Volume 1 — GENERAL DISEASES. (continued 15)

In respect to atmospheric infection by yellow fever, localizations of aërial impregnation are often observable, not common in other air-infecting diseases. A certain district of a large and populous city may become the seat of a sweeping and fatal epidemic, and yet no case occur outside of this area of prevalence. It is customary to speak of these points of epidemic prevalence as infected localities. If unprotected persons visit such infected places, even for a short period of time, they are liable to attacks of yellow fever, although they may take neither food nor drink within the limits of infection and bring no fomites away with them. Under these circumstances atmospheric impregnation is conclusive.

But it is difficult to determine how this infection of a locality has been produced in the first place, and how, in the second place, it is maintained sometimes for periods of from one to three months, with so little apparent diminution or change in the liability to communicate yellow fever to unprotected visitors within the limits of infection.

It seems highly probable that yellow-fever poison, after its exit from the human body, attaches itself to various solid surfaces in proximity to the sick, where, under suitable climatic conditions, it undergoes more or less speedy processes of maturation in toxic qualities. The poison thus matured is capable of being preserved with but little change for the periods indicated above, and is communicable through the atmosphere for short distances. It is also capable, by virtue of some unexplained process or quality, of spontaneously extending its area of infection. But this is at all times slow, and is readily interrupted by streams of water, high walls, or even by much-travelled thoroughfares.

There are no instances in which the water-supply of cities has been shown to have distributed yellow fever.

The periods of time which may intervene between exposure to yellow-fever poison and attacks of the disease are extremely variable. The shortest period of incubation which has come under my observation was about twenty hours. In three cases in which I was able to fix the hours of first exposure with precision attacks followed in 72 hours, 83 hours, and 101 hours, respectively. Of 55 unacclimated physicians who exposed themselves at Memphis during the epidemic of 1878, 54 suffered attacks of yellow fever. In these cases the periods of incubation varied from one to twenty-five days, the average duration being ten days. These physicians all remained steadfastly at their posts of duty; consequently, the attack which occurred on the twenty-fifth day was postponed for that length of time during constant exposure in a locality most intensely infected.

It must be true that many cases of individual resistance to the effects of yellow-fever infection depend upon states of the system or idiosyncrasies which diminish liability to the action of the poison. In other words, their personal receptivity to it is lessened by certain constitutional states.

That this position is correctly taken is proved by the fact that many circumstances which violently disturb the system determine attacks in persons who may have for a long time enjoyed immunity from them. Anxiety, grief, fright, fatigue, or exposure to sudden wettings or cold may precipitate attacks, either by disturbing vital processes by which the system is ridding itself of the poison—so far, at least, as to prevent an accumulation great enough to occasion attacks—or by lowering powers of resistance through enfeeblement of nerve-force.

But it can be affirmed in regard to yellow-fever poison that it is not more capricious or eccentric in its behavior as an infection than that of scarlet fever. Each of these diseases may appear in a large family of unprotected persons with a degree of violence which results in death in every instance, and suddenly cease, leaving a greater or less number of the household without attacks, though equally exposed with those who have died.

One attack of yellow fever confers immunity from the disease during after life. A person who has suffered an attack is said to be acclimated or protected. Neither of these terms should be applied to those who have not suffered attacks, however long they may have withstood exposure during epidemics. It often occurs that persons who have escaped attacks through many years of renewed exposure at last succumb to the disease. On the other hand, I know of three well-authenticated instances of immunity in a sweeping epidemic of persons whose mothers had suffered attacks during the gestations which respectively resulted in their births.

While negroes are susceptible to yellow-fever infection, attacks are far less fatal than among whites.

SYMPTOMS IN MILD OR SIMPLE CASES.—Yellow fever is usually sudden in its onset. Persons are liable to be seized while pursuing their ordinary avocations, or, as often occurs, the attack may begin during the night. The initial symptoms are chilliness or cold sensations, seldom amounting to a decided rigor. Reaction is usually prompt and decided, the temperature reaching within a few hours 102° to 105° F. Yellow fever is not a disease in which it is very common to observe excessive body heat.

As the fever is established, the countenance becomes flushed and the eyes injected and glistening. Frontal headache and lumbar pain are experienced very early in the attack, and are liable to become more intense during the progress of the fever. Muscular neuralgias, especially in the lower extremities, are not uncommon.

During the early period of the attack the tongue is indifferent as a symptom. It is generally moist and free from any coating. In cases attended by much furring of the tongue careful investigation is pretty sure to disclose the fact that it has been brought about by some pre-existing state of disease.

The bowels are generally inactive, though naturally impressible to cathartic drugs. The stomach is querulous from the inception of the attack to its conclusion. Vomiting may not occur spontaneously, but it is easily provoked by repletion of the stomach with any description of ingesta or by harsh or disgusting medicines. The acts of emesis are sudden and short in duration. Bile is a very uncommon constituent of the matters ejected. Whether vomiting has occurred or not, patients nearly always express repugnance to the weight of the physician's hand over the epigastrium. In the very mildest cases it seems to excite gastric distress and a tendency to emesis. The stomach and bowels are liable to distension by flatus, sometimes to the extent of producing colicky pains. Gaseous eructations are common.

During and shortly succeeding the cold stage the urine may be somewhat increased in amount, but after the fever is established both the quantity and the specific gravity are notably lessened. Albumen seldom appears in the urine during the first twenty-four hours of an attack. In very mild cases it is altogether absent throughout.

Delirium is not unusual during the fever. Among children attacks are often ushered in by convulsions. In such cases delirium may be persistent and alarming in violence.

The pulse in the early stage of yellow fever is slower in proportion to the temperature than in most other acute diseases. This is more especially true in respect to mild cases. Another characteristic feature of the pulse in yellow fever is that it declines in frequency before the fever has reached its maximum. In the mildest forms of the disease the temperature will attain its highest record within twelve hours. It then rapidly defervesces, never to return again. But in some cases of a moderately mild form the body heat does not reach its acme of intensity until the second day, occasionally not until the third or fourth day. In these cases also the pulse is apt to decline in frequency before the fever has culminated. There are therefore no fixed laws which govern the duration of the hot stage of yellow fever. Those which relate to the pulse are more uniform.

The following clinical reports of two cases support this statement. The detailed account of the symptoms establishing their diagnosis as mild cases of yellow fever is omitted.

Susie W——, white, aged seventeen years, was admitted to Charity Hospital on August 28, 1878. First observation, nine hours after the beginning of the attack, pulse 100, temperature 104.6°. Morning of 29th, pulse 94, temperature 102.8°; evening, pulse 80, temperature 101.5°. Sanguineous discharge from vagina began on 29th; patient supposed it to be her proper period. Aug. 30th, pulse 80, temperature 99.2°; convalescent and dismissed from further observations. In this case the urine presented a trace of albumen early on the second day, but as the menses appeared shortly after the urine was obtained, the presence of albumen may be in that manner accounted for.

Bessie L——, white, age twenty-seven years, admitted to Charity Hospital on August 28, 1878. First observation, twelve hours after beginning of attack, pulse 100, temperature 100.6°. 29th, pulse 76, temperature 102.3°. 30th, pulse 64, temperature 101.5°. Sanguineous discharge from vagina began on 30th and continued until Sept. 4th; this was two weeks before the patient's regular period. The urine showed traces of albumen at date of admission. Discharged, cured, Aug. 31st.

It may also be stated of the pulse of yellow fever that it is easily compressible and often gaseous in character.

Perspiration is probably an incident in the natural clinical history of a case of yellow fever. It occurs spontaneously if the patient's surface is protected from those influences which conflict with its appearance. It is not critical in any sense of the word, and may coexist with high temperature.

Yellow fever is considered to have two clinical stages. The first is the paroxysm. This is made to include the cold stage and succeeding fever. The cold stage is often almost or quite inappreciable, and when this is not the fact it is in simple cases a very unimportant event. It is therefore quite convenient to include it with the fever under the term paroxysm. The paroxysm of a simple case is terminated by a subsidence of the fever to nearly or quite a normal temperature. Sometimes the temperature falls below the normal standard.

The neuralgias and subjective sufferings are greatly mitigated or cease altogether. Thirst and restlessness are relieved, and the patient sees before him a delicious, but too often treacherous, mirage of restoration to perfect health. This is termed the stage of calm, perhaps because it often precedes a tempest of fatal symptoms.

In mild cases convalescence begins at the termination of the paroxysm, and may proceed without interruption until complete re-establishment of health has been accomplished. But in the very mildest cases the process of recovery is easily interrupted.

In these simple forms the tendency to hemorrhage first manifests itself in the calm stage. The gums become red, tumid, and spongy, the tongue pointed and red at the tip. Epistaxis is liable to occur. The eyes and skin may be slightly yellow, and the urine may show traces of albumen. However mild the other symptoms may appear, the tendency to hemorrhage, to albuminous urine, and to jaundice in the calm stage bears a direct relation in frequency of occurrence and in degree to the blood-stasis, or sluggish capillary circulation, of the first stage.

The foregoing is a recital of the clinical phenomena of typical and simple forms of yellow fever. The departures from type have been divided by different writers into a variety of forms. The most important of these will be referred to in connection with suggestions as to treatment.

PROGNOSIS.—Prognosis is variable in different epidemics, this observation being understood to apply to the same localities. Some of those circumstances which affect epidemic force, so as to increase the mortality-rate, are appreciable. If an epidemic invades a population after an interval of exemption sufficiently long to allow a large number of unprotected persons to have accumulated in its midst, the crowding of the sick will increase the death-rate. We may naturally assume that this is attributable, first, to sheer multiplication of the infection; second, to lack of proper attention to the sick, and to fright, grief, exhaustion, etc.

Tabulated Abstract of Practice in Yellow-Fever Epidemic of 1878, New Orleans Charity Hospital.

AGES. July. August. September. October. Total. Per cent.

White. No. treated. No. fatal. No. treated. No. fatal. No. treated. No. fatal. No. treated. No. fatal. No. treated. No. fatal.

Under 5 ... ... 7 3 3 1 ... ... 10 4 40.0

5 to 10 ... ... 2 1 1 1 ... ... 3 2 66.66

10 to 20 8 3 26 7 25 6 7 ... 66 16 24.2

20 to 40 18 9 246 141 175 91 61 24 500 265 53.0

40 to 60 9 6 75 45 83 45 18 10 185 106 57.3

60 to 80 2 2 7 6 5 1 1 1 15 10 66.66

Total. 37 20 363 203 292 145 87 35 779 403 51.7

Black.

10 to 20 ... ... 2 ... 5 ... 1 ... 8 ...

20 to 40 ... ... 11 3 8 1 5 1 24 5 20.8

40 to 60 ... ... 2 1 1 1 3 1 6 3 50.0

Total. ... ... 15 4 14 2 9 2 38 8 21.0

Grand total. 817 411 50.3

Prognosis is especially bad in hospital practice. The foregoing statistics of cases admitted to the Charity Hospital of New Orleans during the greater part of the epidemic of 1878 illustrate the usual results of hospital practice.

Many of these patients were conveyed to the hospital in extreme conditions; occasionally they were moribund on admission. It is hazardous to the life of a yellow-fever patient to transfer him over the rough streets of a city, often for two or three miles, unless this is done in the very earliest hours of the attack.

Prognosis is seriously influenced by the condition of the patient at the moment of attack. If pregnancy exists or delivery has just occurred, it is, under most circumstances, extremely unfavorable. Fatigue, anxiety, despair, or grief, all render prognosis more gloomy.

The march of temperature is also important in determining fatal results.

The following statistics show the influence of temperature in relation to mortality from yellow fever:

First day. Died. Second day. Died. Third day. Died. Fourth day. Died. Fifth day. Died.

106° ... ... 3 2 1 1 2 2 ... ...

105° 9 3 5 4 2 5 2 2 2 2

104° 18 10 23 13 8 3 2 2 3 2

103° 14 4 11 8 2 2 3 1 2 ...

It will be seen from this table that the danger line of temperature in yellow fever descends as the case progresses.

It may again be stated that yellow fever, like scarlet fever, exhibits such striking contrasts in its mortality-rate that it is hardly possible to assert any average standard. It is true that in this disease, as in all others, statistical accumulations tend to correct their own errors in exact proportion to the magnitude of the collections.

In 1878 some 36,000 cases occurred in Louisiana, of which number not less than 6000 were fatal, a percentage of 16.66. The results of private practice in New Orleans are exhibited in the following statistics: Four of the principal practitioners in the city treated in private practice 975 patients—909 white and 66 colored. Of the former, 92, or 10.11 per cent., died; of the colored only 2 died. The cases and deaths among the whites, classified by age, were as follows:

AGE. Cases. Deaths. Per cent.

Under 5 years of age 206 26 12.67

From 5 to 10 years of age 233 20 8.61

From 10 to 20 years of age 183 9 4.9

From 20 to 40 years of age 232 39 16.7

From 40 to 60 years of age 47 6 12.7

From 60 to 80 years of age 4 2 50

The physicians above quoted lived in different parts of the city. All of them extended their visits and professional services to the sick to the very limits of physical endurance, and consequently included in the above lists some patients who were not able to procure the comforts and attention necessary to the sick. Some cases also were included to which the physician was only brought that he might sign the death-certificate and so avoid the coroner's inquest. After making allowance for increase of mortality on these scores, I think it safe to assert that the best results obtained in private practice varied from 7 to 10 per cent. of mortality-rate.

DIAGNOSIS.—While there is no one symptom pathognomonic of yellow fever in every stage of the disease, its differential diagnosis is nearly always possible. The morbid action of its special poison produces phenomena sufficiently characteristic to prove its presence. The sudden attack, the slight cold stage, the frontal and lumbar pain, and the capillary congestion are important diagnostic symptoms.

Even in mild attacks this capillary blood-stasis is usually sufficient to alter the patient's countenance to such a degree as to attract attention. A great many different adjectives are used in description of the countenances of yellow-fever patients. While no one among them is constantly applicable, the presence of a changed facial expression should enlist the physician's attention and incite investigation. If this altered countenance be associated with watery or glistening injected eyes, the probability of yellow fever is increased.

The slow pulse which coexists with elevated temperature is a point of much diagnostic value. But it must be remembered that this symptom is not peculiar to yellow fever. I have noted this lack of correlation of pulse and temperature in several cases of dengue. It is also not infrequently found in ordinary cases of jaundice. The slow pulse of yellow fever must be attributable to the special action of the poison upon the nervous system. The heart's action may be slowed by influences exerted directly or through the retrograde effects of the delay of blood-currents in the capillary distribution.

Albuminous urine is a symptom of much diagnostic importance.

A tendency to hemorrhage may be safely stated to exist in all cases of yellow fever. In the mildest cases hemorrhage may not actually take place unless the patients be non-gravid females within the ovulating limits of life. These patients seldom pass through yellow-fever attacks without sanguineous vaginal discharges. But even in the mildest cases yellow fever establishes the hemorrhagic diathesis to an extent sufficient to render the occurrence of hemorrhage an imminent event. This fact is shown first, by the congested and tumid gums, from which blood can be readily pressed, and also by the still more important circumstance that medical or hygienic mismanagement is so quickly and certainly followed by black vomit or by hemorrhages from other parts of the system. Capillary congestion is undoubtedly an important factor in the production of hemorrhages in yellow fever, since we cannot otherwise account for the liability to hemorrhage which is so general in this disease.

The yellow color of the skin and eyes during life, and of the tissues and serum of the cadaver, is probably due to the coincident influence of two causes: first, to the coloring matter of the red corpuscles diffused in the serum of the blood; second, to an accumulation of secondary blood-poisons. The occurrence of the yellow color and its intensity bear a direct relation to the sluggishness of capillary circulation during the paroxysm. It appears likely, therefore, that the yellowness is principally ascribable to coloring principles derived from dissolution of the blood, to which capillary obstruction would so strongly predispose this fluid.

Schmidt has made a very careful résumé of the pathological changes found after death from yellow fever. The most important and uniform of these affected the nervous system, liver, and kidneys. They consisted for the most part of hyperæmic conditions, not infrequently attended by points of extravasation and of degenerative changes. The latter are principally found in the liver, and bear some relation to the duration of the case, and it may be also to the degree and persistence of the pyrexia. When the liver is the seat of fatty degeneration, it is yellowish in color in whole or in parts. It is then sometimes spoken of as the café au lait or the box-wood liver.

In cases which run a very rapid course these changes are not observed, but only those which indicate congestion are found, and often hemorrhagic puncta. In these instances the depending portions of the body have dark or livid ecchymoses.

TREATMENT.—There are two propositions to which due attention should be given before formulating rules for the treatment of yellow fever. The first of these is, that yellow fever is strictly a self-limited disease, and therefore is insusceptible of jugulation. Both clauses of this proposition are indisputably true. Cases have been observed in which mitigation of symptoms and abridgment in duration appeared to follow spontaneous diarrhoea. Such events must be extremely uncommon, since in my large experience I know of but one such instance supported by good testimony.

Efforts to abort the disease by purgatives, bleedings, cold baths, quinia, etc. have all signally failed. Among the possibilities of the future is the discovery that some drug or combination of drugs is capable of meeting yellow-fever poison in the field of the circulation and antagonizing it sufficiently to rescue the victim from its fatal toxic effects.

The second proposition is, that the formative stages of the disease—that is, the early hours of the paroxysm—afford the most precious moments for instituting such medication as may be considered proper. This proposition applies no doubt to a number of other acute affections, but in no one among them all is it so important to be regarded as in yellow fever. The primary effects of the poison are so boldly outlined that it appears highly probable that the damage it exerts upon the economy is chiefly inflicted during the paroxysm. This affords an additional reason why efforts at medication should be principally restricted to the paroxysm and to the earliest periods of that stage.

It is probable that during an attack of yellow fever the patient's hold upon life is more or less secure in direct ratio to the number of functions which retain their physiological integrity fairly well. The suggestion of such a fact should exclude all scholastic or routine rules of treatment.

In simple forms of yellow fever the first desideratum of the practitioner is to become acquainted with the patient's condition at the moment of attack. If this has occurred after eating indigestible food or after a hearty meal of any description, the stomach should be emptied. Ipecacuanha may be given in warm water or chamomile infusion until this result has been accomplished. After emesis, provided this should have been considered necessary or as a first step of treatment under other circumstances, a purgative is usually given. The benefits of purgation are, in my opinion, limited to the act of ridding the bowels of any fecal accumulations present. For this purpose those purgatives which combine a due degree of efficiency with inoffensiveness in operation have appeared to me to be the best. Castor oil is at the head of this class. An ounce may be given to an adult in some acceptable vehicle. This may be followed by an enema of tepid water when required. Salines are more agreeable to the palate, but far too unmanageable in their cathartic effects to be adopted generally.

Some very good practitioners believe that a mercurial purge at the onset of the attack impresses the subsequent career of the case in some favorable manner. I do not share in this opinion, but I do select calomel as the preliminary purgative in cases where much gastric irritability attends the early periods of the attack. I exhibit it also in those cases in which previous indisposition had occasioned coating of the tongue, or in which other conditions of systemic derangement existed for which calomel is usually prescribed.

In many cases it is desirable to avoid the disgust at taking a purgative or the perturbation it may occasion by its action. Enemas of tepid infusion of linseed or of milk and water may be substituted, with the addition of castor oil when necessary.

In the early hours of the attack warm pediluvia are always grateful and proper. They are to be given by placing a basin of warm water near the foot of the bed, beneath the covering of a light blanket or sheet, and allowing the patient's feet to remain immersed for ten or fifteen minutes. If the feet are cold, mustard should be added. During the foot-bath the patient usually falls into a perspiration which is sometimes profuse and general.

Perspiration is a desirable event during the paroxysm, although it is not, like the sweatings of the malarial fevers, critical, in the sense of being accompanied by a marked decline in temperature. The idea that sweating is beneficial is so strongly and generally prevalent as to give countenance to the erroneous practice of resting the cure of the disease upon its production and maintenance. I have seen valuable lives sacrificed by obstinate persistence in measures to promote diaphoresis, more especially in the later hours of the paroxysm or in the succeeding or calm stage. It is quite sufficient to encourage the perspiration by the pediluvia and by a moderate allowance of cool, palatable drinks. Much value is attached by non-professional persons to a warm infusion of orange-leaves or some other warm and grateful beverage. When agreeable to patients I permit them in moderate amounts, but do not regard them as especially valuable.

Jaborandi has been used in yellow fever. Strong hopes were quite naturally based upon the action of this drug in exciting excretory functions, especially diaphoresis, but the observations of my friend Dr. Thomas Layton and of others show that it possesses no special value, while it frequently increases the vomiting and has to be discontinued.

After the bowels have been relieved of fecal accumulations it is good practice to exhibit a scruple of quinia in solution with ten to thirty drops of tincture of opium, by rectal injection. Infusion of linseed or mucilage of elm-bark or gum-arabic are the best vehicles.

The combined action of the quinia and opium mitigates the patient's headache and lumbar pains. But the influence of these drugs is not limited to their effect on the nerves of sensation. In quite a proportion of cases reaction is not so prompt or complete as usual; or reaction may be quite pronounced, and still the surface may alternate between a dry and a perspiring state. These oscillations of function of the organic nerves are also often corrected by this prescription. In the great majority of simple cases no other medication than this is requisite or proper, for no medication is proper in yellow fever unless it is requisite.

When the neuralgias are excessively violent, opium may be again administered, preferably by enema, and in combination with bromide of potassium or chloral hydrate. But the effects of opium in limiting excretory function must always be borne in mind and carefully avoided.

External applications are very efficacious in relieving the neuralgias. In the southern part of this country the "eau sedative" of Raspail is greatly used. This is a mixture of ammonia, camphor, and common salt in solution, and may be prepared extemporaneously. The applications may be made hot or cold, but if used cold they must be continuously kept up. It is therefore better to use them warm if sufficiently effective. Stimulating embrocations of turpentine or mustard, or dry or wet cups, are sometimes resorted to for relief of pain.

Excessive temperature demands attention and antagonistic treatment in direct measure with its persistence, its degree, and its occurrence in advanced periods of an attack.

In the epidemic of 1867, I used gelsemium as an antipyretic in fifty cases or more, but the results were so unsatisfactory that I have quite abandoned its exhibition. I have given quinia as an antipyretic, but never in doses of more than a scruple. In these doses it has failed to accomplish the desired result in the great majority of the cases. Perhaps its antipyretic effects are limited to those cases in which malaria is a known or an unknown complication.

I have exhibited small doses of digitalis with apparent benefit, but aconite and veratrum viride I have long since discarded. The physician cannot afford to sacrifice gastric quietude and competency of function to the use of remedies whose value as antipyretics is, to say the most, quite doubtful.

Cold has for a long period of time been brought into use as an antipyretic in yellow fever. Its positive value and instantaneous action should be constantly borne in mind, and in the hyperpyrexia of yellow fever it constitutes by far the most reliable remedy, though its mode of application must be carefully adapted to the degree of fever present and to the susceptibilities of the patient. Cold drinks in limited quantities, but frequently repeated; cold spongings of the surface, or the use of the cold pack, especially in very high degrees of body heat; large injections of cold water per rectum, which may be passed off and repeated once in two to four hours,—form safe and effective modes of treatment.

Hemorrhages are a constant source of anxiety in yellow fever. It is very true that persons do not often die from actual loss of blood. I do not know that I have ever witnessed such an event except when the blood was poured out from a recently-emptied uterus. But the chances of recovery are lessened, because the hemorrhagic state indicates a degree of spoliation of both the fluids and solids of the system incompatible with maintenance of life. When this condition of constitution is once established, the stomach rarely escapes, and in a majority of instances it is the first, and sometimes the only, bleeding surface. The treatment should be directed, first, to the great indication of correcting the hemorrhagic diathesis; secondly, to quiet gastric irritability, in order that vomiting shall not cause rupture of capillaries. To meet the first indication I regard nutrition and stimulants as the most important measures of treatment. The mode of administration will be specially referred to under the head of alimentation.

Hæmostatic remedies, given as specific treatment, generally fail in accomplishing the purpose for which they are administered. It has always appeared to me that those therapeutic agents which are capable of controlling hemorrhage where yellow fever is not present are completely neutralized by the effects of its toxic agent upon the vaso-motor nerves. Consequently, while ergot, turpentine, gallic acid, and other like remedies may be resorted to, too much hope should not be entertained as to their good effects.

Some excellent practitioners rely greatly on preparations of iron. The tincture of the chloride is undoubtedly the best. This may be given in water or upon shaved ice in doses of five or ten drops every half hour. To allay the gastric irritability pellets of ice should be swallowed. Effervescing drinks may be given with benefit.

I have often used with good results the following prescription:

Rx. Sodii Bicarb. gr. xx;

Morphiæ Sulph. gr. ss.

Aquæ Lauro-Cerasi,

Aquæ Menth. Pip. aa. fl. drachm iv. M.

S. Teaspoonful after every act of emesis.

Occasionally I have given the following prescription:

Rx. Creasoti gtt. viij;

Tinct. Opii Deodorat. gtt. xl.

Aquæ Menth. Pip.,

Muc. Acaciæ aa. fl. drachm iv. M.

S. Teaspoonful after every act of emesis in iced Seltzer or Apollinaris water, or in champagne.

Sometimes a few drops of chloroform in a spoonful of iced mucilage of acacia act favorably.

In cases which appear utterly hopeless the physician, acting desperately, is sometimes able to save life by treatment which could scarcely be safely recommended. I once administered a fourth of a grain of morphia to a child of seven years, who, after a sleep of ten hours, ceased to throw up black vomit and recovered.

External applications to the epigastrium usually afford some relief to nausea at any stage of yellow fever. Mustard or aromatic cataplasms may at all times be used with hopes of favorable effects. Towels wrung from cold water are very efficacious. Sometimes a drachm or two of chloroform dashed over them increases their anti-emetic action.

Suppression of urine is generally a symptom of fatal import. Attempts may be made to establish the secretion by dry or wet cups in the lumbar region, by warm applications around the loins, or by mustard cataplasms or blisters. If the condition of the patient's stomach is such as to permit this practice, copious diluent drinks and diuretics should be given. Lemonade holding bitartrate of potassium in solution is generally the most acceptable, and probably the most efficient. Some physicians think they oftener obtain good results from small and frequently repeated doses of turpentine. I can bear testimony to the good results which sometimes follow large rectal injections of warm or cold water, the latter being preferable when there is high fever.

In certain cases of yellow fever reaction from the cold stage is feeble and imperfect, or perhaps may not occur at all. This departure from type is very fatal. The patients are stupid, sometimes semi-comatose and incoherent, from the earliest hours of the attack. The face is listless, drunken, or idiotic in expression. The color of the skin is dark olive and almost livid. The print of a hand on the chest is very slowly effaced. Sometimes the surface is covered with a peculiarly unctuous perspiration. The pulse is feeble and compressible; the temperature seldom more than one or two degrees above the normal standard. Albuminous urine is found during the first day. Death, attended by convulsive rigors, generally closes the scene within seventy-two hours from the moment of seizure.

Hot mustard-baths should be resorted to. Blood may be drawn by cups or leeches from the back of the neck or temples, and this may be followed by the application of a blister. Morphia and atropia may be exhibited subcutaneously in small doses, to be repeated as often as proper. Quinia may be administered per rectum or by the hypodermic method. Lastly, pilocarpine may be thrown into the tissues in sufficient doses to procure its vigorous physiological action.

Almost in precise symptomatic contrast with these cases of failure in reaction is another form of attack, in which violent disturbances of nerve-function occurs; such cases often being characterized as congestive in type. The most typical of these attacks are among children or adolescents. If attended by noticeable chill, it is ordinarily slight. Reaction is quick and excessively violent. The face is flushed, the eyes injected, and convulsions with delirium are liable to occur as early symptoms. I have watched with much interest the alternate flushings and pallor of the countenance occurring in these cases, such as are often observed in basilar meningitis.

The treatment in this type of attacks should include chloroform by inhalation in sufficient amount to control convulsions. Chloral hydrate may be administered by enema, or morphia hypodermically. Cathartic doses of calomel often exert a beneficial effect. Leeches or cups, to be followed by cold applications or by blisters, may be applied about the head or neck. But cupping and leeching should only be resorted to in the treatment of grave symptoms, since obstinate hemorrhage is liable to occur from any and every point from which the cuticle has been removed.

Yellow fever is often masked during the paroxysm by some pre-existing disease. Malarial fevers, the febrile states of pulmonary consumption or of the recently-delivered female, may all mask the early clinical phenomena to such a degree that the most experienced and vigilant practitioners are sometimes astonished to find black vomit, suppression of urine, and all those symptoms which mark the last stages of the disease, suddenly developed.

Walking cases should be classed in the same category as masked forms. In these instances the early symptoms are so slight as to be overlooked or neglected by their subjects. They continue to prosecute their usual pursuits until, by sheer exhaustion, they are driven to beds from which they seldom arise.

The hygienic and dietetic management of yellow-fever patients is extremely important, and the strictest attention must be paid to the condition and discipline of the sick chamber. In this disease those occurrences and circumstances which in other affections would be reckoned as unimportant and trivial become matters of serious magnitude.

The physician, by a composed and cheerful demeanor, often decides which end of the balance shall go down. But an intelligent, experienced, and faithful nurse is equally as important as the excellent physician.

The patient should be confined in strictly recumbent positions, and all drinks and foods must be given through tubes or from pap-cups. It frequently occurs that patients are unable to void the bladder in such positions. In these cases the catheter should be used, rather than suffer any violation of the rule which demands a maintenance of unbroken decubitus.

The sick room should be kept freely ventilated, and the patient's bedding should be changed, when requisite, by removing him to one side of the bed while the other is renovated. If the patient's night-shirt becomes soiled and disagreeable, it may be cut so as to remove it, and another, cut in the same manner, may be substituted and stitched together. The room must be kept quiet, and useless visiting entirely forbidden.

Cool and grateful drinks may be given in any stage or state of yellow fever if demanded by patients. The quantity allowed at one time should be small, since over-distension of the stomach almost certainly causes vomiting. Effervescing drinks are nearly always grateful, and are better tolerated than others. Seltzer-water and lemonade, or Seltzer or Apollinaris on shaved ice, are to be recommended. Sometimes patients call for sparkling wines or beers. I never refuse them or any other alcoholic drink asked for in any stage of the disease. Wine surely possesses valuable therapeutic effects in yellow fever.

Alimentation must be severely controlled by the physician, and the tolerance and effects constantly watched. Even to the most experienced physician the kind of food to be selected, and the time and manner of administration, constitute difficult problems. In simple forms of the disease food had better be strictly withheld during the continuance of the paroxysm. Even after the stage of calm has been reached, sufficient time should be allowed to elapse to enable the physician to form some estimate of the degree of damage his patient has suffered and his competency to retain foods and be nourished by them. This question can seldom be answered in a decided manner, except through a cautious trial of some bland and inoffensive food.

On the third or fourth day of sickness a single tablespoonful of iced milk may be given, and the immediate consequences closely watched. If no retching or gastric uneasiness should ensue, it may be repeated at the end of thirty minutes. Some physicians prefer to begin with spoonful doses of equal parts of sweet milk and thin barley-water. In my own experience chicken-water has proved to be the most universally acceptable, as well as the most beneficial, of all the various forms of nutriment to be chosen as a first venture. I have frequently combined this with barley-water when first given. In this cautious and tentative manner even the most experienced physician prefers to proceed, rather than to attempt to prescribe rules of diet in an abstract and arbitrary manner.

If these light articles of diet are well borne, they are to be gradually and watchfully exchanged for beef-essences, the blood of a rare beefsteak, and the more substantial broths. Solid articles of food should not be allowed during the first ten days after an attack, and for still longer periods patients should be admonished against excesses in eating, and especially in respect to indigestible articles. Those lesions of the blood and of the stomach, and those grave disorders of nerve-function which occasion hæmatemesis in yellow fever, are slowly repaired. Instances are reported in which black vomit and death have followed excessive eating and drinking ten or twenty days after dismissal from treatment.

There are, however, certain conditions which are liable to complicate yellow fever which demand a course of dietetic procedure different from that which I have recommended. Thus, children cannot bear privation of food until the paroxysm is over if its duration is long. In like manner, a more supporting course is required in most of those cases in which yellow fever occurs as an intercurrent affection, in all those cases which are termed typhoid or adynamic per se, and, more emphatically still, in every case in which hemorrhages are occurring. A failing pulse should in all instances admonish us to resort to nourishment and stimulants.

It is a fortunate circumstance that in yellow fever the lower bowel is generally in a state favorable for the retention of nutritious enemas. In the most trying and critical hours of desperate cases I have seen patients tided through by the use of skilfully prepared and skilfully administered injections of some suitable meat-essence. When insomnia exists, chloral hydrate or bromide of potassium may be conveniently given in these vehicles.

It is evident that the discussion of the vastly important sanitary questions pertaining to the prevention of yellow fever cannot be appropriately discussed in the present article.

DIPHTHERIA.

BY A. JACOBI, M.D.

DEFINITION; SYNONYMS; HISTORY.—Diphtheria is a specific, infectious, and contagious disease, characterized principally by epithelial changes in, and the exudation of fibrin on and into mucous membranes, the surface of wounds, and the rete Malpighii, thereby constituting the so-called pseudo-membrane. Under the names ulcus syriacum, ulcus ægyptiacum, garotillo, morbus suffocans, morbus suffocatorius, affectus suffocatorius, pestilentis gutturis affectio, pedancho maligna, angina maligna, angina passio, mal de gorge gangréneux, ulcère gangréneux, angina polyposa, angine couenneuse, cynanche, croup, diphtheritis, and diphtheria, the disease has been known and described at different periods by the writers of different nations. The Hippocratic writings and some remarks in the Talmud allow of some doubt in regard to their explanation. Whether their authors observed or recognized diphtheria cannot be proven. There is less doubt in regard to Archigenes, quoted by Oribasius. Aretæus of Cappadocia is notably the first, if we except Asclepiades only, who is said to have performed laryngotomy. The description of the pharyngeal and laryngeal manifestations furnished by the former, however, can leave no doubt in our minds that he knew diphtheria and recognized it. Galen, in his remarks on the Chironian ulcer, tells us that the pseudo-membrane was gotten rid of by coughing when the respiratory passages were affected by the disease, and by hawking when the disease was in the pharynx. Cælius Aurelianus recognized diphtheria of the pharynx and larynx, as well as the diphtheritic paralysis of the soft palate; it is to him we are indebted for the information that Asclepiades resorted to scarification of the tonsils, and even to laryngotomy. Aëtius in the fifth century distinguished white and grayish patches and gangrenous degeneration, observed paralysis of the soft palate, and advised against energetic local treatment and the forcible removal of the deposits before they were in a condition to fall off spontaneously. The Arabs and Arabists contain no allusions to the subject, but early chronicles tell of an epidemic raging in St. Denis in 580, subsequent to a great inundation. There appear to have been memorable epidemics in Rome in 856 and 1005, in Byzantium in 1004. The former are mentioned by Baronius, the latter by Cedrenus.¹

¹ Haeser, Lehrb. a. Gesch. du Med. u. d. Epidem. Krankh., 3d ed., vol. iii., p. 434.

According to Morejon, Gutierrez wrote his Tradado del enfermedad del garrotillo in the second half of the fifteenth century. A malignant form of angina raged in 1517 in Switzerland, along the Rhine, and in the Netherlands; in 1544 and 1545 in Northern Germany and on the Rhine; in 1557 in France, Germany, and Holland; to the latter refer the reports of Tetrus Fosterus. Antonio Soglia, quoted by Chomel, describes an epidemic in Naples and Sicily (1563), which spread in the following year as far as Constantinople; Joannes Wierus, epidemics in Dantzic, Cologne, and Augsburg (1565); Ballonius (Baillon), in Paris (1576). At the same time this disease was frequent in Denmark. From Spain there are reports on severe epidemics between the years 1583 and 1618; the year 1613 was long known as the year of diphtheria (anno de los garrotillos).

Mercado (1608) speaks of a child that had communicated the disease to his father by biting his finger. Casealez advised gargles containing alum and sulphate of copper. Herrera described diphtheria of the skin and of wounds, and looked upon the pseudo-membrane as the essential characteristic of the disease. Heredia, in 1690, recognized the suffocative and asthenic forms, as well as the paralysis of the soft palate, the pharynx, and the limbs; he also called attention to the occurrence of relapses, which he attributed to the absorption of the morbid products, and endeavored to prevent by cauterization.

Naples had diphtheria 1610-45, in its worse form 1618-20, together with erysipelas, and diphtheritic affection amongst cattle. About those times tracheotomy was often performed by Severino, the same who found pseudo-membrane in the larynx at a post-mortem examination made in 1642. In 1620 the disease was in Portugal, Sicily, and Malta; in 1630 in Spain, according to Fontechu, Villa Real, and Herrera. It was remarked that in some instances no membranes were perceived in the throat, but the cases were liable to terminate fatally with large glandular swellings round the neck and general symptoms of adynamia. Sicily was again invaded in 1632, Rome in 1634, Italy from 1642 to 1650, Spain in 1666. The Italian reports emphasize the marked contagiousness of the disease and its tendency to depress the vital powers, also the weakness of the mental faculties left behind. In Germany the disease was described by Wedel in 1718. The epidemics observed by him were not very instructive, yet they sufficed to teach the importance of isolating the sick.

In the New England States diphtheria appeared in the seventeenth century. Samuel Danforth lost the four youngest of his twelve children by the "malady of bladders in the windpipe" within a fortnight in December, 1659, in Roxbury, Mass. John Josselyn mentions an epidemic in New England, mainly in Maine, which lasted at least until the year 1671. Mr. Douglass reports another, which commenced on the 20th of March, 1735, in Kingston township, about fifty miles east of Boston, and extended all over, and also to Boston, where it was mild at first. But in 1738 it was very severe, and remained so for some time. Indeed, it did not abate for a long time, to judge from a letter of Cadwalader Colden written in 1753 to Dr. Fothergill, and the two letters of Dr. Jacob Ogden, written in 1769 and 1774 to Mr. Hugh Gaine of New York; as also from John Archer's "Inaugural Dissertation on Cynanche Trachealis, commonly called Croup or Hives," published in 1798.² In 1809 there was a severe epidemic in Philadelphia;³ in 1816 in Crete.

² For extensive quotations from these and other writers on diphtheria at a very interesting period of our medical literature, see A. Jacobi, A Treatise on Diphtheria, New York, 1880.

³ Caldwell, in ed. of Cullen's First Lines of the Practice of Physic, Philadelphia, 1816, 1, p. 260.

The reports of Le Cât concerning epidemics in Rouen in 1736 and 1737 being doubtful, the first great epidemic must be set down, in France, for 1745. It commenced in Paris, and invaded the provinces afterward. Chomel gave an accurate description of the diphtheritic paralysis of the soft palate, and reports a case of strabismus. Epidemics are reported from the Netherlands in 1745, 1746, 1769, 1770, 1778-86; from Spain in 1764-71; from England in 1744-48 (by Starr), from Plymouth, England, in 1751-53 (Thurham) and 1776. Dropsy and glandular swellings were frequent; emetics and pure air were the sheet-anchors of treatment. The Netherlands, France, and the West Indies were invaded from 1770-80 by the disease, which was found often complicated with scarlatina; Portugal in 1786 and 1787; France again in 1787 and 1788; Northern Germany in 1790. At that time, particularly in France, the main reliance was had on the internal administration of cinchona and the insufflation into the throat of alum.

Epidemics have been described since from different localities in different years: in Glasgow, 1812 and 1819; Switzerland, 1823-26; Norway and St. Helena, 1824; New York and Kentucky, 1826 and 1828; French provinces, 1834; Paris, 1841; several parts of Europe and North America, 1845-56; Paris, 1853-55; England, 1854 and 1859, when 95 per cent. of all the cases of nasal diphtheria proved fatal; Netherlands and Sweden, 1855; all Western Europe, 1855-65, up to the present time, and all Europe since; California, 1856 and 1857; Portugal and France, 1856; Eastern Prussia, 1850, 1852, 1856, 1857; and all the countries with a cold or moderate climate to this very day.

During the second half of the eighteenth century but two writers are worthy of especial notice—Home, a Scotchman, 1765, and Samuel Bard, an American, 1771.

Home deserves credit for having distinctly drawn the line between the pseudo-membranous and the gangrenous affections. He also endeavored to prove that croup and angina maligna were two distinct diseases, notwithstanding all that had been said since the time of Aretæus in favor of their identity. The false membrane of croup he looked upon as an aggregation of mucus. He sought for it exclusively in the respiratory tract, and disregarded any connection between it and the false membrane found in the pharynx.

Bard's experience was very extensive; he saw membranous pharyngitis, laryngitis, and pharyngo-laryngitis; he speaks of the membrane as met upon the skin, of paralysis of the muscles of deglutition and of the larynx, and likewise of paralysis of the lower extremities, as sequelæ. He looked upon the morbific process as the same whichever were the mucous membranes attacked, and made a distinction only according to the localization of the disease. The influence which he might have exercised in shaping the professional opinion on the nature of the disease did not make itself felt, partly because of his classical modesty, and partly because of his remoteness from the centres of European learning. Not before 1810 was his book translated into French (by Ruette). While his style is classical in its simplicity, his observation is astonishingly correct, and his conclusions as to the actual identity of all the diphtheritic processes in the most various clinical symptoms unimpeachable this very day. His description of the various forms of pharyngeal diphtheria is painfully good, his observations on cutaneous diphtheria very accurate, his few dissections well recorded, particularly when he speaks of tracheal and tracheo-laryngeal diphtheria, and his historical reviews very judicious indeed. "Upon the whole, I am led to conclude that the morbus strangulatorius of the Italians, the croup of Home, the malignant ulcerous sore throat of Huxham and Fothergill, and the disease I have described and that first described by Douglas of Boston, however they may differ in symptoms, do all bear an essential affinity and relation to each other, or are apt to run into each other, and, in fact, arise from the same leaven. The disease I have described appeared evidently to be of an infectious nature, and, being drawn in by the breath of a healthy child, irritated the glands of the throat and windpipe. The infection did not seem to depend so much on any prevailing disposition of the air as upon effluvia received from the breath of infected persons. This will account why the disorder sometimes went through a whole family, and yet did not affect the next-door neighbors. Here we learn a useful lesson—viz. to remove young children as soon as any one of them is taken with the disease, by which many lives have been saved and may again be preserved."

Jurine, in his prize essay of 1807, denies the gangrenous nature of angina maligna and emphasizes the frequent complication of membranous croup with membranous pharyngitis. It was reserved for Bretonneau to enforce attention to the ideas of Bard by asserting (though he did not mention either his monograph or its French translation of 1810) the identity of angina maligna, or by whatever other title it may be known, with membranous laryngitis, and by inaugurating his theory with a new name for the disease to perpetuate the views expressed therein. First and foremost, he called attention to the continuity of the membrane (according to him, composed of coagulated mucus and fibrin) of the nose, pharynx, and respiratory tract, its identity with certain morbid conditions of the skin, and promulgated the theory that "diphtherite"—the name dates from that time—is a specific disease, an affection sui generis, and differs both from a catarrhal and a scarlatinous inflammation.

The modern history of diphtheria may be dated from June 26, 1821, when Bretonneau read his first essay on that subject before the French Academy of Medicine, and gave to the disease the name it now bears. His second and third (Nov. 25th) papers belong to the same year; his fourth was read in March, 1826; his fifth appeared in the Archives gén. of January and September, 1855. It was only in 1826 that the material, previously gathered, was summed up in his celebrated monograph.⁴ Before this time, however, the separate essays had received prominence from the reports and commentaries of Guersant, who laid particular stress on the statement that diphtheria was a non-gangrenous affection, identical, and even synchronous, with croup in the majority of epidemics. Since that epoch the literature on the subject has assumed enormous proportions. It is a matter of regret that the limited space allotted to this subject should exclude much historical detail of the etiology, pathology, and therapeutics of diphtheria. If the history of any disease is interesting, and the neglect of its study has ever punished itself, it is diphtheria. Particularly would the treatment have been more successful if the knowledge of former times had been available and more heeded. As long ago as in the seventeenth century depletion in diphtheria was condemned, and in the seventeenth and eighteenth centuries the local treatment with muriatic acid and the internal administration of cinchona, camphor, and roborant diet were held to be the only admissible ones. Bretonneau urged the same principles, and still in our own times, for want of historical knowledge, we had to learn the old lesson over again.⁵

⁴ P. Bretonneau, Des Inflammations spéciales du tissu muqueux, et en particulier de la Diphthérite, etc., Paris, 1826.

⁵ See history and bibliography of diphtheria in Chatto; Sanné, Traité de la Diphthérie, Paris, 1874; Jacobi, in Gerhardt's Handb. d. Kinderk., vol. ii., 1877; Seitz, Diphtheric und Croup gesch. u. Klin. dargest, Berlin, 1879; Index-Catalogue of the Library of the Surgeon-General's Office, U.S.A., vol. iii., Washington, 1882.

The following is a brief review of the main points of discussion upon subjects connected with the symptomatology and pathology of diphtheria since Bretonneau's first paper:

Bourquoise and Brunet express their belief (1823) in the contagious character of this disease. Desruelles (1824) sees a diagnostic difference between the sporadic and the epidemic forms in the participation of the brain in the latter. Louis referred a number of cases of croup in adults to pharyngeal diphtheria as their source. Mackenzie considers that croup has its origin in the fauces, and urges the employment of lunar caustic. Billard (1826) denies the specific character of diphtheritic inflammation. Hamilton describes cases that terminated in suppuration, and which he therefore distinguishes from Bretonneau's cases. He describes two modes of termination of the disease—one in croup, the other in a state of debility arising from the effect of the absorbed secretion on the respiratory nerves. Pretty looks upon those cases of croup that have their original seat in the tonsils as contagious. Bland (1827) explains the difference between croup and diphtheria. Deslandes declares them to be identical. Bretonneau publishes a work in which he compares diphtheria with scarlatina anginosa, and recommends the use of alum. Emmangard is the first one of the physiological school who, likening diphtheria to typhoid and claiming its origin in a malarial infection, calls it angina gastro-enterica. Abercrombie is in favor of distinguishing diphtheria from croup, but reports a number of cases of diphtheria of the pharynx that terminated fatally by stenosis of the larynx. Ribes, who encountered the disease in nine members of a single family, asserts that croup rarely occurred without a preceding diphtheria in his experience; he advises an examination of the throats of apparently healthy individuals. Fuchs relates the history of epidemics of angina maligna, and declares croup to be a genuine angina maligna trachealis, which only does not run through all the stages. Broussais opposes the identity of croup and diphtheria (1829), and gives a report of cures by means of antiphlogistic regimen and laryngotomy. Diphtheria and gangrenous angina are synonymous with him. Gendron expresses a belief in the identity of diphtheria and gangrenous angina. Roche considers the membrane rather of hemorrhagic than of inflammatory origin, and consisting of discolored fibrin. About the same time Trousseau is endeavoring to clearly establish the diagnosis between diphtheria and scarlatinous angina. Shortly after (1830), he reports cases of diphtheria which originated in blistering wounds, and of diphtheria of the skin giving rise to throat affections, and diphtheria of the throat followed by skin disease. T. F. Hoffmann cites a severe case, that ultimately recovered, with consecutive paralysis of certain cranial nerves. Cheyne (1833) makes a stand against the "confounding of croup and cynanche maligna under the name of diphtheritis." Bourgeois witnessed an epidemic succeeding mumps.

Fricout and Burley (1836) declare their belief in the contagiousness of the disease. Bouillaud attacks the theory of its specific character on the ground that abstraction of blood produced favorable results. Stokes makes a distinction between primary and secondary croup according to the original seat of the affection (1837). Kessler advocates (1841) the view of its contagious nature, and Rilliet and Barthez adduce evidence of the occurrence of ulceration and gangrene in the course of the disease. Taupin, like Ribes, enjoins a methodical examination of the throat of every patient during the prevalence of an epidemic of diphtheria, whatsoever be the disease from which the child suffers. Boudet (1842) opposes Bretonneau's hypothesis that croup is a descending diphtheria, and holds to the identity of diphtheria and gangrenous angina. In this contest Durand (1843) also takes sides against Bretonneau, and lays particular stress on the point that the diphtheritic patient succumbs rather from the severity of the constitutional symptoms than from suffocation. Rilliet and Barthez, on the other hand, rally to the support of the attacked master, asserting that the usual form of croup and that resulting from a descending diphtheritis are one and the same, while they claim that diphtheritis and gangrenous angina are distinct affections.

Meanwhile, the strife regarding the nature of the disease continued. Guersant and Blache (1844) describe the stomatite couenneuse (noma, stomacace, according to them, the rarest kind of gangrenous angina) as a form of Bretonneau's diphtheritis, and Landsberg raises the question whether a nerve-inflammation, present in a certain case, was to be looked upon as an accidental or an essential feature of the disease, and finally comes to the conclusion, with Schönlein, that it was a neurophlogosis dependent on the disease. Bouisson (1847) reports a case of diphtheritic conjunctivitis resulting in loss of the eye. Robert publishes his observations on diphtheria of the skin and of wounds, which he attributes to an atmospheric contamination in crowded wards of hospitals, and looks upon it, with Delpech and Eisenmann, as a form of hospital gangrene. Virchow, in the same year, distinguished the catarrhal, croupous, and diphtheritic varieties of the disease. Meanwhile, reports of paralysis of the soft palate after diphtheria came from Morisseau, from Trousseau and Lasegue, and lastly (1854-59) from Maingault. The subject of diphtheritic conjunctivitis was studied by A. v. Graefe (1854), who encountered the disease as a complication of diphtheria of the pharynx, nose, and skin, and hence considered it a part of the general disease rather than an independent local affection. Diphtheria, in its effects on the system, had at the same time been investigated by Trousseau, who sums up with the statement that the principal source of danger lies in the invasion of the larynx, and that the large majority of cases of croup began as a diphtheria of the pharynx, but that, even without the occurrence of a laryngeal localization, many cases terminate fatally owing to adynamia.

Outside of France, too, the subject had attracted attention. West, who had never seen the disease occur primarily, describes diphtheria as a complication of measles. Bamberger (1855) divides the inflammations of the mouth and pharynx into the catarrhal and croupous forms, and considers croup and diphtheria to be subdivisions of the latter form, differing only in degree. The paralysis of the muscles of deglutition is discussed by Dehænne (1857) who had contracted the disease, and the paralysis of other muscles by Faure. A case of diphtheria of the tonsils, nipples, and vagina in a woman recently confined, followed by infection of the new-born and the death of both, is reported by Mathieux; and cases of diphtheritic conjunctivitis by Grichard, Warlomont, and Testelin. The same year Isambert published a work in which he divided the diphtheritic affections into three forms—viz. angine couenneuse, scarlatinous angina, and diphtheritic angina. The last-mentioned is further subdivided into a croupous-diphtheritic angina, in which croup of the larynx plays an important part, and into that form in which death results from adynamia; in the latter form there is a marked swelling of the lymphatic glands. Apparently, at this time the epidemic in Paris underwent a considerable change, for the croupous form does not occur by far so frequently as Bretonneau had asserted, and croup of the larynx without a preceding diphtheria of the pharynx was observed more frequently than he would lead us to believe.

The various changes in the symptoms of the epidemics of diphtheria which were observed in different places and countries, and at different times, explain many of the differences of opinions in regard to the nature of the disease. The literature of that subject is in the last twenty-five years simply stupendous, and a few more notes must suffice for the elucidation of the drift of theories and observations. Beale was the first to look for organic beings as the cause of the disease, without finding any. Laycock sees it in the bacilli and spores of oidium albicans; Wilks, however, found the same parasite in other affections. Cammack declares the diphtheritic membrane to be herpetic. Feron also calls Bretonneau's mild form of the disease a herpetic angina with pseudo-membrane; so does Gubler. Bouchut writes against the identity of diphtheria, croup, and gangrene. Condie describes the disease as occurring with scarlatina. Litchfield claims that it is a concealed scarlatina, and Hillier that it has some connection with it. Millard cites one case in the course of which gangrene occurred, and another in which skin, mouth, pharynx, respiratory passages, oesophagus, and vulva were affected at the same time. Harley vainly endeavored to inoculate the disease in animals. Stephens declares the disease to be infectious. Sanderson looks upon it as identical with the angina maligna of the aged. Farr considered the exhalations from sewers an important etiological factor. Sellerier, Kingsford, and Harley (1859) report paralyses as sequelæ. Maugin speaks of a specific eruption; Ward, of an accompanying purpura. Bouchut and Empis remarked the frequent presence of and danger from albuminuria; so did Wade. Maugin calls attention to the fact that, when present in diphtheria, it occurs early, whereas in scarlatina it is seen during the period of desquamation, and is not of frequent occurrence even then. Gull gives an account of cases in which death resulted from asthenia, and speaks of a nerve-lesion which he attributes to the severity of the local inflammation. Hildige describes diphtheritic conjunctivitis as seen in Graefe's practice, and looks upon it as contagious. Magne denies its contagious or infectious character. Mackenzie, while probably having seen false membrane appear on the conjunctiva when in a state of inflammation, yet refuses to recognize diphtheritic conjunctivitis as a distinct disease.

In the same degree that observations of cases and epidemics increased in number, the nature of the disease and its cause commenced to be studied. The assumption that the latter was a chemical poison was soon doubted, and the parasitic nature of diphtheria considered by many as proven.

After Henle had (1840) expressed his belief in the existence of a contagium animatum, and morbid processes had for some time been compared with the phenomena of fermentation, Schwann demonstrated the presence of lower organisms in fermentation and putrefaction. The discovery of the cause of the silk-worm disease by Bassis, of the achorion by Schönlein, of the acarus by Simon, of bacteria in malignant pustule by Pollender, Brauell, and, above all, by Davaine, in relapsing fever by Obermeier, the teachings of Pasteur concerning the conditions under which putrefaction occurs,—all tended to explain the various infectious and contagious diseases by analogy also, and to stimulate the search for a vegetable organism in diphtheria. Buhl was the first to discover schizomycetæ in diphtheritic membrane, but expressed no opinion as to the part they played in the process. Hüter found them in the gray diphtheritic covering of wounds, in the surrounding apparently healthy tissues, and in the blood. Hüter and Tomasi found them in the diphtheritic membranes of the pharynx and larynx, inoculated them on the mucous membranes of animals, and described them as small, round or oval, dark-colored, active little bodies. The latter observers look upon these organisms as a part of the infectious element. Oertel found them in diphtheritic membrane and in inflamed mucous membranes in the lymphatic vessels, lymphatic glands, kidneys, and other organs; he considers them as the contagious element of diphtheria. Nassiloff, too, after inoculations in the cornea resulted in an enormous multiplication of the microscopic organisms and their appearance with pus-cells in the lacteals and in the lymphatics of the palate, and even in the bones and cartilages, asserts that the development of organisms is the primary step in the diphtheritic process. Eberth made successful inoculations in living tissues; the micro-organisms, introduced into the cornea, proliferated actively and caused an inflammation of irritative character in the surrounding tissue. He asserts, with the positiveness of an evangelist, that diphtheria cannot occur without bacteria. Klebs inoculated the micrococci in pigeons and dogs, and found them in the blood of the animals after death. Orth found them in the pleura, lungs, kidneys, and urinary bladder. But what their action is, whether they are directly pernicious, or deprive the body of certain elements (as of oxygen in malignant pustule, according to Bollinger), or injure mechanically by acting on the coats of the blood-vessels (either directly or by means of altering the blood), thus depriving whole territories of their blood-vessels, is a question upon which the principal advocates of the parasitic theory have not yet agreed. Even Oertel acknowledges the impossibility of explaining the manner in which bacteria act (Ziemssen, Handbuch, ii., 1, p. 581, 2d ed.). This much is positive, at any rate: that no one has yet proven that the vegetable organisms alone, and not other, free or fixed, parts of the diphtheritic membrane, are the vehicles of the infecting elements (Steudener); and even now the question has not been decided whether the bacteria met with in diphtheria constitute the cause of the disease, or are a part of the process, or co-effects of the poisonous action—whether they are the carriers of the poison or entirely indifferent entities.

The most important observations made by those who deny a direct etiological connection between micro-organisms and septic diseases in general, and diphtheria in particular, are those of Hiller and Billroth. The latter has proven the morphological identity of the various kinds of bacteria, although it cannot be denied that the apparent similarity may mask a yet unknown difference. Hiller calls attention to the fact that large numbers of micrococci have been found in the cadaver where death has not been the result of septic disease, and also that septic infection is not always severest where the bacteria most abound, but where an extensive chemical decomposition or a mass of putrefying tissue is found. This would indicate that the septic process is rather dependent on chemical decomposition than on the presence of bacteria.

Panum, Bergmann, and Schmiedeberg have isolated poisons that contained no bacteria. Rawitsch and many others prove that septic infection is not dependent on the existence of bacteria. Davaine has shown that an infinitely small amount of a chemical poison, free from bacteria, can kill quickly.

The presence of cocco-bacteria (Billroth) in the blood during life has not once been proven, not even in pyæmia or septicæmia. Yet their being swept into the lungs with the atmospheric air is indisputable. It would therefore seem as though living blood had a greater tendency to destroy bacteria than to allow itself to be decomposed by them. Not only, however, would it seem so, but P. Grawitz (Virch. Arch., vol. lxx., p. 546) proves that sporules do not grow in the (tissue and) blood, but that they are in part dissolved, in part eliminated through the kidneys, and that this result is accomplished through the combination of the following four factors—viz. the elasticity of the blood, its constant motion, the absence of oxygen in sufficient quantity in the circulating blood, and the presence of living animal cells. All of these factors appear to be of great importance. Thus it is that, where the constant motion of the blood and the animal living cells are not present (as in the anterior chamber of the eye or in the humor vitreous) a rapid proliferation and accumulation of bacteria can take place. They are also known to increase rapidly and emigrate into the liver when deposited in the abdominal cavity.

The destruction of bacteria in the circulating blood, into which they may have penetrated, accounts for some microscopical facts in connection with (actually or apparently morbid) blood. Their remnants are probably the pale and dark particles which are discovered in the blood alongside the red and white blood-corpuscles. They could not be identified as micrococci, while in the tissue they are more recognizable. In autopsies they have been found in the urinary tubules, pressing forward and piercing the walls, not occupying a nidus of inflammation, however, and probably are even here a post-mortem phenomenon. A direct necrosis or inflammation by the inoculation of diphtheritic elements can only be produced in the cornea, as was shown by Recklinghausen, and particularly Eberth. Besides, there is nothing characteristic in the cocco-bacteria of diphtheria, with the exception, perhaps, of their browner color, to justify their being looked upon as a distinct variety, certainly not as another species. It is more likely that a difference of action is not so much to be sought for in a different parasite as in the peculiarity of the corneal tissue. When fluid containing cocco-bacteria was injected into the eye of a rabbit, in twenty-four hours the eye was destroyed. If injected into the eye of a dog or guinea-pig, only a slight inflammation resulted (Billroth and Ehrlich). If these experiments were continued on a larger scale, we might eventually, by analogy, infer, and even prove, that the immunity against certain diseases enjoyed by some animals is owing to peculiarities in the very structure of their own tissues. In a similar manner I shall prove hereafter that even peculiarities and variations in the tissue and epithelium of the human body give rise to different shades and variable clinical symptoms in the diphtheritic processes.

The views of Curtis, Satterthwaite, and Charlton Bastian fully agree with those of the above observers. The latter is rather inclined to look upon bacteria as an effect of the disease than as a cause. Similar views were expressed by Burdon Sanderson.

Nor are the researches of Weissgerber and Terls, Lukomsky, Weigert, Lücke, any more conclusive; and, finally, Fürbringer, in his most recent and careful studies of diphtheritic nephritis, insists upon this, that it is not caused by immigration of fungi into the kidneys, that the very best methods employed for the finding of parasites result in the absence of micrococci from the inflamed organ, and that the renal inflammation following diphtheria is the result of a chemical process.

H. C. Wood and Henry F. Formad, in Supplement 7 of the National Board of Health Bulletin (1880), declare it altogether improbable that bacteria have any direct function in diphtheria—i.e. that they enter the system as bacteria and develop as such in the system, and cause the symptoms. It is, however, possible that they may act upon the exudations of the trachea as the yeast-plant acts upon sugar, and cause the production of a septic poison which differs from that of ordinary putrefaction, and bears such relations to the system as to, when absorbed, cause the systemic symptoms of diphtheria. Now, these bacteria may be always in the air, but not in sufficient quantities to cause tracheitis, but enough when lodged in the membrane to set up the peculiar fermentation; whilst during an epidemic they may be sufficiently numerous to incite an inflammation in a previously healthy throat.

The same authors publish a number of other experiments and conclusions in Suppl. 17 (Jan., 1882): "There is no proof as yet that the micrococci are the cause of the disease. Their presence in the exposed dead tissue is no evidence, for the membrane represents but the necrotic mucous lining.... Indeed, when the healthy mucous membrane of the mouth or trachea is destroyed by caustics—for instance, ammonia—the eschar into which it is converted—really a pseudo-membrane—contains the same micrococci as are found in true diphtheria, as Wood and Formad have learned. Moreover, in the scrapings of the healthy tongue the same micrococci can be seen. Of more significance is the detection of the same or similar micrococci in the blood of the living patients during severe attacks. But since these parasites were found only in the more severe cases, and not in all instances of the disease, were seen also in the blood of other septic disorders, and since no cultures have been made with the fresh blood, there is not yet enough evidence for any decision. In the internal organs bacteria are not found with any regularity in diphtheria."⁶

⁶ H. Gradle, Bacteria and the Germ Theory of Disease, Chicago, 1883, p. 186.

O. Heubner, while studying both the local affection and the general infection of diphtheria, availed himself of the methods of Cohnheim and Litten, who produced diphtheritic deposits by cutting off the circulation of the blood. He ligated the neck of the bladder in rabbits for two hours. On the first day he noticed a hemorrhagic oedema of the mucous membrane, with loosened and tumefied epithelium; on the second a firm and coagulated exudation took the place of the normal tissue; on the third there were genuine diphtheritic spots in the mucous membrane. The newly-formed pseudo-membrane exhibited all the morphological elements of human diphtheria (genuine or scarlatinous) and epidemic dysentery.⁷ Thus Heubner's results agree with the definition of diphtheria as the compound of severe inflammation and necrosis. The inoculation of his diphtheritic artefacts he found sterile. Animals, however, which were inoculated with diphtheritic masses taken from the diseased human patient fell sick with tumor of the spleen, hemorrhages, and general sepsis, besides a local diphtheritic affection. Scarlatinal diphtheria used for the same purpose had the same effect. Bacilli were developed, but they were not found in the blood-vessels (differing in that respect from the bacilli of anthrax), in spite of continued examination. Thus, Heubner refuses to accept the bacilli as the diphtheritic poison; they are, in his opinion, the result of the morbid process, and not its cause. Thus, though he believes the diphtheria poison to be organic, he concludes that its nature is not yet explained; contrary to the assertions of many prolific prophets of the bacteria literature, who now and then claim for this year's microscopic revelations the same infallibility which was claimed for last year's opposite views.⁸

⁷ Die Experimentelle Diphtherie, Leipzig, 1883.

⁸ L. Letzerich recognized in former years the specific parasites of diphtheria, whooping cough, and typhoid fever as if they were labelled. Then, again (Arch. f. Experim. Pathol. u. Pharmacol.), he admitted the great difficulty in discriminating the specific schizomycetæ of diphtheria, croupous pneumonia, epidemic influenza, and typhoid fever.

E. Rindfleisch⁹ expresses himself as follows: "The microphytes of diphtheria, septicæmia, and pyæmia have not been isolated and cultivated as yet. But experimenters are convinced that there are a great many species of microphytes underlying genuine putrefaction. In producing septicæmic conditions in animals their efficacy differs. Not every animal is influenced by the same microphyte. Thus it becomes probable that the human organism is endangered by a certain number of the putrefaction microphytes. Some one may have a particular predilection for granulating wounds and mucous membranes, and thereby produce a diphtheritic inflammation. Another may enter the blood from a recent wound and give rise to a septicæmic fever with rapidly fatal termination. The third may invade the body by means of a phlegmonous inflammation, purulent infiltration, thrombosis, embolism, and metastatic abscesses, accompanied with a pyæmic fever of a remittent type."

⁹ Die Elemente der Pathologie, Leipzig, 1883, p. 301.

After all, it does not appear to me that the bacteria question has come any nearer its solution in the last few years, in spite of the most eager researches and the fact that some of the best medical names in the world of medicine take the parasitic nature of diphtheria for granted. For instance, in the second Congress for Internal Medicine (Wiesbaden, 1883) C. Gerhardt rises in its favor. He makes the statement, or rather admits, that several parasites have been found by different men, that every one considers his the genuine one, that several writers assume that there are several diphtheria parasites, and suggests that, in his opinion, the disease may be produced by different varieties of bacteria. At the same time, he contends that the essence of the disease consists in the erosion (and change) of the epithelium and the emigration of leucocytes. If that be the case, I understand less than ever why diphtheria is, or is to be called, a parasitic disease.

Panum's words seem still to be the soundest expression of all our knowledge on the subject when he says: "It is a matter of rejoicing that physicians have come to the conclusion that certain microscopic organisms, be they considered vegetable or animal, and designated as bacteria, fungi, monads, micrococci, or vibriones, do not exist merely in the minds of theorists as causes of disease, but are in reality enemies that must be combated with all the known efficient weapons in our possession. But, while thus rejoicing, it must be borne in mind that we have but a feeble insight into the relation between these organisms and diseases, and in order to effect that much-desired advance in scientific knowledge—a matter of considerable importance in the practice of medicine—it is necessary not only to grasp at isolated data, but carefully and deliberately to observe and study all the facts before us, and even to devote some attention to those which would tend to prove that there are bacteria and fungi which, under certain circumstances, are perfectly harmless, and that even some of the malignant ones among them do not commit all those outrages with which they are charged, directly and personally."

SYMPTOMS.—In the majority of cases the disease has a prodromal stage, which usually lasts a day or two, and may run a similar course to that of a catarrhal pharyngitis. The patient feels somewhat indisposed, has slight fever, is dejected, complains of painful deglutition, more marked when swallowing fluids than solids or semi-solids, has headache and occasionally vomiting. The occurrence of the latter, however, is very much less frequent than in the outbreak of scarlatina. In very severe cases convulsions have been observed, chills very rarely; elevations of temperature of from 102.5° to 104° F. are frequent; higher ones, from 105° to 107°, rare. At this time it is often difficult or impossible to distinguish a catarrhal angina from a diphtheritic by the subjective symptoms. Slight glandular swellings under the jaw may occur in either. The characteristic objective symptom of the latter disease is the presence of membrane on the reddened mucous membrane of the fauces, which, usually, is markedly injected over all or part of the surface. The arches of the palate and the tonsils, less frequently the posterior wall of the pharynx, are so affected. A distinctly localized redness cannot be but either traumatic or diphtheritic. Larger or smaller deposits are found thereon, lying loose on the surface or deeply imbedded according to the locality. At times the first examination reveals their presence in large numbers; at other times but a single one can be detected, which is soon followed by others, however. Within a certain period of time, as a rule twenty to twenty-four hours, the single deposits coalesce and form a membrane of greater or less extent. Mostly in the same proportion to its increase in size it increases in thickness. On the uvula, soft palate, and the posterior wall of the pharynx the membrane is located superficially, and at times can be easily removed; on the tonsils it has a firmer hold, and is usually amalgamated with their uppermost tissues. On the other hand, there are cases in which no actual membranous formation is observed; in such cases the tissues are more or less swollen, the surrounding portions more or less reddened, and the grayish-white discoloration is the result of an infiltration of the tissues themselves, and cannot be removed.

There are still other cases in which deposits of membrane and tissue infiltration are found at the same time, and where both history and evidence indicate that these two phenomena are the result of one and the same process. When the uvula takes part in the process the swelling is, as a rule, more marked than when the remaining parts of the fauces only are implicated. Its circumference is very considerable, and amounts sometimes to the treble or quadruple of the normal, in consequence of the oedematous condition of the entire tissue.

We have to deal, then, with three different manifestations of the diphtheritic process: first, with a membrane lying on the mucous membrane, and removable without causing much injury to the epithelium or any to the basement membrane; such membranes were given by some the name of croupous deposits; secondly, with a membrane implicating the epithelium and upper layers of the mucous membrane; to this the title of diphtheritic membrane has been given by preference; thirdly, with a whitish or grayish infiltration of the surface and the deeper tissue, which, if abundant, may give rise to a necrotic destruction of the tissue.

The severity of the disease does not always depend on the predominance of one of these three forms, for any of them may accompany a mild or a severe attack. By a severe attack we understand one attended with chills, temperatures as high as 105° and 107° F., and marked nervous symptoms, such as vomiting and convulsions. It is characteristic of such cases that when the membrane is accidentally or forcibly removed it is speedily reproduced; the lymphatic system, in addition, takes an active part in the process. The neighboring glands become swollen; the periglandular tissue does likewise, so that the circumference of the neck becomes enormous, and the space between the lower jaw and the clavicle appears one immense tumefaction. These are the cases in which, as a rule, loss of strength and general debility speedily ensue, and death occurs from exhaustion. The membrane in cases of this description frequently undergoes changes in appearance; under the influence of the atmosphere and of foreign substances, and by admixture of blood, its color becomes yellowish or brownish. The odor of the membrane and surrounding parts becomes sweetish and musty, and occasionally so fetid that it contaminates the atmosphere of the room, and the air in its transit through the nose and over the pharynx becomes by inhalation dangerous to the patient. His throat becomes more swollen, his respiration loud; he keeps his mouth open constantly, has an indifferent expression; the saliva dribbles continually, the color of the skin is sallow and livid, the appetite very poor, and pulse both frequent and small. When the symptoms are of long duration, and a deep infiltration of the affected parts occurs, hemorrhages not infrequently make their appearance. These may be slight although frequent; occasionally, however, larger blood-vessels are encroached upon in the process of destruction, and dangerous, nay even fatal, hemorrhages may be the result. The septic forms which I have here described are more dangerous than the mild ones previously mentioned. Still, even in the latter bad results may ensue from a direct absorption into the blood of putrid substances and by the penetration of fetid gases to the lungs.

Occasionally, where the infiltration has been extensive, we meet with a condition that can only be considered as gangrene. In such cases we see collections of a grayish pulpy mass, which on falling off leaves a considerable loss of tissue, the further course of the disease being either favorable, or dangerous through absorption of septic material, or accompanied by local hemorrhages. When, after a time, health is completely restored, marked cicatrices are left behind. Such loss of tissue is generally seen in the tonsils only, but it may also be encountered in the soft palate. Its cicatrices on the soft palate are always a source of inconvenience, partly in swallowing, partly in speaking. Actual local perforation of the soft palate I have seen but five times in twenty-five years, sloughing without perforation very often.

The diphtheritic membrane not infrequently spreads from the pharynx to the neighboring organs. From the posterior aspect of the soft palate or pharynx the disease gradually ascends to the nasal cavities; this is particularly apt to occur when the uvula is the seat of extensive deposits, and by forced inspiration and deglutition its posterior surface becomes affected. In such cases the membrane which extends thence to the nasal cavities is very dense, and capable of narrowing the capacity of the nasal cavities anteriorly, and occasionally even to close them entirely; as a rule, however, several days elapse before the membrane assumes such a condition. Usually, when this form of nasal diphtheria is in its incipient stage, it is impossible to diagnosticate it; the most important sign thereof, besides a more nasal articulation and sometimes greater difficulty in deglutition, and the result of close ocular examination while the uvula is turned sideways or drawn forward, is a swelling of the deep facial glands at the angle of the lower jaw; when these swell rapidly it can be asserted positively that the nasal cavities have been invaded. There is little or no discharge from the nostrils under these circumstances.

The picture is a very different one, however, when the nose becomes primarily affected. This usually occurs only where an acute catarrh with but little secretion, not so often where a chronic catarrh, has preceded infection. When the secretion is thin and serous, the diphtheritic infection renders it no thicker, but makes it slightly flocculent, and it may become very profuse. This form is frequently attended with a disagreeable odor, equally unpleasant to the patient and to those around him. During the prevalence of an epidemic one must always be prepared to see an acute nasal catarrh or an influenza, or even a chronic nasal catarrh, become complicated with diphtheria or pass into it. Schuller reports the case of a five-weeks-old male child who, having had a nasal catarrh since birth, became affected with diphtheria of the nose. The glandular swelling of which I spoke above is a very important diagnostic, and likewise a decidedly unpleasant symptom, which becomes very marked inside of twenty-four hours; frequently a partial swelling remains long after the disappearance of the diphtheritic membrane. Such glands rarely suppurate or undergo a necrotic degeneration; sometimes they become permanently indurated. This induration and a chronic pharyngeal and nasal catarrh are very serious matters in many instances. Both of these conditions are starting-points for a number of acute or subacute attacks of diphtheria in the same person. It is they which constitute the liability of persons once affected to be taken sick again. Not only are they liable to be affected themselves, but they are a constant danger to all around them. Diphtheria, in a large family of children living in one of the best houses of the city, after having returned half a dozen times in the course of a year, disappeared instantaneously, not to return, when a seamstress living in an infected neighborhood and suffering from occasional sore throats was relieved of her daily work in the house. Oedematous swelling of the mucous membrane and submucous tissue is often observed for a long period to come; elongated uvulæ, enlarged tonsils, often date back to such an acute attack. Thus it is with the upper portion of the larynx about the posterior insertion of the vocal cords (see below); its large amount of loose submucous tissue is liable to swell considerably in acute attacks. Frequent spells of croupy cough and a certain degree of dyspnoea are often observed for years afterward. Though the cases of genuine cicatrization between the arytenoid cartilages, as described by Michael,¹⁰ be rare, with their result of permanent paresis of the thyroarytenoid interni muscles, when they do occur they are either obstinate or altogether incurable.

¹⁰ Deutsch. Arch. f. klin. Med., 1879, xxiv. p. 618.

Diphtheritic conjunctivitis occurs either primarily or as a complication of pharyngeal or nasal diphtheria. Fortunately, it is not of frequent occurrence; the cornea may become destroyed either by pressure through the considerable swelling of the eyelid or by diphtheritic keratitis. Usually the upper eyelid is the first to suffer; it is red, rigid, swollen. In the beginning the conjunctiva palpebræ is smooth, dry and pale, while that of the eye is chemosed; afterward diphtheritic deposits take place either in floccules or in solid masses. Knapp distinguishes between croup and diphtheria of the eyelid according to the facility or impossibility of removing the deposit. In favorable cases the membranes begin to macerate and the eyelids to soften after a few days. In those less favorable perforation of the cornea, prolapse of the iris, or total destruction of the eye take place.

The ear is but rarely the primary seat of diphtheria. A girl of three years died of laryngeal diphtheria on Sept. 6, 1882, after an illness of four days. A girl of seven years was removed from the house on Sept. 6th and returned on Sept. 8th. On the afternoon of the 10th an earring taken from the corpse was attached to the left ear of the sister, after having been washed with soap and water only. About noon on the 11th the lobe of the left ear reddened, on the 12th it exhibited a membrane and became swollen, and some glands enlarged in the neighborhood. On the right mastoid process the skin was not quite healthy, a vesicatory having been applied three weeks previously. This surface became diphtheritic on the 12th, without consecutive glandular swelling. On the 13th the membranes grew thicker; on the 14th the pharynx was also affected, and the physician called in.

Most diphtheritic affections of the ear, however, are secondary. In pharyngeal and nasal diphtheria the narrow orifice of the Eustachian tube is easily obstructed by either catarrhal swelling or diphtheritic deposit. The disease may invade the middle ear and the drum membrane with perforation, caries, and deafness following.

The descent of the diphtheritic process into the respiratory organs may give rise to various conditions. The membrane is not always found to pass uninterruptedly from the mucous membrane of the fauces into the larynx; not infrequently isolated diphtheritic spots are found in the pouches on either side of the attached extremity of the epiglottis, or on the epiglottis, or in the larynx. At such times the epiglottis is moderately swollen, its margins hard and reddened. Occasionally the redness is interrupted by small diphtheritic deposits, which may remain isolated for a considerable time, but generally coalesce so as to coat the edges of the epiglottis with a continuous membrane. As a rule, the upper surface of the epiglottis is not completely covered by membrane, while only now and then diphtheritic deposits are found on its under surface.

The subjective symptoms accompanying the affection of the epiglottis are not always in direct proportion to the extent of the membranes. Dyspnoea and hoarseness occasionally occur where the only abnormal condition is a marked oedema at the entrance of the larynx, particularly of the posterior wall near the arytenoid cartilages and the attachment of the vocal cords. The oedematous condition causes a functional paralysis of the vocal cords, together with marked dyspnoea on inspiration. The difficulty of breathing may become so excessive that the clinical diagnosis of croup is unquestionable, and tracheotomy resorted to, while expiration is comparatively free and the voice not markedly affected. Furthermore, cases occur in which there is no marked oedema, but merely a general catarrh of the epiglottis and larynx; here, too, the subjective symptoms of hoarseness and dyspnoea may become severe and necessitate the performance of tracheotomy. Still, bearing this in mind, I have on several occasions refrained from performing this operation where I judged that, aside from the diphtheria of the pharynx, I had to deal with a moderate oedema of the glottis or a laryngeal catarrh.

Frequently, however, membranes form in the larynx in the same way as in the pharynx or nose; then inspiration and expiration are equally interfered with, and hoarseness is a more constant symptom than in the above-mentioned cases. Fever and pain are not necessarily prominent symptoms; in fact, they are frequently unimportant, but in proportion as the degree of narrowing of the larynx increases the respiration becomes more difficult, long-drawn, and loud.

It may happen that the trachea and bronchi may become affected, although diphtheria of the fauces does not exist. This does not occur as rarely as Henoch and Oertel seem to believe. They think that diphtheritic tracheo-bronchitis is mistaken for the primary condition, because the throat is not examined early enough.

Oertel is of the opinion that the membrane in the fauces is overlooked in such cases. Steiner,¹¹ too, asserts that "the tendency of the times is to question, nay, rather to deny, the existence of croup extending from below upward." Now, on the contrary, repeated experience enables me to assert with positiveness that diphtheritic tracheo-bronchitis may occur without an affection of the pharynx at the same time. I do not deny that it may last for days without giving rise to dangerous symptoms. I know it does. But when the process reaches the larynx, the symptoms of suffocation become so urgent that tracheotomy may be absolutely required at once, and, in spite of the operation, death soon after occurs.

¹¹ Ziemssen's Handb., iv., 1, 126.

Of course these cases are exceptions; as a rule, laryngeal and tracheal diphtheria result from a descent of the disease from the fauces. More or less uncomplicated cases of primary laryngeal diphtheria, or so-called sporadic membranous croup, were, however, observed before the end of the sixth decade of this century. They were then almost the only cases of diphtheria, and linked former epidemics and the present one together.

Inflammatory affections of the lungs may occur at various times and in various forms during an attack of diphtheria. That which appears after tracheotomy is usually a broncho-pneumonia, and results from rarefaction of the air in the respiratory passages during the period of impeded respiration, with consequent collapse of pulmonary tissue and dilatation of the blood-vessels, and hence a disturbance of the circulation. It may not fully develop until after tracheotomy, and is a frequent cause of death on the second or third day after the operation. Now and then a case of lobular pneumonia will result from the aspiration of pieces of membranes into the smallest bronchi. It can be easily recognized when the trachea is opened, but previous to the operation the auscultatory signs are of little or no value, being masked by the laryngeal râles. Percussion is equally useless, for a dulness may just as well indicate collapse of the lung as infiltration. The second form of pneumonia associated with diphtheria is from the beginning fibrinous in character. Here, too, auscultation and percussion are of little assistance in establishing a diagnosis when there is a laryngeal diphtheria at the same time, for the above reasons. Where, however, the dulness on percussion is accompanied by high fever, and the long-drawn inspiration is replaced by rapid respiratory movements, the diagnosis of pneumonic complication is justified.