CHAPTER III. NATURE'S REVENGES: THE SLEEPING SICKNESS.

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Among the strange and mysterious diseases to which mankind is subject in regions less familiar to the civilised world than Western Europe, none is stranger or more appalling in its quiet, inexorable deadliness than the Sleeping Sickness of the West African coast. Apparently it has existed among the natives of that region from time immemorial; but the first printed record we have of it is due to Winterbottom, who, writing in 1803 of Sierra Leone, said, “The Africans are very subject to a species of lethargy which they are much afraid of, as it proves fatal in every instance.” One of the latest notices of the disease, before it became the subject of active investigation within the last five years, is that of Miss Kingsley, who saw a few cases near the Congo estuary, but, though she was impressed by the mysterious fatality of the disease, she did not describe it as very prevalent or as a general source of danger to life. The opening up of the Congo basin and increased familiarity with the inner lands of the West African coast have shown that this disease is widely scattered—though rarely so abundant as to be a serious scourge—through the whole of tropical West Africa. Writers in the early part of the last century described the disease as occurring in the West Indies and in Brazil. Its presence was almost certainly due, in those days of the slave trade, to the importation of negroes already infected with the disease; and a curious theory obtained some favour, according to which the sleeping sickness of the West Indian slaves was a kind of nostalgia, and, in fact, the manifestation of what is sometimes called “a broken heart.”

The signs that a patient has contracted the disease are very obvious. They are recognised by the black people, and the certainly fatal issue accepted with calm acquiescence. The usually intelligent expression of the healthy negro is replaced by a dull apathetic appearance; and there is a varying amount of fever and headache. This may last for some weeks but is followed more or less rapidly by a difficulty in locomotion and speech, a trembling of the tongue and hands. There is increased fever and constant drowsiness, from which the patient is roused only to take food. At last—usually after some three or four months of illness—complete somnolence sets in; no food is taken; the body becomes emaciated and ulcerated; and the victim dies in a state of coma. The course of the disease, from the time when the apathetic stage is first noticed, may last from two to twelve months.

It is this terrible disease which has lately appeared on the shores of the Victoria Nyanza, in the kingdom of Uganda, administered by the British Government. Until the early part of the year 1901 there was not the slightest suspicion that sleeping sickness occurred in any part of the Uganda Protectorate; nor was it known in East Africa at all, any more than in the north and south of that great continent. It seems gradually to have crept up the newly opened trade-routes of the Congo basin, and thence to have spread into the west of Uganda, the territory known as Busoga. Numbers of Soudanese and Congo men are known to have settled in this region after the death of Emin Pasha. First noticed in 1901, it was estimated in June 1902, by the Commissioner of Uganda, writing officially to the Marquess of Lansdowne, that 20,000 persons had died of this disease in the district of Busoga alone, and several thousands in the more eastern portion of Uganda. At this moment it is probable that the number of deaths in this region due to sleeping sickness since 1901 amounts to more than 200,000; and this though, most fortunately, the disease has not yet spread eastward from Uganda into British East Africa,[23] nor, so far as has been reported, down the Nile. No curative treatment for the disease has yet been discovered; nor is there any authenticated instance of recovery.

The appalling mortality produced by this disease in Central Africa naturally caused the greatest anxiety to his Majesty’s Government, which had but just completed the railway from the East Coast to the shores of lake Victoria Nyanza, and had established a prosperous and happy rule in that densely populated region. The official medical men on the spot, though capable and experienced practitioners, were unable to cope with this new and virulent outbreak. The Foreign Office, having no imperial board of hygiene and medical administration to apply to in this country, sought the assistance of the Royal Society of London.

A committee of that society had already undertaken the study of malaria at the request of the Secretary of State for the Colonies, and had sent out young medical men as a commission to make certain enquiries and experiments on that subject and report to the committee in London. The sleeping sickness enquiry was undertaken by the same committee; but unfortunately very insufficient funds were placed at its disposal. When the South African cattle-owners found their herds threatened six years ago by a new form of mortal disease—‘the East Coast fever’—the South African Government accepted the offer of Dr. Robert Koch, of Berlin, to undertake the investigation of the disease and the discovery, if possible, of a remedy, for the sum of £10,000. No such sum was at the disposal of the committee of the Royal Society. They were obliged to send out young and enterprising medical men, practically without pay or reward, to see what they could do in the way of determining the cause of, and, if possible, the remedy for, the terrible sleeping sickness raging in Uganda and destroying daily hundreds of British subjects. The committee set to work in the summer of 1902, and sent out Drs. Low, Christy, and Castellani to Entebbe, the capital of Uganda.

The guesses as to the cause and nature of sleeping sickness at the time when this commission set forth were very various. Some highly capable medical authorities held that it was due to poisonous food. The root of the manioc, on which the natives feed, was supposed to become infected by some poison-producing ferment. A more generally received opinion was that it was caused by a specific bacterium which invades the tissues of the brain and spinal cord. Several totally different micro-organisms of this sort had been described with equal confidence by French and Portuguese investigators as the cause of the sleeping sickness studied by them in West Africa or on the Congo. Sir Patrick Manson, the head of the British Colonial medical service, an authority of great experience in tropical disease, had put forward the suggestion that the sleeping sickness was due to the infection of the patient by a minute thread worm (allied to the ‘vinegar-eel,’ and one of a great class of parasites) which he had discovered in the blood of negroes and had named Filaria perstans.

The occurrence of minute worms (true worms, neither unicellular plants nor protozoa) in the blood of man was first made known by Dr. Timothy Lewis, who described the Filaria sanguinis hominis, as well as some other most important blood-parasites, some years ago (1878), when officially engaged in an enquiry into the cause of cholera in Calcutta. Subsequently, in China, Manson found that these little blood-worms were sucked up by mosquitoes when gorging themselves on the blood of a patient. It is, indeed, difficult to imagine how they should escape passing into the mosquito with the blood. Manson suggested that the minute worms (known to be the embryos of a worm which, when adult, is about one fifteenth of an inch long) are obliged to pass through a mosquito in order to accomplish their development; but no proof of this suggestion has ever been made. We know by abundant and repeated demonstration and experiment that another blood-parasite—the malaria parasite—must pass through a mosquito, in whose body it develops, and by which it is carried to a new victim of infection. This was suspected long ago by both peasants and doctors, and experimentally proved by Ross; but no such proof has been given of the relation of Lewis’s blood-worm to a mosquito. The so-called Filaria perstans, discovered by Manson in the blood of negroes, appears to be very different from the Filaria sanguinis hominis of Lewis. It is not known how it gets into the blood; and it is very astonishing, and much to be regretted, that none of the medical men who have had it under observation have given a proper anatomical account of it. It appears that this worm is very common in the blood of negroes in tropical Africa; and as it was found in several cases in the blood of individuals attacked by sleeping sickness, Sir Patrick Manson was justified in entertaining the view that this parasite was the cause of the disease.

One of the first results obtained by the commission sent by the Royal Society committee to Uganda was the proof—which had, indeed, been already furnished by the resident medical officers of the Uganda Protectorate—that Filaria perstans, though remarkably abundant in the blood of the negroes of Uganda, can have nothing to do with sleeping sickness, since, though it often occurs in persons attacked with that disease, it also exists in districts where sleeping sickness is unknown; and, further, many cases of sleeping sickness have been observed in which no Filaria perstans has been discovered in the blood or other parts of the body.

While Drs. Low and Christy occupied themselves with settling this question as to the connexion of Filaria perstans with the disease and carried out a careful study of its clinical aspects, Dr. Castellani examined the brain and spinal cord of those who died from sleeping sickness, for bacteria. He found again and again an extremely minute globular vegetable parasite—of the kind known as streptococcus—which he concluded to be the cause of the disease, although he had not produced the disease experimentally by inoculating an animal with this microbe.

In the early part of 1903 these were the only results obtained by some six months’ work of the medical men sent out by the Royal Society’s committee; and it was felt that something more must be done. The investigation of a disease hitherto little known and studied is one of the most difficult tasks in the world, requiring the highest scientific qualities. Any serious attempt to deal with the sleeping sickness in Uganda would, it was at length recognised, require the dispatch of a man of proved capacity and experience, provided with full powers and with trained men as his assistants. No such men are provided by the public service of the British Empire. To detach a medical man of recognised insight and experimental skill from his practice—even were it possible to find one specially qualified for the present enquiry—would involve the payment of a large fee, which neither the Royal Society nor the Foreign Office could command.

What, then, was to be done? Fortunately there was one man in the public service, recently appointed to be one of the chiefs of the educational arrangements of the Army Medical Department, who had shown himself to be especially gifted in the investigation of obscure diseases. This was Colonel David Bruce, F.R.S., who, some fifteen years ago, established the existence of Malta fever, as an independent disease, by his clinical observations and by the isolation and cultivation of the parasitic bacterium causing it; and who, further, when employed by the governor of Zululand a few years later (1895) to investigate the celebrated tsetze-fly disease of South Africa, had discovered, contrary to the assertions and prejudices of a large number of African sportsmen and explorers, that the horse and cattle disease known as nagana or tsetze-fly disease was due to the presence in the blood of the affected animals of a peculiar cork-screw-like animal parasite, the Trypanosoma Brucei. This is carried by the bite of the tsetze-fly from the blood of wild game, such as buffalo and antelope, where it does no harm, to the blood of domesticated animals, in which it multiplies and proves to be the source of a deadly poison causing death in a few weeks. The experiments by which Colonel Bruce demonstrated this relationship of tsetze-fly, trypanosome parasite, wild big game, and domesticated animals, were universally regarded as masterly both in conception and execution, and absolutely conclusive.

The committee of the Royal Society came to the conclusion that the thing to be done was to get Colonel Bruce to consent to proceed to Uganda, and to recommend the Foreign Office to obtain from the War Office the temporary detachment of Colonel Bruce for this service. Accordingly Colonel Bruce arrived in Uganda in the middle of March, 1903. Dr. Low and Dr. Christy had already departed, but Dr. Castellani was still at Entebbe engaged in the study of his streptococcus. He mentioned to Colonel Bruce on his arrival that he had on more than one occasion seen a trypanosome in the cerebro-spinal fluid of negroes suffering from sleeping sickness; but, inasmuch as Dutton on the West Coast and Hodges in Uganda had described a trypanosome as an occasional parasite in human blood, he had not considered its occurrence in sleeping-sickness patients as of any more significance than is the occurrence of Filaria perstans. Castellani regarded the trypanosome, like the filaria, as a mere accidental concomitant of sleeping sickness, the cause of which he considered to be the bacterial streptococcus which he had so frequently found to be present.

Naturally enough, Bruce was impressed by the fact that trypanosomes, of the deadly nature of which he had had ample experience, had been found, even once, in the cerebro-spinal fluid of sleeping-sickness patients; and he immediately set to work to make a thorough search for this parasite in all the cases of sleeping sickness; then under observation at Entebbe. He generously allowed Castellani to take part in the investigation, which resulted in the immediate discovery of the trypanosome in the cerebro-spinal fluid of twenty cases, out of thirty-four examined, of negroes afflicted with the disease; whilst in twelve negroes free from sleeping sickness the trypanosome could not be found in the cerebro-spinal fluid. Castellani returned to Europe three weeks after Bruce’s experiments were commenced, and announced the discovery, which has been, in consequence, erroneously attributed to him, although mainly due to Bruce.

Bruce continued his work in Uganda until the end of August, 1903, having been joined there by Colonel Greig of the Indian Army, who has continued the work of the Royal Society’s commission since Bruce left. Other valuable observations have been carried out by various medical men officially connected with the Uganda Protectorate. Bruce soon showed that in every case of sleeping sickness, when examined with sufficient care, the trypanosome parasite is found to be present in the cerebro-spinal fluid. He also showed that it is absent from that fluid in all negroes examined who were not afflicted with the disease, but made the very important discovery that the trypanosome is present in the blood (not the cerebro-spinal fluid) of twenty-eight per cent. of the population in those areas where sleeping sickness occurs, the persons thus affected having none of the symptoms of sleeping sickness, but being either perfectly healthy or merely troubled with a little occasional fever. The subsequent history of all the cases thus observed has not as yet been recorded. But in many such, even in some Europeans, the earlier presence of the trypanosome in the blood has been followed by its entry into the cerebro-spinal lymphatics, and by the fatal development of sleeping sickness.

As already indicated, it was found by Bruce, on recording the cases of sleeping sickness brought into or reported in Entebbe, that there were certain “sleeping-sickness areas” and other areas free from sleeping sickness. The theory now took shape in Bruce’s mind that the trypanosome first gets into the blood, and then after a time, makes its way into the cerebro-spinal system, only then producing its deadly symptoms. Very generally, when once in the blood, the trypanosome multiplies itself, and sooner or later—apparently, in some cases, even after two or three years—gets into the cerebro-spinal fluid. It is probable that it may be destroyed by natural processes in the human body before this final stage is reached; and thus the infected person may recover and escape the deadly phase of the disease. But nothing certain is known, as yet, on this head. Later observations show that the trypanosome is found alive and in large quantity in the lymphatic glands, especially those in the region of the neck in infected persons. These glands were known to be enlarged in persons suffering from the disease.

Colonel Bruce’s next step was to ascertain the mode in which the trypanosome is introduced into the blood. Naturally he looked for a kind of tsetze fly, such as carries the trypanosome in the nagana disease of horses and cattle already studied by him in Zululand. It is a fact that the Glossina morsitans and Glossina pallidipes, which are the tsetze flies of the “fly-districts” where nagana disease is rife, are unknown in Central or Western Africa; and also it is a fact that no tsetze fly had been observed in the neighbourhood of the Victoria Nyanza when Colonel Bruce began his enquiries. He employed, through the good-will of the native chiefs and rulers, a large number of natives to collect flies throughout the country forming a belt of twenty or thirty miles around the north of the lake. Many thousands of flies were thus brought in, and the localities from which they came carefully noted. Among these flies Colonel Bruce recognised a tsetze fly; and when these collections were received at the Natural History Museum in London, it was at once determined by Mr. Austen, the assistant in charge of our collections of Diptera (or two-winged flies), that the Uganda tsetze fly was not the same species as that of Zululand and the fly country, but a distinct species previously known only on the West Coast and the Congo basin, and described by the name Glossina palpalis. The story thus developed itself: the trypanosome of sleeping sickness is probably carried by this West Coast tsetze fly just as the trypanosome of nagana is carried in the south-east of Africa by the Glossina morsitans and pallidipes, the regular and original “tsetze” flies.

Sleeping sickness thus presented itself as a special kind of human tsetze-fly disease. To test this hypothesis, Colonel Bruce pursued two very important and distinct lines of enquiry. In the first place he found that those places on his map which were marked as “sleeping-sickness areas” were precisely those places from which the collected flies included specimens of tsetze fly, whilst he found that there were no tsetze flies in the collections of flies brought in by the natives from the regions where there was no sleeping sickness.

His second test inquiry consisted in ascertaining whether the tsetze flies of Uganda are actually found, experimentally, to be capable of carrying the trypanosome from one infected person to another. For this purpose it was necessary to make use of monkeys, certain species of which were ascertained to be liable to the infection of the sleeping sickness trypanosome when this was introduced by means of injection through a syringe. Such monkeys were found to develop the chief symptoms of sleeping sickness, and ultimately died of the disease, their cerebro-spinal fluid being invaded by the parasites. Accordingly it was possible to use monkeys as test animals. It was found by Colonel Bruce that tsetze flies (Glossina palpalis) which had been made to bite infected negroes could carry the infection to the monkeys; and it was also found that even when a number of tsetze flies, not specially prepared, were allowed to bite a monkey, the latter eventually developed the trypanosome in its blood and cerebro-spinal fluid, thus showing that the tsetze flies, as naturally occurring in the country around Entebbe, contain many of them, the trypanosome ready to pass from the fly to a human or simian victim, when casually bitten by the fly.

Experiments such as these of infection by the fly, and the use of monkeys in the research, require very great care; and it is quite reasonable to ask that they shall be repeated and most carefully checked before they are considered as demonstrative and absolutely certain. It may, however, be considered as practically certain that the sleeping sickness is due to the presence in the cerebro-spinal fluid of quantities of a minute parasite, the Trypanosoma Gambiense, which is carried from man to man by the palpalis tsetze fly, which sucks it up from the blood of an infected individual and conveys it to previously uninfected individuals. The natives in Uganda lie about and sleep under the shade of trees where the tsetze flies are especially abundant; and they are quite indifferent to the bites of flies of one kind and another.

It is the dislike to the mere touch of a fly, still more to its bite, which has protected Europeans almost entirely from the sleeping sickness. Unfortunately there is no immunity for Europeans in the matter; and the existence of half a dozen or more cases of white people infected with the trypanosome, who have ultimately died in England or elsewhere in Europe from sleeping-sickness contracted through the bite of a fly in Africa, is abundant proof that there is not, as has been supposed, any special freedom from the disease for white people.[24]

The foregoing description of the nature and mode of the infection of sleeping sickness will not cause any astonishment to the layman of the present day who knows anything of recent medical science. We are all familiar with the danger of fly-bites, even in this country, where deadly bacteria are occasionally carried by biting flies, such as the horse-flies, into the human subject; and nowadays every one is more or less familiar with the discovery of the minute blood-parasite which causes malaria or ague and is carried by a particular kind of gnat in the interior of which it multiplies by a process of sexual conjugation. At the same time the reader who is interested in sleeping sickness will probably desire to know more about the nature of the tsetze flies and some further details as to the parasite spoken of as trypanosome.

Tsetze flies—Glossina morsitans—magnified two diameters. This is the “fly” of the Nagana or horse and cattle disease of South Africa. The Glossina palpalis, which carries the Trypanosoma Gambiense causing sleeping sickness, is very closely similar to it in appearance.

The tsetze flies form a genus called by Wiedemann (in 1830) “Glossina.” They are only found in Africa; and some seven species in all are known. They are little bigger than a common house-fly, and much like it in colour (fig. 48). They differ in appearance from the house-fly in the fact that the wings, when the insect is at rest, are parallel to one another, and slightly over-lap in the middle line, instead being to a small extent divergent at their free extremities. The bite, like that of all flies, is rather a stab than a bite, and is effected by a beak-like process of the head, the blood of the animal pricked in this way being drawn into the fly’s mouth by a sucking action of the gullet. The tsetze flies appear to be especially greedy and are said to gorge themselves to such an extent that the blood taken in from one animal overflows the gullet, and so contaminates the wound inflicted by the fly on the next animal it visits. It is at the present moment assumed very generally that this is the way in which infection is produced. But it is not at all improbable that the trypanosome undergoes some kind of multiplication and change of form when sucked into the tsetze fly as happens in the case of the malaria parasite when swallowed by the Anopheles gnat. No such change has yet been discovered in regard to the trypanosome of sleeping sickness: but it cannot be said that the matter has been exhaustively studied, or that a negative conclusion is justified.[25]

Fig. 49.

The earliest discovered Trypanosome, described by Gruby in 1843 as “Trypanosoma sanguinis” and found by him in the blood of the common esculent Frog.

It was not noticed again until it was re-discovered by Lankester in 1871, who published the above figure of it in the Quarterly Journal of Microscopical Science in that year.

As to the parasite itself—the trypanosome—a long and very interesting story has now to be told. The first blood-parasite ever made known to naturalists and medical men was that to which Gruby, in 1843, gave the name Trypanosoma sanguinis. He found it in the blood of the common frog. We have here reproduced a figure of this original trypanosome (fig. 49). Similar parasites had been seen, but not named, in the blood of fishes. These trypanosomes are all very minute and of a somewhat elongated form, a fair average length being one thousandth of an inch. They are simple protoplasmic animals, consisting of one single nucleated corpuscle. The protoplasm is drawn out at one end of the creature into a motile undulating thread, and from the point where this joins the body a membranous undulating crest extends along the greater part of the animal’s length. There is no mouth, nutrition being effected by the imbibition of soluble nutrient matter.

After a long interval Gruby’s trypanosome was re-discovered in 1871; and then several kinds were described in the blood of tortoises, fishes and birds. In 1878, Dr. Timothy Lewis found a parasite in the blood of rats, at first in India, and subsequently in the common rats of London sewers. This parasite resembles a trypanosome in many respects (fig. 46A), but was very properly given a distinct name by Savile Kent, who called it “Herpetomonas.” This name has, however, been dropped; and the rat’s-blood parasite is spoken of as a trypanosome. It is the Trypanosoma Lewisii, and was the first of these trypanosomes to be found in the blood of a mammalian animal. The Trypanosoma Lewisii of the rat’s blood seems to do no harm to the rat, in which it swarms, multiplying itself by longitudinal fission; nor is it at present known to produce any trouble in other animals when transferred to their blood. Similarly, the frog’s trypanosome seems to exist innocently in the frog’s blood.

The next trypanosome discovered (1880) was, however found in the blood of camels, horses, and cattle suffering from a deadly disease known in India by the name “surra.” It is called Trypanosoma Evansii, after the observer who detected it. Trypanosomes now began to get a bad name, for the next was discovered in animals afflicted by a North African disease known to French veterinaries as “dourine.” This trypanosome was called T. equiperdum.

A little later, namely, in the year 1895, came Bruce’s discovery of a trypanosome associated with a tsetze fly in the production of the terrible nagana disease of the “fly-belts” of South Africa, which renders whole territories impassable for horses or cattle (fig. 46B). The remarkable and important observation was made by Bruce that this trypanosome (known as T. Brucei) inhabits the blood of big game without injuring them, just as the rat’s trypanosome inhabits the rat’s blood without producing disease; and that it is only when the trypanosome is carried from these natural wild “hosts” to domesticated animals introduced by man, such as horses asses, cattle, and dogs, that disease results. The wild animals are “immune” to Bruce’s trypanosome; the introduced animals are poisoned by the products of its growth and fissile multiplication in their blood.

Since Bruce’s researches on nagana, a trypanosome, T. equinum (fig. 46D), has been discovered in the horse-ranches of South America, where it causes deadly disease, the mal de caderas, among the collected horses; and a curiously large-sized trypanosome has been found by Theiler in the blood of cattle in the Transvaal. Down to a recent date no trypanosome had been found in the blood of man; and indeed it is almost certain that none of the kinds hitherto mentioned can survive in his blood. But in 1902 Dutton discovered a trypanosome in the blood of a West African patient; and a few other cases were noted. This trypanosome of human blood was called by Dutton T. Gambiense. It was not found to be connected with any serious symptoms, a little fever being the only disturbance noted. It now, however, appears that this trypanosome in the blood is the preliminary stage of the infection which ends in sleeping sickness; and, as we have seen, in a population seriously attacked by sleeping sickness, as is that of Uganda, as many as 28 per cent. of the people have trypanosomes in their blood.

There is no ground at present known for distinguishing Dutton’s T. Gambiense of human blood from that which Bruce has found to be so terribly abundant in Uganda, and to be the cause of sleeping sickness. Indeed all the trypanosomes of the blood of the larger mammalia are singularly alike in appearance; and the figure which is here given (fig. 50) of the trypanosome of sleeping sickness (T. Gambiense) might quite well serve to represent the T. Evansii of surra disease, the T. Brucei of nagana disease, or the T. equinum of the South American mal de caderas.

Fig. 50.

Trypanosome Gambiense, from the blood of men suffering from the early symptoms of sleeping sickness. A, after Bruce and Navarro; B, after Castellani. They show a large oval nucleus (drawn as a black mass), and a small black “micronucleus,” or “blepharoplast” in front.

A most characteristic feature, which has been made out by the careful study of these trypanosomes by means of colouring reagents and very high powers of the microscope, is that, whilst there is a large granular nucleus there is also a small body at the anterior end of the animalcule which readily stains and is placed at the end of the root (so to speak) of the vibratile flagellum or free thread. This smaller nucleus has been variously called the “micronucleus,” the “centrosome,” and the “blepharoplast.” It is identical with a structure similarly placed in non-parasitic microscopic animals to which trypanosoma is undoubtedly related. We find it in the phosphorescent noctiluca of our seas, and in various animalcules called “Flagellata.”

Fig. 51.

The Trypanosome (T. equiperdum) of the disease called “Dourine,” as seen alive in the blood of a rat, eight days after inoculation.

A, the actively wriggling cork-screw-like parasites; B, the blood-corpuscles of the rat. This figure, of comparatively low magnification, gives an indication of the relative size of the parasites and the blood-corpuscles.

The blood-corpuscles are about 1/5000th of an inch each in diameter.

The creature drawn in our fig. 50 is, then, the typical trypanosome. It is this which the medical investigator looks for in his human or animal patients; it is this which he has regarded as the sign and proof of infection. Experiments have shown that, though so much alike in appearance in the different diseases we have named, yet each trypanosome has its own properties. Human blood-serum is poisonous to one and not to another; an animal immune to one is not immune to another. At present no treatment has been discovered which will destroy the parasites when once they have effected a lodgment, or act as an antidote to the poison which they produce in the infected animal or man. But the fact that in some cases an animal may become immune to the attack of the parasite which usually is deadly to its kind, gives hope of an eventual curative treatment for trypanosome infection; as does also the fact that the serum of some animals acts as a poison to trypanosomes which flourish in other animals.

With regard to immunity, it must always be remembered that we are liable to confuse two different conditions under this one term. An animal may be said to be immune to blood-parasite because that parasite is actually unable to live in its blood. On the other hand an animal is often said to be immune to a parasite when the parasite can and does flourish in its blood or tissues but produces no poisonous effect. A more precise nomenclature would describe the attacked organism in the first case as “repellent,” for it repels the parasite altogether; in the second case as “tolerant,” for it tolerates the presence and multiplication of the parasite without suffering by it.

We have yet to learn a good deal more as to the repulsion and the toleration of the trypanosome parasites by mammals and man. Still more have we to learn about the life-history of the trypanosome. At the moment of writing, absolutely nothing has been ascertained as to the life-history of the trypanosome of mammalian blood, except that they multiply in the blood by longitudinal fission. Our ignorance about them is all the more serious since other trypanosomes, discovered by Danilewesky in birds, have been studied and have been shown to go through the most varied phases of multiplication and change of size and shape, including a process of sexual fertilisation like that of the malaria parasite, to which, indeed, it now seems certain the trypanosomes are very closely allied.

It is to Dr. Schaudinn[26], that we owe a knowledge of some most extraordinary and important facts with regard to the trypanosomes parasitic in the blood of the little stone-owl of southern Europe (Athene noctua). These facts are so remarkable that, were Dr. Schaudinn not known as a very competent investigator of microscopic organisms we should hesitate to accept them as true. Supposing, as is not improbable, that similar facts can be shown in regard to the trypanosomes of mammalian blood, the conclusions which our medical investigators have based upon a very limited knowledge of the form and life-history of the trypanosomes occurring in diseases such as sleeping sickness, surra, and nagana, are likely to be gravely modified, and practical issues of an unexpected kind will be involved.

As has already been pointed out in this article, the British Government has no staff of public servants trained to deal with the world-wide problems of sanitation and disease which necessarily come with increasing frequency before the puzzled administrators of our scattered Empire. There is no provision for the study of the nature and history of blood-parasites in this country, that is to say, no provision of laboratories with the very ablest and exceptionally-gifted investigators at their head[27]. We play with the provision of an adequate army, officers, and equipment to fight disease, which annually destroys hundreds of thousands of our people, much as barbarous states or bankrupt European kingdoms play with the provision of an ordinary army and navy. Their forces exist on paper, or even in fact, but have no ammunition, no officers, and no information; and there is no pay for the soldiers or sailors. Dr. Schaudinn, on the other hand, carried on his researches as an officer of the German Imperial Health Bureau of Berlin; and the account of them was published in the official Report of that important department of the German imperial administrative service three years ago.

Fig. 52.

Trypanosoma Ziemanni, from the gut of the gnat (Culex), having been sucked in with the blood of the owl (Athene noctua). A, fertilized vermiform stage. B, multiplication of nucleus. C, elongation and coiling, with increase of nuclei (after Schaudinn).

Fig. 53.

Minute neutral Trypanosomes in the gut of the gnat liberated from the coiled form of Fig. 52, C (after Schaudinn).

It is not possible here to give a full report on Dr. Schaudinn’s work; but it appears that he has studied two distinct species of trypanosoma, both occurring side by side in the blood of the little stone-owl, and already seen but incompletely studied, by Danilewsky and Ziemann. The second of the two species of trypanosome is in some respects the more remarkable. Schaudinn calls it Trypanosoma Ziemanni; and from the figures which are here given (figs. 4, 5, 6, and 7), copied from his article, with the explanations below the figures, the reader will at once see what an extraordinary range of form and mode of multiplication is presented by this one species of trypanosome. Space will not permit us to comment on these various phases beyond noting how assuredly such forms would have escaped recognition as belonging to the trypanosome history if seen, before Dr. Schaudinn’s memoir was printed, by any of our medical commissioners blindly exploring round about the diseases caused by trypanosomes in man and mammals.

Fig. 54.

A, B, C, D, Elongated spiral forms of Trypanosoma Ziemanni (some intertwined) developed from those of Fig. 53—showing transverse division, nucleus, and blepharoplast.

E, F, pear-shaped forms resulting from the contraction of forms like A; G, a cluster of very minute individuals.

These forms are observed in the gnat and also in the blood of the owl, into which they pass when the gnat bites that bird, and there give rise to the large male and female Trypanosomes seen in Fig. 55 (after Schaudinn).

One very astonishing and revolutionary fact discovered by Schaudinn we must, however, especially point out. Medical men have long been acquainted with the spirillum, or spiral threads, discovered by Obermeyer in the blood of patients suffering from the relapsing fever of eastern Europe. These were universally and without question regarded as Bacteria (vegetable organisms) and referred to the genus “SpirochÆta” of Ehrenberg. They were called SpirochÆta Obermeieri; and relapsing fever was held to be a typical case of a bacterial infection of the blood. It is now shown by Schaudinn that the blood-parasite spirochÆta is a phase of a trypanosome (fig. 54); that it has a large nucleus and a micronucleus or blepharoplast, neither of which are present in the spiral Bacteria; and, further, that it alters its shape, contracting so as to present the form of minute oval or pear-shaped bodies, each provided with a larger and a smaller nucleus (fig. 54, E, F). These oval bodies are often engulfed by the colourless corpuscles (phagocytes) of the blood; and it is in the highest degree probable that in this condition they have been observed in some tropical diseases without their relation to the spiral forms being suspected. The corpuscles lately described by Leishman, in cases of a peculiar Indian fever, are very probably of this nature, as are also similar bodies recently described in Delhi sore. On the whole, it may safely be said that the researches of Dr. Schaudinn, of which only a preliminary account has yet been published, have widely modified our conceptions as to these blood-parasites, and must lead to important discoveries in regard to diseases caused by them in mammals and in man.

Fig. 55.

Trypanosoma Ziemanni, from the blood of the little owl. The stages shown in Figs. 52–54 are passed inside the gnat. The spiral and pear-shaped bodies of Fig. 54 pass from the gnat’s proboscis into the blood of the little owl, and grow there into the large forms here figured. A, B, and C are females, destined to be fertilized by spermatozoa (see Fig. 21) when swallowed by a gnat. D and E are male Trypanosomes, which will give rise each to eight fertilizing individuals or spermatozoa as shown in Fig. 56—when swallowed by a gnat.

The facts that wild game serve as a tolerant reservoir of trypanosomes for the infection of domesticated animals by the intermediary of the tsetze fly, and that native children in malarial regions act the same part for the malarial parasite and mosquito, suggest very strongly that some tolerant reservoir of the sleeping-sickness trypanosome may exist in the shape of a hitherto unsuspected mammal, bird, or insect. The investigation of that hypothesis and the discovery of the reproductive and secondary forms of the mammalian trypanosomes are the matters which now most urgently call for the efforts of capable medical officers. But we must not be sanguine of rapid progress, since men of the scientific quality needful for pursuing these enquiries are not numerous; and those who exist are not endowed with private fortunes, as a rule. At the same time no attempt is made by the British Government to take such men into its pay, or to provide for the training and selection of such officers.[28]

Fig. 56.

Male Trypanosoma Ziemanni, giving rise by nuclear division to eight spermatozoa or microgametes. From the stomach of the gnat (Culex).

Each of these penetrates and fuses with the substance of a female Trypanosome, swallowed at the same time or already taken in by the gnat. The fertilized animalculÆ is the vermiform motile stage of Fig. 52, A; and so we return to the starting-point of the cycle (after Schaudinn).

The relations of parasites to the organisms upon or in which they are parasitic, and the relation of man, once entered on the first steps of his career of civilisation, to the world of parasites, form one of the most instructive and fascinating chapters of natural history. It cannot be fully written yet, but already some of the conclusions to which the student is led in examining this subject have far-reaching importance and touch upon great general principles in an unexpected manner.

Before the arrival of man—the would-be controller, the disturber of Nature—the adjustment of living things to their surrounding conditions and to one another has a certain appearance of perfection. Natural selection and the survival of the fittest in the struggle for existence lead to the production of a degree of efficiency and harmonious interaction of the units of the living world, which, being based on the inexorable destruction of what is inadequate and inharmonious as soon as it appears, result in a smooth and orderly working of the great machine, and the continuance by heredity of efficiency and a high degree of individual perfection.

Parasites, whether microscopic or of larger size, are not, in such circumstances, the cause of widespread disease or suffering. The weakly members of a species may be destroyed by parasites, as others are destroyed by beasts of prey; but the general community of the species, thus weeded, is benefited by the operation. In the natural world the inhabitants of areas bounded by sea, mountain, and river become adjusted to one another; and a balance is established. The only disturbing factors are exceptional seasons, unusual cold, wet, or drought. Such recurrent factors may from time to time increase the number of the weakly who are unable to cope with the invasions of minute destructive parasites, and so reduce, even to extermination the kinds of animals or plants especially susceptible to such influences. But anything like the epidemic diseases of parasitic origin with which civilised man is unhappily familiar seems to be due either to his own restless and ignorant activity or, in his absence, to great and probably somewhat sudden geological changes—changes of the connexions, and therefore communications, of great land areas.

It is abundantly evident that animals or plants which have, by long Æons of selection and adaptation, become adjusted to the parasites and the climatic conditions and the general company (so to speak) of one continent may be totally unfit to cope with those of another; just as the Martian giants of Mr. H. G. Wells, though marvels of offensive and defensive development, were helpless in the presence of mundane putrefactive bacteria and were rapidly and surely destroyed by them. Accordingly, it is not improbable that such geological changes as the junction of the North and South American continents, of North and South Africa, and of various large islands and neighbouring continents, have, in ages before the advent of man, led to the development of disastrous epidemics. It is not a far-fetched hypothesis that the disappearance of the whole equine race from the American continent just before or coincidently with the advent of man—a region where horses of all kinds had existed in greater variety than in any other part of the world—is due to the sudden introduction, by means of some geological change, of a deadly parasite which spread as an epidemic and extinguished the entire horse population.

Whatever may have happened in past geological epochs, by force of great earth-movements which rapidly brought the adaptations of one continent into contact with the parasites of another, it is quite certain that man, proud man, ever since he has learnt to build a ship, and even before that, when he made up his mind to march aimlessly across continents till he could go no further, has played havoc with himself and all sorts of his fellow-beings by mixing up the products of one area with those of another. Nowhere has man allowed himself—let alone other animals or even plants—to exist in fixed local conditions to which he or they have become adjusted. With ceaseless restlessness he has introduced men and beasts and plants from one land to another. He has constantly migrated with his herds and his horses, from continent to continent. Parasites, in themselves beneficent purifiers of the race, have been thus converted into terrible scourges and the agents of disease. Europeans are decimated by the locally innocuous parasites of Africa; the South Sea islanders are exterminated by the comparatively harmless measles of Europe.

A striking example of the disasters brought about by man’s blind dealings with Nature—disasters which can and will hereafter be avoided by the aid of science—is to be found in the history of the insect phylloxera and the vine. In America the vine had become adjusted to the phylloxera larvae, so that when they nibbled its roots the American vine threw out new root-shoots and was none the worse for the little visitor. Man in his blundering way introduced the American vine, and with it the phylloxera, to Europe; and in three years half the vines in France and Italy were destroyed by the phylloxera, because the European vines had not been bred in association with this little pest, and had not acquired the simple adjusting faculty of throwing out new shoots.

But it is not only by his reckless mixing up of incompatibles from all parts of the globe that the unscientific man has risked the conversion of paradise into a desert. In his greedy efforts to produce large quantities of animals and plants convenient for his purposes, and in his eagerness to mass and organise his own race for defence and conquest, man has accumulated unnatural swarms of one species in field and ranch and unnatural crowds of his own kind in towns and fortresses. Such undiluted masses of one organism serve as a ready field for the propagation of previously rare and unimportant parasites from individual to individual. Human epidemic diseases as well as those of cattle and crops, are largely due to this unguarded action of the unscientific man.

A good instance of this is seen in the history of the coffee plantations of Ceylon, where a previously rare and obscure parasitic fungus, leading an uneventful life in the tropical forests of that country, suddenly found itself provided with an unlimited field of growth and exuberance in the coffee plantations. The coffee plantations were destroyed by this parasite, which has now returned to its pristine obscurity. Disharmonious, blundering man was responsible for its brief triumph and celebrity. Dame Nature had not allowed the coffee fungus more than a very moderate scope. Man comes in and takes the reins; disaster follows; and there is no possibility of return to the old rÉgime. Man must make his blunders and retrieve them by further interference—by the full use of his intelligence, by the continually increasing ingenuity of his control of the physical world, which he has ventured to wrest from the old rule of natural selection and adaptation.

The adjustment of all living things to their proper environment is one of great delicacy and often of surprising limitation. In no living things is this more remarkable than in parasites. The relation of a parasite to the “host” or “hosts” in which it can flourish (often the host is only one special species or even variety of plant or animal) is illustrated by the more familiar restriction of certain plants to a particular soil. Thus the Cornish heath only grows on soil overlying the chemically peculiar serpentine rocks of Cornwall. The two common parasitic tape-worms of man pass their early life the one in the pig and the other in bovine animals. But that which requires the pig as its first host (TÆnia solium) cannot use a bovine animal as a substitute; nor can the other (TÆnia mediocanellata) exist in a pig. Yet the difference of porcine and bovine flesh and juices is not a very patent one; it is one of small variations in highly complex organic chemical substances. A big earth-worm-like stomach-worm flourishes in man, and another kind similar to it in the horse. But that frequenting man cannot exist in the horse, nor that of the horse in man. Simpler parasites, such as are the moulds, bacteria, and again the blood-parasites, trypanosoma, etc., exhibit absolute restrictions as to the hosts in which they can or can not flourish without showing specific changes in their vital processes. Being far simpler in structure than the parasitic worms, they have less “mechanism” at their disposal for bringing about adjustment to varied conditions of life. The microscopic parasites do not submit to alterations in the chemical character of their surroundings without themselves reacting and showing changed chemical activities. A change of soil (that is to say of host) may destroy them; but, on the other hand, it may lead to increased vigour and the most unexpected reaction on their part in the production of virulent chemical poisons.

We are justified in believing that until man introduced his artificially selected and transported breeds of cattle and horses into Africa there was no nagana disease. The Trypanosoma Brucei lived in the blood of the big game in perfect harmony with its host. So, too, it is probable that the sleeping-sickness parasite flourished innocently in a state of adjustment due to tolerance on the part of the aboriginal men and animals of West Africa. It was not until the Arab slave raiders, European explorers, and indiarubber thieves stirred up the quiet populations of Central Africa, and mixed by their violence the susceptible with the tolerant races, that the sleeping-sickness parasite became a deadly scourge—a “disharmony” to use the suggestive term introduced by my friend Elias Metschnikow.

The adjustment of primaeval populations to their conditions has also been broken down by “disharmonies” of another kind, due to man’s restless invention, as explained a few years ago in the interesting book of Mr. Archdall Reid on the “Present Evolution of Man.” Not only does the human race within given areas become adjusted to a variety of local parasites, but it acquires a tolerance of dangerous drugs, such as alcohol and opium, extracted by man’s ingenuity from materials upon which he operates. A race thus provided and thus immune imposes, by its restless migrations, on unaccustomed races the deadly poisons to the consumption of which it is itself habituated. The unaccustomed races are deteriorated or even exterminated by the poisons thus introduced.

Infectious disease, it was long ago pointed out, must be studied from three main points of view: (1) the life history and nature of the disease-germ or infective matter; (2) the infected subject, his repellant or tolerant possibilities, and his predisposition or receptivity; (3) the intermediary or carrying agents. Whilst it is true that little or nothing has been done by the State in acquiring or making use of knowledge as to the first and second of these factors, with a view to controlling the spread of disease, it is the fact that much has been done both in the way of investigation and administration in relation to the third factor. The great public-health enquiries and consequent legislation in this country, in which scientific men of the highest qualifications, such as Simon, Farr, Chadwick, and Parkes, took part during the Victorian period, have had excellent results; to them are due the vast expenditure at the present day on pure water, sewage disposal, and sanitary inspection. But little or nothing has been done in regard to the first and second divisions of the subject, in which the less organised portions of the British Empire are more deeply concerned than in waterworks and sewer-pipes. It is still contested whether leprosy (which is a serious scourge in the British Empire, though expelled from our own islands) is a matter of predisposition caused by diet or solely due to contagion; and yet it is left to individual practitioners to work out the problem. The State prepares vaccine lymph in a cheap and unsatisfactory way for the use of its, till recently, compulsorily vaccinated citizens; but the State, though thus interfering in the matter of vaccine, has spent no money to study effectively and so to improve the system of vaccination. Here and there some temporary and ineffective enquiry has been subsidised by a Government office; but there is no great army of investigators working in the best possible laboratories, led by the ablest minds of the day, with the constant object of improving and developing in new directions the system of inoculation. Surely if compulsion, or every pressure short of compulsion, is justified in enforcing vaccine inoculation on every British family, it would be only reasonable and consistent to expend a million or so a year in the perfection and intelligent control of this remedy by the most skilled investigators. Yet not a halfpenny is spent by the British Government in this way. Medicine is organised in this country by its practitioners as a fee-paid profession; but as a necessary and invaluable branch of the public service it is neglected, misunderstood, and rendered to a large extent futile by inadequate funds and consequent lack of capable leaders. The defiant desperate battle which civilised man wages with Nature must go on; but man’s suffering and loss in the struggle—the delay in his ultimate triumph—depend solely on how much or how little the great civilised communities of the world seek for increased knowledge of nature as the basis of their practical administration and government.

Postscript, December, 1906.—Messrs. Thomas and Breinl, of the Liverpool School of Tropical Medicine, two years ago discovered and published the fact that an arsenical aniline product known as “atoxyl” when injected into patients suffering from Sleeping Sickness destroys the parasite and promises to be a cure for this terrible infection. Experiments are in progress in many quarters in regard to this treatment, but certainty can only be arrived at by prolonged observation of the patients. The newspapers have lately, in error, attributed this discovery to Dr. Robert Koch of Berlin, who has merely confirmed the observations of the earlier workers.—E. R. L.


                                                                                                                                                                                                                                                                                                           

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