of the origin of pulmonary consumption,
beside the results of infantile and puerile infections, there must
still be considered
(_a_) Additional virile Tb. infections (cf. Romberg, _Deutsch.
Arch. f. klin. Med._, 1903).
(_b_) Combined action of a complicating infection.
(_c_) The co-action of general hygienic and dietetic injuries.
39. For my plans for suppression of tuberculosis, therefore, the
following points are essential:
(_a_) Prevention of the introduction of Tb. with food,
especially with milk, during infantile life.
(_b_) Introducing Tb. anti-bodies with the milk in earliest
infancy in order to render innocuous any inhaled tubercle
bacilli.
40. I have made separate communications regarding feeding with Tb.-free
milk. The production of such a milk will be very easy if my method of
cattle immunization in practice fulfils the hopes, which I have for it;
and these hopes I am convinced are fully justified.
41. In order to produce immunity by means of anti-bodies it is probable
that anti-bodies derived elsewhere will have to be added to the milk
given to infants.
SUGGESTIONS CONCERNING THE HYGIENE OF COW-STABLES AND THE PRODUCTION OF
MILK FOR INFANT-FEEDING, WITH SPECIAL REFERENCE TO TUBERCULOSIS.
THE BONN RULES.
1. Until it has been definitely decided whether or not my protective
cattle inoculation protects cattle against tuberculosis when these are
kept in stalls or herds strongly infected with Tb. virus, it should
be sought to reduce the danger of infection as much as possible by
following Ostertag’s recommendations and segregating all the cattle
with an open tuberculosis.
2. The milk of cows which react positively to tuberculin must not be
used for feeding calves, nor, of course, for infant-feeding.
3. Whenever the circumstances permit, the separate housing of the
protectively inoculated animals in a stable free from tuberculosis is
to be recommended. In constructing new stables it is strongly urged
that in place of _one large_ stable, several small ones be erected;
besides this, attention should be paid to the placing of the animals.
They should be placed with the heads toward the lateral walls, and not
head to head, facing a common feeding-trough along the middle of the
stable.[7]
4. Particular attention should be paid to the cleanliness of the
feeding-troughs. Every fourteen days they are to be filled with hot
water and freed from any adherent dirt by mechanical means. The
feeding-buckets are to be similarly cleansed from time to time.
5. The drinking-water supplied to cattle should meet essentially the
same requirements as are demanded of water supplied to dwellings.
6. In maintaining the health of the young cattle an important factor is
the pasturage. For larger dairies an arrangement used at our Marburg
experimental station, consisting of a lightly constructed shelter
within a large enclosed pasture, is to be recommended.
7. The disinfecting of infected stables is to be done in accordance
with the government regulations.[8] [This refers to the German
regulations of June 23, 1880, and May 1, 1894.] Here it is to be
remarked that disinfection of the stables by means of formaldehyde
generation is not even then accomplished when one far exceeds the
requirements formulated by Flügge for the Breslau method. Utilizing the
opportunity presented by a number of courses given at Marburg in the
method of making protective inoculations, etc., we have found that even
in the stable of the pest laboratory here, which is very easily closed
off, the above-mentioned formaldehyde fumigation is ineffectual; for
by treating the disinfected objects with ammonia water it was found
that neither anthrax virus nor cocci, in the dry state, were certainly
destroyed by the fumigation.
8. More important than the disinfection by means of chemicals is the
prevention of the accumulation of infectious materials on the stable
utensils, in the food, on the body surface of the cattle, on the body
and clothing of the stablemen. Training the stablemen to the use of
warm or hot water and soap; the use of towels and dishcloths which
have been rendered germ-free by means of hot water or dry heat before
throwing them among the soiled clothes; special regard to a rational
care of the milker’s hands, including the removal of the dirt under the
nails; all of these are the most important measures for the prevention
and suppression of stable infection.
9. If it is desired to secure a milk as free from dirt and germs as
possible (not over 400 germs per c.c.), the following additional
measures must be taken:
I. Presupposing that the milk is to be used for infant-feeding, the
same is to be filled into bottles holding 250 to 500 c.c. All parts of
the bottle, including the air-tight and germ-tight closing contrivance,
must be constructed so as to be readily cleansed, and further, so that
they can, without injury, be sterilized by heat.
II. In order to meet all the requirements for cleansing and sterilizing
milk-bottles, the following rules are recommended. The bottles returned
by the consumers are in a soiled condition and contain fluid remnants
of milk:
(_a_) The cleansing of the bottles should be undertaken in a
well-ventilated room which can readily be kept clean and which
may also serve as the bottling room. This room is to be so
separated from the stables that the stable odors cannot gain
access.
(_b_) The following manipulations are required to clean the
bottles:
(α) Energetic rinsing with 10% warm soda solution.
(β) Rinsing with quartz gravel by means of a stream of hot
water.
(γ) Cold rinsing.
(δ) Sterilization in the dry chamber. These cleansing
manipulations occupy about forty-five minutes.
III. The stable itself should be so built that it can readily and
thoroughly be cleansed, with special regard to the following points:
(_a_) Draining of the fluid excreta, etc., by means of drains
with sufficient pitch.
(_b_) Ready removal of solid refuse without raising dust.
(_c_) A plentiful supply, by means of pipes, of pure, wholesome
water. Also a hot-water supply for cleansing purposes.
(_d_) Good ventilation for the high lying stalls.
(_e_) Broad alleys separating the rows of stalls.
(_f_) Each stall to be constructed in such manner that the cow
is obliged after feeding to step back, thus compelling her to
empty her excreta into an open drain connected with the main
drain. This is effected by means of the so-called “drop-railing
contrivance.”
(g) Water-tight flooring.
IV. The spreading of peat instead of straw to keep the stalls dry.
10. Another deciding factor in the production of a pure milk for
infant-feeding is the cleanliness of the stable and dairy attendants,
the milkers, the cows, and the stable and dairy utensils.
I. Aside from general body cleanliness, particular attention is to be
given to a healthy condition of the milking person’s hands. Before
proceeding to milk, these persons are to don a clean gown made of white
linen.
II. The cows are to be kept scrupulously clean. The udders and tails
are to be so clean that they can be touched with white-kid gloves
without causing appreciable amounts of dirt or of odorous substances to
soil them. In order to keep the udder and teats clean the following is
recommended:
Just before milking, the udder, which should always be kept dry, is to
be rubbed off with a clean flannel cloth which has been greased with a
little lard. By this means dirt and odorous substances are most readily
removed. Following this, the parts are rubbed dry with the aid of a
little bran.
III. The milk vessels should be of tinned sheet iron.
IV. The milk should be strained through aluminium-nickel gauze or brass
gauze, which is then to be cleaned and disinfected.
V. All the milk of one milking period is pumped high into the bottling
room and conducted into a collecting reservoir. This passage to the
reservoir, during which it is cooled and aired, occupies only a few
minutes and the milk reaches the reservoir at a temperature of 4°-5° C.
VI. From this reservoir the milk is bottled without delay by means of
a bottling-machine, the milk having a temperature of about 5°-7° C. on
bottling. _A temperature of less than 2° C. has an injurious influence
on the anti-bacterial substances in the milk, and should therefore be
avoided._
11. If the milk hygienic rules above mentioned are carefully followed,
and if attention is paid to the experiences regarding a rational method
of feeding milch cows, it is possible, without any further method of
preserving the milk, to have the same capable of being transported and
kept for sixteen hours without losing its adaptability as infant food.
In Berlin I saw such a milk reach the consumer with a germ-content of
not over 1000 germs per cubic centimeter. On the other hand, I have
seen milk derived from dirty cows and collected without particular
hygienic precautions, after being transported six hours, contain a
hundred to a thousand times as many germs. In such cases, soon after
milking, the milk often contains from 30,000 to 100,000 germs per cubic
centimeter.
In the strictly fresh milk from my own cows the number of germs per
cubic centimeter varies from 10 to 50 to 200. Such milk kept at room
temperature does not coagulate until after three to five days.
At present I regard 1000 germs per cubic centimeter at the time of
feeding to be a safe limit for milk fed to infants.
12. If a milk collected in accordance with the preceding regulations
is to be made capable of being transported and kept for three days (in
which case coagulation factors must be reckoned with) without losing
its qualifications as an infant food, the addition of formaldehyde in
the proportion of 1:40,000 (B. f. milk) is to be recommended.
The following manipulations are then to be carried out:
I. Preparing a formaldehyde stock solution containing 0.5%
formaldehyde. (One part of commercial formaldehyde and 79 parts of
boiled water.) This solution will keep for two or three days.
II. Pouring 50 c.c. of this 0.5% stock solution (= .25 gramme
formaldehyde) into an empty tin pail in which a mark has been made at
the 10-liter level.
III. Milking into this pail up to the mark.
IV. Straining, airing, cooling, etc., according to paragraph 10, IV, V,
and VI.
13. In order not to conflict with the government sanitary regulations
the milk producers at present delivering this B. f. milk have agreed to
supply it only to certain private institutions designated by me.
14. Should the authorities later decide to allow the sale of this B. f.
milk, it is recommended that licenses be issued, out of the proceeds
of which veterinary physicians be appointed to see that this B. f. milk
is produced in accordance with these regulations.
15. Containers for B. f. milk should have trademarked labels indicating
that the milk has been produced in conformity with the requirements.
Beside this the label should bear in clear figures the time and date of
milking.
16. Whenever for any reason it is impossible to raise a calf directly
on the udder, B. f. milk should be preferred to milk sterilized
by heat. In the production of B. f. milk tubercular and suspected
tubercular cows are to be excluded on principle.
17. Where it is desired to suppress an infectious process in the
digestive system of cattle, the temporary employment of a stronger
formaldehyde milk (1:25,000 to 1:16,000) under the direction of a
veterinary physician is recommended.
18. In the suppression of “_Kälbersterbe_,” beside the increased
requirements regarding the cleanliness of attendants’ clothing and
body, of stable and stable utensils, the proper care of the navel with
the aid of ⅖% aqueous solution of formaldehyde is recommended.
19. The radical suppression of bovine tuberculosis by means of my
protective inoculation is to be sought for.
20. The following article shows the method of making these inoculations
at present in use at Marburg.
SYNOPSIS FOR PROTECTIVE INOCULATION OF CATTLE IN AGRICULTURAL PRACTICE.
GENERAL CONSIDERATIONS.
For the protective inoculation carried out by us in practice we make
use of “Mxt. Tb.” in the form of our “Culture No. 1,” which has been
studied by us for years and which we have minutely described in the
_Beiträge_, Nos. 5 and 6. The accumulation of orders for this virus on
the one hand and the multitudinous experimental labors in the institute
here on the other, compelled us to rid ourselves of the technical
labor of manufacture, weighing off and shipping of the virus, which
accordingly has been undertaken by the local firm of Drs. Siebert &
Ziegenbein. The virus, however, continues to be tested as to purity,
virulence, etc., in the scientific department of the institute at
Marburg.
The virus is accompanied by directions for use which have already
appeared in the _Zeitschrift für Thier-medicin_. These are as follows:
I. SELECTION OF THE ANIMALS TO BE INOCULATED.--As a rule only animals
without external evidences of disease, from three weeks to three months
(for the first inoculation) should be inoculated. In healthy animals of
this age a previous tuberculin test is unnecessary, even if the animal
comes from a notoriously tubercular herd.
II. NUMBERING THE INOCULATED ANIMALS.--Every inoculated animal must be
marked with a running number. The marking must be of such a character
as to be distinct, not liable to be mistaken for some other, and to
last the lifetime of the animal. (Ear-marking, tattooing, etc.) If
necessary, the marking is to be repeated should the first mark become
indistinct.
III. KEEPING OF RECORDS.--See under “Conditions governing the
distribution of the virus, etc.,” p. 75.
IV. TECHNIQUE OF TAKING THE TEMPERATURE.--The body temperature is
determined by means of a self-registering thermometer completely
inserted into the rectum. Before introducing it, the rectum is to be
cleared of any hard fecal masses. A tape about a foot long, having
a clamp at its end, is tied to the neck of the instrument. The
thermometer is left in the rectum for four minutes, the clamp meanwhile
being fastened to the hairs at the root of the tail. In order to save
time, thermometers are introduced into a number of animals (about six)
consecutively. When the last thermometer has been inserted it will
usually be time to extract and read the first. In this way one can take
the temperature of fifty head of cattle in 1-1½ hours.
V. THE VIRUS.--The inoculating virus consists of living tubercle
bacilli whose action has been accurately tested in the Marburg
Institute for Experimental Therapy. The tubercle bacilli have been
dried without losing their vital powers in any way. These dry tubercle
bacilli (Trocken Tb.), kept in sealed glass tubes, will retain their
action on cattle unchanged for a period of thirty days. If, therefore,
a tube of Tb. bears the date VII-1-02, the contents can be used for
cattle immunization until VIII-1-02. After thirty days, although the
immunizing power is not entirely lost, it is so far decreased as to
render it ineffective in the dosage recommended.
VI. DOSAGE OF THE VIRUS.--For the first inoculation, one immunizing
unit, 1 I. E. [= 1 Immun Einheit] is used for each calf; for the second
inoculation, which is not to be undertaken until at least twelve weeks
after the first, five units (5 I. E.) are used for each calf. As a rule
the dose of 1 I. E. is 0.004 gramme dry Tb., that of 5 I. E. for the
second inoculation is therefore 0.02 dry Tb.
If the tube contains the quantity requisite for the first inoculation
of twenty cattle, it will bear the label 20 I. E. In order at all times
to control the manner of production of the dry Tb. each tube also
bears in Roman numerals the consecutive laboratory number thus:
+-------------+
| Op. No. IV. |
| 20 I. E. |
| VII-17-02 |
+-------------+
This label is interpreted as follows:
Dry Tb., which in the records of the Marburg Institute bears
the laboratory number IV, contain on the day of delivery, i.e.,
on VII-17-02, twenty immunizing units, and retain this strength
until VIII-17-02.
For the inoculation the virus is uniformly mixed with 1% salt solution
which has previously been boiled and cooled. The procedure is as
follows:
The entire contents of the tube are placed in a small mortar and
crushed with the pestle. Then 2 to 3 c.c. salt solution are added and
the whole rubbed into a uniform mixture or emulsion, after which it is
poured into a graduated cylinder holding 50 c.c. A little more salt
solution is then added to the mortar, and thus the remaining particles
of virus are added to the previous mixture. The fluid in the graduate
is then made up to 30 c.c. with salt solution, and then poured into a
sterile wide-mouthed bottle holding 100 c.c. Any remaining emulsion
is then washed out of the graduate with an additional 10 c.c. salt
solution and added to the 30 c.c. in the bottle. The bottle thus
contains virus ready to inoculate, and each 2 c.c. will be the dose
for the first inoculation of a calf, provided that the tube originally
contained 20 I. E. The dose for a second inoculation would then be
contained in 10 c.c. of this fluid.
VII. INSTRUMENT CASE.--In order to carry out the inoculations in
agricultural practice, the instrument case constructed by W. Holzhauer,
Marburg, is to be recommended. It contains the following:
(_a_) Two bottles for the virus, each 100 c.c., made of colored
glass.
(_b_) One bottle lysol.
(_c_) One bottle alcohol.
(_d_) One Erlenmeyer flask (for 1% salt solution).
(_e_) One mortar and pestle.
(_f_) One graduated cylinder 50 c.c.
(_g_) One graduated cylinder of 10 c.c.
(_h_) One basin to hold disinfectant solutions.
(_i_) Six thermometers with tapes and clamps. (Price 10.50
marks or 1.75 marks each.)
(_k_) Two virus syringes with two strong canulas. (Price 11
marks.)
(_l_) One small hand-scale and weights.
(_m_) One alcohol stove and cover.
(_n_) Sterile cotton.
(_o_) One wire basket.
The entire box is supplied with a canvas cover and a leather handle.
The lid, which bears four movable legs, can, when the same is removed
from the box, be set up like a saucepan and used as a sterilizer. For
this purpose the vessels and instruments are placed into the wire
basket, the sterilizer half-filled with 2% lysol solution, and the
whole heated just to boiling by means of the alcohol stove.
The price of the complete outfit is 85 marks. By omitting the
thermometers and syringes the price is reduced to 63.50 marks.
VIII. METHOD OF MAKING THE INTRAVENOUS INJECTION.--The injection is
best made by means of a 5-c.c. glass syringe with an asbestos plunger
(paragraph VII, _k_), which is cleaned by means of the lysol solution
and rinsed in sterile salt solution. The canula attached to the
syringe is cleaned in the same manner. One immunizing unit (1 I. E.)
is then drawn up into the syringe and any air-bubbles are expelled,
care being taken that any drops of fluid expelled in this manner do
not fall on the floor but are caught up in the basin. The filled
syringe, together with the canula, which is now detached, is then
placed on the previously mentioned basin. The virus is injected into
the left jugular vein. When possible the cattle should be inoculated,
each in its own stall, so as to avoid exciting them. After washing
the left side of the neck with 2% lysol solution, the operator, by
pressing his thumb on the jugular vein, stops the circulation, causing
a distinct, sausage-shaped, fluctuating swelling to appear. With his
right hand he now takes the canula from the basin and thrusts it, just
above the compressing thumb, upward into the vein at an angle of 45°.
One recognizes that the vein has been entered, by the blood that at
once flows through the canula. If no blood flows, the vein has not
been entered. In that case the canula is withdrawn slightly but not
completely, and again thrust into the fluctuating swelling. As soon
as blood flows, the left hand ceases making pressure and grasps the
canula, whilst the right hand fits the syringe thereto. Then the virus
is slowly and uniformly injected into the vein. When the syringe is
emptied, the skin at the site of injection is pressed together and the
syringe and canula withdrawn. As a rule, bleeding ceases almost at
once. The region is then rubbed over with 2% lysol solution and the
inoculation is completed.[9]
CONDITIONS GOVERNING THE DISTRIBUTION OF THE VIRUS PROTECTIVE AGAINST
TUBERCULOSIS.
1. The virus is supplied by the firm of Drs. Siebert & Ziegenbein in
Marburg a. d. Lahn, Germany.
2. This firm supplies the virus in packages containing 5 I. E. and 20
I. E. The price for the former at present is 40 pf. per I. E. and for
the latter 25 pf. per I. E. In ordering, the style of package is to be
specified.
3. The recipients bind themselves to fill out and return the following
records:
A. Temperature charts: The temperature is to be recorded as a curve.
B. Other data as per blank herewith enclosed (see next page).
+---+--------------------------------------+-------------------+
| A | Consecutive Marburg Number. | |
+---+--------------------------------------+-------------------+
| B | Consecutive Inoculation Number. | |
+---+--------------------------------------+-------------------+
| C | Breed, Herd and Designating Number. | |
+---+--------------------------------------+-------------------+
| | | I.|Owner. | |
| | +----+-----+---+----------------+-------------------+
| | | | | A |At Birth. | |
| |Natio-| II.|Loca-+---+----------------+-------------------+
| D |nali- | |tion.| B |At Time of | |
| |ty. | | | |Inoculation. | |
| | +----+-----+---+----------------+-------------------+
| | |III.|Breed. | |
| | +----+--------------------------+-------------------+
| | | IV.|Sex. | |
+---+--------------------------------------+-------------------+
| | | I.|Natural (Suckling Calf). | |
| | |----+------+--+----------------+-------------------+
| E |Manner| | |a |With Non- | |
| |of | |Arti- | |sterilized Milk.| |
| |Rai- | II.|fi- +--+----------------+-------------------+
| |sing. | |cial. |b |With Sterilized | |
| | | | | |Milk. | |
+---+--------------------------------------+-------------------+
| | | I.|Laboratory Number of | |
| |Pro- | |the Virus. | |
| |tec- +----+--------------------------+-------------------+
| F |tive | II.|Dose in Grammes or in c.c.| |
| | +----+--------------------------+-------------------+
| |Inno- |III.|Date and Manner | |
| |cula- | |of Inoculation. | |
| |tion. +----+--------------------------+-------------------+
| | | IV.|Degree of Reaction. | |
+---+--------------------------------------+-------------------+
| |Tuber-|Date. | |
| G |culin +-------------------------------+-------------------+
| |Test. |Degree of Reaction. | |
+---+--------------------------------------+-------------------+
| H | |Weights. | |
+---+--------------------------------------+-------------------+
| I | |Special Remarks. | |
+---+--------------------------------------+-------------------+
DIRECTIONS FOR FILLING THIS BLANK.--Column A is to be left
blank by the attending physician; column B contains the running
number of the animal inoculated; C is to be recorded only in
fitting cases; D, on the other hand, is never to be omitted;
under E the fitting column is to be marked thus: “!”; in column
F, IV, the degree of reaction following the inoculation is to
be noted by signs, thus: O = Failure of any reaction whatsoever
(R = O); I = short febrile reaction; II = 2-4 days of fever;
III = 5-8 days of reaction associated with other disturbances
of health (cough, loss of weight, diminution of appetite,
diarrhœa, etc.).
In the same manner the degree of the reaction to a later
tuberculin test is to be recorded (column G). In column H the
weight is always to be accompanied by the date.
_The returns are to be made as soon as the data for about 100
cattle have been secured._
C. General report: This includes a report on the manner of keeping the
inoculated cattle, the hygienic conditions of the stables, previous
occurrence of _perlsucht_ in the cattle of the herd, previous use of
other means of suppression of tuberculosis and their result, etc., etc.
4. The owners of the cattle must see to it that the inoculations are
properly made and they themselves must bear all consequences resulting
from defective inoculation. Drs. Siebert & Ziegenbein can in no way
accept responsibility for this.
* * * * *
The preceding conditions are still adhered to in many large dairy
farms. To a number of smaller dairies we have allowed easier
conditions. An example is afforded in the following order of the
Ministry of the Interior of the Grandduchy of Hesse.
MINISTRY OF THE INTERIOR OF THE GRANDDUCHY OF HESSE,
DEPARTMENT OF PUBLIC HEALTH.
To the Grandducal County Veterinarians:
Whereas, following the proclamation of the Ministry of the Interior
dated Aug. 19, 1902, a large number of replies has been received from
the farmers, it is ordered that the inoculations be hereafter made in
accordance with the following principles:
1. The protective inoculation consists in the intravenous
injection of a _single_ immunizing unit of tubercle germs
(derived from man), rubbed up with sterile salt solution; and
in a second intravenous injection, three months later, of
_five_ immunizing units of the same germs.
2. The germs in question can be obtained in glass tubes
containing 5 or 20 units.
3. As a rule only cattle without external manifestations of
disease, aged from three weeks to four months (at the first
inoculation) should be inoculated. With healthy animals of this
age it is unnecessary to test them previously with tuberculin,
even if they belong to a notoriously tubercular herd.
4. In exceptional cases older animals (from four months to two
years) may be inoculated with the virus, but only when they are
entirely free from disease, _and when a tuberculin test made on
them results without any reaction whatsoever_.
5. The inoculated animals are to be kept in their stalls two
days before and two weeks after the inoculation.
6. In all cases in which the owners can manage the rectal
temperatures, the same are to be taken two days before the
inoculation (morning and evening) and again on the morning of
the inoculation. After this they are taken once more in the
evening and then once daily for the next five days. If, after
this, the animals still have temperatures above 39.2° C., the
temperatures are to be taken daily until the same reach 39.2° C.
7. In animals not over four months old at the time of the first
inoculation, the temperature may be omitted if there be any
difficulties in taking it. In those, however, which are over
that age at the time of the first inoculation, the temperature
must invariably be recorded according to paragraph 6. Even
when inoculating animals in infected herds the above-mentioned
measurements should be taken whenever practicable.
8. If possible, the inoculated animals should be weighed every
fourteen days on a cattle scale.
9. Owners of cattle are to keep record of all the temperatures
and weights. You are to collect the records concerning
temperatures as soon as they have been completed; the records
of the weights, however, only after three months. The results
noted in the temperature returns are to be entered by you on
the charts herewith provided, and a temperature curve plotted.
These charts are to be made in duplicate, one copy to be
sent to our representative and the other to the Experimental
Division of the Hygienic Institute, Marburg.
10. The inoculated animals are all to be permanently marked.
Those on which temperature and weight observations have been
made should also be numbered.
The method of thus marking and numbering the animals is left to
your judgment.
11. Should you not be informed in regard to the previous
notifications respecting the inoculations, kindly place
yourself in communication with the grand-ducal “Kreis Amt.”
Following this, as soon as you have informed yourself regarding
the age and health of the animals to be inoculated, notify our
representative as to the number of these animals suitable for
inoculation. The reports for each village are to be made out
separately.
12. The necessary virus and utensils, as well as explicit
directions for use, will be furnished by us.
13. We shall see that your first inoculation is attended by our
representative.
(Signed) ----
DARMSTADT, Nov. 16, 1903.
APPENDIX.
NOTE TO PAGE 28.
... Nowadays, however, there are few authorities who do not admit that
tubercle bacilli which have gained lodgment in the nasopharynx or in
the oral cavity may cause _primary lesions in the lung_ in an entirely
different way [different from direct infection by inhalation], namely,
through _lymphogenous_ or _hæmatogenous channels_ after an _intestinal
infection_ (the intestine reckoned from the pharynx down through the
stomach to the rectum).
Whether this inhalation of tubercle bacilli from the air into the
nasopharynx is followed by a pulmonary tuberculosis, and whether,
if it be demonstrated that this actually occurs, the disease is to
be ascribed to _intestinal_ or _pulmonary_ infection, is the thema
probandum.... How little I deny the possibility of an inhalation of
tubercle bacilli and the consequent danger of infection to many persons
can be seen from two quotations, one from my Vienna lecture, March 12,
1903, and the other from the lecture held at Cassel, Sept. 27, 1903.
“In my plans for the suppression of tuberculosis I give the central
place to the feeding of infants with milk both harmless and capable
of healing. But as already stated in my previous communications, it
is absolutely important to keep coughing consumptives away from the
nursing infant. The tubercular virus scattered throughout the dwelling
of the consumptive surely finds its way in one way or another into the
mouth of the nursling, and then, just like the tubercle bacilli in
the milk, it reaches the lymph-vessels and the circulation. It will,
of course, also get into the infant’s milk, and when, therefore, in
my lecture in Cassel, I stated that ‘the milk fed to infants is the
chief cause of consumption,’ I presumed that my auditors and readers
were familiar with the following paragraph of my Vienna lecture:
‘If I may apply the experiences gained in studying the conditions
under which tubercular and other cattle are housed, etc., I must say
that model hygienic housing can do little to prevent the spread of
tuberculosis, if at the same time the scattering of tubercle bacilli
by the cattle with open tuberculosis is not prevented or at least
lessened. It is absolutely impossible to determine all the numerous
ways in which tubercle bacilli coughed up, or otherwise scattered
about by the tuberculous animals, will finally reach the organism of
the other cattle in the stable; and I regard it as almost impossible,
by means of mechanical or other measures, to prevent the spread of
virus from a case of open tuberculosis to the other inmates of the
same room. For adults who, in healthy circumstances, possess a strong
protection against the action of the tubercle bacilli, in the form
of the epidermis, the epithelial covering of the mucous membranes,
and the anti-bacterial ferments, I regard the danger of infection as
not particularly great, provided, of course, the dose introduced is
not as large as in our laboratory experiments. On the other hand, the
new-born, whose mucous membrane is so very permeable and lacks the
protective ferments, are so very much exposed to the danger that I
cannot conceive such individuals escaping infection if they be in the
same room with a coughing consumptive. It has been amply proved that
the air can carry not only dry but also moist tubercle bacilli. If,
then, this virus be present in the air (in a measure ‘volatile’), its
introduction into the mouth and so into the intestinal tract cannot be
avoided.
“These facts apply equally well to infants and to new-born calves.”
NOTE TO PAGE 51.
Mar. 3, 1904.
Excellence E. von Behring, Marburg, Germany.
My dear Professor Behring:
I have seen in recent discussion, reported in the medical journals,
a reference to Dr. Knopf in regard to the infection of record-books,
which he attributed to an occurrence in the Health Bureau of Lansing,
Michigan, and seems to have reported in one of the French journals.
Dr. Henry B. Baker, who is the Secretary of the State Board of Health
of Michigan, and who is a personal friend of mine, has been applied to
for more particular information, and it appears that the matter refers
to a newspaper (published in Detroit Oct. 14, 1899) and _undoubtedly
refers to a claim made by some one in Russia, where such an infection
is said to have taken place_.
I send you herewith a copy of the notice that has been sent out by
the Lansing Health Bureau, and may say that Dr. Baker writes me that
nothing of the sort has occurred in the office at Michigan.
I would be greatly pleased if you could send me a copy of Dr. Knopf’s
publication in the _Press Medicale_ to which you have referred.
Thanking you in advance, I remain
Sincerely yours,
KARL VON RUCK.
NOTE TO PAGE 75.
... One unpleasant possibility [in the making of inoculation] is to
be mentioned, one which I did not originally think of and which was
called to my attention by Ober-med. Rath Lorenz. It consists in the
general collapse of the inoculated calf, of very threatening aspect,
when the inoculating fluid has been injected _too cold_. This happened
on a Hessian farm on a cold winter day, and resulted in the collapse of
_all_ the inoculated calves. (It would, by the way, have happened if
only the cold fluid without the virus had been injected.) As it was,
all the inoculated animals had recovered by the following day. This
teaches us to warm the inoculating fluid to about body temperature
before injecting it. This is readily done by placing the bottle
containing the fluid into a little lukewarm water.
FOOTNOTES:
[1] Address delivered at the seventy-fifth meeting of Naturalists and
Physicians in Cassel, September 25, 1903.
[2] On the other hand, certain stages in the development of various
malaria parasites resemble each other very closely; but we distinguish
the parasites definitely because they are of different origin.
[3] Formula for the digesting fluid:
Pepsin 1-2 gm.
Glycerin 10 c.c.
HCl 22° Baumé 10 c.c.
Sodium fluorid 3 gm.
Distilled water 1000 c.c.
[4] The intestine reckoned from the pharynx down through the stomach to
the rectum. See appendix, p. 81.--TRANSLATOR.
[5] See appendix, page 84.
[6] It will be well to retain the name “Scrofula” for those tubercular
processes _outside_ of the lung which go on with cheesy degeneration.
Only in that way can the connection between the histogenetically so
important results of earlier investigations be maintained.
[7] Rules 1, 2, and 3 have been _purposely_ neglected in certain
dairies in Savár, Teschen, and Mecklenburg, as can be seen by the
reports of Messrs. Strelinger, Rösler, and Ebeling (_Beiträge zur
experim. Therapie_, No. 8, 1904), without, thus far, injuring the
inoculated animals.
[8] §2 includes the following disinfecting agents:
1. Water, steam, hot water, boiling for one hour.
2. Soap-suds.
3. Soda-lye solution (at least 2 kilos soda in 100 liters water).
4. Freshly slaked lime, powder, and milk of lime, 1:2 aq. and 1:20 aq.
5. Sol. chloride of lime, 1:3 aq. and 1:20 aq.
6. Sol. carbolic acid, 5%.
7. Sol. crude cresol, 5% (Liquor cresoli saponatus of the German
pharmacopœia).
8. Coal-tar and wood-tar.
9. Fire.
The most reliable and cheapest agent for rendering harmless Tb. virus
in stables is hot 2% soda solution, whenever a surface disinfectant is
desired. Disinfection of the stable air is as yet to be classed only as
a pious wish.
[9] See appendix, page 84.
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