Leprosy

by G. Armauer Hansen; Carl Looft

There is, therefore, no other course open to us but to assume the infectiousness of the disease, and thus the spread of leprosy is readily understood; while by the assumption of heredity, or Baumgarten’s latent germinative infection, it remains absolutely inexplicable. These two last causes are to our thinking absolutely proved to be non-existent by the case of Father Damien; by the results of our investigations in North America; and by the diminution of the disease in the descendants of lepers in the Norwegian towns.

But direct proofs of its contagiousness may also be obtained. Such are given by Drognat-Landré in his book, and also by many other observers. Norway can supply many proofs; but against these it can always be urged that it is impossible to exclude the possibility of inheritance on account of the widespread nature of the disease. But we think we can supply from Norway a still better proof in the shape of the gradual diminution of the disease during the last thirty-five to forty years.

Up to 1856 leprosy probably increased in Norway; we cannot speak more definitely, as previous to that year there was no exact or sufficient enumeration of the lepers. But we have grounds for believing that we have obtained, by means of the yearly census begun in 1856, a pretty exact knowledge of the number of new cases in the years 1851-55, and this shows that the number is considerable, and almost exactly corresponds with the number of new cases in the next five years, 1856-60. This, we think, indicates that the total number of lepers in the two quinquenniums was pretty much the same. Now we know that there were in Norway in 1856 over 2800 lepers. The number was estimated in 1836 at 659, and in 1845 at 1122. According to this estimate a considerable increase had taken place. We can, however, with certainty say that the numbers for 1836 and 1845 are too low. In the first place, the enumeration was not undertaken by medical men, and secondly, even now, there are many lepers overlooked at every enumeration, or, to speak more correctly, they are not discovered because the patients conceal their condition. But that the number of those overlooked in the years 1836 and 1845 can have been so great as the difference between the numbers for those years and that for 1856 is scarcely credible, and it therefore appears probable that the number of lepers in Norway increased during the first half of the century.

In the year 1856 the first Leper Asylum was opened in Bergen. Previously to this we had in Bergen the St. Georg and Lungegaard’s Hospitals, which together served for 200 patients. In Molde there was also a small hospital, for lepers, so that altogether in the year 1856 there were about 235 lepers in hospital. In 1861 were opened two new asylums, one in Molde, the other in Trondhjem (Drontheim), and as is seen in [Table IV] (p. 145), since that time a large number of lepers have been admitted to these institutions.

We may regard the numbers in this Table up to 1885 as accurate; for the later years corrections will have to be made from the later enumerations, which may detect older, concealed cases. But these can only affect the figures to a limited degree.

If we consider the Table closely, we see that in the first quinquennium (1856-60) the total number of lepers is 76 less, while those in their own homes are 380 less; during this period 585 lepers were admitted to the asylums. The number of lepers as a whole, then, was not much reduced, but at the end of the period there were 380 lepers fewer at home, or, in other words, there were among the people 380 fewer sources of infection, and to this we ascribe it that while the number of new cases was 1,148 in the years 1856-60, it fell in the years 1861-65 to 1,028. The mortality of the year 1856 we do not know; in the four following years 981 died—668 at home, in the asylums 313. If we assume that there died at home as many in 1856 as in 1857, viz., 230, then the number of deaths at home during the quinquennium would have amounted to 898, and the whole mortality, adding the 313 who died in the asylums, would have been 1,211—only 109 more than the new cases. But one must not so reckon. There died, especially in the early days, a much larger proportion in the asylums than outside; and it is evident, secondly, when one observes the figures in a district from which at the commencement only very few cases were sent to the asylum, that the new cases are much more numerous than the deaths. In Nordmoere, for example, the number of new cases from 1856-60, was 81; that of deaths, 46; only 14 were sent to the asylums, and the disease increased during the quinquennium, the cases rising from 105 to 119. One finds the same thing in Soendmoere—new cases 104, deaths 42, sent to asylums 28; number of cases in 1856, 178; in 1860, 195. In these two districts, then, the disease was evidently on the increase, and this would probably have been the case throughout the country, had many cases not been removed from their homes to the asylums; as, for example, in Soendfjord. Here there were, in 1856-60, 214 new cases, 116 deaths, 211 sent to the asylums; number of cases 1856, 431; 1860, 306. If we examine in this way the numbers in the different districts, we find everywhere that decrease of the disease depends on the numbers isolated in the asylums. Where isolation was insufficient or absent, there was no decrease, but either the numbers increased or remained stationary; where, on the contrary, isolation was thorough, the decrease was invariable. This can only be explained in one way, viz., that isolation is the cause of the decrease, and isolation can only have effected improvement by removing from the homes of the people the sources of infection. Further, during the next five years, the number of new cases in those districts where isolation was good continued to sink; where there was none, or it was insufficient, the numbers either rose or remained almost stationary. We will once more compare Nordmoere with Soendfjord. In Nordmoere, in 1856-60, 81 new cases, 14 sent to the asylum; 1861-65, 88 new cases. In Soendfjord, 1856-60, 214 new cases, 211 sent into asylums; 1861-65, 146 new cases.

We consider it superfluous to point out further how the isolation of the patients has caused the decrease of Leprosy in Norway. It is not possible to explain the action of isolation by the elimination of heredity; the time is too short for that. The only one possible solution is that which we have given, and therefore we regard this decrease of Leprosy in Norway following on isolation as the best proof of the contagiousness of Leprosy. Leprosy is, then, according to our view, a contagious disease, and only contagious, not hereditary.

How Leprosy is “caught,” we do not know, but we think it is probably by inoculation; and the nodular form must be more dangerous than the maculo-anæsthetic. This last statement seems to be confirmed by the fact, that in Sogn, where 56.6 per cent. of the cases are nodular and 43.4 per cent. maculo-anæsthetic, the increase varies between 8. and 10.8 per cent., while in Soendfjord, with 72.6 per cent. nodular, and 27.4 per cent. maculo-anæsthetic, it is between 14.4 per cent. and 19.5 per cent. In the nodular form there are incomparably more bacilli than in the maculo-anæsthetic, and in the latter there is no discharge containing bacilli, which in the former is almost always present. It is not improbable that Leprosy may be conveyed by the clothes. We know of one case in which a young man became affected one year after he had worn a pair of old drawers given him by a leper. The same thing happened to another young man who wore several pairs of his leprous father’s stockings.

Although we are not acquainted with the spores of the Lepra bacillus, it is quite conceivable that the bacilli are spore bearing. Unfortunately, we know of no method of determining whether the bacilli are alive or dead, and therefore Arning’s observation of the bacilli in the fæces does not decide the question as to whether the bacilli can live for any time outside the body, even admitting that the bacilli which Arning found were actually Lepra bacilli.

After completing this work I received “The Recrudescence of Leprosy and its Causation,” by William Tebb. The author seeks to prove that leprosy is everywhere on the increase as the result of the introduction of vaccination. The book as a whole is directed against vaccination as dangerous. Distinct proofs for his contention that leprosy may be conveyed by vaccination from arm to arm, the author, to our thinking, does not supply. Since Dr. Arning found lepra-bacilli in the contents of vaccine vesicles in lepers, the possibility of the communication in this way can scarcely be denied. But that it can be frequent, I cannot possibly believe. In Norway, vaccination has been compulsory during all those years in which leprosy has steadily diminished. In 1891 I put the question to all those doctors in Norway who had anything to do with leprosy, whether they had ever met in their practice with a case which could be ascribed to vaccination. Not a single one had observed such a case. And yet, here in Norway, lymph must often be taken from the children of leprous families. But since leprosy is very rare in children, it is evident that leprosy cannot be conveyed in this way. That vaccine vesicles in the non-leprous members of leprous families contain lepra-bacilli is incredible.