1IOWA MEDICAL JOURNAL
IOWA MEDICAL JOURNAL
(Vol. 17, Issue 5. November 15, 1910)
Discussion of the
EPIDEMIC OF ANTERIOR POLIOMYELITIS
At a Meeting called by the Iowa State Board of Health, and held at the House Chamber, State Capitol, August 17, 1910
DR. FROST: Mr. President and Gentlemen, I feel that I have to preface my remarks with an apology, in that I have not been able to prepare any paper for this meeting. I have not known exactly what was expected of me, as a matter of fact, and have not had time to prepare a paper if I had known.
Also as to any report of the work at Mason City, that work is still incomplete. About one-third of the cases which need to be investigated have not been investigated yet, and the work there being primarily statistical, it seems useless to base statistics on two-thirds of the total cases. So that I am only going to give rather general statements as to the conditions at Mason City.
I understand from members of the State Board that they want a brief review of the subject of poliomyelitis, and in connection with that some with that some discussion of the conditions at Mason City, chiefly in so far as they differ from those of other reported epidemics. Anterior poliomyelitis, as you all know, is by no means a new disease in this country, although it has recently attracted much more attention here. So far as I can learn, the disease was first reported in epidemic prevalence some thirty years ago by Bergenholz. Since that time numerous epidemics have been described and the disease has been reported with increasing frequency. That, of course, is due, in part, to the increase in ability to recognize the disease, but, especially within the last five years, the increase in the number of cases reported all over the world shows that there must actually have been a very great increase in the number of cases occurring. The increase can not be accounted for simply by the increased accuracy of diagnosis.
I have taken the following figures from an abstract of a report of the Massachusetts State Board of Health.
From 1890, 150 cases were reported as occurring in epidemics from the medical literature at large; from 1895 to 1899, 345 cases, comprising 23 epidemics; from 1900 to 1904, 349 cases in nine epidemics, the epidemics being an average larger; and from 1905 to 1909, inclusive, 8,054 cases, including 25 epidemics. These cases have been reported from a large part of the civilized world. Norway and Sweden had quite and extensive epidemic of a good many hundred cases around 1905. that was where probably the first start was made at really good epidemiological study of this work by Wickman, whose work on this subject has become a classic. Epidemics have also been reported from Austria and from parts of Germany. In Westphalia they had some 450 cases last year.
The point that is of special interest to us, is that of the 8,000 cases reported in the last five years, over 5,000 have been from the United States; that is, five-eighths of all cases of epidemic poliomyelitis that have occurred within the last five years have been found in the United States, and the vast majority of these cases have occurred in a few states on the northern border of the United States. The epidemic in this country started, apparently, in New York City, in 1907, spreading from there over the state and over adjacent New England states. It is estimated that there were some 2,500 cases in New York. The Massachusetts State Board of Health has collected 600 odd cases occurring in 1909. In Nebraska last year there were of over 600 cases, and in Kansas about 100. In Minnesota, they had several hundred; I have not been able to get the exact figures. It is of interest to note, in this connection that there was an epidemic of about 140 cases, in Cuba. The exact date I don’t remember but it was subsequent to 1907. In practically every state from Maine to California there have been more or less cases in the last five years—not epidemics, but at least sporadic cases. So that while the disease is in general most prevalent in northern countries, it can not be said to be strictly limited geographically, as, for instance, yellow fever is.
The disease has been very carefully studied; I think there has been as much careful work done on it as on most diseases. The nature of the studies has been, first, clinical studies of the symptoms of the disease, the symptoms of onset, the extent of paralysis, and the various types of paralysis. Besides that there have been pathological studies of the lesions, not only of the cord and brain, but of the body generally. There have been probably even more extensive epidemiological studies, whish have been largely statistical. The model for these was set by Wickman in Norway and Sweden, who followed up practically all the cases occurring there in more than a year, (over 1,000), tried to trace the origin of cases from one to another, and succeeded in doing so in a large proportion of the cases. He carefully considered the effect of geographical location and of climate, race, sex, age, etc., the possibility of insect transmission, the period of incubation, the varying degrees of virulence of the disease, and other circumstances which might have a bearing on epidemics. He was the first to point really clearly to the infectious, transmissible or contagious nature of the disease, if you do not object to the latter word.
Wickman’s views have since been confirmed by another line of work, that is, experimental laboratory work. It is only within the last year that we have been able to prove in the laboratory what had been inferred from the study of epidemics, viz: that epidemic poliomyelitis is due to a specific micro-organism and is transmissible. For many years cultures had been made from cerebro-spinal fluid and various organs, with not negative, but varying results. Many varieties of bacteria were cultivated, but with not constancy; so that we can consider all these results as due to errors of technique or to secondary infections.
During the past year Landsteiner and Popper in Austria succeeded in transmitting the disease to monkeys by inoculating into them a portion of the spinal cord of a child which had died of acute anterior poliomyelitis. They did not succeed, however, in transmitting this disease from the first monkeys to other monkeys. The monkeys showed perfectly characteristic paralysis and characteristic microscopic lesions in the cord; and their work is generally accepted as being an undoubted reproduction of the disease in monkeys. The work was then taken up by a number of observers, notably by Flexner and Lewis of the Rockefeller Institute in this country, who have confirmed Landsteiner and Popper by inoculating monkeys with virus from two cases of human anterior poliomyelitis. They have further succeeded in transmitting the disease from monkey to monkey, through seven passages—possibly more by this time. That, of course, proves beyond all peradventure the transmissible nature of the disease and that it is a specific infection, the lesions in all these monkeys being absolutely characteristic. It has further been found that the virus is not confined to the spinal cord. The original work was done by taking portions of the spinal cord and inoculating monkeys with that. It has since been shown, however, that the virus exists in various organs of infected monkeys; in the salivary glands, in the mesenteric glands, in the regional lymphatic glands, and in the cortex of the brain. It is inferred from this, that the distribution of the virus through the body is quite general.
Some more very interesting work which has been done by Flexner and Lewis and others shows the various avenues of infection in experimental poliomyelitis. The first experiments were done by intra-cerebral and intra-peritoneal inoculation of monkeys with portions of the spinal cord and brain. It was found that monkeys could be inoculated not only in this way, but sub-cutaneously; and more recently successful inoculations have been made by rubbing the virus into the nasal mucous membrane; also, by feeding it to monkeys, when their intestines had been practically paralyzed with opium, I forgot to mention that the virus has been found in the nasal mucous membrane. These facts are all of extreme importance, as showing the possible means of transmission of the disease.
It has been proved, then, that epidemic poliomyelitis is due to a specific infective agent, or germ; that this germ is present not only in the spinal cord, but in the mesenteric glands, in the salivary glands, and in the nasal mucous membrane of animals which are infected; and we can presume that the same is true of persons. It has been shown that the disease can be transmitted through the nasal mucous membrane and through the stomach. That gives us a very good idea of the possible means of spread of the disease. It is strongly suspected from the pathology of the disease that the excretions of the bowels are infective also but this has not been proved. It is a difficult matter to prove in the laboratory but I think it probably will soon be settled one way or the other.
As to the nature of the germ which causes the disease, it belongs to the class of ultra-microscopic organisms. It is not visible in any preparations made by the ordinary laboratory methods. Whether the invisibility is due altogether to its extremely small size or to some other properties is not known. Certainly, however, it is an organism of extremely small size, being able to pass through fine filters which will hold back the smallest known bacteria. It is presumed, then, that this germ does not belong to the class of bacterial organisms, but is probably protozoan, belonging to the same class as the organism of yellow fever, the foot and mouth disease of cattle, rabies, and other so-called “filterable viruses”.
A few important facts have been worked out regarding the viability of this organism. It has been found very resistant to the action of glycerine. The ordinary pathogenic bacteria are killed by long exposure to glycerine. This fact as you are all aware, is used in preparing vaccine virus: to mix it with glycerine, which destroys a large portion of the bacteria but does not destroy the vaccine virus. In it’s resistance to the action of glycerine, the virus of poliomyelitis is analogous to the virus of vaccine hydrophobia, etc.
It is found, also, that the virus of poliomyelitis is very resistant to drying. It was supposed from its analogy to rabies that the process of desiccation similar to that employed in the drying of cords for the Pasteur treatment would alter the virus of poliomyelitis very much. It has been shown, however, that a portion of cord dried for 28 days, retained its virulence. This is another important fact in the epidemiology of the disease, as it points to the possibility of the organism remaining virulent for a long time in the dust in dwellings and other places where the disease has been present.
The ordinary process of formaldehyde disinfection will apparently destroy the virus. It is comparatively easily destroyed by heat at a temperature of 45˚ Centigrade, but extreme cold does not diminish its virulence to any appreciable degree.
We know little enough about the biology of bacteria which can be readily isolated. For instance, we know little about the conditions which affect the virulence of the bacilli causing typhoid fever, pneumonia, diphtheria, etc., so with an organism which can not be cultivated or even seen, we must admit that there are very many possibilities of conditions affecting its length of life and its virulence outside of the human body, as to which we can only make surmises from circumstantial evidence derived from the study of epidemics.
The experimental workers on poliomyelitis have aimed further to demonstrate an immunity, and if possible, to utilize this immunity. It has been a clinical observation that there is an immunity after an acute attack of anterior poliomyelitis. The disease has been so comparatively rare that we would not expect one person to be attacked twice, but the fact of immunity after one attack has been proven by laboratory experiments on monkeys, so that we can assert that there is quite a definite immunity after the disease. It is probable that there is immunity also after an abortive attack which does not result in paralysis. It is suggested, and apparently proven by the few experiments which I have seen up to date, that the serum of recovered animals has certain anti-toxic properties. Whether this property can in the future be utilized or not is not known—that is, whether the serum of an animal recovered from poliomyelitis will have any effect on the course of the disease in human beings. It was suggested that we might use the process of vaccination to immunize persons against this disease, as is done in hydrophobia. This has not been found practicable so far. In the first place, the drying of the cord does not seem to sufficiently attenuate or destroy its virulence so that we are in danger of actually producing the disease in persons whom we intend to immunize, although this has never yet been tried on people. More over, the incubation period is so short that we would have to immunize people before they were exposed, which would seldom be practicable. On the whole, protective vaccination does not appear, at present, to be very promising; it may be worked out in the future.
The disease to which poliomyelitis is most analogous is rabies, in its pathology, in its affinity for the nervous system, in the nature of the organism producing it, and apparently in the comparative insusceptibility of a large number of persons. Human beings are comparatively insusceptible to rabies. Only 15 to 20 percent of persons definitely exposed to the infection develop rabies. That seems to be true also of poliomyelitis.
The pathology of this disease is characteristic, as is true of other infectious diseases. The characteristic lesions are located in the central nervous system. In a general way, the lesions are first a congestion of the pia mater, with very little congestion of the dura mater and practically no exudates into the meninges. Following this is an infiltration of the substance of the cord, chiefly of the gray matter, most marked in the motor area of the anterior horns. This infiltration of the substance of the cord which is, at first, around the vessels finally results in the degeneration of some of the cells of the anterior horn of the cord. Whether this degeneration is due to pressure or to specific toxic action, I will not undertake to discuss. It is of interest, however, that the primary lesion in the cord is one of congestion and of infiltration, and that the whole of the cord is affected more or less, not simply the motor cells of the anterior horn, although these are the ones that suffer most. The motor cells of the cervical and lumbar enlargements are usually more severely damaged than the cells in other portions of the cord. The whole of the cord may be affected, however, and quite frequently there is damage, usually temporary, to the medulla and the brain, especially in the region of the nuclei of the cranial nerves. It is to be remembered, too, that the lesions of poliomyelitis are not confined to the central nervous system. Fairly constant lesions have been found in the intestines, namely, congestion, especially of Peyer’s patches; also, congestion and enlargement of the mesenteric glands. General enlargement of the lymphatic glands has been described in some cases. Lesions of the respiratory tract are not uncommon. I some epidemics angina has been a prominent early symptom; and a broncho-pneumonia has been found in some autopsies. The pathology of the disease indicates, therefore, that it is a general infection with characteristic localization in the central nervous system.
The symptoms of the disease are extremely variable, as we should expect from its pathological anatomy. The primary symptoms of most infectious diseases are quite variable, and as the involvement of the central nervous system in poliomyelitis is very irregular both in location and in extent, it is to be expected that the nervous symptoms resulting will likewise be variable. The symptoms may best be considered in the early stage prior to paralysis, in the stage of acute paralysis, and in the stage of repair.
Previous health seems to have no relation to the occurrence or severity of an attack. In the stage prior to paralysis the onset may be either sudden or gradual or unnoticed; there may be a chill, which is quite commonly found in the cases in Mason City. Fever is one of the most common of all symptoms. It is not always noted, but is practically always present. The range of the fever may be very various, sometimes as high as 103˚ or in a child even higher; in other cases the temperature may not exceed 100˚. As to this point I have been able to obtain very little information in Mason City, as I have not been able to make any clinical observations, but have had to rely on the statements of the family. There is usually very marked malaise and prostration.