Chapter XXIII: Part II: , Showing Predominance of Malarial Element . . . . 617 (22)

Contagion is, however, the essential cause of the spread of relapsing fever when the virus has once been developed. It seems clear from the distinct periods and from the widely-separated localities in which different outbreaks of relapsing fever have occurred that its special poison is capable of being called into existence or activity by favoring conditions. Murchison held the belief that it was very intimately connected with, if not generated by, destitution, and, as already stated, much evidence exists to show that the disease is most apt to break out after periods of scarcity; but no just and convincing proof exists that destitution, any more than over-crowding and other depressing influences, can actually engender a specific contagium capable of being transported to great distances and of originating widespread outbreaks of the specific disease among differently situated populations. It appears necessary to assume the existence of some unknown special virus which finds its suitable nidus for development in the conditions attendant on filth and overcrowding, and which attacks with greatest facility the systems of those who are enfeebled by want and depressed by vitiated air. When once this specific poison has been called into active existence, however, there can be no doubt as to the fact that it can be carried by fomites, and that it is given off from the bodies of relapsing-fever patients so as to affect any who may approach. Although a few observers have doubted this contagiousness of relapsing fever, the evidence in its favor is overwhelming. In many epidemics, as in Philadelphia in 1869, its contagiousness is at least as intense as that of typhus fever. A single case may, indeed, be admitted to a healthy family among the better classes or into the wards of a well-ventilated hospital without propagating the disease, although striking cases of contagion are on record where a patient has communicated the disease to all the members of a family favorably situated and living at a distance from any other possible source of contagion. On the other hand, if admitted to an overcrowded and filthy lodging the disease is apt to spread rapidly. Wyss and Bock report seventy-one cases as having occurred in a single lodging-house during the course of the Breslau epidemic of 1868, and in Philadelphia single houses in several instances furnished more than a score of cases, and several short streets more than one hundred cases each.

In the Philadelphia Hospital twenty-three persons lying sick in the wards with other affections contracted relapsing fever from the patients {373} admitted with that disease; two of the visiting staff, five resident physicians, and nine nurses also suffered attacks of varying severity. This corresponds with the general experience of those connected with fever hospitals during the prevalence of relapsing fever.

As in the case of typhus and other contagious diseases, the distance at which relapsing fever can be contracted by direct contagion through the atmosphere is a very short one, not exceeding a few feet at most.

The poison may be carried by fomites. Instances are on record where persons having visited infected districts have conveyed the disease to others at a distance without contracting it themselves.

When rooms which have been occupied by relapsing-fever patients are subsequently occupied by other persons, these are very liable to acquire the disease. Parry relates two remarkable cases in which relapsing fever was transported to a distance by infected clothes; and it has been more than once observed that during epidemics of this disease laundry-women engaged in washing the clothes of fever patients, but without any means of more direct communication with the sick, were frequently attacked (Cormack, Wyss and Bock).

In connection with the etiology of relapsing fever it is necessary to consider the rôle played by a minute organism which has been frequently detected in the blood of patients suffering with this disease. This spiro-bacterium was first observed in relapsing fever by Obermeier[7] in 1873, and has since been identified as a spirillum or spiroechete. The very numerous observations of Obermeier, Albrecht, H. V. Carter, Motschutkoffsky, Koch, Cohen, Holsti, Enke, Meschede, and others leave no doubt that this peculiar parasite does occur at least very frequently in the blood of patients with this disease. The failure to detect it, which has been reported by several good observers, may readily have been due to the extreme delicacy of the organism, or to the neglect of the proper method of preparing the slides of blood for examination, or to delaying the examination of the blood until after death, when it rapidly disappears. Thus no value can be attached to the negative observations of Rhoads and myself, made prior to Obermeier's discovery, since our method of examination was not sufficiently exact.

[Footnote 7: _Centralbl. f. die med. Wissensch._, 1873, No. 10.]

The following description of the mode of examining the blood, and of the spirillum, is condensed from H. V. Carter's account: It is necessary to employ magnifying powers of not less than 500 diameters. The fresh blood may be examined immediately after obtaining it by pricking the washed finger of the patient. For preservation dried specimens are needed: a very thin layer of fresh blood is evenly spread with the needle over the glass cover, exposed to the weak fumes of a solution of osmic acid, and allowed to dry under protection from dust; the dried film of blood may then be treated with glacial acetic acid or may be stained.

The spirillum [See Fig. 19] is a colorless, slender, twisted filament, which when quiescent has a length of 2.66 times the diameter of a blood-disc (1/1500 to 1/500 inch = 0.012 to 0.043 millimetre). When unfolded they become distinctly elongated. They are very narrow (not more than 1/40000 inch), and present four to ten spiral turns; when fresh they are in active movement and unfold in part, becoming wavy or bent. They {374} resist the action of concentrated acetic acid, and are readily stained by certain dyes. In number, five or ten may be visible in a field or they may be too numerous to count. They have not been detected either in the secretions or in the evacuations. Both Koch and Carter have succeeded in cultivating this special form of bacteria outside of the body.

To judge from the observations thus far made on this difficult question, the parasite is found first toward the close of the period of inoculation or soon after the beginning of the fever, or it may be detected throughout the febrile stage; but shortly before the cessation of the fever it quickly disappears, to reappear at the time of the relapse. There would seem, therefore, to be some close connection between the febrile paroxysms and this organism, and it is not remarkable that many observers have concluded that this spirillum is the essential and specific cause of the fever, and that it is impossible to have this disease present without the appearance of the parasite in the blood; nor that the name spirillum fever has been applied to the disease by Carter.

Such conclusions appear to be premature, however, and we prefer to regard the undoubted existence of the spirillum in the blood of relapsing-fever patients as at present only an important aid in diagnosis, and to await the occurrence of other epidemics and the repetition of careful studies upon this organism, both within and without the human system, before venturing to decide whether it is merely one of the phenomena of the disease or whether it is its true cause and specific contagious principle.

It must be added that both Carter and Koch have succeeded in inoculating monkeys with relapsing fever, and Motschutkoffsky[8] of Odessa, who had the opportunity of inoculating a human being, asserts that he succeeded in producing the disease, and found the incubation period to be not less than five nor more than eight days. Carter also gives an interesting table[9] of six instances of inoculation, four of them by cuts while making autopsies, with consequent development of relapsing fever in each instance. Some allowance must be made for the fact that in all the instances of this series there had been exposure to contagion by close communication with fever patients, though this exposure had existed for several months previously without leading to the development of relapsing fever.

[Footnote 8: _Centralblatt f. d. med. Wissenschaften_, 1876, No. 11, p. 194.]

[Footnote 9: _Op. cit._, p. 403.]

GENERAL CLINICAL DESCRIPTION.--After a period of not less than five or six days from the reception of the contagion the disease begins {375} abruptly with a chill of variable severity, accompanied by headache and aching pains in the back and limbs. The patient feels weak and is often giddy, but is not always obliged to go to bed the first day. Nausea and vomiting are among the earliest symptoms, and distress at the epigastrium, with tenderness, may attend or even precede the chill. Fever quickly follows; the pulse runs up from 110 to 130 in a few hours; the temperature reaches from 103.5° to 106° by the end of twenty-four hours; the pains increase, and there are insomnia and great restlessness; appetite fails; thirst is extreme; the tongue is moist and furred, and the bowels quiet. During the subsequent six days these symptoms persist. The temperature presents a daily remission at some period of the twenty-four hours amounting to one or two degrees, the maximum reached in fully-developed cases varying from 104° to 108°. The pulse continues very rapid, and not rarely exceeds 140; the respirations are hurried and rapid, and cough attends many cases. Delirium is rare, but insomnia, restlessness, headache, and rheumatic pains in the back and limbs may prove constantly annoying. Appetite is variable, more frequently lost; nausea and vomiting are common; thirst is very troublesome; and the bowels are constipated or loose. No characteristic eruption appears, but sudamina are frequently present, since in a large proportion of cases there is more or less sweating, even during the continuance of high fever. Abdominal pain, tenderness in the epigastrium and hypochondria, and demonstrable enlargement of the liver and spleen are almost invariable. The urine is concentrated and dark or bile-stained. Jaundice is a common symptom, though its frequency varies greatly in different epidemics. The same may be said of epistaxis.

While these symptoms are at their height and the patient is suffering severely the paroxysm suddenly ceases, and in a few hours he is entirely relieved. This remarkable crisis occurs usually at the close of the seventh day, but may occur as early as the third or as late as the fifteenth day. It is attended with a critical discharge, copious sweating being by far the most common, though diarrhoea, free epistaxis, or hemorrhage from some other surface may replace it. The patient feels weak and languid; the temperature and pulse have fallen below the normal, and remain so for a day or two. Soon there is a rapid improvement in the appetite and the appearance of the tongue, and the patient regains strength day by day, and often feels so well that it is difficult to persuade him that he must avoid exertion and exposure. The enlargement of the spleen subsides rapidly, that of the liver more gradually; epigastric tenderness subsides, but in many cases some degree of it persists for several days. This interval or apyretic period lasts about a week, when, again without warning or provocation, the patient relapses, and is seized abruptly with the same set of symptoms which attended the first attack. This relapse does not usually last more than three days (one to five are the limits), and is terminated by a similar crisis, after which a slow convalescence is entered upon, or else after an apyretic interval of some days' duration a second relapse ensues, and this may, in rare cases, be in turn followed by a third, fourth, fifth, or even sixth similar relapse. In addition, it must be noted that many serious complications are liable to occur. The total duration of the disease thus varies from eighteen to ninety days. Convalescence is often tedious, and there are many troublesome sequelæ. {376} The mortality, however, is not great, averaging 5 or 6 per cent. Death may occur suddenly from collapse at the close of the first paroxysm or from heart-clot; it may be produced by exhaustion in protracted cases; or be hastened by any serious complication; or the patient may sink into a typhoid condition, with low delirium, coma, and suppression of urine for several days before the fatal termination.

DETAILED STUDY OF SPECIAL CONDITIONS.--It is usually difficult to determine the period of incubation. In the unique case in which Motschutkoffsky is said to have produced relapsing fever by inoculation the initial symptoms occurred seven days after the inoculation. Wyss and Bock had several good opportunities of determining the minimum period of incubation, and found it to be six days. We may assume that the ordinary period is six to eight days, but that it varies, in accordance with the virulence of the virus or the susceptibility of the system, from four to fourteen days. During this time the patient feels as well as usual, or at most suffers for a day or two from slight malaise, with vague rheumatoid pains, headache, giddiness, and anorexia. In only 13 out of 181 of our cases in which this point is noted was the invasion gradual. Examination of the blood prior to the invasion does not discover any spirilla.

The invasion is usually abrupt and during the daytime; the patient can often fix the very hour of its occurrence, a severe chill attacking him while at work or at meal-time. This is the most common initial symptom (138 out of 168 our cases of sudden invasion); less commonly, obstinate vomiting and nausea or sudden vertigo are the first symptoms (each 8 times out of 168), or violent headache (14 times out of 168), or sharp epigastric pain. Parry also observed that the occurrence of obstinate and profuse vomiting as the initial symptom was especially frequent in children.

The physiognomy is carefully noted in one hundred and seventy of our records. The countenance is often flushed, with watery eyes and anxious, suffering expression. The flush is less dingy and dull than in typhus; the eye is comparatively rarely injected; and the expression is much less dull and stupid than in that disease. In cases where grave nervous symptoms supervene and the typhoid condition is developed the facies assumes all the characteristics of that state.

The livid bronzing of the face, described by Cormack in 1843 and by Carter (Bombay epidemic of 1877), was noticed in a moderate degree in only nine of our cases, and seems to be of infrequent occurrence. When we observed it it seemed due to an admixture of a faint jaundice tinge with a deep flush. Jaundice, as already stated, is of common occurrence, though its frequency varies greatly in different epidemics. It was present in 25 per cent. of our cases, rather more frequently in the negro patients than in whites, and in degree varied from a slight tinge of the conjunctiva and skin to the deepest staining of the entire body. The presence of jaundice in combination with the general features of high fever imparts a most peculiar and alarming appearance to such patients.

With the occurrence of the crisis the flush rapidly subsides and the face becomes pale, or, if the discharges have been profuse, it may appear sunken, haggard, and almost choleraic. Parry described a peculiar puffed, velvety look at this stage, as though the skin had been much thickened and softened at the same time.

{377} There is no characteristic eruption in relapsing fever. In 150 out of 180 cases where the condition of the skin was carefully noted there was no eruption of any kind; in 4 cases there were small roseolar spots, with peculiar subcuticular mottling, which resembled the early stages of typhus eruption, but soon faded away without becoming petechial. A similar eruption was noticed by Murchison in 8 out of 600 cases. It appears from the third to the seventh day of the first paroxysm; it may or may not recur in the relapse, or it may occur then only. Eruptions apparently similar to this have been described by others as quite common in certain epidemics. Carter describes minutely an eruption which was noted in at least 10 per cent. of his Bombay cases, the spots of which were at first small, slightly raised, and pinkish or rose-colored, and which either faded away soon or changed into purplish, more persistent stains. In a valuable report on the Königsberg epidemic of 1879-80, Meschede[10] remarks that roseola was observed in cases complicated by exanthematic typhus, which prevailed simultaneously, but in no case of uncomplicated relapsing fever. While, however, this suggestion may apply to some few of the cases of eruption observed by others, it is certainly inapplicable to the vast majority of them. We also noticed an eruption of pale-reddish, slightly elevated papules in seven cases. It must be borne in mind that persons of such a low class as are the great majority of relapsing-fever patients would naturally be expected to present a variety of cutaneous eruptions from filth or vermin, and that in consequence some of the appearances above described may have been of such origin. It is certain that the bites of either mosquitoes, fleas, or bedbugs may in this disease be followed by persistent reddish papules passing into petechiæ. Apart from this, however, true petechiæ have been quite common in some epidemics, while very rare in others. Parry saw "small spots of purpura" once only, in a delicate girl; and we did not observe petechiæ once in several hundred cases, many of which had extensive internal ecchymoses. On the other hand, they have been found in as much as 30 per cent. of all cases (314 out of 1000 cases, Smith at Glasgow). They do not appear on any fixed day, but are more common in the first paroxysm than in the relapses; and although sometimes associated with a tendency to hemorrhages from other surfaces, they have been so often observed in cases of ordinary severity that scarce any unfavorable prognostic value can be attached to them.

[Footnote 10: _Virchow's Arch._, Bd. lxxxvii., p. 405.]

Vibices and extensive ecchymoses of the surface are of much more grave import, and in cases where fatal sinking is threatened they may appear accompanying a purplish lividity of the countenance.

Herpetic eruptions about the mouth or nostrils were observed in 20 out of 181 of our cases in which this point is noted. They appeared usually toward the close of the febrile stage, and their development was found to have value in determining the approach of the crisis. Bärensprung mentions especially the occurrence of herpes labialis in cases of irregular relapsing fever which bore considerable resemblance to typhus. Sudamina are, as might be expected in a disease attended with so much sweating, of quite common occurrence, though much more so in some epidemics than in others, unless searched for with greater care by the one set of observers. Desquamation was noted in 42 out of 181 of our cases, and {378} invariably at the close of the relapse. It was usually confined to the hands and face, and occurred in the form of comparatively small flakes. This is more frequent than has been the case in most epidemics. Murchison quotes a case in which a piece of epidermis ten inches square separated from the body of a lad convalescent from relapsing fever.

A peculiar odor exhaling from patients with relapsing fever has been repeatedly noticed. A description of this unpleasant symptom, given by Kelly, as quoted by Murchison,[11] accords closely with what was frequently manifest in our own cases: "The smell was peculiar, not fetid or heavy, but somewhat like burning straw with a musty odor." Carter, in describing a similar odor in some of his cases, notes that the skin was not in these instances in a particularly foul state.

[Footnote 11: _Op. cit._, p. 346.]

From what has already been said, it will be anticipated that the variations of the temperature in relapsing fever constitute the most peculiar and characteristic feature of that disease. A careful study of the accompanying charts will convey a more accurate impression than can be given by any description. The temperature begins to rise before the chill is fully developed, and when there is no initial chill the patient may be found within a few hours of the appearance of giddiness and headache with a temperature of 102.5° to 103.5°. Before twenty-four hours have passed it has risen to from 104° to 106°. During the paroxysm the febrile movement is continued, presenting merely a diurnal variation of one to two degrees, sometimes attended with sweating and partial relief of distressing symptoms, the minimum being observed at different hours in different cases, or even in the same case, though more frequently it occurs in the morning.

In a case reported by Parry a chill recurred at the same morning hour on three successive days. Wyss and Bock report some unusual cases in which a brief intermission occurred, with a fall of pulse and temperature to the normal, most frequently on the day before the real termination of the paroxysm. The highest temperature varies from 104.5° to 108.75°; in our cases the highest observed was 107.5°. This occurs, as a rule, on the last day or the day before the last of the initial paroxysm, and Obermeier has observed a sudden rise of four degrees in half an hour just before the crisis. Meschede,[12] however, found the highest temperature on the corresponding days of the first relapse.

[Footnote 12: _Loc. cit._]

The duration of the primary paroxysm is usually six or seven days; but this is subject to considerable variations, as will be seen from the following table of 160 cases in which the duration was accurately ascertained: Initial paroxysm lasted--2 days in 1 case; 3 days in 2 cases; 4 days in 10 cases; 5 days in 19 cases; 6 days in 40 cases; 7 days in 58 cases; 8 days in 18 cases; 9 days in 2 cases; 10 days in 5 cases; 11 days in 2 cases; 14 days in 2 cases; 15 days in 1 case; and Parry, observing the same epidemic, found the duration of the first paroxysm to vary from 4 to 11 days. It is, however, rare for the duration to exceed ten days unless some complication be present.

{379}

With the beginning of the crisis there is a prodigious and sudden fall of temperature, unequalled in any other condition of disease. Within a few hours it may fall six or eight degrees (going down at the rate of 1.5° or 2° an hour); and falls of 12°, 13°, or even 14.4° (Murchison), in the course of twelve hours have been noted. In our own cases the greatest {380} fall was from 107.2° to 95°, or 12.2°; and this is as low a point as is usually reached, though temperatures of 94°, 93°, or even 92°, have repeatedly been observed. Murchison refers to one case in which collapse supervened, where the rectal temperature was 90.6°. In nearly all of our cases a subnormal temperature occurred at the crisis, and lasted for a day or two subsequently, when it gradually rose and remained normal until the relapse, unless some transient complication caused a temporary rise in the interval.

Occasionally, there is no relapse whatever, but convalescence follows {381} the initial paroxysm. This occurred in 10 out of 181 of our cases, and Murchison found that of 2425 cases reported by various authors no relapses occurred in about 30 per cent. Carter describes these under the name of the abortive form, and found them to constitute 23.8 per cent. of all his cases. It is probable, however, that in many cases so regarded either a relapse of very transient duration has been overlooked, or else that an attack of ephemeral fever has been regarded as of specific nature. In ordinary cases the duration of the intermission averages six or seven days, but here, again, considerable variation occurs. In 139 of our cases where its duration could be accurately determined it was as follows:

3 days in 4 cases. 7 days in 64 cases. 11 days in 1 case.
4 " " 3 " 8 " " 22 " 12 " " 1 "
5 " " 12 " 9 " " 9 " 13 " " 1 "
6 " " 12 " 10 " " 9 " 20 " " 1 "

Despite these variations in the duration of the initial paroxysm and of the first intermission, the average date of the occurrence of the relapse in any large series of cases is about the twelfth day from the primary chill.

The relapse is ushered in with the same striking abruptness as the initial attack. The temperature again rises rapidly to 104° or 106°, and then pursues a continuous course resembling ordinarily that of the primary paroxysm. The difference between the maximum of the two paroxysms is rarely more than 1.5° or 2°, though either may be much milder than the other; as a rule, the highest temperature is attained on the last or penultimate day of the first attack. The duration of the relapse averages three or four days, though it may last but a few hours or a single day, and yet exhibit a rise of 5°, 6°, or 7°; or, on the other hand, it may be prolonged to six, seven, or even more days. Lyons, observing the disease in the Crimea, reports some relapses as having lasted twenty-one days, though it is improbable that a greater duration than seven days occurs without the presence of some complication. The relapse usually terminates by crisis, with an abrupt fall to an abnormally low temperature; though we observed at this time, much more frequently than at the close of the first paroxysm, a gradual subsidence of fever, or lysis. Again the patient regains strength and appetite, but in a considerable proportion of cases subsequent relapses ensue. As a rule, the second, third, and later relapses are attended with a febrile movement of shorter duration and of less severity than the first two paroxysms, and are also separated by intermissions of increasing length. Meschede[13] found from a study of 360 cases that the average duration was for the first paroxysm six or seven days; second paroxysm, four or five days; third paroxysm, three or four days; fourth paroxysm, one or two days; fifth paroxysm, one day.

[Footnote 13: _Loc. cit._]

In a remarkable case given in full at page 394, the duration of the paroxysms and intermissions were as follows:

First paroxysm, 8 days; first intermission, 9 days.
Second " 5 " second " 1 "
Third " 1 " third " 6 "
Fourth " 6 " fourth " 8 "
Fifth " 5 " fifth " 9 "
Sixth " 4 " sixth " 10 "
Seventh " 3 " seventh " 11 "
Eighth " 3 " followed by convalescence.

{382} The proportion of cases in which more than a single relapse occurs appears to vary in different epidemics. Murchison found that in 1500 cases reported by various authors a second relapse occurred 109 times (1 out of 14); a third relapse, 9 times (1 out of 166); and a fourth relapse, once. Of 182 cases noted carefully by ourselves, a second relapse occurred 24 times (1 out of 7-1/2); a third relapse, 5 times (1 out of 36); a fourth relapse, once; and in the above-mentioned case six or seven relapses.

It follows that the total duration of the morbid process varies from the average of about eighteen or twenty days, in cases with a single relapse, to forty, sixty, or even ninety days. Of course the occurrence of complications may lead to very great modifications of the febrile movement and of the total duration of the disease.

There are several additional points about the febrile process requiring mention. In all the paroxysms there is a greater tendency to local or general perspirations than is met with in other continued fevers, and occasionally there are rigors or slight chills about the same hour on several days after the invasion or on the day preceding the crisis. It has been noted also that, even when the temperature is very high, the quality of the heat, as judged by the feeling of the skin, is different from that in typhus fever, and that the peculiar pungent irritating sensation known as calor mordax is rarely marked. But a more important peculiarity is the fact that the extreme temperatures (106°, 107°, or 108°) that are frequently observed in relapsing fever for several days in succession do not appear to involve any great increase of danger, and in particular are not attended with the production of the grave nervous symptoms so often met with in connection with hyperpyrexia in typhus and typhoid, and often regarded as the direct result of the exalted temperature itself. This striking fact is of much interest in its bearing on the theory of hyperpyrexia, and may possibly be explained by some marked difference in the conditions of heat-dispersion in these different diseases.

The pulse in relapsing fever is very rapid, and on the whole the rate corresponds with the movement of the temperature. It usually rises above 110, the limits being 90 and 140, the lower rate being noticed in the milder and uncomplicated cases and in subjects of phlegmatic constitution. The pulse rises rapidly at the invasion, and may reach 120 in the course of a few hours. Its maximum is usually noticed when the temperature is highest, shortly before the crisis; and when this actually begins the pulse may fall with a rapidity as remarkable as that of the decline of the temperature. Thus, within twenty-four hours it may fall from 152 to 80, or in even a shorter time from 140 to 54, or even as low as 48 (Obermeier) or 44 (Muirheid), or even 30 (Stillé). While this great fall is often noted, it is by no means constant. In our own cases it was frequently observed that the critical fall in temperature was not accompanied by a commensurate fall in pulse. Thus, at the close of a very severe initial paroxysm lasting nine days the temperature was 107°, and fell in the course of twenty-four hours to 99°, and in twenty-four hours more to 96°; during the first day of this fall the pulse was from 96 to 100, and during the second it fell to 76.

This want of correspondence was more marked at the close of the {383} relapse than of the primary attack; thus, in a well-marked case, where the maximum temperature (105.4°) occurred eighteen hours before the crisis of relapse, the temperature fell in four hours from 104.4° to 96.2°, while the pulse, which was 130, fell in twelve hours to 108, and in twelve more to 92. In another case, in a man aged twenty, the temperature at the close of the second relapse was 106.4°, with a pulse of only 100; after the crisis, as the temperature fell, the pulse rose to 120, and did not descend until the end of twenty-four hours; and later, at the close of thirty-six hours, the temperature was 98° and the pulse 72, lower than which it did not go. Carter[14] states that in the Bombay epidemic it was invariably the case that the pulse did not decline to an extent corresponding with the temperature.

[Footnote 14: _Op. cit._, p. 140.]

During the remainder of the intermission the pulse may be normal, or it may continue accelerated in consequence of some irritative condition; as the time for the relapse approaches it frequently again becomes abnormally slow. In either event it is found that any muscular exertion causes marked acceleration of the pulse.

During the paroxysm the character of the pulse is full and bounding, and there is considerable arterial tension. This is well shown in some of the sphygmographic tracings by Carter;[15] while in one of our tracings from the right radial of a man æt. 32, taken on the fourth day of a severe initial paroxysm, the line of ascent is steep and the summit sharp. During the crisis, and for a day or two thereafter, the pulse may be weak, compressible, and dicrotic, and occasionally irregular.

[Footnote 15: _Op. cit._, p. 103.]

The sounds of the heart and its impulse are weakened, except possibly during the first few days of the primary paroxysm. Blood-murmurs over the base of the heart and along the great vessels in relapsing fever were first noticed by Stokes, and have been frequently observed in subsequent epidemics. They were found in a large proportion of our cases, not rarely in both paroxysms, and during the early stage of convalescence when anæmia was marked; but during the intermissions they are rarely audible, and when the action of the heart was slow they were replaced by prolongation of the first sound.

It must be further noted that the pulse-rate is not a reliable indication of the danger in this disease, since, just as is the case with the hyperpyrexia, extreme rapidity of pulse may be present when the general symptoms denote no unusual danger, and when the patient ultimately recovers most satisfactorily.

There is a remarkable disproportion and dissimilarity between the cerebral and peripheral nervous phenomena in relapsing fever and those familiar to us in typhus and typhoid fevers. We have seen that patients almost invariably complain of headache. When prodromes are present it is commonly among them, and it may be the initial symptom to usher in each paroxysm. When the attack is fully developed headache is usually very severe, and no symptom is more bitterly complained of. It varies in seat and character. More commonly it is frontal or general; occasionally we found it occipital, and still more rarely it was unilateral, constituting hemicrania. It rarely continues during the relapse. Headache of an equally acute and violent character may be present in typhoid, but the headache of typhus is much more dull and contusive.

{384} The mental condition is only exceptionally affected, a circumstance which greatly increases the patient's perception of his sufferings. Delirium is not present in ordinary cases, even though very severe and attended with hyperpyrexia; or if present is limited to the period immediately preceding the crisis, when there may be violent and noisy delirium of transient character. In some of our cases forcible restraint was necessary under these circumstances.

There are numerous instances on record showing the abruptness with which noisy, demonstrative, or even destructive delirium may appear, and the equal suddenness with which in the course of a few hours, or even of fifteen minutes, the patient may become rational and composed. Such attacks resemble hysteroidal spells, and probably occur more readily in patients of a nervous or hysterical temperament. They were certainly more common when the patients had been of intemperate habits; and, further, we had opportunities of noting that the occurrence of relapses in habitual drunkards who had previously suffered with delirium tremens was apt to develop a form of delirium which was to all appearance of that nature.

Delirium of a different and much more grave type may appear in connection with the symptoms of the typhoid state. In some cases this results from the presence of serious complications which induce a state of great prostration, while in others it is associated with great diminution or entire suppression of urine. The delirium under these circumstances is apt to be low and muttering, with a tendency to pass into stupor or profound coma.

Vertigo is present more frequently and in a more persistent form than in any other febrile disease. It was noticed as among the occasional prodromes, and was especially severe for the first few days of the initial paroxysm, though it often continued throughout this stage and recurred with the relapse. Occasionally it was complained of in the recumbent position, but usually it was excited only by a change of position.

Wakefulness was one of the most distressing symptoms in all cases, and appears to have been noted in all epidemics. Although the severity of the pain in various parts of the body and the absence of blunting of the perceptions would naturally cause much loss of sleep, the degree of the insomnia and the obstinate resistance it offers to the action of anodynes are apparently far in excess of what could thus be accounted for. Parry found that several of his patients could take as much as three grains of opium every second hour throughout the afternoon and night without either inducing sleep or causing contraction of the pupils.

Convulsions are rare and of very grave import. They may occur at the period just preceding crisis, when the nervous irritation is most intense, and are then somewhat less indicative of a fatal result than if occurring in the course of the paroxysm, when they are apt to be associated with extreme prostration of the nervous centres, with a tendency to subsequent fatal coma. No connection has been observed between their occurrence and the presence of albumen in the urine.

General tremor is rare, and was observed only in those of our cases where there had been habitual intemperance, with presumably a tendency to delirium tremens. Muscular rigidity was noticed occasionally, but may have been only apparent, being induced by the hyperæsthesia and {385} soreness which were marked in some cases. The hyperæsthesia which was observed was both cutaneous and muscular, and was attended with tenderness of the body of the muscle, and also of the nerve-trunk supplying it. Meschede speaks of opisthotonos as a rare complication in his cases.

Motor paralysis involving single muscles or groups of muscles is occasionally noticed, as of the deltoid or of one arm (Meschede). Parry observed transient loss of power of the extremities in several cases, chiefly during the intermission or the period of convalescence. In one of our cases temporary hemiplegia occurred, with partial loss of sensation on the affected side.

The bladder and rectum are rarely affected, except in cases where the typhoid state with tendency to coma is present. Disorders of sensation are, however, much more common. When motor palsy occurs the affected part may also be the seat of impaired sensibility, while in a large proportion of all cases numbness of the extremities, with or without a sense of tingling, is complained of; out of 182 cases we noted this symptom in 94, affecting the fingers alone in 62, the feet alone in 6, and all the extremities in 25 cases. Cutaneous hyperæsthesia or partial anæsthesia are also occasionally observed. But the most noteworthy and constant symptom of this class are the pains in the muscles and joints which are bitterly complained of by nearly all patients with relapsing fever. They constitute, indeed, one of the highly characteristic features of the disease, and possess a diagnostic value. They may occur among the rarely present prodromes, but usually they appear with the chill and increase in intensity during the paroxysm; they may persist with even greater severity during the intermission, or, if they have then subsided, recur with the relapse, and may constitute one of the most troublesome hindrances to convalescence. It will thus be seen that in frequency, severity, and persistency they differ widely from the aching pains in the extremities complained of in typhus and other specific fevers. They are one of the most potent causes of the extreme insomnia, and are apt to dwell in the mind of the patient so vividly that he dreads each relapse on this account, and consequently looks back upon his attack of relapsing fever as a terribly painful experience. These pains are usually described as rheumatic in character, and several times patients presenting themselves at the hospital on the second or third day of the initial paroxysm stated that they had inflammatory rheumatism. As a fact, we observed the utmost intensity of these pains in a few cases where the patients were of marked rheumatic diathesis. The nape of the neck, the muscles of the trunk or extremities, or the large or small joints, or lower parts of the spinal region, may be the seat. At times they extend along the course of nerve-trunks. In character they are described as a deep intense aching, with occasional severe or excruciating, sharp, lancinating pains. Pressure or movement increases them. The joints are not red or swollen (though swelling may appear as a sequel), and the pains seemed to us rather to be referred to the joints than to be caused by any local irritation therein. As already stated, there is often tenderness of the body of the muscles, and this was especially marked in many of our cases on pressure along the course of the nerve-trunk.

Murchison suggests that they are due to the circulation in the blood of an {386} abnormal substance, such as uric, lactic, or phosphoric acid; but it appears to us altogether probable that they are rather to be connected with states of congestive irritation of the sheaths of the nerve-trunks (early stage of perineuritis), or possibly in some cases of the spinal membranes also. It is true that they are sometimes shifting in their seat and fluctuating in their severity, but this is not inconsistent with the above suggestion, while the widespread irritative processes found in this remarkable disease, the resemblance of these pains and the frequently attendant numbness and tingling to the sensations caused by other forms of perineuritis, and the occasional development of local palsies of a single muscle or group of muscles, all are in its support.

The special senses are acute, sometimes painfully so. The eyes are watery and occasionally injected, but this latter condition is rare and slight in relapsing as compared with typhus fever. At the crisis and for a few days subsequently wide dilatation of the pupils is not infrequently observed. Dulness of hearing was present during the paroxysm in 14 of our cases, and a few patients complained of tinnitus; but these symptoms are not at all common in the disease, although it will be seen hereafter that affections of the middle ear are among its sequelæ.

Debility is not such a prominent symptom as in typhus and typhoid fevers. Patients manage to drag themselves about for several days during the initial paroxysm with all the symptoms fully developed, and after admission to the hospital will often be able to help themselves, or even to rise from bed, unless prevented by the severe pains or the vertigo. Still, there are many cases, not necessarily of very grave type, in which there is a marked sense of weariness and exhaustion, and of course in all cases of typhoid character the prostration is great. It must constantly be borne in mind that even when the patient feels or seems able to sit up he must on no account be permitted to do so, since the occurrence of sudden and fatal syncope is one of the accidents constantly to be apprehended. It is not only during the pyrexia that this precaution must be enforced; we meet with extreme debility during the intermission in some cases, and syncope has followed exertions made at that period as well as at others.

During the paroxysms the respirations are much accelerated, at times to a greater degree than would correspond with the pulse-rate, while at others extreme rapidity of pulse may be associated with moderate elevation of the rate of respirations.

As examples of the relation between temperature, pulse, and respirations we quote the following from our records of adult cases:

(_a_) Temperature, 108°; pulse, 124; respiration, 40. In the relapse; no chest trouble.

(_b_) Temperature, 107.5°; pulse, 120; respiration, 28; falling to temperature, 96°; pulse, 68; respiration, 18, within twelve hours, during which crisis occurred.

(_c_) Temperature, 107°; pulse, 144; respiration, 31. In the relapse.

(_d_) Temperature, 107°; pulse, 108; respiration, 44. Initial paroxysm; no pulmonary congestion.

Temperature, 106°; pulse, 116; respiration, 28. Relapse; no pulmonary congestion.

Temperature, 97°; pulse, 76; respiration, 24. Critical fall; cough, {387} congestion of lungs posteriorly, and left one relatively dull on percussion, but pneumonia did not develop.

In many epidemics bronchitis, hypostatic congestion, and pneumonia are of rare occurrence, while in others, as in Philadelphia in 1870, they are comparatively frequent and lead to serious respiratory symptoms. While the pyrexia was high there was very frequently an irritative dry cough, with the fine crepitant and subcrepitant râles attending congestion and imperfect expansion of the lungs heard at the middle and lower portions of the chest posteriorly. In numerous instances the râles would disappear entirely after a few full inspirations in the sitting posture, just as in the corresponding condition in typhoid fever. But in a considerable proportion of all the cases (fully 35 per cent.) there was more troublesome bronchial cough, associated with sonorous, sibilant and subcrepitant râles, with mucous or muco-purulent expectoration.

Bronchitis of this character was a source of serious annoyance to many patients. In several cases there was impaired resonance at the lower margins of the lungs posteriorly, with imperfect bronchial respiration, but without the symptoms of fully-developed pneumonia. Such conditions were regarded as due to hypostatic congestion, and proved amenable to treatment. Pneumonia occurred in eleven cases out of 200 recorded with reference to this complication. It will be more fully discussed under the head of Complications. It was attended with the usual physical signs, and gave rise to extremely rapid and labored breathing, especially when associated with painful enlargement of the liver and spleen. In a case of double pneumonia, with enlarged and ruptured spleen, the respirations were from 80 to 90 for two days, the pulse being 130 to 136. It was a very fatal complication, death resulting in all but two instances.

Leyden[16] has shown that though the percentage of carbonic acid in the air expired during the pyrexia is diminished, the total quantity exhaled is increased, the proportion being as 1.5 to 1 in the non-febrile state.

[Footnote 16: "U. d. Resp. in Fieber," _Deutsch. Arch. f. klin. Med._, 1870, 536, quoted by Murchison.]

Elaborate investigations have been made of the condition of the urine in relapsing fever by numerous observers, and in the Philadelphia epidemic of 1870 we had the great advantage of being assisted by the distinguished chemist, the late Horace B. Hare, who conducted an extensive series of analyses in our cases. In a number of cases quantitative analyses were continued daily throughout the entire course of the disease.

As a rule, the quantity of the urine is comparatively free during the febrile periods, very scanty at the time of crisis, except in the cases where critical discharges of urine occur, and excessive for some days after the crisis.

Still, there were not rare exceptions, especially to the first of these statements. Thus on four successive days of the relapse of a severe case with delirium, but without albumen, and which ultimately recovered, the analysis gave--

Temperature. Amount in ccm. Sp. gr. Urea in Grm. Na. Cl.
103 400 1024 23.8 2.64
105 300 1025 15.27 1.95
106 500 1024 24.7 4.3
106 to 97 850 1021 24.735 5.525

{388} And in another severe case, also resulting in recovery, the analysis was, for two days preceding the crisis of the initial paroxysm--

Amount. Sp. gr. Urea. Na. Cl.
500 1014 12.9 Traces of albumen.
650 1014 15.85 1.365

After the crisis:

2250 1004 18.9 15.75 No albumen.

And again, in another case at the height of the initial paroxysm, within twenty-four hours of the crisis, no vomiting, purging, or epistaxis being present; temperature 105°; only 500 ccm. was passed of dark reddish colored urine, non-albuminous, and with sp. gr. 1011.

In a fatal case there was total suppression of urine for three days, the catheter drawing off only a few drops of almost pure liquid blood.

When crisis occurs by copious urination the discharges are frequent, large, and of light color and low specific gravity.

The urine of the intermissions is of similar character, and for several days after crisis it is not rare to have 2000 to 2500 ccm. passed. The largest amounts we noted were in a man who recovered, and who passed at the crisis of the relapse and during the following days the amounts here given.

Amount. Sp. gr. Urea. Na. Cl.
1000 ccm. 1010 14.9 2.6
2000 " 1003 20.2 42.8
3550 " 1002 26.625 130.995
2600 " 1002 19.24 27.30
2800 " 1005 24.96 22.66
2500 " 1013 47.25 11.25
2700 " 1014 59.13 7.29

Carter reports a case where the patient continued for two weeks after the relapse to pass 130 oz. of sp. gr. 1002.6.

The amount of urea varies considerably, and is evidently under the influence of complicated conditions. The rule appears to be that it increases during the paroxysms, diminishes during the crisis, increases during the few days following crisis, and then falls off again. These results are stated upon the authority of Murchison, quoting from Pribram and Robitschek, Wyss and Bock, and others. Our own observations, however, while agreeing in the main with these, show that there are numerous and important exceptions, especially to the occurrence of the post-febrile increase in the elimination of urea.

The largest amount of urea excreted in twenty-four hours by any of our patients was 59.13 grammes, or 912 grains, on the sixth day after the end of the relapse, but as much as 74 grammes (1142 grains) have been found.

Deposits of urates were very common in the urine of the paroxysms and of the crisis. The uric acid has been found increased, and so also have the phosphates, crystals of which are frequently found mixed with the urates.

The chlorides diminish during the paroxysms, until just before the crisis their amount is very small, or they may even have disappeared. Immediately after the crisis they reappear slowly or quickly, and even {389} very large amounts may be discharged, as seen in the figures given by Hare's analyses: 2.6 grm. on day of crisis, 42.8 grm. the following day, and the enormous amount of 130.995 grm. on the next day. A copious flow of urine corresponds with great augmentation in the amount of the chlorides.

Bile-pigment was constantly present in jaundiced cases, the amount being proportioned to the depth of the jaundice and the quantity of the urine. Bile-acids have been detected (Carter and Schmidt), and also leucin and tyrosin (Pribram and Robitschek).

Albumen, with or without tube-casts, is not uncommonly found, and traces of sugar have been detected in a few cases. More careful consideration will be given to these under the head of Complications.

The following appearance of the tongue has been repeatedly described, and when present may be regarded as possessing some diagnostic value: The body of the tongue slightly swollen, so as to show the impressions of the teeth, and by the second day the central part of the dorsum covered with a peculiarly white fur, while the edges and a small triangular space at the tip are clean and red. Such a tongue was seen in many cases at the beginning of the Philadelphia epidemic, but later it was present in but a small proportion. We find it specially mentioned in 97 of our recorded cases, or about 50 per cent., the general description being given that it was moist, rather large, with pink, clear edges, and a triangular clear space at the tip, and with heavy white fur in the centre.

Some accurate observers, as Wyss and Bock, did not notice anything peculiar about the tongue, but merely described it as moist and coated with a thick white fur. The tongue often remains moist throughout the case, the coat becoming yellowish, and later brownish. Of course if there is nasal obstruction from epistaxis or catarrh, and the patient breathes through the mouth, the tongue will soon become dry and brown; but in addition, this state of the tongue with sordes on the teeth and lips, appears in a small proportion of cases (3 per cent., Zuelzer; 12 per cent. of our own patients) in conjunction with grave typhoid symptoms.

During the intermissions the tongue clears off quite rapidly, unless marked gastric disturbance persists, but regains its former state as soon as the relapse occurs.

In rare cases the tongue is red and glazed, and Parry and ourselves observed peculiar painful cracks continuing obstinately after the relapse. It is apparent, therefore, that the tongue presents evidences of vitiated secretions, of local catarrh of the buccal mucous membranes, and of the high grade of gastric irritation so constantly attendant on this disease.

As a rule, there is complete anorexia during all of the febrile paroxysm, while in the intermission the appetite soon returns, and is sometimes truly ravenous. We did not, however, observe in any case a voracious appetite during the febrile paroxysms, such as was very often present during the London epidemic of 1843 and the Irish epidemic of 1847, and is particularly mentioned by Murchison.[17]

[Footnote 17: _Op. cit._, p. 360.]

Thirst is constant and intense, and is excited not only by the high temperature, but by the irritation of the stomach; it may continue through {390} the intermission, when natural appetite and the power of digesting solid food have returned.