Chapter XXXVI: Part II: , Showing Predominance of Malarial Element . . . . 617 (35)

HISTORY.--A rapid glance at the interesting historical evolution of rötheln to a specific position among the acute infectious diseases is all that our space will allow. Some writers have attempted to show that this affection was known to the Arabian physicians; but since it is only in comparatively recent times that the contagious epidemic exanthemata in general have been thoroughly differentiated, it is quite likely that the modern conception of it was not held by them nor by other medical men till many centuries later. Indeed, in our day, physicians are yet to be found, though the number is rapidly diminishing, who refuse to recognize in rötheln a distinctive specific malady. Certain German observers in the middle of the last century (De Bergen, 1752; Orlow, 1758) favored the idea of specificity, but these views were soon disputed. In the years following a number of other physicians announced their belief in the specific nature of rötheln, while, on the other hand, various noted authorities still insisted upon its connection with scarlet fever or measles. In 1815, Maton, an English physician, most unequivocally declared that he had observed cases of an eruptive disorder which resembled neither measles, scarlatina, nor roseola, and which was worthy of a new designation.[2] In the second and third decades of this century Hildebrand, and afterward the celebrated Schönlein, taught that rötheln was a hybrid of measles and scarlatina, although at this time Wagner (1834) advocated the essential independence of rötheln. There is no doubt that under the name of rubeola sine catarrho Willan, Bateman, and later writers described what we now call rötheln, for they stated that this variety of measles was not self-protective. Space will not allow of a detailed mention of the various writers who, during the first half of this century, {583} have contended for or against the autonomy of rötheln. It will be well to state, however, that Hebra, from the standpoint of the dermatologist, very properly regards the manifold roseolæ of Willan as in many instances merely symptomatic erythemata, or else as irregular forms of measles or scarlatina; but he also fails to recognize the distinctive features of rötheln. Even so recent a writer as Niemeyer declares that roseola arising from infection consists in a modification of measles or scarlet fever. It is only in the last twenty years that our present exact ideas of rötheln have obtained. For example, while Trousseau[3] asserts that rubeola (rötheln) is a perfectly distinct nosological species, he speaks of the rash as appearing and disappearing alternately for some days, of its frequent recurrence in the same individual, etc. American physicians were almost entirely ignorant of rötheln till within the last ten years, when they were made acquainted with it through the medium of a careful paper on the subject from the pen of J. Lewis Smith of New York.[4] Before this time, however, cases had been described by Homans, Sr., of Boston (1845), and in 1853 and 1871 by Cotting. Very few authorities now dispute the distinctive specific nature of rötheln; which statement is borne out by the fact that at the last meeting of the International Medical Congress, held at London in 1881, there were but two dissentients to this view in the section before which it was discussed.[5]

[Footnote 2: Squire, _Trans. Internat. Med. Congress_, London, 1881.]

[Footnote 3: _Clinical Medicine_, vol. ii.]

[Footnote 4: _Archives of Dermatology_, Oct., 1874.]

[Footnote 5: See especially Kassowitz's paper, "Die Wirkliche Stellung der sogenannten Rubeola," etc., _Trans. Internat. Med. Cong._, 1881.]

ETIOLOGY.--The contagium of rötheln is unknown, but that the disease is contagious has been fully demonstrated by numerous observations of epidemics and sporadic cases. From my own experience I should judge that unprotected persons are not so susceptible of it as is known to be the case under similar conditions in measles;[6] yet cases are recorded which would prove that the contagion may be conveyed through a third person and for some distance. It is probable that the vehicles of contagion are the same as in measles. At what period of its course the disease is most capable of transmission has not been satisfactorily determined. Squire is of the opinion, however, that the disease is contagious before the appearance of the rash, and may continue so for some days or for two or three weeks. Rötheln may be called a disease of childhood for the same reason that the other contagious exanthemata are--namely, that the majority of adults have already been attacked. From an examination of available statistics I am inclined to regard the ages between five and fifteen--the years of school attendance--as the period of life most susceptible of the influence of rötheln, although, of course, no time of life is entirely exempt. The non-susceptibility of sucklings, as in measles, holds true as a rule, although I am in a position to supply exceptions to this from my own experience, as well as from that of others. Sex seems to be without influence in determining liability to the disease.

[Footnote 6: In this regard it resembles scarlatina more than measles, for I have a number of times seen the disease introduced into families, where it would attack one or two of a number equally exposed. J. L. Smith regards it as feebly contagious, and quotes Chadbourne's experience to the same effect. Liveing declares that rötheln is more distinctly epidemic in Great Britain than either measles or scarlet fever, although probably less contagious.]

The period of incubation is not very definitely settled, and, indeed, {584} owing to the generally trivial character of the affection, evidence on this point is difficult to obtain. Taken as a whole, it is probably longer than is observed in measles. According to J. Lewis Smith, in the epidemic observed by him the incubation period varied from seven, or less than seven, to twenty-one days; Emminghaus places it at from two to three weeks; Thomas, from two and a half to three weeks; Squire, mostly a fortnight, the extreme being twenty-one days; Cheadle, from eleven to twelve days.

There is nowhere recorded a trustworthy instance of a second attack of rötheln, although from analogy such an event is to be expected. As in measles, true recurrences of rötheln--that is, the result of a fresh infection--are not to be confounded with relapses. I have never witnessed a relapse, but cases of such a nature have been recorded by other observers (Lindwurm, Emminghaus, Körtlin, Kingsley).

Rötheln is a disease sui generis, and is in no way related to either measles or scarlatina; that is to say, it is not an irregular form of either of these nor a hybrid of them, nor has it ever been observed to propagate anything but itself. That it is not connected with any of the symptomatic skin eruptions--the so-called roseolæ--is proved by its contagiousness and epidemic character. I quite agree with other observers in declaring that rötheln has very little clinical resemblance to scarlatina, and that, on the other hand, in the greatest number of cases the points of likeness are with measles. In the section on diagnosis the differential points between rötheln, measles, and scarlatina will be considered; therefore in this place it will only be necessary to call attention to certain general facts. Thus, aside from the marked divergence in clinical symptoms--incubation, invasion, fever, eruption, complications, and sequelæ--we are at once met by the positive fact that epidemics of rötheln, while always presenting identical features, prevail without regard to the existence of similar epidemics of measles and scarlatina--following or preceding them--and that attacks of rötheln offer no bar to the reception of their contagions, or vice versâ. Literature is so full of examples of this statement that it need scarcely be dwelt upon. By way of illustration, however, the accurate observations of J. Lewis Smith may be quoted in this connection. Of 48 cases recorded by him prior to May 1st in the New York epidemic of 1874, 19 had had measles. Rötheln in the N.Y. Foundling Hospital in 1873-74 followed an epidemic of measles. During the epidemic of 1880-81 the same fact was observed--namely, that a previous attack of measles, as well as scarlatina, afforded no protection from rötheln. I could multiply such examples from my own experience. A single interesting instance may be noted here. A physician asked the writer to examine his child, suffering, as he thought, from measles. A careful investigation revealed a typical rötheln. A number of weeks later an older child got measles, from which the rötheln patient acquired a characteristic attack of the same. In the following year both children were taken with scarlet fever.

The only escape for those who would deny the autonomy of rötheln is in the bold assertion that both measles and scarlatina more frequently recur in the same individual than universal experience and observation will allow; and this leaves them in the dilemma of determining to which group rötheln must be relegated. The hypothesis of the hybrid nature {585} of rötheln cannot be accepted by the pathologist nor the clinician, if for no other reason than that no one has ever seen rötheln generate anything but rötheln, and in no case give rise to either scarlatina or measles.

SYMPTOMS AND COURSE.--As already stated, the probable average duration of the incubation period in rötheln is about fourteen days, varying, however, within the limits of from six to twenty-one days. In this respect rötheln resembles scarlatina more than measles, the period of latency in the latter observing considerable uniformity. No deviations from the general health are to be noted in the incubation stage.

In most cases prodromal symptoms are entirely absent, the presence of the eruption being the first thing to show the existence of rötheln in the system. On the other hand, in a certain proportion of cases there will be present for a half day, or even longer, the general symptoms of malaise, such as slight nausea, some sore throat, pain in the limbs, stiffness of the neck, etc. Vomiting is generally absent. J. L. Smith records one case of convulsions in the stage of invasion, and I have notes of a single case in which the prodromal stage was initiated by mild delirium and fever, the latter anticipating the eruption for two days and a half, and disappearing when the rash came out. As Thomas well observes, however, such cases are anomalous, and indicate either abnormal sensibility on the part of the patient or are due to a secondary rötheln.

Most observers (Emminghaus, Thomas, Smith, Squire) describe the rash as coming out in the order usual in measles--namely, first upon the face, scalp, and neck, then the trunk and arms, and finally the legs. Others (Liveing, Morris) have stated that the rash first appears upon the back and chest. In many cases in my own experience this has seemed to be true. It is quite probable that the situation of the exanthem in rötheln, as in measles and scarlatina, may present various irregularities; but I am inclined to believe that a careful investigation will in most instances show that the normal course of the eruption is as first stated. Now, a marked characteristic of the rash of rötheln is that, unlike that of measles, there is no period, however short, in which its maximum is simultaneous over the whole body; on the contrary, the eruption will have reached its full development upon the face, and will be almost or quite faded again, before the exanthem, for example, will have blossomed upon the trunk, and especially upon the lower extremities. The duration of the eruption upon individual parts of the body is probably from a few hours to half a day at most (Thomas). A consideration of these facts explains, according to Emminghaus, how different observers have described the eruption as having its seat upon this or that region of the body; in other words, it is probable that in a certain proportion of the cases in which the rash was supposed to have begun on the chest it had already run its course upon the face. The eruption usually continues altogether about four days, sometimes disappearing sooner, and sometimes being visible, especially as a fine mottling, for some days longer. So far as the individual lesions of the eruption are concerned, there is no question that they present, within a certain range, varying aspects; and this clinical fact has been taken advantage of by the opponents of the idea of specificity in order to make it appear that the disease is not sui generis, inasmuch as it lacks uniformity of expression. Such an argument wants force when we consider that in making up a given diagnosis we lay stress {586} not upon special, but upon the ensemble of, symptoms. For example, no one would deny to measles an independent position because the eruption, as is well known, may assume this or that form (morbilli lævis, m. papulosi, etc.); on the contrary, we recognize a particular case or series of cases to be measles from a due appreciation of all the symptoms present. So it is to be expected that while the cutaneous lesions will present a certain similarity of feature, as they do, there will also exist minor differences in detail.

In the greatest number of cases in my own experience the exanthem is composed of ill-defined, roundish, punctate macules, without special grouping. These are usually discrete, but in certain situations they may coalesce. The color is of a pale rosy red, quite difficult to describe, but less purplish than in measles, and not so livid a red as in scarlatina. I have occasionally observed large irregular spots not unlike those of measles.[7]

[Footnote 7: According to Emminghaus (_op. cit._, p. 345), the eruption generally forms roseolæ of pin-head, lentil, or small bean size. They are mostly round, sometimes oval, and bordered by well-defined or by blurred edges. The intervening skin is not always unchanged, for here and there we find upon it small dilated blood-vessels, and from the spots processes extend with a certain regularity to other spots in such a way as to give the skin a marbled appearance.]

Thomas distinguishes three types of eruption--one with large spots, which is rare; one with medium-sized spots; and one with small spots. Emminghaus describes a discrete and a more confluent variety. I have observed one case where the maculæ on the back had undergone a vesicular transformation. Others have mentioned this occurrence. Itching of the skin is marked in some cases, and a fine desquamation is observed after the rash, but by no means invariably.

The mucous membranes are implicated to a slight degree in rötheln, but the amount of involvement varies considerably. In some cases that I have observed the catarrh of the mucous membranes has been barely appreciable. As a rule, however, the eyes are somewhat suffused, and there is slight lachrymation and photophobia. Sneezing may be noted, but there is little discharge from the nose. Sore throat is not uncommon, perhaps the most constant feature, and, according to Liveing, is apt to persist after the subsidence of the rash. The fauces are injected, and the tonsils are red and swollen, but with no evidence of ulceration. J. Lewis Smith and others state that the buccal mucous membrane shows a more or less diffuse patchy and spotted redness. The tongue may be, and usually is, covered by a white fur, through which protrude a few enlarged red papillæ. There may be slight cough. Loeri[8] describes the mucous membranes of the pharynx, larynx, and trachea as presenting a spotted or uniform hyperæmia. There is no marked participation of the intestines in the catarrh. Some few writers have noted a transient albuminuria, but it is safe to say that such cases are entirely anomalous, if not, indeed, in some instances, examples of mistaken diagnosis.

[Footnote 8: _Jahrb. f. Kinderk._, xix. Bd., 1 Heft.]

A very constant feature is the swelling of the lymphatic glands of the neck, especially those back of the sterno-mastoid; the swellings may come on before the rash appears. In all the cases that have fallen under my notice this symptom has not been absent in a single instance. Less constantly, and it would seem in proportion to the development of the rash, engorgement of the glands may be noted elsewhere.

{587} There is but slight disturbance of the temperature in rötheln, and when it does occur it is usually limited to the first few hours of the eruption. This has been the rule in my observation, and certainly holds good for the majority of cases. In a minority, varying degrees of fever may be present; thus, the temperature may reach 102° F. or 103° F., and then rapidly sink by the second day of the disease, or, having fallen a degree, it may continue at this point till the subsidence of the rash, or, it is said, may retain its initial height till the end of the disease. During the following week Squire states that the temperature may be readily disturbed--either elevated by exertion or depressed by fatigue or chill. A relapse or recrudescence of the rash may be looked for at this time.[9]

[Footnote 9: Cheadle (_Trans. Internat. Med. Congress_, London, 1881) has reported an epidemic of rötheln of a very severe type, all the symptoms of the disease as ordinarily recognized being very much exaggerated.]

COMPLICATIONS AND SEQUELÆ.--In the vast majority of cases neither complications nor sequelæ have been observed in connection with rötheln. J. Lewis Smith has recorded instances of diphtheritic inflammation as a complication, which, however, as he justly remarks, may, when prevalent, attack any inflamed surface. Pneumonia and bronchitis have been occasionally reported as complicating or following rötheln. Liveing and Duckworth mention albuminuria, but, so far as I know, they are alone in this experience. I have known otorrhoea and ciliary blepharitis to occur as sequelæ. It would not be a matter of surprise that in weakly children various chronic ailments should be set up by rötheln, as by any other disturbance of the general health.

DIAGNOSIS.--There is no other disease which so much resembles rötheln as measles. Especially is this true of atypical cases occurring sporadically. In rötheln the whole course of the disease is much milder than in measles, the incubation is longer as a rule, and the fact of a previous attack of rubeola is of much importance, since we know that recurrences are very rare. In measles there is a prodromic period, having a characteristic temperature curve, and presenting pathognomonic catarrhal symptoms, which precedes the eruption for three or four days; in rötheln the appearance of the rash is often the first sign of the affection. The sore throat of rötheln resembles that seen in scarlatina more than the angina of measles, and the general catarrhal implication of the mucous membranes, so marked a feature of measles, is either absent in rötheln or exists to a very trivial extent. Measles is essentially a febrile disease, having a peculiar type of fever; rötheln may run its whole course without appreciable rise of temperature. As will be seen in the preceding pages, the development and progress of the exanthem of measles differs materially from that witnessed in rötheln. In measles the lesions are larger, more vivid, more angular and indented, more frequently provided with processes, and therefore more apt to assume the crescentic arrangement, than in rötheln. Finally, it must be urged that the tout ensemble of the case should be taken into consideration, and not some special feature of the skin eruption.

The incubation period of scarlet fever is much shorter than in rötheln, and all of the constitutional symptoms are, as a rule, infinitely graver. In scarlatina there is a febrile invasion stage of twenty-four hours; in rötheln, if fever is present at all, it is most generally simultaneous with {588} the rash, and rapidly disappears, while in the former it persists for a number of days longer. Vomiting is common in scarlet fever, rare in rötheln. In scarlet fever the lymphatic glands are notably involved at the angles of the jaw, in rötheln at the sides and back of the neck. Sore throat is a feature common to both scarlet fever and rötheln, but it is very much less marked in the latter. Thomas[10] says that in scarlatina only the posterior parts, the uvula, the arches of the palate and their vicinity are affected, while in rötheln the anterior parts are also affected, and both in much the same degree. In scarlet fever the rash, which mostly begins on the neck and chest, is made up of large patches formed of minute red spots on a bright-red hyperæmic base; in rötheln the eruption is composed of roundish pea-sized macules, with normal integument intervening. In cases of doubt--for example, when the rash of rötheln consists of very small spots which have become confluent--the further development and persistence of the scarlatinal efflorescence, the temperature, the pulse, the angina, and the character of the desquamation must be taken into consideration. The complications and sequelæ are very different in the two diseases.

[Footnote 10: Article "Scarlatina," _op. cit._]

The symptomatic eruptions of the skin which pass under the name of roseola bear no resemblance to rötheln. They usually occur as the result of some trivial derangement of the system or in the course of some primary affection. They are not contagious, the lymphatic glands and the mucous membranes are not involved, and the rash is quite different in character.

PROGNOSIS.--The prognosis of simple uncomplicated rötheln is invariably good. Complications arising in delicate children necessarily affect the prognosis, as would any other disturbance of the general health.

TREATMENT.--Simple cases of rötheln require no treatment, as the patients are rarely sick enough to be confined to bed. Graver forms of the disease must be met by such measures as are indicated by the symptoms present. The after-management must be conducted on general principles having reference to the previous and present condition of the person attacked.

{589}

MALARIAL FEVERS.

BY SAMUEL M. BEMISS, M.D.

In the medical nomenclature of this country the term malaria is synonymous with swamp or ague poison.

Malarial affections, therefore, comprise all those diseases or morbid manifestations which the swamp poison produces in the human organism.

This article is not designed to notice in a systematic manner any of these disorders which are not properly classifiable under the head of malarial fevers. It will, however, be necessary to make such references to the pathology of chronic malarial toxæmia as may serve to explain the influence this condition exerts in occasioning departures from type in the febrile attacks.

When a poison generated outside the human system obtains admission to it, and produces deleterious effects, three questions naturally arise: What is the essential character and natural history of this noxious agent? How does it obtain access to the human system? What is its mode of action when received?

In reference to the first of these questions, it must be admitted that the substantive essentiality of the malarial poison remains as yet undemonstrated. It is true, however, that the attempts at an objective study of this poison by means of the microscope and the cultivating retort point to the conclusion that it is an organism.

Its subjective or analogical study affords quite incontestable evidence in support of this conclusion. The leading features in the natural history of malaria are closely coincident with those of certain known organisms. It requires for its production suitable conditions of moisture, temperature, and a properly circumstanced breeding-place. Within certain bounds these conditions are requisite to the life and perpetuity of all organisms.

Again, when all the above-enumerated conditions correspond apparently in the most favorable degree, their continuous concurrence for a lapse of time is necessary before the poison manifests its presence. It is not improbable that this period of development may differ in different climates, but in this country we assume it to be about thirty days. If these facts related to some noxious organism visible to the eye, no doubt would be entertained that the presence of its germs in the places where it appeared was the indispensable condition. It would then follow that the concurrence of suitable meteorologic and telluric conditions with sufficient time for its growth and maturity were merely accessories to its perfect development. According to this theory, the coincidence of five circumstances is necessary before malaria can be fully matured--viz.: Its own {590} specific germ; suitable soil or pabulum; suitable moisture; suitable temperature; sufficient time for its growth and development.

Certain physical qualities which pertain to the malarial poison can also be profitably made points of subjective study. These are very closely connected with the answer to the second question, or "How the malarial poison obtains access to the human system." They will therefore be briefly noticed in relation to the instrumentality of each in conveying malaria into the system.

The first to be mentioned is ponderability, which the following facts prove that malaria possesses:

Those different atmospheric states which affect the range of diffusion of known air-borne yet ponderable substances exert similar influences upon the malarial poison.

Altitude illustrates the ponderability of malaria by powerfully retarding its diffusion.

High readings of the barometer favor its aërial dissemination.

Fogs, smoke, dust, or floating particles presumably more buoyant than this poison may exert greater or less influence in overcoming the obstacle which ponderability attaches to malaria as an air-borne agent.

Currents of air passing continuously and steadily in one direction over the breeding-places of malaria increase the limits and intensity of toxic range.

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.

The sweating stage terminates a malarial paroxysm. The intermission now begins, and lasts until the inauguration of another paroxysm. The intermission is longer or shorter accordingly, first, as the paroxysm occupies less or more time; and, second, as the interval may affect it. The interval is that period of time which reaches from the beginning of one paroxysm to the beginning of another. It therefore furnishes the basis of classification of simple intermittents into the following forms: quotidian, tertian, and quartan.

Statistics gathered from a great many sources and relating to many countries and climates indicate that quotidian intermittents are more common than tertian. It may then be assumed that the natural type of intermittents is that form characterized by diurnal paroxysms. It must be remarked, however, that if any natural law does exist establishing the quotidian as the typical form of intermittent fevers, it is very often set aside by unknown influences. In certain epidemics the tertian cases preponderate, and under all circumstances convertibility may be witnessed between the various forms.

It is probable that the statistics gathered by the medical staff of the United States Army during the late Civil War afford the most valuable data which we possess touching these points, in so far as they relate to this country. During three years of the war 724,284 cases of intermittent fever were recorded, tabulated as follows:

Quotidian, 370,401 cases, 388 deaths--equivalent to 1047 + deaths per 1,000,000 cases.

Tertian, 318,704 cases, 324 deaths--equivalent to 1007 + deaths per 1,000,000 cases.

Quartan, 35,179 cases, 79 deaths--equivalent to 2245 + deaths per 1,000,000 cases.

It has been remarked by several writers that quartan attacks have a smaller ratio in the Southern States than in other parts of the Union. My observations on this point have not been sufficiently well recorded to make them especially authoritative, but they support such a conclusion.

The morbid anatomy of malarial fevers is more properly discussed in treating of the graver forms, since the paroxysms of simple intermittent do not often occasion death.

TREATMENT.--This must necessarily vary with the stage of the paroxysm and condition of the patient at the time of the first visit.

Let us suppose this to be the incipiency of the paroxysm, or the early part of the cold stage. However little the danger to life from the paroxysm of a simple intermittent attack, the practitioner should not forget that whatever danger does exist is to be ascribed to damages suffered during or in consequence of the chill. There are few exceptions to this rule, and those will be noticed presently. With this fact in view the practitioner's duties are much simplified. He should first endeavor to remove any complications present which tend to aggravate the cold stage. If the chill has come on after a full meal or after eating indigestible food, the stomach should be promptly emptied; otherwise the cold stage will {595} be prolonged and rendered more violent. Large draughts of warm water will frequently produce sufficient emesis. If this should fail, ipecacuanha may be added. The warm infusion of eupatorium perfoliatum answers well as an emetic, producing also a laxative effect. But it is disgusting to the palate, and sometimes prolongs its action beyond desired results. The effect of an emetic in abridging a chill by revulsive action are uncertain, and I avoid resorting to them for this purpose alone in simple intermittents.

The patient's subjective complaints of suffering should receive a due degree of attention. Additional blankets and warm applications should be allowed when solicited. I always discourage hot or heating drinks, except for the purpose just mentioned. I especially oppose alcoholic stimulants, because they seldom do any good in mitigating the chill, oftener aggravating the patient's symptoms during the hot stage, particularly the headache and vomiting, and sometimes directly occasioning perplexing perturbations. For example, I have seen convulsions speedily follow a strong brandy toddy given to shorten a chill.

While the removal of complications is imperatively indicated, it is also important to use promptly those means which are designed to modify and shorten the chill. It is a remarkable fact that all the agents found to be useful for this purpose are such as directly influence nervous function. Opium in some form enters into all prescriptions which I have found efficient in modifying a chill. It is quite efficacious when given alone, but I think its therapeutic energy and certainty are increased by the addition of other agents of the same class. I have often exhibited twenty to thirty drops of chloroform with an equal quantity of laudanum with excellent results. The tincture of opium may be combined with aromatic spirit of ammonia, or with bromide of potassium, or with chloral hydrate. In combination with either of the latter medicines it may be given by rectal injection. If the stomach is intolerant, or by preference because of facility of dosage and quickness of effect, the opiate may be given hypodermically. For this purpose one-sixth to one-quarter of a grain of morphia may be given, together with one-sixtieth to one-fortieth of a grain of atropia. It is rarely necessary to repeat the dose whichever form may be adopted.

After much experience in these methods of mitigating and abridging the chills of intermittent fever, I feel entitled to say that, whether the objects be achieved or not, no injurious consequences ensue.

The conditions of the circulatory and digestive organs are not favorable for the introduction of quinia or of any preliminary purgative which may be supposed to be necessary, and I therefore delay their exhibition. It may be excepted, however, that sometimes a very obstinately irritable stomach or exceedingly vitiated state of the fluids can be appropriately met by gr. x to xx of calomel.

The hot stage of a simple intermittent seldom calls for medical interference on account of excessive temperature. If the headache is very violent or the vomiting troublesome, a subcutaneous dose of morphia will bring speedy relief. The existence of high temperature does not contra-indicate its use.

I am in the habit of giving opium in the following combinations:

Rx. Morphiæ Acet. gr. ss;
Liq. Ammon. Acet. fl. oz. iv. M.

S. Two tablespoonfuls every second hour.

{596} Or, occasionally, the following:

Rx. Sodii Bicarb. gr. xx.
Morphiæ Sulph. gr. i;
Aquæ Lauro-Cerasi,
Aquæ Menth. Pip. _aa._ fl. drachm iv. M.

S. Teaspoonful pro re nata.

I do not limit the use of opiates in the hot stage to old and infirm subjects, as Dickson suggests, but give them in all cases where vomiting, headache, or other neuralgias are excessive, or where unusual restlessness and jactitation are present.

The propriety of giving purgatives as a preliminary measure of treatment during the hot stage must be determined by symptoms connected with individual cases. In the majority of cases falling under my care purgatives are avoided. When regarded necessary, gentle purgation is solicited by administering bitartrate of potassium in lemonade or by combining mild mercurial doses with antiperiodics when these latter are resorted to during the fever. In some cases a very furred tongue, sallow skin, and costive bowels indicate more active purgatives, which may be exhibited during the febrile stage.

The most important question which relates to medication during the hot stage is in respect to the administration of antiperiodics. It may be safely stated that practitioners of this country were the first to adopt this method of procedure in malarial fevers. Here it has been well demonstrated that a competent dose of quinia, given during any part of the hot stage, is so often followed by the defervescence of the fever that it would be illogical to attribute the change to any other cause. Sometimes the remedy fails in producing this result; then excessive physiological disturbances may follow, and perhaps some general aggravation of the patient's symptoms.

There are four different circumstances, each of which, in my opinion, calls for the exhibition of quinia during the hot stage, whether the fever has reached its maximum point or not:

_First._ If the period which has elapsed since the beginning of the paroxysm is so considerable that further delay might prevent sufficient cinchonism to intercept the next accession.

_Second._ When the fever is so excessive that quinia should be given as an antipyretic.

_Third._ When apprehensions exist that the fever will occasion some complication or accident.

_Fourth._ When the tongue is clean and the state of the system is favorable to absorption.

The hot stage is not usually favorable to absorption, and consequently the economical use of quinia must not be attempted. It should be given in doses varying from ten to twenty grains, preferably in solution. I may remark that I have seldom failed in getting good results from the powder or pills if lemonade or some fluid facile of absorption be given at the same time. The mixtures previously formulated answer this purpose very well, and at the same time mitigate the disagreeable physiological effects of the quinia.

Allusion has been made to certain symptoms occasionally connected {597} with the hot stage which involve danger. Convulsions are among the most important of these. They occur most often among children, but occasionally with adults. They should be met by chloroform, cold to the head, hypodermic injection of morphia, and cupping or leeching if the face is flushed, the eyes injected, and the carotids pulsating forcibly.

The sweating stage may be classed with the intermission in respect to medication. No time should be lost in securing cinchonism. From the moment the sweating stage announces itself the fluids of the system begin to resume their normal physiological functions. Absorption from the intestinal surfaces is again restored, and remedies may be administered with confidence in their effects.

The question is now no longer whether antiperiodics should be administered, but how they shall be given. Many practitioners prefer exhibiting them in one large dose; others think it better to give them in repeated small doses. I have usually adopted the latter method. Beginning with the sweating stage, I give three grains of quinia every hour or two hours, until eighteen grains have been taken. This would occupy periods of five to ten hours to complete the doses, ordinarily quite a sufficient length of time to obtain cinchonism before the advent of another paroxysm. If the physician elects to give his antiperiodic in one or two large doses, he should not trust to so small an amount as eighteen grains. Allowance must be made for the loss incident to the probable over-taxation of the power to dissolve and receive a large amount into the circulation.

Purgation should not be induced to a sufficient degree to hurry the quinia off before absorption takes place. Some practitioners favor the employment of adjuvants to the quinia. Very few of these have appeared to me to be of service except opium. A very convenient formula is a solution of quinia in peppermint-water by addition of dilute sulphuric acid, in such proportions that fl. drachm j of the solution shall represent five grains of quinia and seven and a half drops of laudanum.

But, however we may boast of the efficacy of cinchona as the anceps remedium for malarial diseases, we are forced to admit that it is not certainly an immediate cure, and very commonly fails in producing a permanent curative effect. If we could in all cases discern and remove the impediments to its immediate or temporarily curative action, its claims to be regarded as a practical specific would be undeniable. It is probable that these impediments generally rest upon the fact that either the remedy does not gain admission to the circulation or that some complication exists not within the range of its therapeutic action.

The failure of cinchona to cure a malarial attack in such a permanent manner that it shall not be liable to return is probably owing to the incompetent action of the drug because of its transitory stay in the system as compared with that of the malarial poison. Some objections apply to this theory, because when the succession of intermittent attacks is broken by quinia and it is continuously administered afterward, the paroxysms occasionally recur in spite of its presence in the system. These objections may be answered by pleading that under these circumstances secondary blood-poisons precipitate the attacks, and cinchona should not be expected to cure these conditions.

The best methods of practice I know of to prevent a recurrence of {598} intermittent fever after having interrupted the succession of attacks are, first, to continue the cinchona for at least forty-eight hours, giving at least three three-grain doses a day. After this no medicine need be given except such as may be required to correct chronic toxæmic states of the system or to act as blood-restoratives until such time as prodromes of another paroxysm may exhibit themselves. At the instant when these manifest themselves ten to fifteen grains of quinia in solution should be taken. In order that no loss of time should occur in applying this method, I always advise patients to keep a solution of quinia within immediate reach. The following prescription has sometimes appeared to effect a permanent exemption from recurrence of paroxysms:

Rx. Ferri Redacti gr. xl;
Acid. Arseniosi gr. j;
Quiniæ Sulph. gr. xl;
Ol. Pip. Nigr. gtt. x. M.
Ft. pil. No. xx.

S. One pill three times daily.

It seems sometimes to occur that intermittent attacks so impress the nervous system that they become, like epilepsy, more liable to recur because of an established habit. I have known chills to occur when the ears were ringing with quinia. Strychnia fails to arrest them; arsenic has more value, but frequently fails. Pure nitric acid, properly diluted, in doses of six to ten drops, given every four to six hours without regard to the stage of the paroxysm, succeeds more often than any medication I have ever resorted to.

Before dismissing the subject of the treatment of simple intermittent fever it may be proper to mention that I have made trials of cure by carbolic acid, administered by mouth and subcutaneously, and also of the sulphites, with no results worthy of recommendation.

Remittent Fever.

The difference in definition between the words remittent and intermittent expresses the clinical distinction between these two forms of fever in a very satisfactory manner.

Remittent fever exhibits oscillations of temperature regulated as to hours of recurrence by laws similar to those which govern the periodic returns of intermittent fever; but there is no complete defervescence of the fever. While the lowest angles of the fever curve approximate the normal body heat more or less closely, they never decline to a standard of apyrexia.

That remittent fever is a malarial disease, produced by a cause identical with that which produces intermittent fever, is well proven by the following facts:

First. Cases occur in close relation with cases of intermittent fever in populations similarly exposed to malaria, and at the same periods of the year.

Second. The two forms of disease are readily convertible, the one with the other.

In non-tropical countries remittent fever cannot be regarded as the {599} natural type of malarial fevers. At least, it may be affirmed that the proportion of cases which begin as remittent attacks is so small that we are warranted in looking upon them as departures from type. In the United States army during the years 1861-66, inclusive, there occurred 286,490 cases of remittent fever. The fatal cases were 3853, being a mortality-rate of 13,450 per 1,000,000 cases. By comparing these statistics with those of intermittent fever recorded in a previous section it will be found that remittent fever is more than twelve times as fatal to life as the simple intermittent forms.

If we accept this view of the pathology of remittent fever, it is of interest to the sanitarian or practitioner to endeavor to arrive at the causes which occasion these departures from type. Some of these are undoubtedly extraneous to the system, and relate wholly to circumstances affecting the malarial poison as a disease-producing agent. Increased quantity of malaria is well understood to enlarge the ratio of remittent cases. There is also strong presumptive evidence supporting the hypothesis that different annual crops of malaria vary in respect to the noxious qualities of this agent. The same presumption relates to all crops produced in certain localities as contrasted with others. Other causes which determine remittent rather than intermittent attacks are personal to patients. They may be classed as follows:

First. Unusual personal receptivity or impressibility to malaria may exist, either because of some constitutional idiosyncrasy or of some state the system at the time of exposure.