those in the liver. It is enlarged with rare exceptions, and
especially so if death has occurred during the febrile stage. Upon the
subsidence of the fever the spleen probably returns to its normal size
more rapidly than the liver. The more common extent of the enlargement
in our own cases was from ten to eighteen ounces, though we found the
spleen in one case weighing twenty-nine and a half ounces and in
another forty-four and a half ounces. In neither of the latter
instances was there any reason to suspect malarial complication. The
most extensive enlargement we have found recorded is sixty-eight
ounces in a case reported by Küttner.[34]
[Footnote 34: _Schmidt's Jahrb._, 1865, vol. cxxvi.]
There is usually a correspondence between the stage and extent of the
splenic and hepatic lesions, but this is not invariable, and one or
the other organ may present a far higher degree of enlargement or much
more intense interstitial changes. It may be mentioned, moreover, that
in some unusual cases the lesions of the lungs, such as ecchymoses and
hemorrhagic infarctions, may be disproportionately marked as compared
with those of either the liver or spleen.
The capsule of the spleen often presents a mottled look, with at times
large purplish ecchymoses; it is apt to be more or less opaque, and
local peritonitis, with thin layers of plastic exudation often forming
friable adhesions with the abdominal wall, may exist.
In one of our cases the capsule presented a small perforation or
rupture, with an exudation of plastic lymph over an area of four by
six inches, and diffuse peritonitis, with effusion of bloody liquid
with shreds of lymph throughout the abdominal cavity. This fatal
termination is fortunately rare, but there are several other instances
on record. The splenic pulp may retain its consistency and firmness,
even in cases that have run a long course; but more frequently it is
softened, and may be almost diffluent. The pulp is often swollen, so
that when cut it projects above the section. The color is darker than
normal, and often is of a deep maroon color. This swelling is due to
enlargement of the blood-vessels, associated with great increase of
the cellular elements of the pulp and with enlargement of the
Malpighian corpuscles.
When death occurred early in the disease we found these bodies grayish
or grayish-yellow in color and of the size of hempseed, so that the
section very thickly studded with them closely resembled shad-roe, and
this stage of the lesion is frequently described in our notes as the
shad-roe spleen. Subsequently, the Malpighian bodies enlarge still
more, and stand out above the section a line or more in diameter, and
of a lighter color; not rarely, several of them come in contact, and
thus form a considerable mass of irregular shape, resembling the
infarctions described below.[35] It is probable that central softening
may occur later in the {417} Malpighian bodies, though we are inclined
to regard the puriform collections frequently found as chiefly due to
the disintegration of hemorrhagic infarctions or of embolic patches.
Of these, hemorrhagic infarctions are by far the most common and
present the familiar appearances. They may be quite numerous,
superficial, or deep-seated, and of variable shape and size. At first
dark reddish, firm, and sharply separated from the surrounding pulp,
they grew reddish-yellow or yellowish later, softened in the centre,
and eventually were transformed into puriform collections. Doubtless,
in a large proportion of cases that recover such infarctions exist and
are slowly absorbed. Ponfick has shown that these are venous
infarctions, the arterioles leading to them being patulous. True
arterial embolism does, however, occur, though much more rarely
(Ponfick, Murchison), giving rise to firm, wedge-shaped infarctions at
the periphery of the spleen, which may undergo degenerative changes
similar to those above described. The resulting abscesses may burst
into the peritoneum, pleura, lung, or bowel. The microscopic
appearances have been most fully described by Ponfick, our own
comparatively meagre observations having accorded entirely with his
subsequent accurate description. The cells of the swollen pulp contain
red blood-discs and pigment, and some present collections of bright
granules. The lymphoid cells of the Malpighian corpuscles are at first
in a state of cloudy swelling with multiplication of their nuclei, and
later show marked granular fatty degeneration.
[Footnote 35: Thus, Wyss and Bock describe "multitudes of minute
abscesses as large as poppy or hempseed, and containing a single drop
of pus."]
The lymphatic glands present no lesions, and the pancreas is normal.
The peritoneum is not affected as frequently as other serous membranes
in this disease. Superficial ecchymoses are, however, quite common,
especially so over the solid viscera; and more rarely effusions of
blood have been found in the subperitoneal connective tissue,
involving the muscular or glandular tissues beneath. We have already
mentioned (p. 406) the occasional occurrence of local peritonitis,
most frequently of the splenic capsule, and also the rare accident of
diffuse inflammation from rupture of the spleen.
The marrow of the bones was carefully examined by Ponfick, who first
called attention to the presence of important changes in relapsing
fever, which have since been confirmed by other observers. These
changes consist in proliferation and subsequent degeneration of the
lymphoid cells of the marrow, with multiplication of the nuclei in the
walls of the minute vessels and fatty degeneration of their coats. As
a result of these changes, spots of puriform softening may form,
chiefly in the cancellous tissue of the extremities of the long bones,
with the production of localized necrosis, and possibly with extension
of inflammation to the neighboring articular cavity.
Considerable space has been devoted to the detailed consideration of
the pathological changes in relapsing fever, partly because we believe
the fact has not been sufficiently recognized that the disease is
constantly attended with important and characteristic lesions. These
consist, in brief, of remarkable changes in the blood; of widespread
ecchymoses and infarctions, which not rarely undergo puriform
disintegration; of hyperplasia and subsequent degeneration of the
Malpighian corpuscles of the spleen, with changes in the cellular
elements of the splenic pulp; of cloudy swelling of the gland-cells of
the liver and kidneys, with a {418} marked tendency to fatty
degeneration; of changes in the marrow of the long bones; and,
finally, of granulo-fatty degeneration of the muscles, and especially
of the heart.
DIAGNOSIS AND RELATION TO OTHER DISEASES.--The entire question of the
diagnosis of relapsing fever is dominated by that of spirillar
infection. Before Obermeier's discovery the differential diagnosis of
the initial paroxysm, and to a less extent that of the subsequent
events of a case of relapsing fever, was attended with considerable
difficulty. But if, as now seems established, immediately before and
throughout the initial paroxysm and subsequent relapses a
characteristic spirillum is to be detected in the blood upon proper
examination, while it rapidly disappears after the crisis, it is
evident that as soon as a suspicion is aroused as to the possible
presence of relapsing fever the question may be settled conclusively
by the microscope.
None the less is it important to consider carefully, but briefly, the
symptoms by which relapsing fever is to be distinguished from various
affections which may simulate it, because even the most experienced
observers admit that the spirillum cannot be invariably detected;
because it is not yet known that a similar organism may not be found
in some other affections; and, finally, because on the outbreak of an
epidemic of relapsing fever, especially in America, where its
occurrence has hitherto been so rare, there is strong probability that
the nature of the early cases will not be even suspected until the
relapse occurs.
Typhus fever often prevails in an epidemic form simultaneously with
relapsing fever, so that it was inevitable they should have been for a
time confused. Their essential non-identity is, however, now too well
recognized to require any lengthy demonstration. The following
statement of the heads of the argument may therefore suffice.
In typhus there is no characteristic spirillum, and the lesions which
are truly characteristic of relapsing fever are totally wanting. There
are convincing differences in the symptoms, course, and results of the
two diseases. There is no evidence to show that when fever has been
imported into a locality by a single case, typhus fever has ever
produced other than typhus, or relapsing other than relapsing fever.
The two diseases often prevail together, and may coexist in the same
house, each preserving its own distinct characteristics; and persons
exposed to the double contagion may contract one or the other, or
first one and then the other at a shorter or longer interval, so that
an attack of either exerts no protective power against the other. It
must be noted, however, that in a large majority of such cases of
successive contagion it is relapsing fever which has been followed by
typhus, while the reverse has been observed much more rarely.
In 1869-70 the two diseases were prevalent in Philadelphia, and the
wards of the municipal hospitals constantly contained a considerable
number of cases of both. Three instances came under our care in which
after recovery from relapsing fever the patient contracted typhus. All
of these patients were employed as assistant nurses, and were
continuously under observation from the early part of their attack of
relapsing fever to the end of the attack of typhus. In one case the
interval of health between the close of the relapse and the onset of
typhus was forty-four days; in the second it was thirteen days. In
both cases the original disease was {419} thoroughly characteristic
and the subsequent attack of typhus was typical. In both death
followed, and the post-mortem examination verified the above
statement. The third patient had severe relapsing fever, from which he
recovered and returned to work, though with pains in the legs,
shoulders, and forehead. After an interval of apparent health of
eleven days he developed a well-marked attack of typhus, which
terminated on the twelfth day in recovery. It may be added that
although typhus is not of frequent occurrence in any portion of North
America, there have been a number of epidemics unattended with a
single case presenting the features of relapsing fever.
Between well-marked cases of the two diseases there should be no
difficulty in making a prompt diagnosis. Relapsing fever is
distinguished from typhus clinically by the severity of the initial
chill; the rapid elevation of the pulse and temperature; the
comparative infrequency and mildness of cerebral symptoms, despite the
intense fever; the severity of the gastric symptoms, nausea and
vomiting; the enlargement of the liver and spleen, with marked
abdominal pain and soreness; the frequency of jaundice, of epistaxis,
and of other hemorrhages, and of anæmic murmurs over the heart and
large vessels; obstinate insomnia; vertigo; peculiar rheumatoid pains
and perversions of sensation; the frequency of sweating during the
high pyrexia; by the occurrence of crisis, subnormal temperature,
apyretic interval, and relapse; the rarity of measly eruption and of
bed-sores; the frequency of pneumonia, diarrhoea, ophthalmia, oedema,
and desquamation as complications and sequelæ; the usual occurrence of
abortion in pregnant females; the protracted course of the disease,
and its remarkably low mortality despite the severity of the symptoms,
except in cases of complicated or typhoid type; and, finally, by the
modes in which death occurs. Of course to this must be added the
specific result of examination of the blood in relapsing fever.
Doubt will arise only in very rare cases where a measly eruption
appears on or before the fifth day of relapsing fever, with headache
and mild delirium, but without severe gastric symptoms, epistaxis, or
jaundice. If no relapsing fever were prevalent at the time, such a
case might well be regarded as one of mild typhus until the crisis and
the relapse disclosed its real nature. But if the two diseases were
known to be prevalent in the community, examination of the blood would
properly be made at once and the diagnosis be established.
The diagnosis between ordinary cases of relapsing fever and typhoid is
readily made by the gradual onset and peculiar course of the pyrexia
in the latter disease, as well as by the frequency of delirium, of
abdominal distension, and of diarrhoea, and by the characteristic
eruption. The occurrence of epistaxis, bronchial irritation, and
splenic enlargement is common to both, and an eruption of small
rose-pink spots has been noted by some observers (Carter, pp. 194,
317). But jaundice, enlargement of the liver, hypochondriac pain and
soreness, excessive nausea and vomiting, severe rheumatoid pains, and
numbness and tingling of the extremities, are very significant
symptoms of relapsing fever. Attention has already been called to the
grave type of relapsing fever in which the typhoid state is fully
developed, and to the fact that in such cases the pyrexia is often
modified, the onset less abrupt, the crisis imperfect, and the
interval occupied by an irregular post-critical {420} symptomatic
fever. It is altogether probable that such cases have not rarely been
regarded as of true typhoid character; and indeed the attempt has been
made by Griesinger to establish as a separate and independent
affection, under the name of bilious typhoid fever, a group of cases
which close examination seems to show to be chiefly composed of grave
complicated relapsing fever with a certain proportion of true typhoid
fever, complicated with jaundice.
The recognition of the bilious typhoid type of relapsing fever is
based upon the history of the case; the mode of onset; the greater
severity of the pains, arthritic and abdominal; the early appearance
and intensity of the jaundice; the more marked enlargement of the
liver and spleen; the marked tendency to hemorrhages from various
surfaces; the peculiarities which careful study of the temperature
curve will show, especially about the time of crisis; the rarity of
eruption; the characteristic spirillum;[36] and the totally different
anatomical lesions, which are, unfortunately, often demonstrable, as
this form of relapsing fever is fatal in from 33 to 50 per cent. of
cases.
[Footnote 36: As first demonstrated by Motschutkoffsky.]
Since the discovery of the spirillar test for relapsing fever it may
be said that Griesinger's bilious typhoid must be stricken from
medical nosology as an independent affection.
The case of Charles Hood, on page 396, is a good example of the
bilious typhoid form which occurred not rarely in the Philadelphia
epidemic.
Murchison points out that, owing to the frequent occurrence of
jaundice in relapsing fever, this disease has been mistaken for yellow
fever by such good observers as Graves, Stokes, and Cormack.
Difficulty in diagnosis would be likely to arise only in regard to the
bilious typhoid type of relapsing fever, and since its clinical
history has become so well known, a mistake is not likely to occur.
The geographical distribution of the diseases is widely different.
Yellow fever is influenced powerfully by season and temperature, while
relapsing fever is independent of both. Negroes are but slightly
liable to yellow fever, while relapsing fever attacks them with
special violence. Yellow fever is not contagious, but infectious, and
second attacks are extremely rare; relapsing fever is one of the most
contagious of the zymotic diseases, but one attack does not protect
against a subsequent one. The mortality, the anatomical lesions, the
course of the pyrexia, the leading clinical symptoms, are all widely
distinct in the two affections; and, finally, no spirillum has been
found in the blood in yellow fever. Yellow fever is an extremely fatal
disease; the ordinary form of relapsing fever has a mortality of 2 to
10 per cent.; the bilious typhoid form, one of 33 to 50 per cent. In
yellow fever the spleen is but slightly enlarged, and the liver is
pale and softened; in relapsing fever the liver and spleen are greatly
enlarged, and there is great tenderness over the hypochondriac region.
In yellow fever albuminuria is much more common, and the urine more
frequently suppressed, than in relapsing fever.
The sudden onset, the severe headache and pains in the limbs, the
vomiting, jaundice, epigastric tenderness, enlargement of the liver
and spleen, occasional epistaxis, hematemesis, or hematuria, absence
of characteristic eruption, liability to herpes facialis, pneumonia,
and diarrhoea; the occasional occurrence of remissions in the pyrexia,
and even of more or less fully-developed chills for several successive
days during the initial paroxysm or {421} the relapse, suffice to
explain the difficulty which may arise in distinguishing the bilious
form of relapsing fever from bilious remittent fever. But the latter
disease arises exclusively from malaria, and is therefore powerfully
influenced by season and locality; is not contagious; does not present
anything approaching to the crisis, the apyretic interval, or the
abrupt relapse of relapsing fever; presents pigmentary changes in the
blood, instead of the spirillum; and lesions of the spleen and liver
totally unlike those characteristic of relapsing fever; can be
promptly controlled by antiperiodic doses of quinine, and therefore
should have a mortality far less than that of the grave form of
relapsing fever. It is not necessary to pursue this subject further,
but a reference to the temperature charts of Carter[37] or of
Litten[38] will show that in some epidemics single paroxysms
resembling those of quotidian ague might occur during the interval
between the initial paroxysm and the relapse, or a series of two,
three, or more such paroxysms of quotidian or tertian type might
represent an entire relapse. Such phenomena are wholly uncontrollable
by quinia, and are presumably dependent upon irregularities in the
specific infection, instead of upon a blending of malaria with the
poison of relapsing fever. There is some ground for believing,
however, that those who have recently passed through an attack of the
latter are highly, perhaps unusually, susceptible to malarial
infection, as we have already seen they are liable to contract typhus.
[Footnote 37: _Op. cit._]
[Footnote 38: _Deut. Arch. f. klin. Med._, xlii. 1874.]
The chill, the sudden and high fever, the acid sweat, the high-colored
urine, the intense pains and soreness, and the occasional murmur over
the heart, will in some cases of relapsing fever suggest the idea of
severe rheumatic fever, with illy-developed articular inflammation and
with a tendency to hyperpyrexia. The urgent danger presented by the
latter condition and the necessity for immediate recourse to cold
baths and large doses of quinine or of the salicylates, render it
highly important that no such error of diagnosis should be made. It
will usually be avoided readily by observing that in relapsing fever
there are great nausea, repeated vomiting, insomnia, peculiar
formication of the extremities, jaundice, early enlargement of the
liver and spleen, with abdominal pain and soreness, and a tendency to
epistaxis; and, further, that despite the high temperature, cerebral
symptoms such as result from rheumatic hyperpyrexia are not
threatened, except in grave typhoid cases or just preceding the
crisis.
The onset of relapsing fever may suggest forcibly the invasion period
of small-pox, with its marked rigors, high fever, lumbar pain, aching
in the head and limbs, nausea and vomiting, and if the patient is
known to have been exposed to the contagion of both diseases a
diagnosis would be impossible until the third day. But such a dilemma
can rarely occur, and under ordinary circumstances the patient's
antecedents will enable a correct opinion to be formed.
Severe cases of simple febricula with marked gastric disturbance may,
as remarked by Jenner, closely simulate relapsing fever; and the same
is true of attacks of acute gastro-hepatic catarrh, with severe
headache, sharp fever, cholæmic eye, epigastric tenderness, and
frequent vomiting. Of course there is no danger under ordinary
circumstances of these simple conditions being regarded as relapsing
fever, but when the latter is prevalent in epidemic form it is
probable that the mistake is frequently made. {422} Although an
immediate diagnosis might be possible only by microscopic examination
of the blood, the peculiar clinical symptoms of relapsing fever would
soon be found wanting, and suitable treatment would bring the simpler
affection under control.
Acute yellow atrophy of the liver occurs chiefly in pregnant women,
though it is also met with in men and children; but it is so rare that
should a case of it come under observation during the prevalence of
relapsing fever there is considerable danger that its nature would be
overlooked. It resembles relapsing fever in the occurrence of jaundice
and other signs of hepatic disorder, of delirium, and of a tendency to
hemorrhage from various surfaces. The temperature, however, is more
moderate, and does not exhibit the sudden remission of relapsing
fever; the liver is usually demonstrably diminished in size; severe
nervous disturbances, such as convulsions followed by stupor and then
by coma, are more constant; while the occurrence of spirilla in the
blood of relapsing fever and of leucin and tyrosin in the urine of
acute yellow atrophy serves to distinguish completely the two
diseases. Acute yellow atrophy is, moreover, invariably fatal.
With ordinary care there is but little danger that any of the local
complications of relapsing fever will so absorb attention as to lead
to a neglect of the specific general disease, so that the cerebral
symptoms should be readily distinguished from the onset of any acute
intracranial affection; the parotitis which occasionally appears early
in the disease should not be confounded with idiopathic mumps; and so
for other complications. There is far more danger, indeed, lest some
of the complications may be overlooked; and this is especially true of
pneumonia, one of the most frequent and most important of them all.
Its occurrence is the cause of the supervention of grave typhoid
symptoms or of the modification of the normal course of the pyrexia in
so many cases that nothing but a systematic daily examination of the
lungs will avert serious oversights.
MORTALITY AND PROGNOSIS.--The rate of mortality has varied in
different epidemics from 2 or 3 to 24 per cent. Murchison shows that
out of 2115 cases admitted to the London Fever Hospital during a
period of twenty-two years, and embracing two distinct outbreaks, only
39 proved fatal, making 1.84 per cent. mortality. Adding to these the
results of Scotch and Irish epidemics, a total of 18,859 cases, with
761 deaths, is reached, giving the rate of mortality for Great Britain
as 4.03 per cent. The great Indian epidemics studied by Carter gave
111 deaths out of 616 cases, equal to 18.02 per cent. Recent German
epidemics have given from 5 to 10 per cent. The above rates are
obtained where all the cases observed during an epidemic are included.
If, however, the mortality of the ordinary form of relapsing fever is
computed separately from that of the bilious typhoid form, it does not
exceed 2 to 5 per cent., whilst the mortality of the latter form rises
to from 33 to 50 per cent., or even higher.