Part 92

The atmosphere is undoubtedly the medium by means of which malarial poison is most frequently brought into the human system. Liability to intoxication is increased in direct ratio to the proximity of points of exposure to places of development; to similarity of level; to situation in the line of prevailing winds which have traversed the breeding-ground; and, lastly, to the extent and fertility of the locality of production.

Whether malaria passes through the respiratory apparatus directly into the circulation, or is lodged upon the fauces and absorbed through some other surface, is not clearly ascertainable. It is certainly not deprived of its noxious qualities by stomach digestion, and therefore, sometimes at least, may reach the blood through the alimentary canal.

Malaria is miscible with water. It is capable of being carried by currents of water through distances and periods of time altogether undetermined, without losing either its toxic effects or, perhaps, the faculty of reproduction. It is more than likely that this means of conveyance has effected its distribution to continents and islands too widely separated to justify a belief that it was wind-wafted. No observations need be adduced to establish the water-borne habit of the malarial poison, or the positive liability to its toxic effects when received into the stomach through this medium. These facts have been well understood from the time of Hippocrates.

The matter of communicability of malaria by means of drinking water should not be dismissed without some allusion to the great probability that other fluids or solids are open to a similar charge. There is a widespread popular prejudice, especially notable in the southern part of the United States, that drinking milk occasions attacks of the endemic fevers. It is the usual custom to pour the evening supply of milk into broad uncovered pans, and allow it to remain exposed in the open air for {591} consumption at the morning meal. This viscid fluid, so tenacious of ordinary air-borne particles, may well be suspected of entangling sufficient quantities of swamp poison to produce sickness if exposed where it is rife during a whole night.

A similar popular prejudice exists in regard to the muscadine grape, which flourishes best in swampy localities. The rough skin of this fruit, frequently covered with its own juice, offers favorable conditions for the adhesion of air-borne particles.

The malarial poison is not reproduced within the human system. This proposition is undeniable, since no intensification of the poison is produced by any degree of crowding of the sick which can be practised; neither do any conditions of contact with the sick ever impart malarial affections.

Malarial poison is specific. This allegation is sufficiently established by its specific effects on the human economy. There is no other agent known which is capable of originating morbid phenomena characterized by such marked diurnal periodicity.

It is not interchangeable with other specific poisons. This statement may be rested upon all fairly collected clinical observations.

There are no facts which justify the belief that malaria is capable of becoming mixed in the atmosphere, or outside the system, with any other specific morbific germ, so as to produce a third something which may give rise to compound forms of disease.

The answer to the second question which is best supported is, that the malarial poison is brought into the system principally by breathing an atmosphere impregnated with this miasm.

It is also ingested by being held in suspension in fluids used as drink or food; perhaps also by eating certain fruits or vegetables in their natural state whose external surfaces afford favorable conditions for its lodgment.

MORBID EFFECTS AND PHENOMENA WHICH FOLLOW ITS INTRODUCTION INTO THE HUMAN SYSTEM.--The discussion of the morbid process established by the malarial poison involves some difficult problems. A period of incubation must be admitted to follow the inception of the ague germs. But this period has no definitely marked limits. Perhaps it is a shifting one, according to the quantity or quality of the poison received, or the sudden or gradual manner in which it is received, or the state of receptivity of the system.

Certain facts seem to indicate very clearly that malarial poison is very slowly removed from a system which has been brought under its influence. These evidences of long systemic residence of the poison are principally displayed in those attacks which occur after long periods of removal from any surrounding where intoxication was possible. Vernal attacks may be classed in the same connection. In many instances the subjects of these long-delayed attacks have never suffered a paroxysmal seizure, and yet when some accidental derangement of health occurs, as from a fit of indigestion or a sudden wetting, they fall sick with one or another form of malarial fever.

It does not appear to me that we are justified in assuming that such attacks as I refer to are to be ascribed to secondary changes produced in either the fluids or solids of the system by the malarial poison. In so {592} far as the clinical phenomena are worth anything in demonstrating the presence and agency of the specific malarial poison in these deferred attacks, they are precisely similar to those observed in paroxysms arising after a few hours' or a few days' exposure to marsh miasm.

But we find further proofs of the long-continued and silent manner in which malaria exerts its pathological influences in those enlargements of the spleen which occur without specific attacks of sickness. The alterations of nutrition in this organ are so characteristic of malaria that they can scarcely be supposed to depend upon those chances which determine the nature of secondary blood-impurities.

Intermittent Fever--Simple Forms.

The clinical phenomena of intermittent fevers afford strong support to the opinion that this type of malarial attacks illustrates more strongly than any other the primary influence of the poison upon the human system. Fits of ague often occur very shortly after exposure in infected localities, and the persons thus suddenly attacked may present little or no evidence of cachexia before or after the paroxysm. Indeed, they frequently resume their ordinary avocations after the paroxysms, apparently as well as if they had not occurred.

It is therefore my opinion that the pathology of an intermittent fever does not necessarily involve an hypothesis that the attacks are the results of certain changes which the poison undergoes after its inception, nor, on the other hand, that certain perversions of systemic chemistry are required to inaugurate the paroxysms.

In accordance with these conclusions, it seems likely that the phenomena of intermittent malarial fever result from the primary effects of its specific poison exerted directly upon the fluids and solids of the system, and disturbing their functions, and especially the nerve-function.

Those malarial attacks which ensue almost immediately after exposure are principally manifested in persons exposed at points of unusually abundant evolution. The rule of malarial attacks in temperate latitudes is, that they require repeated exposure to infection for their production. The long residence of the poison in the system may render additional doses possible, until a point of saturation is reached which occasions paroxysmal explosions. In these cases the period of incubation is reckoned from the first date of exposure, thus forming the most striking contrast with the incubative periods of the cases occurring almost immediately after exposure.

Whether the quiescent period after exposure to malaria be long or short, attacks are seldom abrupt in their announcement. The symptoms which usually precede pronounced attacks consist, for the most part, in some derangement of the functions presided over by the organic nervous system. Derangement of digestion, vitiated taste, coating of the tongue, loaded urine, and sallow skin are ordinarily found among the prodromic symptoms. Next in succession come feelings of malaise, hot and cold flushes, and those neuralgias which precede and attend malarial paroxysms.

The symptoms of an ordinary or typical malarial paroxysm are so characteristic, as to be generally readily interpreted. Creeping, chilly, {593} sensations over the surface, especially along the spine, yawning, livid coloration beneath the finger-nails, retreat of blood from superficial capillaries, and that consequent papillary elevation which is commonly called goose-skin, comprise the earliest symptoms. Then decided shiverings with chattering of the teeth come on, and the patient asks for blankets to be heaped upon him and hot applications to be made, even though the atmospheric temperature may be decidedly elevated.

Nausea and vomiting are frequent symptoms, no doubt due to the fact that the portal system of blood-vessels is so often the seat of congestion during a chill. No intelligent practitioner can watch a patient during the cold stage of a malarial paroxysm without realizing how important the attendant congestion is as a pathological state. It should first be considered that every chill necessarily implies a condition of congestion in some part of the system. The blood driven from the surface and extremities must be accounted for elsewhere; and the amount of blood which is lost from one part of the circulatory tree must correspond with that accumulated elsewhere. But in treating of the pernicious forms of malarial fevers this question will again receive notice.

In our present state of knowledge we are no more able to explain those perversions of the normal action of the physical forces of the system which occasion the phenomena of a chill than we are to explain how the altered circulation in the first steps of an inflammation is brought about. The theory which Cullen adopted is quite as explanatory and consistent as any which has been promulgated since his time. According to this, a state of spasm of the arterioles and capillaries causes the chill, while the fever is merely the rebound of functions held in abeyance during the chill.

After a variable length of time there occurs a change in these symptoms: the patient begins to remove the blankets which covered him; the face shows signs of returning circulation; the veins of the whole surface gradually fill again, apparently beyond their normal state. But the reaction goes far beyond any normal physiological state. The face becomes flushed and the eyes injected, and the patient complains of headache, thirst, dryness and heat of the surface; he will not permit any covering, and constantly shifts his place in the bed in the hope that some new position may afford him more comfort. Nausea and vomiting are commonly present. If the fever runs high, delirium is apt to occur. The thermometer seldom shows a temperature above 105°, but I have seen 106.5° recorded in the axilla in the hot stage of a paroxysm of simple intermittent fever.

The duration of the hot stage is different in different cases. According to Aitken, the mean duration is three to eight hours.

There is a very old and quite well-supported opinion, that the cold stage is shorter in the quotidian than in the tertian type, and also that the hot stage is longer in the former than in the latter. It may certainly be affirmed that in individual cases of either type there is no fixed relation between the duration of the chill and that of the hot stage.

The decline of the hot stage begins by the appearance of a gentle perspiration, limited at first to the forehead, face, and neck. This gradually extends itself over the surface and increases in quantity until the whole body is bathed in a profuse sweat. During this period the {594} patient's symptoms, both subjective and objective, undergo wonderful mitigation, and, although this stage is usually short, it often happens that by the time it is concluded a restoration to ordinary health seems to have occurred.