ring in other infectious diseases are found present in Weil's disease. Degeneration of the kidney and liver is prominent. Bacteriologic investigation has yielded no positive results. Symptoms. The onset is marked by chill and a rapid rise in temperature. On the fourth or fifth day a remission usually occurs. The disease lasts three or four days longer than this, and defervescence comes on with a well-marked crisis. Occasionally, a relapse takes place. The pulse early in the disease is rapid and full, and as is so characteristic of jaundice, decreases in frequency as the disease advances. Prostration is a prominent symptom. Delirium and coma may occur, and there is usually mental dullness and apathy. Pains in the back of the neck and legs appear. The tongue is coated. There may be vomiting and either diarrhea or constipation, an enlarged and tender liver resulting in one-half of the cases.

The spleen is early enlarged. Jaundice is invariably present, and may be the first symptom of the disease. It varies in intensity in different cases. The urine is decreased in amount, containing bile pigment, albumin, and hyaline and granular casts. The stools are clay colored.

Complications and Sequels.—Catarrhal affections occur in the mucous membrane. Occasionally, purpuric manifestations are present. Secondary bubo appears in some cases.

Prognosis. The prognosis is generally good, death, however, occasionally resulting.

Treatment. The diet should consist exclusively of milk. Violent purging should be avoided. Alkaline mineral waters should be used. In the early stages fractional doses of calomel should be given. Enteroclysis of cold water is useful in many cases.

MALTA FEVER.

Definition. A specific infectious disease, due to the micrococcus melitensis of Bruce, characterized by irregular fever, pain in the joints, free sweating, and other constitutional symptoms. The disease commonly lasts from three to six weeks. Relapses are frequent.

Synonyms.-Mediterranean fever; rock fever; Neapolitan fever; undulant fever.

Etiology. The disease appears to be endemic in Malta and parts of the Mediterranean coast. It has recently been noted as occurring in some of the islands of the Gulf of Mexico and in Puerto Rico. It especially affects young adults.

The specific cause is the micrococcus melitensis of Bruce. (See p. 121.) Inoculation experiments have been successful in monkeys.

The period of incubation is from a few days to twenty or thirty.

Pathology. The pathology is by no means settled. Perry, who made 100 autopsies of cases occurring in Gibraltar, found the typical lesions of enteric fever in every case. According to Bruce, the disease is rarely fatal, and upon autopsies no characteristic lesions are found.

Symptoms. The onset of the disease is characteristic, marked by prodromes. Some authorities describe the onset identically with that of enteric fever. There are headache, general malaise, loss of appetite, epistaxis, sleeplessness, and thirst. Diarrhea is not common. After a day or two of these symptoms slight chills occur, followed by more or less fever. The fever is often of a remittent type, lasting from one to three weeks. A period of apyrexia then takes place, which varies in duration from one to three days, and is followed by a relapse, in which marked rigors, high fever, delirium, diarrhea (the stools sometimes containing blood), and great prostration occur. The relapse may last several weeks and then, after a remission of a week or two, a second relapse takes place with a return of the initial symptoms. In the second relapse there are marked sweating, muscular and joint pains are more pronounced, and the prostration is extreme. The disease now often terminates in recovery, or after a lapse of one or two months all the symptoms may reappear. In severe cases the temperature is high,—105° F.,-its course subcontinuous, and death may be due to hyperpyrexia. Complications are

rare.

Diagnosis. The disease may be differentiated from malaria by the microscopic examination of the blood.

Prognosis. The mortality is low, estimated at about 2%. The course of the disease may be very protracted, and may last six months or longer.

Treatment. The treatment is symptomatic.

PART II.

DISEASES OF THE CIRCULATION.

CONGENITAL MALFORMATION OF THE HEART.

ASIDE from abnormality in the size and position of the heart, defects in its development and structure occur. The heart may even be entirely absent in some individuals called acardiac monsters. There have been instances in which the heart has been found in the neck or in the abdomen. It may lie immediately beneath the skin, only covered by the pericardium. The heart has been found in the right side of the chest, with the blood-vessels reversed, the venous blood entering the left auricle, the pulmonary blood the right auricle, and the aorta having its origin at the right ventricle. This condition is known as dextrocardia. It is usual in such cases to have the abdominal organs also reversed, so that the liver is found upon the left side and the spleen upon the right side.

Complete absence or only a slight indication of the auriculoventricular septum has been observed, in which the entire heart may consist of practically only two chambers, with one blood-vessel springing from each. Defects in the interauricular and interventricular septa may be present. Stenosis of the pulmonary artery is the commonest of the malformations. of the heart. Atresia or obliteration of the pulmonary artery is a much rarer condition.

rare.

The same conditions may be found in reference to the aorta, but are here even rarer than in the pulmonary artery. A patulous foramen ovale, or ductus Botalli, is by no means so Valvular defects are common; thus, there may be but two semilunar cups, and sometimes four have been observed. A similar state of affairs has been met with in the mitral and tricuspid valves.

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Congenital deformity and fetal endocarditis are the most prominent causes of these conditions. With dextrocardia the individual may be perfectly normal otherwise.

Symptoms. The child is apt to be weakly, does not thrive well, and soon after birth presents signs of disturbance of the circulation, consisting of lividity of a bluish tint, affecting the face, hands, and feet. The respiration is labored and paroxysmal, and is apt to be increased by screaming, suckling, and exposure to a cooler atmosphere. The extremities are cold and the terminal phalanges of both hands and feet are often clubbed. The surface temperature is subnormal, although the rectal temperature may be 99° F.

Convulsions and cerebral attacks may take place independently of those induced by screaming, movement, and suckling, merging into coma, and often rapidly proving fatal.

Cyanosis is by far the most common symptom and occurs in about 90% of the cases. The blood shows marked alterations, the red corpuscles and the hemoglobin commonly being above normal.

Physical Signs.-A loud, prolonged systolic murmur is heard all over the cardiac region, being transmitted in all directions. If there be stenosis of the pulmonary artery, a thrill will be noticed in the pulmonary area.

Prognosis.-Grave in nearly all cases in which there is marked circulatory disturbance.

Treatment. The child should be kept warm and exertion should be controlled. General good hygiene is necessary. The treatment by drugs is unsatisfactory.

DISEASES OF THE PERICARDIUM.

PERICARDITIS.

Divisions.-Acute and chronic pericarditis.

ACUTE PERICARDITIS.

Definition. An acute inflammation of the pericardium. Etiology.-Etiologically, it may be divided into primary and secondary pericarditis.

Primary Pericarditis.-Primary pericarditis includes those cases which can not be referred to any previous underlying It is occasionally found in persons without apparent

disease.

cause, but such cases are extremely rare, and in the present state of knowledge they had better be classed as cryptogenetic.

Those cases following injury, such as blows, wounds of the heart, or from internal causes, such as trauma of the esophagus, etc., may be classed as primary pericarditis.

Secondary Pericarditis. By far the greater number of cases belong to the secondary variety. In these rheumatic fever plays the greatest causative rôle; it is associated with renal disease; with extension from neighboring structures, as from the pleura or diaphragm; with cardiac disease, such as myocarditis; occasionally, with direct disease of the aorta; with new growths, such as sarcoma; and, finally, it is frequently associated with various diseases, such as scurvy, tuberculosis, scarlet fever, diphtheria, septicemia, erysipelas, gout, or diabetes.

Pathology. In acute pericarditis the visceral or the parietal layer may be involved; often the condition is general or may be localized to certain areas.

In the early stages the membrane becomes opaque, lusterless, and the surface roughened. Soon a fibrinous exudation appears upon the membrane or a serous exudate may result. The constant friction of the surface will cause a "honeycombed" condition of the fibrin or a “bread-and-butter ” appearance.

If the irritant be severe, a hemorrhagic exudate is present or it may go on to suppuration and a pyopericardium be produced. The inflammatory process may subside at any time during the process of the disease and the exudation be absorbed or it may in some cases be retained. When absorption takes place, there are adhesions of the two surfaces, and fibrous connective tissue develops, called adhesive pericarditis. These adhesions may be general or local. General adhesive pericarditis, as a rule, causes hypertrophy of the heart; rarely, atrophy results from the contraction of the connective tissue.

Various micro-organisms are associated with acute pericarditis, such as the staphylococcus pyogenes aureus, albus, or citreus, the bacillus coli communis, the bacillus typhosus, Klebs-Löffler bacillus, the bacillus of Pfeiffer, and others.

Microscopically, the first change noticed in acute pericarditis is a parenchymatous degeneration of the endothelial cells. The blood-vessels under the endothelial layer show the