The temperature in diphtheria is not characteristic, and is not usually especially high; in moderately severe cases it may reach 102° or 103°, and in severe cases 104°.

As the disease progresses the pseudomembrane becomes thicker and darker in color, and infiltrates the mucous membrane to such an extent that, if forcibly removed, the surface beneath is seen to be raw and bleeding, and in a few hours becomes covered with a fresh layer of membrane. The pseudomembrane may remain localized or may spread over the whole interior of the throat or extend thence to the nose, larynx, or bronchi.

Toward the end of the first week or a little later the pseudomembrane separates by a process of sloughing, leaving a raw surface behind it; the throat is less swollen, the pulse and general strength improved, and the symptoms (barring sequels) indicate an early convalescence.

Albuminuria is present in upward of one-half the cases of diphtheria. The amount varies greatly from a mere trace to so large a quantity that the urine becomes semisolid upon the application of heat. It appears most frequently on the third or fourth day of the disease; its duration is frequently not more than one to three days, and seldom continues more than 10 days.

Nasal diphtheria, whether primary or secondary to a deposit in the throat, is characterized by more or less complete obstruction of the nasal passages, accompanied by an acrid mucopurulent and sometimes bloody discharge, which excoriates the nares and lip. The inflammation of the lymphglands and ducts, in which the nasopharyngeal mucosa is very rich, favors systemic infection, and usually results in a marked aggravation of the constitutional symptoms.

Laryngeal diphtheria presents a very different clinical picture from the conditions just described. Owing to the limited absorptive power of the laryngeal mucous membrane the toxemia is not materially increased, by extension of diphtheritic inflammation to the larynx. The obstruction to respiration from laryngeal stenosis, with gradually deepening

cyanosis and threatened asphyxia, indicate the most serious complications of the disease. The first symptoms of laryngeal involvement are huskiness of the voice, a brazen cough, and noisy stridulous inspiration. Gradually the cough becomes more and more hoarse, the voice fails steadily until aphonia is complete, the stridor at first only affecting inspiration, becomes louder and is heard with expiration, and every effort to fill the chest becomes more and more labored; with each inspiration there is depression of the suprasternal and supraclavicular spaces, and the epigastrium. The face is pale, the lips livid, the finger-tips blue, and, as the patient struggles to overcome the increasing obstruction to respiration, the body is bathed in perspiration. As the difficulty in breathing further increases the patient instinctively sits up, and with elbows supported and widely separated rests the head upon the open palms, in order to give free play to the muscles of respiration. In such a case, unless quickly relieved by treatment or operative interference, the cyanosis deepens, the respiration becomes more and more labored, drowsiness supervenes, and the patient sinks into a stupor which is relieved only by death.

If

The characteristic and diagnostic feature of diphtheria of the larynx is the progressive dyspnea with aphonia. aphonia is absent the obstruction to respiration is not laryngeal.

The clinical picture which I have endeavored to exhibit to you is that of pure diphtheria, but unfortunately such cases are seldom seen. There is in most cases another factor that adds greatly to the gravity of the disease; an added infection due to the various organisms causing pseudodiphtheria, that find in the local inflammatory lesions suitable conditions for growth.

Under favorable conditions the streptococci may penetrate the tissues beneath the pseudomembrane, enter the lymphatics, and gain wide access to the body, to the serous cavities as well as to the mucous membrane. We may find ourselves face to face with suppurative inflammations in various parts

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of the body, "empyema, arthritis, endocarditis, pericarditis, and bronchopneumonia." As the result of mixed infection the pseudomembranes become darker and more friable, and may be detached in places to interfere with acts of respiration or excite violent paroxysms of cough. "The peculiar and fetid odor of decomposition is now present, the face is pallid, the pulse feeble, and blood-poisoning is marked by apathy and profound adynamia.”

The lymphatics and the submucous and interglandular tissues are invaded by the septic process, "so that indurated glands tender to pressure may stand out prominently above the general surface of the neck, or the natural outline of the neck be obliterated in a universal tumefaction." Parenchymatous changes may occur in the heart and kidneys, "so that heart failure in the course of the disease; endo and pericarditis with subsequent valve-lesions; albuminuria with subsequent Bright's disease, may attend the course, complicate the progress, or protract the convalescence, if they do not directly take life." (Whitaker.) (Whitaker.) One of my own cases, a boy of twelve, who had diphtheria with albuminuria and grave cardiac conditions, was found four years later to have a typical case of cyclic albuminuria. The most striking and characteristic sequel of diphtheria is paralysis. Indeed it has been proposed to define diphtheria as an acute infectious disease produced by the action of the Klebs-Loefler bacillus, and characterized by the development of nerve degenerations. Paralysis occurs in about 25% of non-fatal cases. It is rare in infancy. Liability to it increases with years. "It occurs alike in the strong and feeble; the mild as well as severe cases." It is customary to speak of it as a neuritis, but ordinary forms of neuritis are attended with pain, while the condition under consideration develops and continues without pain. As remarked by Whitaker, we are better informed as "to its results than its lesions."

While it may be intercurrent with the disease, it does not as a rule appear until the second or third week after convalescence has begun, and may be deferred that many months.

The first indication is loss of "patellar reflex,” a phenomenon of great diagnostic significance, as well as an indication of the probable development of paralysis elsewhere. After loss of knee-jerk it usually first shows itself in the palate, in difficulty of phonation and deglutition. Fluids regurgitate through the nose, and particles of solid food may pass in the same direction, to the great discomfort of the patient.

The paralysis may also involve the epiglottis which ceases to protect the larynx during deglutition, and more rarely to the muscles of the pharynx increasing the dysphagia. Next in order of frequency is paralysis of the intrinsic muscles of the eye, causing indistinctness of vision, and frequently resulting in inability to read. Occasionally strabismus, more rarely ptosis, from paralysis of the extrinsic muscles of the eye is seen. In about one-half the cases the paralysis goes still further, involving the extremities; first and more particularly the lower. In some cases there is formication, tingling, or numbness, but more frequently motion alone is impaired. The legs are weak; there is an uncertain staggering gait with frequent falls. The paralysis may be so extensive as to render the patient entirely helpless. Hemiplegia occasionally results. In a single case coming under my own observation the hemiplegia was accompanied by aphasia. After seven years, motion of the upper extremity remains much impaired. Paralysis of the diaphragm, intercostal muscles, and heart is fortunately much more rare. If the diaphragm is paralyzed, respiration is entirely thoracic; if the intercostals, then the diaphragm must do the work. Either affection is characterized by attacks of urgent dyspnea and even cyanosis. By far the most important local paralysis is met with in connection with the heart. It follows tonsilar and nasopharyngeal forms of the disease frequently, but is rare after other forms.

Whether occuring early or late in the disease, the symptoms of involvement of the heart are in general the same. There may be bradycardia or tachycardia, or they may alternate in the same patient. Nausea and vomiting may precede

the cardiac effect. The face and extremities are cold, the pulse feeble, the temperature sinks and may become subnormal, and death may take place in a few hours from syncope. But not all cases of heart failure present the foregoing symptoms. In some cases the patient is seemingly entirely convalescent, and may be up and about, when perhaps following a sudden exertion or excitement, unforeseen paralysis of the heart results in instant death.

It is of the utmost importance that the diagnosis in a case of diphtheria be made early, that proper remedial measures may be employed at the beginning, as well as measures to prevent the spread of the disease. In a large proportion of cases the diagnosis is easy after 24 hours, since in addition to the fever and pain in swallowing the characteristic gray patches have begun to form on one or both tonsils, and there is fullness and tenderness at the angle of the jaw. The diphtheritic exudate, deeply set and surrounded by inflamed and swollen mucous membrane, has been not inaptly compared to the crystal of a watch surrounded by its rim. The diseases most frequently requiring differentiation from diphtheria are follicular tonsilitis and pseudodiphtheria. Follicular tonsilitis is a very common disease, frequently spreading through families as if contagious. Like diphtheria it begins suddenly with headache, fever often reaching 103° or more, pain in the back and limbs, and chilliness. There is dysphagia and the surface of the tonsils is hyperemic.

In a few hours a white cheesy material exudes from the crypts of the tonsils, forming rounded masses of varying size from that of a mustard-seed to that of a small pea. The secretion occurring as small rounded masses, distinct from one another, is distinguished by its appearance from the false membrane of diphtheria, which is at first a thin pellucid film, subsequently becoming thicker. The secretion of follicular tonsilitis, consisting simply of epithelial cells held together by the secretion of the crypts, is usually limited to the tonsils, is friable and easily detached by a swab or brush, and usually disappears in two or three days. If two or more of these