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    "source_title": "Encyclopaedia Britannica (1926)",
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    "title": "SLEEPING SICKNESS",
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    "verified_text": "at the international conference held in london in june 1907 nine problems were stated for future solution. some of these have been completely, others partly, solved (1) and (2).! transmission of infection——it was at first believed that the transmission of trypunosoma gambiense by the tsetse fly, glos- sina palpalis, was direct or mechanical, and that a fly lost its power of infecting 24-48 hours after feeding on an infected man. kleine (1909) showed that this is not the case. in a certain per- centage of flies the germs ingested with the blood do not die but multiply exceedingly in the fly’s gut, change in form, come for- ward and at last invade the salivary glands, where they resume their blood form. during the process, which occupies 14-28 days or more, the fly is not infective, but when the germs are established in the salivary glands it regains its infectivity and may retain it for a long period, for at each feed germs are poured into the punc- ture. unless the salivary glands contain the germs a fly 1s not capable of infecting, but only in a small proportion is this devel- opment completed; in nature the proportion of infected flies rarely exceeds one in 1,000. conveyance is therefore indirect. direct infection may occur in nature, but the failure of the disease to spread in the absence of tsetse, even though biting insects of many kinds are present, seems to show it must be rare, e.g., hundreds of cases of sleeping sickness were recorded in the west indies among slaves brought from africa, but there is no recorded instance of spread in the new world. the discase was formerly rife in the island of principe in the gulf of guinea, where pulpalis abounded, but no cases occurred in the neigh- 1 these numbers refer to the problems discussed in 25.240. 397 bouring island of san thome, with the same insect fauna, but, like america, with no tsetse. duke believes that when the dis- ease is epidemic direct infection is the rule. there is no evidence that the fly can transmit the germs to its offspring. the fly has been shown to be capable of infecting for at least 96 days. other species of glossina, e.g., morsitans, tachinoides, become similarly infected, and it is probable that all the species are capable of conveying sleeping sickness; whether they do so or not depends in part on their habits; e.g., some species rarely attack man. it. rhodestense-——in 1909 a second species of trypanosome was discovered in a case of human infection from rhodesia and called t. rhodesiense. it is found in areas infested not by g. palpalis but by g. morsitans, and was shown by kinghorn and yorke (1911) to be conveyed by this species and to undergo in it a similar development. 7. rhodcsicnse infections are founc in nyasaland, portuguese east africa and tanganyika terri- _ tory, besides northern rhodesia, and, rarely, south of the zam- bezi river. j. rhodesiense cannot be distinguished from gant- biense by its appearance in human blood; after inoculation into animals microscopical differences can be detected; since such inoculations are rarely made it may be more often the cause of sleeping sickness than is believed; its carrier is widely distributed. indeed, a few cases have been found as far north as the anglo- egyptian sudan; and near mwanza, south of lake victoria, a small epidemic occurred in 1922, conveyed by a tsetse akin to morsilans. this type of human trypanosomiasis is rarely epi- demic; cases occur in sporadic fashion. it is more acute and more rapidly fatal than the gambiense varicty, and is more re- sistant to drugs. whether or not 7. rhodesiense is identical with t. brucei, the parasite of nagana, first described by bruce in zululand (1893), is undecided. bruce and yorke consider them to be the same; kleine makes a distinction. they cannot be separated by their appearance under the microscope, the symp- toms and course of the ness produced in animats, or the man- ner and site of development in the tsetse. both complete their development in the salivary glands. if they are the same, man must, as a rule, be refractory to infection, for t. brucei is com- mon in animals over a large fly-infested area of africa. t. brucei and t. rhodesiense are found in big game, especially waterbuck, bushbuck, reedbuck, haartebeest, on which g. mor- sitans feeds. these animals are, therefore, reservoirs of germs capable of infecting man, and much discussion has taken place as to the rele played by big game in the spread of t. rhodesiense, some claiming that the passage of the parasite is game to fly to man; others that it is man to fly to man. a decisive opinion cannot even now be given. | an experiment was made in east africa during the world war in which blood was taken from transport animals infected with 7. brucei and inoculated by taute into himself, his colleague huber and 127 natives. though animals inoculated at the same time always became infected, there was no single instance of infection in man. they concluded that man is immune to infection by 7. brucez. this striking experiment, however, does not convince those who believe man to be susceptible but very resistant. as regards 7. gambiense, it is generally agreed that infected man is the chief reservoir of infection, though bruce (1911) found that antelopes can be infected with this trypanosome by allowing infected palpalis to ieed upon them, and they continue to harbour the trypanosomes in their blood for many months, and though the sitatunga antelope (tragelaphus spcket) is com- monly infected under natural conditions on lake victoria (duke). domestic animals also harbour both trypanosomes, in the case of 7. gambiense without sign of illness; whether they play any appreciable part in the spread of the human disease is unknown. field observations have shown that in northern nigeria and french africa, south of lake chad, another tsetse, g. tachinoides, conveys a human trypanosome, probably t. gam- biense. in these areas fachinoides is the only tsetse. 558 treatmenit.—sleeping sickness is now treated by compounds of arsenic, especially afoxyl and tryparsamide, the latter a prod- uct of the rockefeller institute; by compounds of antimony, as tartar emetic; and by a drug of undisclosed composition called bayer 205, or germanin. the french and belgians use atoxyl largely in the african villages, where doses are injected at the proper intervals by trained natives. a high degree of success is claimed, both curative and preventive,in that the blood is kept free from germs which might be taken up by the tsetse. anitmontals are used as a rule in conjunction or alternation with arsenicals. bayer 205, first employed in the treatment of man in 1921, has remarkable successes to its credit in europeans, especially in cases of the rhodesian type which were refractory to other drugs; unless used with caution it has a harmful effect on the kidneys. it has been less successful in natives, perhaps because infection is usually detected in them at a later stage when the spinal cord and brain are affected, and at this stage treatment nearly always fails. french chemists have prepared the same or a similar drug. tryparsamide, introduced about the same time, appears to be still more potent, and especially in cases in which the nervous system is involved, but it also has a serious effect in that it sometimes affects vision. though sleeping sick- ness in the european is nearly always a fatal disease if left un- treated, in the natives of parts of africa it is very chronic, does not interfere with the patient’s activities, and almost certainly may end in natural recovery. the means of prevention of sleeping sickness have been known in principle for 20 years, and depend upon the fact that infection is conveyed by tsetse flies and in no other way. an international conference—at the instance of the league of nations an international conference on sleeping sickness met in london in 1925. in its recommendations it laid down administrative measures which should be taken on both sides of the frontiers between infected countries for the control of the disease, and advised the dispatch to uganda of an international commission to study certain problems, such as immunity to the disease, the function of wild and domestic animals as breeding grounds for the virus, and the relations between 7. gambiense and t. rhodesiense infections; work with curative and prophy- lactic drugs was also envisaged. the commission started work in 1926. birliography.—report of the interdepartmental committee on sleeping sickness, h1.m.s.0., london, cd. 7349 (1914); sir david bruce, ‘' croonian lectures,” lancet (june and july 1915); b blacklock and w. yorke, “ ‘the trypanosomiases,” in w. byam and r. g. archibald’s practice of medicine in the troptcs, vol. 2 (1922); also tropical diseases bulletin, tropical diseases bureau (london ig12-25). all the scientific publications on slecping sick- ness are abstracted in this periodical. a, w. g. b.) slesvig: see schleswig. small holdings: sec allotments.",
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