B. B. Y., medical student, was much exposed to the contagion of

relapsing fever in the wards of the Philadelphia Hospital during the

spring of 1870, and in May had an attack apparently of this disease,

which, however, subsided in four or five days and was followed by no

immediate relapse. He continued his attendance at the hospital during

the remainder of May and the whole of June; in July took a trip to the

South, where there was no relapsing fever prevailing, and after

exerting himself for several days during intensely hot weather, he

became sleepless and much prostrated. He returned home, and after

recovering from the fatigue felt quite well for about a week, until 3

A.M., August 1st, when he was attacked with a severe chill, followed

by great insomnia, obstinate vomiting, intense headache, especially in

the back of the neck, occasional sweating, violent fever, recurrence

of very severe chill the following day at 11 A.M., epigastric and

hypochondriac tenderness, decided jaundice, costive bowels, and

scanty, high-colored urine. This paroxysm lasted till the morning of

August 9th, when severe vomiting took place, followed by sleep, during

which crisis occurred by drenching sweat lasting several hours.

Appetite and strength soon began to return, though some jaundice

persisted, and by August 17th he felt able to drive out a short

distance, and retired feeling somewhat fatigued. He awoke with pain in

the back of the neck, which continued increasing till 11 A.M., August

18th (second paroxysm), when a severe chill occurred, lasting three

hours and followed by the same train of symptoms, including jaundice,

which persisted five days, till Aug. 23d, when crisis again occurred

by sweating. On the 24th he felt well enough to use slight exercise,

which was followed by prostration and by a return of chill (third

paroxysm) the next day at 11 A.M., with subsequent headache, fever,

irregular sweats, etc., lasting but one day. Again felt well until

Aug. 30th, when he was attacked (fourth paroxysm) at 11 A.M. with

severe chill, lasting three hours, followed by severe paroxysm,

lasting six days, till Sept. 5th, when crisis again occurred by

sweating. Again felt well for eight days, until Sept. 13th, when the

fifth paroxysm occurred, lasting five days, ending Sept. 18th by

critical sweating. This was followed by an intermission of nine days,

until Sept. 27th, at 11 A.M., when the sixth paroxysm occurred,

lasting four days, and less severe than the preceding ones. This was

followed by an intermission of ten days, till Oct. 11th, when the

seventh paroxysm occurred at the same hour of the day, and lasted

three days. He then went sixty miles from home to a fine, pine-bearing

district, and enjoyed an intermission of eleven days, when the eighth

and {395} last paroxysm occurred at the same hour, and lasted three

days, until Oct. 25th. His convalescence was very satisfactory, and he

was enabled to resume his studies by the middle of November. No

sequelæ occurred. In 1878 Dr. Y., who had been working very steadily

with a rapidly-growing practice, was attacked with severe typhoid

fever, with grave nervous symptoms and with albumen and tube-casts in

the urine, and died on the twelfth day.

It will thus be seen that in this unusually protracted case there were

seven distinct relapses, one of which was brief and interrupted one of

the regular intermissions, while the rest were all severe.

Duration of

1st paroxysm, violent, 8 days. 1st intermission, 9 days.

2d " violent, 5 " 2d " 1 day.

3d " less violent, 1 day. 3d " 6 days.

4th " severe, 6 days. 4th " 8 "

5th " severe, 5 " 5th " 9 "

6th " less severe, 4 " 6th " 10 "

7th " less severe, 3 " 7th " 11 days,

8th " mild, 3 " followed by convalescence.

The total duration of the case, which was entirely free from

complications, was therefore ninety days.

VARIETIES.--The foregoing clinical description prepares us to

appreciate the varieties of relapsing fever that may be said to exist.

They consist of--

The abortive form, in which a single paroxysm of variable length and

severity occurs, terminating in a critical fall of temperature and

usually with some critical discharge, but not followed by any relapse.

There can be no doubt of the existence of such cases, although they

are not common; and at times the paroxysm is so slight that were it

not for the known exposure of the individual to the prevalent epidemic

influence, in the absence of any other adequate cause, the case might

readily be regarded as one of non-specific febricula. The caution

must, however, be borne in mind as to the occurrence of relapses of

such extreme shortness of duration (less even than twenty-four hours)

as to readily escape notice unless a careful watch be kept for their

detection.

The ordinary or typical form, including the cases with one or two

relapses, presenting the usual variations in the severity of the

symptoms and in the duration of the paroxysms and of the

intermissions.

The multiple or protracted form, if it be thought desirable to thus

particularize cases presenting an excessive and unusual number of

relapses, as three, four, five, six, or even seven.

The grave or subintrant form, which is designed to include the highly

congestive form of Cormack and the bilious typhoid of Griesinger and

Lebert.

Under another heading (see relations to other diseases, p. 420) we

shall give reasons for regarding the bilious typhoid fever of

Griesinger and Lebert as merely a form of relapsing fever, with which

a certain proportion of cases of true typhoid fever complicated with

hepatic catarrh may have been included.

The characteristics of this grave subintrant form are as follows:

Jaundice, occasionally absent, but usually present in an intense

degree; marked enlargement of the liver and spleen; a tendency to

hemorrhage from various mucous surfaces; extreme prostration;

defective or suppressed {396} secretion of urine; hypostatic

congestion or inflammation of the lungs in a large proportion of

cases; dry brownish tongue; low muttering delirium, often passing into

stupor or coma; hiccough; imperfect crisis; and a continuance of some

morbid phenomena, so that merely a remission occurs to separate the

paroxysms; and a high percentage of mortality. The great modification

of the intermission which is so highly characteristic of typhoid

relapsing fever is doubtless due in chief part to the serious local

lesions developed, and seems to justify the name of subintrant as

above suggested. The course of such fever is well illustrated by the

following case, in which the characters of typhoid relapsing fever

were present in the highest degree, death occurring on the fifteenth

day:

Charles Hood, colored, æt. 28, of temperate habits, was taken ill on

April 5, 1870, after malaise lasting thirty-six hours, with fever,

nausea and vomiting, headache, and general aching throughout body; and

was admitted to the hospital April 6th. There was already marked

jaundice, and epistaxis had occurred; there were also insomnia;

wandering delirium; extreme tenderness over the liver and spleen, both

of which were enlarged; dryness of tongue, vomiting, and distension of

the abdomen. These symptoms continued, his condition becoming daily

more aggravated. Restless delirium alternated with heavy sopor. The

jaundice grew deeper. Marked digital formication existed, but the

arthritic pains were not so severe as in ordinary cases. The tongue

was dry and of a red orange color. Profuse epistaxis occurred on the

seventh day of the disease, requiring plugging of both anterior and

posterior nares, and followed by great prostration. A gradual fall in

the temperature occurred during the sixth, seventh, and eighth days,

reaching 99° on the latter day. During this decline the delirium

ceased and the mind remained merely dull; the jaundice decreased, as

did also the tenderness of the hypochondriac zone. The pulse and

respirations improved, and diarrhoea ceased. The improvement was but

brief; for about eighteen hours he lay apyretic, with cool hands and

feet, and with eyes closed and mind dull but free from delirium. Fever

then reappeared and with the ascent of the temperature the unfavorable

symptoms recurred. The relapse lasted but two days, and was followed

by irregular decline of fever till death occurred on the fifteenth day

of the disease. Obstinate hiccough appeared on the eleventh day, and

continued, accompanied with occasional vomiting on the fourteenth day.

Delirium alternating with sopor reappeared. Jaundice again became

marked, and again there was extreme tenderness over the liver and

spleen. The pulse grew small and feeble, the respirations shallow and

labored, with an expiratory moan. Cough began on the twelfth day, and

was soon followed by the physical signs of pneumonia of the lower lobe

of both lungs. The urine continued free from albumen. The patient sank

into deeper coma, and died on the fifteenth day. Post-mortem

examination showed highly-developed characteristic lesions of the

spleen and liver, with red hepatization of lower lobe of both lungs.

There was no affection of the glands of Peyer. The course of the fever

is shown in the following tracing (see Fig. 22).

[Illustration: FIG. 22. From a case of the bilious typhoid or grave

subintrant form of relapsing fever.]

COMPLICATIONS AND SEQUELÆ.--As would be anticipated from what has been

said of the wide range of the symptoms and of the remarkable course of

the temperature in relapsing fever, there are many complications and

sequelæ liable to occur, and which require special consideration.

{397} They may be classified according as they affect the febrile

movement, the state of the blood, or one or other of the groups of

organs.

We have already described the various irregularities presented by the

febrile paroxysms and the intermissions, and no further allusion need

be made to mere variations in length, severity, or number of the

former. In rare cases, however, a peculiarity is presented, usually in

the first intermission, which is difficult of explanation. About

twenty-four hours after an apparently complete crisis, with a fall of

temperature to a subnormal point, there may be a sudden and rapid rise

or rebound of temperature to 104° or 105°, attended with distressing

symptoms of high fever, but lasting only twenty-four or forty-eight

hours. A good example of this is given in the case described on page

394; and Carter[18] cites several examples of it terminating either in

recovery or in rapid death. He asserts that examinations of the blood

during such post-critical febrile rebounds invariably showed an

absence of spirilla, so that in his opinion such fever must be

considered non-specific. Their explanation seems difficult, since the

pyrexia is too brief to be associated with any local inflammatory

complication.

[Footnote 18: _Op. cit._, p. 172.]

More frequent and serious is the protracted post-critical pyrexia

which we have already described as modifying the interval, so as to

produce a subintrant type by maintaining continuous though irregular

fever until the accession of the relapse, unless cut short by death.

This post-critical fever is non-specific, is unattended with spirilla

in the blood, and is to be associated with the extensive irritative

processes in the liver, spleen, kidneys, lungs, and other parts that

are present in these grave and {398} complicated cases. It is to be

noted that the course of those paroxysms which terminate in lysis

indicates that they may represent a milder type of the above process.

The peculiarities of the delirium, amounting sometimes to maniacal

excitement, which attends some cases of relapsing fever, has been

fully described.

Less common are the following: mental hebetude, lasting some days or

even weeks after the close of the last paroxysm, or, as in a case of

Carter's, gradually increasing mental feebleness, terminating in

imbecility. In such cases suspicion must arise of the occurrence of

some local lesion of the membranes or substance of the brain.

Partial palsy is mentioned by numerous authors as occurring during or

shortly after attacks of relapsing fever. Paralysis of one or both

deltoids has been noted, the latter by Cormack, who saw it continue

ten days after the patient was well in all other respects. Temporary

paralysis of the forearm (Douglas) or of the whole arm (Parry,

Meschede) has been observed; and Parry also describes loss of power in

the legs lasting for one week. In one of our cases temporary loss of

power of the left arm and leg occurred, attended with such impairment

of sensibility that the woman had to feel for the fingers of the left

hand to assure herself of their existence. This loss of power occurred

during the initial paroxysm, and gradually passed away, but she was

unable to stand alone on the thirty-first day of the disease. In a

case reported by Tennent[19] facial palsy was developed six days after

the second crisis.

[Footnote 19: _Glasgow Med. Jour._, May, 1871, p. 379.]

Various explanations have been offered for these local palsies, but,

as already stated (see page 386), it seems probable that they are

referable to morbid conditions of the nerve-trunks, or, less commonly,

of the spinal cord. It must be noted, however, that in a certain

number of autopsies serious intracranial lesions are found, which are

evidently the results of the attack of relapsing fever. These consist

of abscess of the brain, meningitis, and specially cerebral

hemorrhage. This was present in one of our cases, but Carter found

copious hemorrhage in no less than 8 out of 54 autopsies, and in 5

others there were minute capillary cerebral hemorrhages. Still, in

nearly all the cases of large hemorrhage we have found recorded the

effusion was upon the surface of the brain, and this, combined with

the absence of true hemiplegia from the forms of paralysis noted in

relapsing fever, and the transient character of these palsies, makes

it clear that they are not to be explained by any considerable

cerebral hemorrhage. On the other hand, however, it must be admitted

that an additional possible cause of them is to be found in minute

hemorrhage into small areas known to govern the movements of certain

groups of muscles. Again, we have had occasion to note the occurrence

of both thrombosis and embolism among the lesions of relapsing fever,

and it is evident that either of these accidents, if involving a

comparatively small branch of a cerebral vessel in certain motor

areas, might cause transient paralysis, such as has been described.

Nor can we fail to see that, while such symptoms as the delirium,

mania, coma, or subsequent mental impairment may receive other

explanations, it is possible that they may arise from similar

processes of minute hemorrhage, thrombosis, or embolism involving

other parts of the brain.

{399} The frequent occurrence of severe rheumatic pains in the muscles

and joints during the course of the disease has been dwelt upon (p.

385); but in some cases they persisted during the intermissions and

for a considerable time after all other symptoms of disease had passed

away. Occasionally they greatly retarded convalescence by interfering

with exercise and sleep. These pains were mostly in the legs, and were

increased by exercise, and also seemed to be influenced by changes of

weather. Patients who suffered thus were also liable, after exposure

or in consequence of severe atmospheric changes, to sharp attacks of

similar pains elsewhere, and especially in the course of the

intercostal nerves. Occasionally violent and persistent headache

follows the disease, not improbably associated with changes in the

membranes of the brain, although in other cases severe neuralgia

occurs in consequence of the anæmia which may remain in an intense

degree after the fever. Troublesome numbness and soreness of the soles

of the feet and of the palms of the hands, increased by pressure, has

been noted as a sequel persisting for several days or weeks.

Affections of the special senses are not rare. The most remarkable

among these is the affection of the eyes, which is apt to occur far

more frequently in connection with relapsing fever than with typhus or

typhoid. The proportion of cases in which this sequel appears varies

greatly in different epidemics. In the British epidemics of 1826 and

1843, when this form of post-febrile ophthalmia was first accurately

described by Mackenzie of Glasgow, it was very frequent; and it was

equally so in Finland in 1867-68, when Estlander[20] again carefully

studied it.

[Footnote 20: "U. Choroiditis nach Febris Recurrens," _Arch. f.

Ophth._, 1869, Bd. xv., Abth. ii., 108.]

On the other hand, so far as can be stated in regard to a sequel which

may appear after convalescence is far advanced and the patient

discharged from medical care, it was very uncommon in the Philadelphia

epidemic of 1869-70. This ophthalmia may occur during the course of

the fever, but more frequently it begins during convalescence, and

even some months after convalescence has been established. It occurs

in patients of both sexes and at all ages. Usually it affects but one

eye, but both may be attacked simultaneously or consecutively.

Patients who were very ill-nourished and debilitated were most apt to

present this sequel, and Murchison regards previous starvation as one

of its main causes. The exciting cause and true pathology appear

obscure as yet, however, and the existence of a neural origin is not

improbable. In some cases the ophthalmia has seemed to result directly

from exposure to cold. Among our own patients, as already stated, eye

symptoms were less common and severe. A careful record of 184 cases

was kept in reference to this question. Several patients complained of

diplopia during the febrile stage, and one asserted that every object

appeared fourfold to him. Conjunctivitis of moderate severity, usually

associated with otorrhoea, occurred in about 5 per cent. of our cases;

it generally affected only one eye, and occurred in a few instances as

late as the third week after the relapse. In a few cases (four) also

there was dulness of vision in one eye, noted during the course of the

disease and persisting for some time after convalescence began. In

only one instance, however, did permanent impairment of vision ensue,

and this man had passed through a violent attack of the fever with

unusually grave nervous symptoms. {400} It left him with optic

neuritis on the right side, which induced partial atrophy of the nerve

and great limitation of the field of vision. Meschede reports

intraocular affections in 6 cases out of 180 specially examined,

though it is not certain that such affections were directly connected

with the febrile process. Ocular ecchymosis occurs in a small

proportion of cases, especially of the graver types.

Dulness of hearing is not so common in relapsing fever as it is in

typhoid. It was present in 14 out of 184 of our cases during the

course of the disease, and in a few instances partial or almost

complete deafness in one ear persisted after convalescence, owing

doubtless to a slight affection of the middle ear. In one case marked

deafness appeared suddenly on the day after the termination of the

relapse by crisis. Meschede[21] found disease of the middle ear in no

less than 8 per cent. of his cases.

[Footnote 21: _Loc. cit._]

Purulent otorrhoea from one or both ears is of more frequent

occurrence, and without any special exciting cause may present itself

at any time during the course of the disease or more commonly after

the relapse. In the same manner purulent coryza may occur.

The eruptions occasionally present during the fever have been

described. Bed-sores from pressure are much less common than in

typhus, but are met with in a small proportion of cases. As a rule,

they are of moderate size and heal quickly. Superficial gangrene of

the lips, nose, and ears has also been noted in rare cases (Zuelzer)

in connection with gangrene of the extremities, probably from

embolism. The occasional occurrence of painful boils, of abscesses in

the cellular tissues (Wyss and Bock), and the more rare occurrence of

erysipelas may be mentioned among the sequelæ.

As already stated, the severe pains in the joints and members which so

frequently occur during relapsing fever are, as a rule, unattended by

any redness or swelling of the joints. In rare cases, however, there

is effusion into the joints during the fever, or more commonly there

are attacks during convalescence which simulate subacute rheumatic

arthritis. Such attacks may last but a few days, but in several of our

cases there was painful swelling of the knees, wrists, and fingers

which persisted for several weeks after the fever, being attended with

slight crepitation on motion, and altogether behaving like subacute

rheumatism.

As would be expected from the severity of the fever, the marked

disorder of digestion, and the lesions of the spleen and liver in

relapsing fever, anæmia is a common sequel. In cases where there has

also been free hemorrhage, usually in the form of epistaxis, the

anæmia may indeed reach an intense degree.

The cardiac murmurs which have been described as present in a certain

proportion of cases are dependent upon the blood-changes, and when the

anæmia is extreme these murmurs are also audible over the large veins

and the pulmonary artery, and persist after convalescence is fully

established.

Oedema of the lower extremities occurs in a considerable number of

cases. It is clearly due in part to the anæmia, but the cardiac

debility which follows the fever is also largely concerned in its

production. It was, indeed, marked in some of our cases where no

anæmic murmurs existed, but where there was great nervous and muscular

debility. {401} Usually limited to the feet and ankles, it

occasionally extended above the knees, and in one case, where great

anæmia and debility from fever and over-exertion coexisted, there was

oedema of the hands and wrists, with great distension of the legs up

to the hips. It is not associated with albuminuria as a rule, and

yields readily to treatment and rest, in the course of a few weeks.

Hemorrhages from various surfaces have already been mentioned, and a

full account given of epistaxis, which is by far the most common form.

Bloody vomiting has been noticed in a small proportion of cases in

various epidemics. It varies in amount, but is always attended with

great gravity of the attack, and usually is followed by fatal results.

It occurred in four of our cases, two of which presented also black

stools containing altered blood, and suppression of urine; while in

another it occurred at the close of the first relapse, and during the

second relapse was copious and repeated. In this case it was attended

with alarming symptoms of collapse, from which the patient rallied,

and after a desperate struggle recovered.

Blood may also be discharged from the bowels in such large amount as

to constitute actual hemorrhage--a symptom of great gravity; or in

small quantity and completely altered, so as to impart an inky black

color to the stools--a condition not necessarily attended with urgent

danger; or, finally, there may be frequent bloody dysenteric stools.

Hemorrhage has also been observed from the uterus, from the kidneys,

from the ears, and from the old cicatrix of a syphilitic chancre.

Hemorrhage occurred in 87 out of 183 of our cases, or in nearly 50 per

cent. It was from the nostrils in 82 cases, from the uterus in 1 case,

from the stomach in 4 cases, and from the cicatrix of a chancre in 1

case.

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