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with a feeling of oppression in the chest, and a copious flow of clear and watery urine from the congested kidneys. The body temperature will have risen suddenly from the normal to 103° or higher. This first or cold stage of the paroxysm varies much in length; in temperate climates it lasts from one to two hours, while in tropical and subtropical countries it may be shortened. It is followed by the stage of dry heat, which will be prolonged in proportion as the previous stage is curtailed. The feeling of heat is at first an internal one, but it spreads outwards to the surface and to the extremities; the skin becomes warm and red, but remains dry; the pulse becomes softer and more full, but still quick; and the throbbings occur in exposed arteries, such as the temporal. The spleen continues to enlarge; the urine is now scanty and high-coloured; the body temperature is high, but the highest temperatures occur during the chill; there is considerable thirst; and there is the usual intellectual unfitness, and it may be confusion, of the feverish state. This period of dry heat, having lasted three or four hours or longer, comes to an end in perspiration, at first a mere moistness of the skin, passing into sweating that may be profuse and even drenching. Sleep may overtake the patient in the midst of the sweating stage, and he awakes, not without some feeling of what he has passed through, but on the whole well, with the temperature fallen almost or altogether to the normal, or it may be even below the normal; the pulse moderate and full; the spleen again of its ordinary size; the urine that is passed after the paroxysm deposits a thick brick-red sediment of urates. The three stages together will probably have lasted six to twelve hours. The paroxysm is followed by a definite interval in which there is not only no fever, but even a fair degree of bodily comfort and fitness; this is the intermission of the fever. Another paroxysm begins at or near the same hour next day (quotidian ague), which results from a double tertian infection, or the interval may be forty-eight hours (tertian ague), or seventy-two hours (quartan ague). It is the general rule, with frequent exceptions, that the quotidian paroxysm comes on in the morning, the tertian about noon, and the quartan in the afternoon. Another rule is that the quartan has the longest cold stage, while its paroxysm is shortest as a whole; the quotidian has the shortest cold stage and a long hot stage, while its paroxysm is longest as a whole. The point common to the various forms of ague is that the paroxysm ceases about midnight or early morning. Quotidian intermittent is on the whole more common than tertian in hot countries; elsewhere the tertian is the usual type, and quartan is only occasional.

If the first paroxysm should not cease within the twenty-four hours, the fever is not reckoned as an intermittent, but as a remittent.

Remittent is a not unusual form of the malarial process in tropical and subtropical countries, and in some localities or in some seasons it is more common than intermittent. It may be said to arise out of that type of intermittent in which the cold stage is shortened while the hot stage tends to be prolonged. A certain abatement or remission of the fever takes place, with or without sweating, but there is no true intermission or interval of absolute apyrexia. The periodicity shows itself in the form of an exacerbation of the still continuing fever, and that exacerbation may take place twenty-four hours after the first onset, or the interval may be only half that period, or it may be double. A fever that is to be remittent will usually declare itself from the outset: it begins with chills, but without the shivering and shaking fit of the intermittent; the hot stage soon follows, presenting the same characters as the prolonged hot stage of the quotidian, with the frequent addition of bilious symptoms, and it may be even of jaundice and of tenderness over the stomach and liver. Towards morning the fever abates; the pulse falls in frequency, but does not come down to the normal; headache and aching in the loins and limbs become less, but do not cease altogether; the body temperature falls, but does not touch the level of apyrexia. The remission or abatement lasts generally throughout the morning; and about noon there is an exacerbation, seldom ushered in by chills, which continues till the early morning following, when it remits or abates as before. A patient with remittent may get well in a week under treatment, but the fever may go on for several weeks; the return to health is often announced by the fever assuming the intermittent type, or, in other words, by the remissions touching the level of absolute apyrexia. Remittent fevers (as well as intermittents) vary considerably in intensity; some cases are intense from the outset, or pernicious, with aggravation of all the symptoms—leading to stupor, delirium, collapse, intense jaundice, blood in the stools, blood and albumen in the urine, and, it may be, suppression of urine followed by convulsions. The severe forms of intermittent are most apt to occur in the very young, or in the aged, or in debilitated persons generally. Milder cases of malarial fever are apt to become dangerous from the complications of dysentery, bronchitis or pneumonia. Severe remittents (pernicious or bilious remittents) approximate to the type of yellow fever (q.v.), which is conventionally limited to epidemic outbreaks in western longitudes and on the west coast of Africa.

Of the mortality due to malarial disease a small part only is referable to the direct attack of intermittent, and chiefly to the fever in its pernicious form. Remittent fever is much more fatal in its direct attack. But probably the greater part of the enormous total of deaths set down to malaria is due to the malarial cachexia. The dwellers in a malarious region like the Terai (at the foot of the Himalayas) are miserable, listless and ugly, with large heads and particularly prominent ears, flat noses, tumid bellies, slender limbs and sallow complexions; the children are impregnated with malaria from their birth, and their growth is attended with aberrations from the normal which practically amount to the disease of rickets. The malarial cachexia that follows definite attacks of ague consists in a state of ill-defined suffering, associated with a sallow skin, enlarged spleen and liver, and sometimes with dropsy.

Causation.—From the time of Hippocrates onwards the malarial or periodical fevers have engaged the attention of innumerable observers, who have suggested various theories of causation, and have sometimes anticipated—vaguely, indeed, but with surprising accuracy—the results of modern research; but the true nature of the disease remained in doubt until the closing years of the 19th century. It has now been demonstrated by a series of accurate investigations, contributed by many workers, that malaria is caused by a microscopic parasite in the blood, into which it is introduced by the bites of certain species of mosquito. (See Parasitic Diseases and Mosquitoes.)

The successive steps by which the present position has been reached form an interesting chapter in the history of scientific progress. The first substantial link in the actual chain of discovery was contributed in 1880 by History of Discovery. Laveran, a French army surgeon serving in Algeria. On the 6th of November in that year he plainly saw the living parasites under the microscope in the blood of a malarial patient, and he shortly afterwards communicated his observations to the Paris Académie de Médecine. They were confirmed, but met with little acceptance in the scientific world, which was preoccupied with the claims of a subsequently discredited Bacillus malariae. In 1885 the Italian pathologists came round to Laveran’s views, and began to work out the life history of his parasites. The subject has a special interest for Italy, which is devastated by malaria, and Italian science has contributed materially to the solution of the problem. The labours of Golgi, Marchiafava, Celli and others established the nature of the parasite and its behaviour in the blood; they proved the fact, guessed by Rasori so far back as 1846, that the periodical febrile paroxysm corresponds with the development of the organisms; and they showed that the different forms of malarial fever have their distinct parasites, and consequently fall into distinct groups, defined on an etiological as well as a clinical basis—namely, the mild or spring group, which includes tertian and quartan ague, and the malignant or “aestivo-autumnal” group, which includes a tertian or a semi-tertian and the true quotidian type. Three distinct parasites, corresponding with the tertian, quartan and malignant types of fever, have been described by Italian observers, and the classification is generally accepted; intermediate types are ascribed to mixed and multiple infections. So far, however, only half the problem, and from the practical point of view the less important half, had been solved. The origin of the parasite and its mode of introduction into the blood remained to be discovered. An old popular belief current in different countries, and derived from common