Extracted from the 
TRANSACTIONS OF THE COLLEGE OF PHYSICIANS OF 
PHILADELPHIA. 
THIRD SERIES, VOLUME IX. TWO CASES 
OF 
MALIGNANT ENDOCARDITIS. 
By 
J. H. MUSSER, M.D., 
PHYSICIAN TO THE PHILADELPHIA HOSPITAL, ETC. 
[Read March 2, 1887.] 
Both the cases included in this report have been 
named malignant endocarditis, although one of them is 
without the warrant of a microscopical examination. 
The clinical course and macroscopical appearances indi- 
cate such to have been its true nature, however. I 
venture to bring it before you thus labelled, to excite 
criticism, if necessary, and to ask your attention to one 
of the manifold phases of this interesting disease. 
The case was under the observation of Dr. J. Henry 
Musser, of Lancaster County, and seen by my father, 
Dr. Benjamin Musser, in consultation. It occurred in 
their practice, in 1878. I recall the case both from 
conversations and letters concerning it at the time. 
Unfortunately, the notes of the case in Dr. Musser's 
possession have been mislaid. His memory and memo- 106 
MUSSER, 
randa in his case-book feebly supply the deficiency; 
fortunately, we have the morbid specimens. 
Case I. Rheumatism; embolism of large vessels; cardiac mur- 
murs ; gangrene; chills and fever; death. Autopsy: vegetations 
on mitral leaflets ; emboli in brachial and femoral arteries.-H.R., 
male, set. twenty-three, laborer, consulted Dr. J. Henry Musser, 
June 25th, on account of rheumatism. He was visited by his physi- 
cian the first week in July once, the second week four times, and the 
third twice. On the first of August grave symptoms set in, and on 
the third of September he died. It will be observed, therefore, that, 
in July, H. R. was not very ill; in fact, he continued at light work 
on his farm, and on the first of August was in the harvest field when 
the first embolus manifested itself. During that month he had rheu- 
matism, and, for a short time before August 1st, chills and fever. 
August 1. Sudden severe pain occurred in the right brachial 
artery. Could not be removed to his house at once on account of 
collapse. Dr. Musser saw him, and found the pulse absent at the 
wrist, the hand cold and cyanosed. Two days subsequently the 
femoral artery became plugged, much pain being occasioned at the 
time. The circulation in neither arm nor leg was ever restored, 
and gangrene ensued. Attention was at once called to the heart, 
and a distinct systolic murmur was heard at base and apex. During 
the month an irregular fever, with irregularly recurring chills, was 
present. Death took place from exhaustion, September 3d, thirty- 
three days after serious symptoms set in. 
At the autopsy the vessels were plugged with emboli and thrombi, 
as exhibited in the specimens. The heart was enlarged by dilatation, 
and on the posterior cusp of the mitral valve soft fungating vege- 
tations grew. Some of the chordae tendineae were surrounded by 
vegetations. The auricular surface of one cusp was rough, and 
minute ulcers were present. Fibrin clung to the vegetations, and 
recent clots filled the cavities. The aortic valve and the right heart 
were normal. There was no atheroma. 
Remarks.-Without doubt, in this instance, malm- 
' 7 o 
nant endocarditis was associated with rheumatism, and MALIGNANT ENDOCARDITIS. 
107 
the type was essentially pyaemic. One might presume, 
however, that the so-called primary rheumatic symptoms 
were pyaemic in nature, or that the cardiac lesions super- 
vened secondarily to the gangrene. The teachings of 
the autopsy do not sustain either supposition. The 
absence of old cardiac and vascular lesions, and the 
general integrity of the organs, preclude the possibility 
of pyaemia. The normal condition of the arteries (ab- 
sence of atheroma), the absence of primary blood 
dyscrasiae, or of any cause, save cardiac, for the emboli, 
defeat the second supposition. 
Case II. Malignant endocarditis', chills, irregular fever, sweats ; 
cardiac murmur and pain; vomiting and diarrhoea; marked em- 
bolic phenomena; jaundice; death. Autopsy: proliferative bacte- 
rial endocarditis confined to the mitral valve; emboli of skin, 
mucous membrane of mouth, of stomach, and of intestines, of 
spleen, kidneys, peritoneum and endocardium ; embolus and throm- 
bus in left iliac vein.-M. S., female, 8et. twenty-seven, white, Ger- 
man, married, admitted to Philadelphia Hospital August 26, 1886. 
At the same time her husband and children were admitted for a 
febrile complaint, thought to be of malarial origin. M. S. had been 
ill about six weeks, of an irregular fever, also said to be malarial. 
At this time she was nursing an infant which had been born one year 
before. The labor was natural, and she had a good getting up. 
Since birth of child M.S. has not menstruated. Three years pre- 
vious to this illness she had an attack of malarial fever, and at one 
time had rheumatism of the leg. She never had any other ailment, 
was strong and hearty, and of temperate habits. 
The family history of M. S. is very good. Her parents and 
several brothers and sisters are living. One sistei- died of pneu- 
monia ; the cause of death of another is unknown. On admission it 
was noted that the patient was prostrated and complained of chilly 
sensations, she sweated profusely, and suffered from nausea. The 
tongue was clean and moist; the bowels loose, five movements in 
twenty-four hours, thin and greenish in color; the nausea had disap- 108 
MUSSER, 
peared in twelve hours; tenderness of the epigastrium was observed, 
but none in the iliac fossae. The spleen extended, in the axillary 
line, from the sixth rib to the margin of the ribs. There was no 
eruption. Both cheeks were flushed. The skin and mucous mem- 
branes were pale, the hands quite anaemic. She was somewhat 
emaciated. The mind was clear. The lungs and heart were normal; 
the latter rapid in action, and rather feeble. Milk diet, stimulants, 
and quinia ordered. 
Sept. 2. My resident, Dr. Dorland, detected a cardiac murmur 
two days ago, and to-day the following is noted: General symptoms 
and appearances about the same. Apex beat of heart in fifth inter- 
space in nipple line; impulse moderately feeble; no thrill; pul- 
monary second sound accentuated ; high-pitched systolic murmur at 
apex transmitted, to axilla ; no murmur at aortic orifice. Pulse rapid, 
small, and feeble. No cough; no dyspnoea. Ulcerative endocar- 
ditis suspected. 
Sth. The fever has continued in spite of quinine. The patient 
sweats profusely throughout the day, but not at night. Her anaemic 
appearance is striking. She is quite cheerful, but is evidently losing 
flesh and strength. The diarrhoea continues. The cardiac murmur 
has increased in intensity during the past forty-eight hours, and can 
be heard loudly at the angle of both scapulae, louder at the right. 
Marked tenderness on pressure, and some pain complained of in 
the third left intercostal space. At the base of the right lung 
impaired resonance, and fine, moist, crepitant rales are observed. A 
few rales are heard at the right apex also. Short, high-pitched, 
jerking inspiration and prolonged expiration are detected at the right 
apex, and high-pitched inspiration at the left. 
12tA. Two days ago two small purpuric spots were observed 
on each upper eyelid, and to-day hemorrhagic infarcts are seen 
all over the trunk and on the upper extremities, pin-head to split- 
pea in size, bright red, not disappearing on pressure. Hemor- 
rhages in the ocular and palpebral conjunctivae of both eyes at 
inner and outer canthus. Rapidly losing flesh and strength. 
Sweats continue. Abdomen distended in epigastric and umbilical 
regions ; large wavy impulse in epigastrium. Nausea and vomiting 
recurred the past five days ; fluid dark, greenish tinge. The vomiting MALIGNANT ENDOCARDITIS. 
109 
occurs in the morning. Diarrhoea continues. Spleen readily felt 
below the margin of the ribs, tender. Lungs have cleared up. 
No cerebral symptoms. Heart's action irregular. Pulse small, 
feeble, rapid, dicrotic. Tenderness behind the sternum. Impulse 
(systolic) in second, third, and fourth left interspaces. In second 
interspace to the left of sternum very perceptible thrill. Systolic 
murmur not so loud as it has been at apex. Ovei' third rib, left 
auricle, loud, booming systole, with " grinding " murmur. In second 
interspace to the left of the sternum loud, rough, high-pitched mur- 
mur. Pulmonary second sound muffled. Murmur over tricuspid not 
so distinct as at mitral, and probably transmitted; aortic murmur 
low in pitch, conducted from base. No oedema. Mind clear. 
13£A. Physical signs as above. Cardiac dulness extends from the 
left edge of the sternum one inch to the left in the second interspace. 
It extends in the third interspace two inches, and in the fourth 
three inches. Apex beat in nipple line. Intensity of murmur 
greatest in second interspace. Chill this morning. Urine scanty 
and high-colored, and contains blood and epithelial tube casts in 
abundance, and a small amount of albumin. General symptoms the 
same. Extreme prostration. 
Vith. Chill at 7 a.M. A little more drowsy than formerly; no 
delirium. Murmur in second interspace not so distinct. New capil- 
lary infarcts in abundance about the neck. Vomiting and diarrhoea 
continue. Infarcts in lips and on end of tongue. Conjunctivae 
slightly icteric. Dyspnoea severe for half an hour at 2 p.m. Parti- 
ally collapsed state, with gasping and sighing; excessively rapid 
pulse ; stimulants relieved the patient. At 11. p.m. a second attack. 
During the day very irritable, and latter part of day drowsy. Died 
at 2 a.m., September 15th. 
The following record indicates the daily fluctuations in tempera- 
ture. The pulse record was not preserved, but from first to last it 
was rapid, 120 to 130 per minute. 
Aug. 25, p.m., 99.3°. 26^, a.m., 100.4° ; p.m., 103.2°. 27tA, 
a.m., 101.1°; p.m., 103°. 28tA, a.m., 101.1°; p.m., 101.3°. 29^, 
a.m., 102.1° ; p.m., 102.3°. 30tA, a.m., 103° ; p.m., 100.4°. 31^, 
a.m., 100.1°; p.m., 101°. 
Sept. 1, a.m., 102°; p.m., 101.2°. 2d, a.m., 102.1°; p.m., 110 
MUSSER, 
102.3°. 3d, a.m., 102.4°; p.m., 99°. 4^, a.m., 99°; p.m., 101.4°. 
5th, a.m., 101.2°; p.m., 105°. 6th, a.m., 99.2° ; p.m., 105°. 7th, 
a.m., 101.1°; p.m., 97°. 8th, a.m., 97.2°; p.m., 99.3°. 9th, a.m., 
101.2° ; p.m., 105°. Wi, a.m., 105.4° ; p.m., 99.2° (chill at 6.30 
A.M., and 9 a.m. temperature taken). 11th, A.M., 101.3°; p.m., 
99.3°. 12tA, a.m., 101.4° ; p.m., 99.3° (chill, 7.30). 13tA, a.m., 
102.3°; p.m., 102°. WA, a.m., 100.2° ; p.m., 100.4°. 15th, a.m., 
99.2°. 
During the course of her illness careful search was made for local- 
ized purulent inflammation. The pelvic organs were normal, the 
bones were evidently free from disease, and inflammation of the 
middle ear was not detected. 
Autopsy was made by Prof. Osler, Dr. Musser, and Dr. Dorian. 
G-eneral appearance: Medium sized body, somewhat emaciated. 
Skin pale, slightly icteric. Numerous petechiae cover the face, chest, 
and arms ; very numerous on right arm and wrist. Petechiae range 
in size from a pin's head to a split-pea, and vary slightly in color 
from vivid red to dark blue; one or two only present central 
yellowish core. 
Abdomen, thorax: Numerous petechiae on parietal peritoneum. 
Slight serous effusion in both pleural sacs; few adhesions at right 
base; some petechiae in parietal pleura. 
Pericardium, heart: Excess of pericardial fluid, numerous small 
petechiae on visceral layer. Right chamber relaxed, containing fluid 
blood and small clot. Left ventricle, tolerably firm dark clot. Apex 
of the left auricle is long, and can be seen turning round to base of 
pulmonary artery. Before removal of heart, fingers in pulmonary vein 
and pulmonary artery, both of which are free. Further dissection 
of heart: right auricle, little blood, staining of endocardium ; a few 
petechiae. Right ventricle, chamber large; tricuspid segments a 
little thickened ; a distinct nodular thickening at angle of anterior 
and internal cusps. Pulmonary semilunar valve normal. Left auricle 
dilated. Seen from above, mitral orifice plugged by loose black clot 
and large grayish-white vegetations. After removal of auricle, the 
following conditions of valve appear: from base of posterior cusp of 
mitral, large irregular gray-yellow vegetations one inch in length 
extend into the auricle, passing out at right angles to the mitral ring, MALIGNANT ENDOCARDITIS. 
111 
and forming a sort of valve across the orifice. Entire auricular sur- 
face of this cusp covered with vegetations. Anterior cusp at free 
edge a large, warty vegetation projecting into ventricle three-fourths 
of an inch. The anterior part of this cusp is free. One or two of 
the chordae tendineae are encircled with vegetations. No involvement 
of endocardium, other than that of valves. Aortic cusps normal. So- 
called unprotected space below aortic ring presents deep depression, 
is closed, and to its base is attached a nodular thickening at angle of 
tricuspid cusps. Muscle substance of heart is pale, looks fatty; 
numerous ecchymoses. Coronary arteries free. 
Lungs crepitant; ecchymoses on pleura. No infarcts. Bases 
oedematous, somewhat congested. Pulmonary artery normal. • 
Spleen weighs 1 lb. 5 oz., soft, capsule closely adherent at one 
spot. Pulp soft, reddish-brown; four large infarcts of some age, 
yellowish ; others recent, none suppurating. 
Kidneys somewhat enlarged. Capsule free, surface irregular. 
Numerous recent infarcts. Unusual amount of pigment. Right 
kidney, same changes ; not so many large infarcts ; the pigmentary 
changes about many of these infarcts are peculiar. 
Pancreas: Few interlobular hemorrhages. 
Stomach: Numerous ecchymoses. Many with small, central 
grayish spots. Mucosa about cardiac end much reddened. 
Duodenum: Bile duct pervious; in mucous membrane small, 
superficial ecchymoses. 
Small intestine : One or two small infarcts in jejunum. Toward 
valve the ileum was much injected, and the small infarcts were 
numerous. 
Large intestine: Caecum deeply injected; throughout the colon 
they are numerous, in size from two to ten millimetres. Some of 
larger show distinct nodular prominence, which on dissection is 
grayish-red, firm. 
Liver: A little enlarged. No extravasations; tissue soft and 
light brown. No infarcts. Weight 5 lbs. 4 oz. 
Uterus : Medium size. Os shows deep lateral laceration. Mucous 
membrane deeply pigmented. Muscle substance normal. Ovaries 
normal. Small cyst in broad ligament. Pelvic veins are normal. 
No trace of chronic inflammation about broad ligament. No throm- 
bosis of veins. 112 
MUSSER, 
Bladder: Few ecchymoses. 
In the common iliac artery a plug is seen extending into the ex- 
ternal iliac as far as the femoral; in the internal iliac it extends for 
two inches. On slitting up artery the thrombus is closely adherent, 
and at bifurcation it has softened, and has a purulent (?) appearance. 
Clot in internal iliac is one and a half inches long at least. Much 
pigmentation about the internal coats of the artery. No evidence of 
any local disease. Brain, spinal cord, eyes, and ears not examined. 
Microscopical examination of the fresh clot in the artery, and the 
vegetation on the valve, by Dr. Griffiths, revealed the micrococci 
common to ulcerative endocarditis, the Staphylococcus pyogenes 
aureus. 
Sections of the organs after hardening were made for me by Dr. 
William Gray. He reports as follows: 
Heart: Fatty degeneration of the muscular fibre, with almost 
entire obliteration of the strife ; increase of the interfibrillar connec- 
tive tissue, and decided increase of the nuclear elements. 
Spleen : Extensive cirrhosis; obliteration of the cellular elements 
by fatty degeneration and an abundance of blood crystals (section 
from an infarct) are seen. 
Kidney ; Increase of intertubular connective tissue and tissue of 
Bowman's capsule. Proliferation of epithelial cells lining capsules 
and tubes. Cells degenerated and lumen of tubes plugged with 
casts. Section of infarct shows blood infiltrating into the tubules 
and between connective tissue fibres. 
Intestine: Increase of connective tissue in submucous layer and 
of adenoid tissue of villi; extensive lymphoid infiltration into mucous 
layer, villi, and glands of Lieberkuhn. Granular degeneration of 
cells of villi. Infarct between and into submucous and muscular 
coat, blood crystals in infarct. 
Artery : Entire absence of intima, with thickening of middle coat, 
and infiltration of blood into media. 
Unfortunately, Dr. Gray did not get any of the proliferated mass 
on the valves. Dr. Gray was unable to find micrococci in the sec- 
tions he had cut. They were given him without proper labelling, so 
that he did not know the tissue he was cutting. While this is to be 
regretted, it is enough to learn from the early and late examinations MALIGNANT ENDOCARDITIS. 
113 
of Dr. Griffiths, that bacteria were present. Dr. Griffiths readily 
found in the fresh treated preparations that micrococci abounded in 
the granular matter, and about the leucocytes of the vegetation. 
The lesions otherwise found, were myocarditis, glomerulo-nephritis, 
and gastro-enteritis, with the usual histological * changes about an 
infarct. 
Kemarks.-So many thoughts arise in the contempla- 
tion of a case that represents so complete an evolution 
of a morbid process that one is tempted to indulge in 
lengthy remarks. We shall limit ourselves, however, 
and so be content with calling your attention to one or 
two prominent features. 
Diagnosis. Observe, if you please, in the first place, 
the perfect picture of malignant endocarditis presented 
by the case. There was not a moment after the mani- 
festations of the heart lesions were studied, that the 
diagnosis of endocarditis was doubted. It is true that 
before the cardiac murmur had been detected we could 
only say we had to do with a septic process. Who 
would say otherwise in a case of a young person with 
irregular fever, profuse sweats, and extreme exhaustion; 
with vomiting and diarrhoea, and enlargement of the 
spleen; with an acute inflammation of the kidneys with- 
out dropsy; with the physical signs of endocardial 
inflammation; and with the most pronounced appearance 
of capillary hemorrhages in the skin and mucous 
membranes, terminating in suffusion of the skin, con- 
junctive, and mucous membranes with the mild but 
ominous hue of icterus ? It is true we considered at first 
whether, from the history and association with similar 
affections, the case was one of malarial origin. The use 
of quinia without result, the irregularity of the fever, 
the frequent pulse, the extreme sweats, and the diarrhoea, 114 
MUSSER, 
led us to abandon this idea. Typhoid fever was rightly 
thought of, but momentarily. The spots, the tympany, 
and the characteristic stools were wanting; no approach 
to the typhoid state was observed in spite of the high 
fever and rapid pulse; the peculiar features of the tongue 
were absent, and at no time were the faculties dull or the 
mind wandering. The physical signs observed in the 
lungs, the profuse sweats, the quick pulse, and the diar- 
rhoea, naturally induced the question of tuberculosis to 
arise. The disappearance of the lung affection, the 
absence of hurried respiration and of the tubercle bacilli 
in the discharges, were sufficient counter-proofs. 
Thus, by exclusion and by a careful study of the 
disease as it was gradually unfolded to us, we were 
enabled to make a diagnosis. In this, as in many 
instances, unfortunately, with waiting and watching, too 
soon the true nature of the affection was so legibly 
written that he who ran could read. 
Class. So far as can be ascertained, the affection 
was idiopathic-using the term with the modern reser- 
vation. That is, a cause cannot be ascertained for the 
development of the disease in this case unless the slight 
rheumatic attack years previously is sufficient to attach 
the diathesis as cause and effect. 
Type. Recall for a moment the marked symptoms 
present. The fever, the chills and the sweats, the clear 
intellect, the gastric and intestinal disturbances, clearly 
group the case with other examples of malignant endo- 
carditis of the pyaemic type. 
Special symptoms. Enough has been said of the 
symptoms in the history of the case. Your attention 
need not be called again to the vivid temperature range, 
the recurring chills, the grave renal symptoms, and the MALIGNANT ENDOCARDITIS. 
115 
pronounced capillary hemorrhages. The latter were 
striking-at first but a few, each day more and more 
appearing; confined not only to the skin, but seen in the 
lips and the tongue and the conjunctivae, they presented 
a glaring picture of the pathological process. The 
anaemia, which was barely noted, deserves a remark. It 
was profound, and the appearance due to it at once 
excited attention. Certainly the haemoglobin was much 
reduced, yet the patient was so ill we did not care to 
disturb her to ascertain its percentage. 
One class of phenomena deserves more lengthy 
remarks-the physical signs of the cardiac lesion. At 
first, at the mitral orifice a systolic murmur transmitted 
in the usual direction was heard. It varied in loudness 
and pitch. Later it diminished in pitch and volume, 
and at the same time a very loud systolic murmur, high 
in pitch and grinding in character, was heard on the 
third left rib and in the second left interspace one and a 
half inches outside the sternal edge. So loud was the 
murmur in this situation that, especially as it was 
attended by a thrill, we thought the pulmonary valves 
were implicated in the disease. The occurrence, how- 
ever, of an increased area of pulsation, most distinct in 
the second and third interspaces, and of an increased area 
of dulness in the auricular region, led to the conclusion 
that mitral stenosis was present. A presystolic murmur 
was not heard, however, and probably was not present. 
It was not created because of the projection of the 
vegetation over the orifice, in all probability. For a 
similar anatomical reason one can infer that the ven- 
tricle fills, partially at least, prior to and independent of 
contraction of the auricle. For with such an effort, at 116 
MUSSER, MALIGNANT ENDOCARDITIS. 
once, communication would be cut off by the vegeta- 
tion. 
The systolic murmur was heard, in the latter weeks, 
loudest in the second and third interspaces. Two causes 
can be invoked for this peculiar localization of the 
murmur. The projection of the mass from the auricular 
surface of the valve could readily throw the back flow 
of blood-the valve not closing from the situation of 
the second mass-into vibration, and thus murmur and 
thrill be produced and heard loudest over the auricle. 
While such an explanation suffices, a second cause for 
the murmur can be found in the position and dilatation 
of the auricular appendage. If such a view of the case 
is held, then the theory of Nanny n and Balfour to ex- 
plain the mechanism of systolic murmurs in this loca- 
tion is well illustrated. The excessive loudness of the 
systolic murmur at the angle of the right scapula was 
very peculiar. 
The ease of recognition during life, and the peculiar 
physical signs, are the features of prominent note in this 
case.