Part 9 (2/2)
Furthermore, all who have carefully studied the subject are convinced that much of this apparent increase is due to more accurate and careful diagnosis. Up to ten years or so ago it was generally believed that pneumonia was rare in young children. Now, however, that we make the diagnosis with a microscope, we discover that a large percentage of the cases of capillary bronchitis, broncho-pneumonia, and acute congestion of the lung in children are due to the presence of the pneumococcus.
Similarly, at the other end of the line, deaths that were put down to bronchitis, asthma, heart failure, yes, even to old age, have now been shown on bacteriological examination to be due to this ubiquitous imp of malevolence; so that, on the whole, all that we are probably justified in saying is that pneumonia is not decreasing under civilization. This is not to be wondered at, inasmuch as the inevitable crowding and congestion which accompanies civilization, especially in its derivative sense of ”citification,” tends to foster it in every way, both by multiplying the opportunities for infection and lowering the resisting power of the crowded ma.s.ses.
Moreover, it was only in the last ten years, yes, within the last five years, that we fairly grasped the real method and nature of the spread of the disease, and recognized the means that must be adopted against it. And as all of these factors are matters which are not only absolutely within our own control, but are included in that programme of general betterment of human comfort and vigor to which the truest intelligence and philanthropy of the nation are now being directed, the outlook for the future, instead of being gloomy, is distinctly encouraging.
Our chief difficulty in discovering the cause of pneumonia lay in the swarm of applicants for the honor. Almost every self-respecting bacteriologist seemed to think it his duty to discover at least one, and the abundance and variety of germs constantly or accidentally present in the human saliva made it so difficult positively to isolate the real criminal that, although it was identified and described as long ago as 1884 by Fraenkel, the validity of its claim was not generally recognized and established until nearly ten years later.
It is a tiny, inoffensive-looking little organism, of an oval or lance-head shape, which, after masquerading under as many aliases as a confidence man, has finally come to be called the pneumococcus, for short, or ”lung germ.” Though by those who are more precise it is still known as the _Diplococcus pneumoniae_ or _Diplococcus lanceolatus_, from its faculty of usually appearing in pairs, and from its lance-like shape. Its conduct abounds in ”ways that are dark and tricks that are vain,” whose elucidation throws a flood of light upon a number of interesting problems in the spread of disease.
First of all, it literally fulfills the prognostic of Scripture, that ”a man's foes shall be they of his own household,” for its chosen abiding place and normal habitat is no less intimate a place than the human mouth. Outside of this warm and sheltering fold it perishes quickly, as cold, sunlight, and dryness are alike fatal to it.
We could hardly believe the evidence of our senses when studies of the saliva of perfectly healthy individuals showed this deadly little bacillus to be present in considerable numbers in from fifteen to forty-five per cent of the cases examined. Why, then, does not every one develop pneumonia? The answer to this strikes the keynote of our modern knowledge of infectious disease, namely, that while an invading germ is necessary, a certain breaking down of the body defenses and a lowering of the vital resistance are equally necessary. These invaders lie in wait at the very gates of the citadel, below the muzzles of our guns, as it were, waiting for some slackening of discipline or of watchfulness to rush in and put the fortress to sack. Nowhere is this more strikingly true than in pneumonia. It is emphatically a disease where, in the language of the brilliant pathologist-philosopher Moxon, ”While it is most important to know what kind of a disease the patient has got, it is even more important to know what kind of a patient the disease has got.”
The death-rate in pneumonia is an almost mathematically accurate deduction from the age, vigor, and nutrition of the patient attacked. No other disease has such a brutal and inveterate habit of killing the weaklings. The half-stifled baby in the tenement, the underfed, overworked laboring man, the old man with rigid arteries and stiffening muscles or waning life vigor, the chronic sufferer from malnutrition, alcoholism, Bright's disease, heart disease--_these_ are its chosen victims.
Another interesting feature about the pneumococcus is its vitality outside of the body. If the saliva in which it is contained be kept moist, and not exposed to the direct sunlight and in a fairly warm place, it may survive as long as two weeks. If dried, but kept in the dark, it will survive four hours. If exposed to sunlight, or even diffuse daylight, it dies within an hour. In other words, under the conditions of dampness and darkness which often prevail in crowded tenements it may remain alive and malignant for weeks; in decently lighted and ventilated rooms, less than two hours. This explains why, in private practice and under civilized conditions, epidemics of this admittedly infectious disease are rare; while in jails, overcrowded barracks, prison s.h.i.+ps, and winter camps of armies in the field they are by no means uncommon.
This is vividly supported by the fact brought out in our later investigations of the sputum of slum-dwellers, carried out by city boards of health, that the percentage of individuals harboring the pneumococcus steadily increases all through the winter months, from ten per cent in December to forty-five, fifty, and even sixty per cent in February and March. The old proverb, ”When want comes in at the door, Love flies out at the window,” might be revised to read, ”When sunlight comes in at the window the pneumococcus flies 'up the flue.'”
Authorities are still divided as to the meaning and even the precise frequency of the occurrence of the pneumococcus in the healthy human mouth. Some hold that its presence is due to recent infection which has either been unable to gain entrance to the system or is preparing its attack; others, that it is a survival from some previous mild attack of the disease, and the body tissues having acquired immunity against it, it remains in them as a harmless parasite, as is now well known to be the case with the germs of several of our infectious diseases--for instance, typhoid--for months and even years afterward. Others hold the highly suggestive view that it is a normal inhabitant of the healthy mouth, which can become injurious to the body, or _pathogenic_, only under certain depressed or disturbed conditions of the latter. In defense of this last it may be pointed out that dental bacteriologists have now already isolated and described some thirty different forms of organisms which inhabit the mouth and teeth; and the pneumococcus may well be one of these. Further, that a number of our most dangerous disease germs, like the typhoid bacillus, the bacillus of tuberculosis, and the bacillus of diphtheria, have almost perfect ”doubles,”
law-abiding relatives, so to speak, among the germs that normally inhabit our throats, our intestines, or our immediate surroundings. The ultimate foundation question of the science of bacteriology is, How did the disease germs become disease germs? But the question is still unanswered.
However, fortunately, here, as in other human affairs, imperfect as our knowledge is, it is sufficient to serve as a guide for practical conduct. Widely present as the pneumococcus is, we know well that it is powerless for harm except in unhealthful surroundings. There is another interesting feature of its life history which is of practical importance, and that is, like many other bacilli it is increased in virulence and infectiousness by pa.s.sing through the body of a patient.
Flushed with victory over a weakened subject, it acquires courage to attack a stronger. This is the reason why, in those comparatively infrequent instances in which pneumonia runs through a family, it is the strongest and most vigorous members of the family who are the last to be attacked. It also explains one of the paradoxes of this disease, that, while emphatically a disease of overcrowding and foul air, and attacking chiefly weakened individuals, it is a veritable scourge of camps, whether mining or military. When once three or four cases of pneumonia have occurred in a mining camp, even though this consist almost exclusively of vigorous men, most of them in the prime of life, it acquires a virulence like that of a pestilence, so that, while ordinarily not more than fifteen to twenty per cent of those attacked die, death-rates of forty, fifty, and even seventy per cent are by no means uncommon in mining camps. The fury and swiftness of this ”miners'
pneumonia” is equally incredible. Strong, vigorous men are taken with a chill while working in their sluicing ditches, are delirious before night, and die within forty-eight hours. So widely known are these facts, and so dreaded is the disease throughout the Far West and in mountain regions generally, that there is a widespread belief that pneumonia at high alt.i.tudes is particularly deadly.
I had occasion to interest myself in this question some years ago, and by writing to colleagues practicing at high elevations and collecting reports from the literature, especially of the surgeons of army posts in mountain regions, was somewhat surprised to find that the mortality of all cases occurring above five thousand feet elevation was almost identical with that of a similar cla.s.s of the population at sea-level.
It is only when a sufficient number of cases occur in succession to raise the virulence of the pneumococcus in this curious manner that an epidemic with high fatality develops.
That this increase in virulence in the organism does occur was clearly demonstrated by a bacteriologist friend of mine, who succeeded in securing some of the sputum from a fatal case in the famous Tonopah epidemic of some years ago, an epidemic so fatal that it was locally known as the ”Black Death.” Upon injecting cultures from this sputum into guinea-pigs, the latter died in one-quarter of the time that it usually took them to succ.u.mb to a similar dose of an ordinary culture of the pneumococcus.
It is therefore evident that just as ”no chain is stronger than its weakest link,” so in the broad sense no community is stronger than its weakest group of individuals, and pneumonia, like other epidemics, may be well described as the vengeance which the ”submerged tenth” may wreak from time to time upon their more fortunate brethren.
Now that we know that under decent and civilized conditions of light and ventilation the pneumococcus will live but an hour to an hour and a half, this reduces the risk of direct infection under these conditions to a minimum. It is obvious that the princ.i.p.al factors in the control of the disease are those which tend to build up the vigor and resisting power of all possible victims. The more broadly we study the disease the more clearly do the data point in this direction.
First of all, is the vivid and striking contrast between hospital statistics and those gathered from private practice. While many individuals of a fair wage-earner's income and good bodily vigor are treated in our hospitals, yet the vast majority of hospital patients are technically known as the ”hospital cla.s.ses,” apt to be both underfed, overworked, and overcrowded. On the other hand, while a great many both of the very poor and even of the dest.i.tute are treated in private practice, yet the majority of such cases who feel ”able to afford a doctor,” as they say, are among the comparatively vigorous, well-fed, and well-housed section of the community. And the difference between the death-rate of the two cla.s.ses in pneumonia is most significant. In private practice, while epidemics differ in virulence, the rate ranges all the way from five per cent to fifteen per cent, the average being not much in excess of ten per cent, occasionally falling as low as three per cent. In the hospital reports on the contrary the death-rate begins at twenty per cent and climbs to thirty, forty, and forty-five per cent.
It is only fair to say, of course, that hospital statistics probably include a larger percentage of more serious cases, the milder ones being taken care of at home, or not presenting themselves for treatment at all. But even when this allowance has been made, the contrast is convincing.
A similar influence is exercised by age. Although pneumonia is common at all ages, its heaviest death-rate falls at the two extremes, under six years of age and over sixty, with a strong preponderance in the latter.
Under five years of age, the mortality may reach twenty to thirty per cent; from five to twenty-five, not more than four to five per cent; from twenty-five to thirty-five, from fifteen to twenty per cent; and so on, increasing gradually with every decade until by sixty years of age the mortality has reached fifty per cent, and from sixty to seventy-five may be expressed in terms of the age of the patient. One consoling feature, however, about it is that its mortality is lowest in the ages at which it is most frequent, namely, from ten to thirty-five years of age. And its frequency diminishes even more rapidly than its fatality increases in later years. So that while it is much more serious in a middle-aged man, he is less liable to develop it than a younger one.
Where the mortality from pneumonia is highest, is in the most densely populated wards, especially among negroes and foreigners of the hospital cla.s.s, in individuals who are victims of chronic alcoholism, and also among those who are for long periods insufficiently nourished. Lastly, it is only within comparatively recent years that we have come clearly to recognize the large role which pneumonia plays in giving the finis.h.i.+ng stroke to chronic diseases and degenerative processes. It is, for instance, one of the commonest actual causes of death in Bright's disease, in diabetes, in lingering forms of tuberculosis, and in heart disease; and last of all, in that progressive process of normal degeneration and decay which we term ”Old Age.” It is one of the most frequent and fatal of what Flexner described a decade ago as ”terminal infections.” Very few human beings die by a gradual process of decay, still less go to pieces all at once, like the immortal ”One-Hoss Shay.”
Just as soon as the process has progressed far enough to lower the resisting power below a certain level, some acute infection steps in and mercifully ends the scene. This is peculiarly true of pneumonia in old age.
To the medical profession to ”die of old age” is practically equivalent to dying of pneumonia. The disease is so mild in its symptoms and so rapid in its course that it often utterly escapes recognition as such.
The old man complains of a little pain in his chest, a failure of appet.i.te, a sense of weakness and dizziness. He takes to his bed, within forty-eight hours he becomes unconscious, and within twenty-four more he is peacefully breathing his last. After death, two-thirds of the lung will be found consolidated. So mild and rapid and painless is the process that one physician-philosopher actually described pneumonia as ”the friend of old age.”
When once the disease has obtained a foothold in the body its course, like one of Napoleon's campaigns, is short, sharp, and decisive.
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