up and about, and weeks and even months may pass before the signs present indicate a chronic valvular affection. To me personally the gradual increase in the intensity of a murmur (which was at first a mere blurring of the heart sound, gradually growing into a definable new sound-a murmur), is of the greatest possible value in the diagnosis of endocarditis. If symptoms are present, the diagnosis is, of course, more certain, but their presence or absence is not essential to the diagnosis. I lay particular stress upon this gradual increase in the intensity of the murmur because this augmentation gradually of a murmur's loudness apparently represents the onward progress of the anatomical defect being caused by the endocardial inflammation; because if this murmur represented the incipiency of asynchronism it would not increase in intensity gradually, but sporadically; because, if the murmur represented dilatation, as the dilatation and crippling of the heart grows greater the murmur diminishes in loudness. You see, therefore, that I do not rely simply upon the presence of the murmur to diagnose endocarditis, but upon the discovery of that murmur early and upon recognition of the modification in intensity that takes place in the evolution of the murmur. This gradual increase in the intensity of the adventitious sound is true of the vast majority of the murmurs of endocarditis in the early stages of these new sounds, but not of all. Those cases of endocarditis accompanied by a considerable degree of dilatation (a dilatation capable of causing death) is not characterized by an increase in the intensity of the murmur, but rather by a diminution or total disappearance of the adventitious sound. However, here practically the diagnosis of endocarditis is of little importance; the recognition of the dilatation is the important and necessary lesion to discover.

Dilatation of the heart in the young is not at all infrequent, and may complicate diseases that have no direct relationship whatever to the heart or endocardium-diseases that lay stress upon the heart by virtue of their special pathology or the height of the fever, or the contamination of the blood stream, but do not in themselves intrinsically and specifically attack the heart in such a way as to set up what are known technically as heart diseases. The young heart dilates readily, and also recovers its tone, in numberless instances, with remarkable facility. When the heart is seriously dilated you more frequently have symptoms that direct your attention to the heart than you do in most cases of endocarditis. In dilatation, if there be no pulmonary signs, and these often are present, you may be compelled to rely for the diagnosis of the dilatation upon the great relative weakness generally and of the radial

pulse, signs of an enlargement of the heart and a weakening of the muscular element of the first sound, together with slight or severe cyanosis, which is sometimes a symptom of dilatation. Sometimes a murmur, varying very much in intensity from time to time is found with dilatation; but, if the dilatation becomes extreme, this adventitious sound may disappear altogether. If the early signs of dilatation were looked for in the acute, and even the chronic diseases, that is, a lessening of the muscular element of the first sound of the heart, a prolongation of the expiratory murmur at the bases of the lungs, and slight labial cyanosis, and the heart be given proper therapeutic attention, there would be fewer deaths in infancy and childhood.

The myocardial inflammations or degenerations accompany any of the diseases that profoundly affect the character and composition of the blood, notably diphtheria, typhoid fever and severe scarlatina. Myocarditis, according to the books, can seldom be diagnosed with certainly; but practically the action can often be discovered. Most of the cases of acute myocarditis that I have personally seen have been in connection with typhoid and diphtheria. In typhoid, late in the disease, where the death occurs specifically from heart failure, there is no reasonable doubt but that myocarditis has been present. However, sometimes as early as the first week, the heart will become exceedingly rapid, the first sound lose its muscular boom, and this, together with the septic condition of the patient, and the profound weakness, is sufficient evidence upon which to base a diagnosis of myocarditis and a most unfavorable diagnosis. These same signs, possibly minus the sepsis, will diagnose a myocarditis in any acute disease where serious impairment of the heart's power is manifest long before the period when the degenerative changes should normally appear during the progress of the malady. The "time" element, so far as the natural evolution of the disease is considered, is sometimes of vital importance in the diagnosis of myocarditis.

Those cases which I have seen in connection with diphtheria have made themselves manifest about two weeks after the subsidence of the acuter symptoms of the disease. In fact, in two cases, which terminated fatally in twenty-four hours after I had first seen them, the fact that they had had diphtheria was an inference, inasmuch as the reported sore throat had been regarded as of no import whatever, and was not suspected to have been diphtheritic. Indeed, one other case that I now recall, had had what had been called a follicular tonsilitis of a single day's duration and had only required one visit from the attending physician. Heart paralysis undoubt

1

edly occurs during and shortly after diphtheria, but I am inclined. to believe from my own experience that most, if not all, of these cases of so-called cardiac paralysis were cases of myocarditis, and the cardiac paralysis was not recognized as having myocarditis as its basis. It seems to me that the cardiac paralysis was the terminal symptom of an unrecognized myocarditis. The extreme weakness, the pallor, the extremely rapid pulse, and the loss of the muscular element of the first sound of the heart, would be sufficient evidence upon which to base a diagnosis of myocarditis, when that disease occurs early in diphtheria. Sometimes the very first symptom in the later cases of diphtheritic myocarditis, if I may so term it, is a sudden, unaccountable collapse, the patient having apparently seemed perfectly well to the parents. Sometimes death is immediate, but in most of my cases death has occurred in from ten to thirty-six hours after the initial collapse. Weak, relatively lowtensioned pulse, frequent irregularity and intermittency of the heart beats, and loss of the muscular element of the first sound, are the signs I have found in these cases.

The practical lesson to be learned is: If the first sound of the heart is losing its muscular element, your patient, if acutely (or chronically sometimes) ill, is in the throes of pericarditis, hydropericardium, endocarditis, dilatation, myocarditis or some one of the forms of cardiac degeneration, and it at once becomes incumbent upon you to do two things-one is to tell which of these lesions. is present (with its corresponding prognosis), and the other is to keep the patient at rest during the prevalence of the weak first

sound.

This paper is intentionally not an elaborate nor an exhaustive one. It is simply intended to suggest the possibility of recognizing cardiac conditions and diseases at a time when we will have a doctor's grasp on all the factors of a given case, and will not be caught napping by some smarter fellow or by a special dispensation of Providence so-called.

A BRIEF REFERENCE TO UNCINARIASIS (ANKYLOS

TOMIASIS) WITH ILLUSTRATIONS.

BY CHAUNCEY E. TENNANT, M. D., AND GILES F. ROOSEVELT.

ΤΗ

Denver, Colo.

HIS disease is also known as tunnel miners' or brickmakers' anemia, Egyptian or tropical chlorosis or hook-worm disease, and is a specific infection of the intestinal canal by the parasite Uncinaria Americanus (Stiles). It is characterized by gastro-intestinal ir

ritation, anemia of a severe type, dizziness, dyspnoea, oedema and exhaustion.

The recent investigations of Dr. C. Wardell Stiles, Chief of the U. S. Bureau of Animal Industry, Washington, D. C., has made it possible to differentiate this disease from the chronic malaria and other forms of anemia so common in the South. The recognition of a specific cause for this disease makes both diagnosis and treatment quite simple.

While the European type of this disease has been known since 1838 (Dribini), it has not been recognized as a disease common in America until after Dr. Stiles' recent investigation (1902). The

Uncinaria or hook-worm, a nematode parasite belongs to the family strongylidae. The name indicates, as will be seen in exhibit, the dorsal curvature of the body resembling a hook. The mouth differs from the ankylostomum in that it has a pair of semilunar plates in place of the four teeth. Below the conical shaped head will be seen the bulbous enlargement of the stomach from which leads the tortuous intestinal canal.

The male adult worm is usually about one-third, and the female about one-half inch in length. This parasite inhabits principally the duodenum and jejunum. It produces anemia by attaching itself to the mucous membrane and sucking the blood and also by the escape

of the blood from the ecchymotic spots after the worm has let go. The possibility of toxic absorption is also worthy of consideration. The ovum, see illustration number one, does not develop in the intestinal canal, but is discharged in the feces and under favorable conditions of moisture, temperature (25 degrees C.), and culture media (feces preferably) segmentation of the granular mass within the capsule commences and in 24 hours embryos are found.

These embryos form by an agglutination of the granular mass after bursting the thick capsule and the triangular formation as seen in the illustration, number two, is the result, the head being Within a few days a larva is formed, number two,

the base.