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Chapter XVII

Communicable Diseases, Table of Contents



Vincent's disease, as it was known during the World War, was variously designated, according to location or pathological process, as trench mouth, trench gums, trench throat, ulcerative tonsillitis, Vincent's angina, epidemic ulceromembranous stomatitis, ulcerative gingivitis, and angina necrotica. As the disease first received attention on a large scale among troops while serving in the trenches, and it was thought that conditions incident to this service at least predisposed them to infection, it was spoken of most commonly, during the war, as "trench mouth," "trench throat," and "trench gums." By some it was thought to be a new disease. All authorities are not agreed as to the origin and cause of the affection. Some contend that Vincent's angina almost invariably commences as gingivitis, acute ulcerative, sub-acute, or chronic;1 others are of the opinion that it is not a separate entity, a disease in itself, but is a manifestation of some other process, notably syphilis. Sobernheim2 is often referred to as authority for the statement that the Wassermann reaction is positive in Vincent's angina. Further, there is dispute as to the etiological part played by B. fusiformis and Vincent's spirochæta, as well as other spirochætes in the mouth, notably the S.dentium.

Vincent's disease is an acute or chronic, mildly contagious disease of the mucous membrane of the mouth, with occasional manifestations in the throat, bronchi, eye, and genitalia. It is characterized clinically by a rather slow or chronic onset, with a local lesion or lesions, pain in the acute form and little or none in the ulcerative, lymphadenopathy of the glands draining the area involved, offensive breath, interference with deglutition when the lesion is located in the mouth or throat, and comparatively little constitutional disturbance. It is characterized pathologically by the formation of a pseudomembrane or "punched out" ulceration, with a red bleeding base and the presence of the B. fusiformis and the Spirochæta vincenti.

The number of cases of Vincent's disease reported in medical literature prior to the war would indicate that it was rare until the widespread occurrence among troops on the Western Front, described by Bouty.3 Investigation showed that among the British and French troops, especially in the trenches, a disease of the mouth, gums, and tonsils, which came to be called "trench mouth," "trench throat," and "trench gums," was so common that it constituted 23 per cent of all throat complaints. It was found that these conditions were associated with an admixture of fusiform bacilli and spirilla.

Before the entrance of the United States into the war, the ulcerative form of Vincent's disease was practically unknown in the Army. Rarely cases of the acute type, characterized by presence of a pseudomembrane in the throat (rarely on the gums), with severe angina and marked constitutional symptoms, were diagnosed as Vincent's angina. These cases were so few that it was not deemed necessary to record this term in the Army list of diagnoses. Soon after the arrival of American troops in Europe, cases of "trench mouth" appeared on


the sick and wounded reports and the number of reported cases of Vincent's disease greatly increased. Cases appearing under the terms "trench mouth" and Vincent's angina were tabulated and carried separately in the files; however, the statistical tables for the World War show only cases reported as "trench mouth." In this chapter both trench mouth and Vincent's angina will be considered as one and the same disease-Vincent's disease.



In modern American textbooks the statement is made that Vincent's disease is not common among the civilian population. Theisen4 found that, between 1909 and 1910, 687 throat swabs were examined in the Michigan State Laboratory for diphtheria, and that 178 of the cases proved not to be diphtheria at all but were cases of Vincent's disease. Vincent himself found the disease in 2 per cent of all cases of membraneous angina. One is led to believe, therefore, that it is more common among civilians than heretofore believed.


Bouty,3 in 1917, stated that during the two preceding years there had been a gradual and marked increase in the number of cases of Vincent's disease among the troops in France, both British and French. In times of peace the rate was from 2 to 3 per cent of all throat complaints among French troops. Chalier5 reported 46 cases of throat conditions among 2,500 men during 22 months. Of these, 26 per cent were Vincent's disease, while Deglos6 found 21 cases of ulceromembranous stomatitis, Vincent's disease, among 255 men sent with sore throat to his contagious hospital. The acute ulcerative form of gingivitis was found present in about 0.7 per cent of the British troops in France seeking dental treatment, and in about 0.3 per cent among soldiers living under various conditions but not reporting for dental treatment.1

From the available fragmentary reports, it would appear that Vincent's disease, commonly designated by German and Austrian authors as Plaut-Vincent disease, was prevalent among the German and Austrian forces. Sauerwald7 described an outbreak of 45 cases among the German troops in 1917. These cases occurred in a hospital center and were described as Vincent's angina and noma. Sachs8 demonstrated some cases in a military hospital in Vienna in April, 1917.


Table 80 shows the number of primary admissions, deaths, discharges from the service on account of disability, and days lost from duty, by country, race, and year of occurrence, for Vincent's disease during the World War. This table includes enlisted men only. It shows that the number of cases of Vincent's disease, under the designation of trench mouth, was small, the majority having been reported from Europe, while the primary admissions for what was diagnosed Vincent's angina ran into the thousands and were about evenly divided between the United States and Europe. It is of interest to note, however, that the number of primary admissions for Vincent's disease by years increased throughout the war, although the size of the Army fluctuated greatly, being considerably smaller in 1919 than during the preceding year.


TABLE 80.-Vincent's disease. Admissions, deaths, discharges for disability, and days lost, white and colored enlisted men and native troops, United States Army, by countries of occurrence, April 1, 1917, to December 31, 1919, absolute numbers



In 1917 there were 261 primary admissions for Vincent's disease among American enlisted men, 223 in the United States and 9 in Europe. The number greatly increased the following year, with a total of 1,762. Of these, 857 were among enlisted men stationed in the United States and 848 in Europe. This increase continued during 1919, when the primary admissions amounted to 4,159, with 1,770 in the United States and 2,272 in Europe. The Army in Europe was much smaller in 1919, yet the number of primary admissions markedly increased. Not only was the disease more prevalent in Europe, but the vast majority of cases reported from stations in the United States were among troops returning from Europe. It was of rare occurrence in the large military hospitals in the United States until patients were returned from Europe for further hospitalization and troops for demobilization. At the base hospital, Camp Grant, Ill., the disease was first noticed immediately upon arrival of the first consignment of patients from abroad, December, 1918.9 Some 8,000 overseas patients were cleared through this base hospital, in addition to approximately 35,000 patients admitted from commands that had not been abroad. The overseas patients were received between December, 1918, and June, 1919. In addition to these troops, many thousands of overseas troops were sent direct to Camp Grant for demobilization. A chronic ulcerative condition of the gums and tonsils, especially the former, was noticed among the first arrivals and received active attention of the dental surgeons. It was first thought by the internist to be of syphilitic etiology and by the chief of the dental service to be a new disease. The patients spoke of their condition as "trench mouth" and some said it had been diagnosed as the "fourth venereal disease." Finally the internist and the dental surgeons agreed that the disease was Vincent's disease, described more particularly in foreign literature. From January, 1919, until this base hospital closed during the following summer, Vincent's disease was constantly present among overseas patients, but nothing in the archives of this camp or hospital indicates spread from one person to another.

The consensus of opinion among medical officers who served with troops at home before the war and with troops during the war not sent abroad is that Vincent's disease is a rare malady; however, it was quite a common affection among American troops serving in Europe. It is further recognized that the majority of cases did not seek admission to hospital; therefore, the number of admissions does not represent the occurrence. The statistics of an American base hospital at Coblentz, Germany, show Vincent's disease to have been very common and present in at least 20 per cent of cases admitted to the throat wards.10 It is further shown that this disease was not the cause of admission to hospital in the majority of cases.

As shown in Table 80, Vincent's disease was reported among American enlisted men serving elsewhere than in the United States and Europe. In 1917 there were 29 primary admissions reported among such troops, 24 of which were in the Philippines, 2 in Hawaii, and 3 on transports. The same number of primary admissions was reported during the following year. Of these, 7 were reported in the Philippines, 3 in Hawaii, 2 in Panama, 3 on transports, and 14 in countries not specified. In 1919 the number increased three or four fold. The Philippines reported 15 primary admissions; Hawaii, 7; Panama, 3; transports, 4; and countries not specified, 88.


Although occurring among American troops serving in the Philippines and Hawaii, Vincent's disease was of little or no importance among the native troops. There were 6 primary admissions among the Philippine Scouts and 1 among the native Hawaiian troops during the period of the war.

The white American soldier was more commonly affected than the colored. There were 5,873 primary admissions among the former and 157 among the latter. In addition to these, 152 primary admissions were reported where color was not stated. It is a recognized fact that the American negro suffers less from tooth and gum affections than the white man; therefore, it is not surprising to find that the occurrence of Vincent's disease was no exception to the rule. Prevalence in Europe and in the United States, based upon the reported cases, was about evenly divided, not only in the total primary admissions, but also by race.

Vincent's disease was an appreciable cause of noneffectiveness among troops during the war. There were 92,690 days lost from duty by the 6,189 primary cases, with an average of 14.97 days per case. The average days lost was greater in Europe than at home, being 13.52 and 17, respectively. The number of days of hospitalization was greater for white than for colored troops. For the former the average was 14.60 and for the latter 13.43 days. White enlisted men admitted to hospital on account of Vincent's disease lost an average of 13.66 days in the United States and 16.33 in Europe. Colored troops did not show such great variation, being 13.33 in the former country and 14.52 in the latter. When viewed by years of occurrence, it is seen that the average time lost in 1917 was 9.73 days; 1918, 15.67; and in 1919, 14.81 days, for the total Army. With the exception of 1917, the duration of hospitalization was longer in Europe than in the United States. In this year it was 6.33 and 9.84, respectively. Conditions were reversed the following two years. In 1918 and 1919, respectively, the average was 16.77 and 15.87 in Europe and 14.66 and 13.51, respectively, at home.


The whole story in the etiology of Vincent's disease has not been told; however, since the report of Plaut, and later, the contributions by Vincent, it is generally accepted that the Bacillus fusiformis and Spirochæta vincenti are intimately associated as causal factors. Yet these organisms are normal inhabitants of the mouth. Nichols11 states that some strains appear to take on virulent characteristics producing ulceration and are capable of being spread to others. He asks: "How are the two organisms related to each other and to the disease?" "Are they primary or secondary causes? If primary, how can the epidemic be identified?" There is no adequate answer at present to these crucial questions. Fusiform bacilli, other than those of Vincent, have been found in the mouth, some quite indistinguishable, morphologically, from the Vincent bacillus.

According to Zinsser,12 the fusiform bacilli described by Vincent, Plaut, Babes, and others are from 3 to 10 micra in length, and have a thickness at the center varying from 0.5 to 0.8 micron. From the center they taper gradually toward the ends, ending in blunt or sharp points. The length of these bacilli


may vary greatly within one and the same preparation. They are usually straight, sometimes slightly curved. They do not stain very easily with the weaker analine dyes, but are readily stained by Löffler's methylene-blue, carbol fuchsin, or better, by Giemsa's stain. Stained by Gram, they are usually decolorized, though in this respect the writers have found them to vary. Stained preparations show a characteristic inequality in the intensity of the stain, the bacilli being more deeply stained near the ends, and showing a banded or striped alternation of stained and unstained areas in the central body. The staining qualities in this respect are not unlike those of the diphtheria bacillus, and, according to Babes,13 the dark areas are to be interpreted as metachromatic granules. The bacilli are not motile.

The spirilla found in Vincent's angina, according to Zinsser, are usually somewhat longer than the fusiform bacilli, and are made up of a variable number of undulations, shallow and irregular in their curvatures unlike the more regularly steep waves of Spirochæta pallida. They are stained with even more difficulty than the bacilli and usually appear less distinctly in the preparations. The stain, however, is taken without irregularity, showing none of the metachromatism observed in the bacilli.

The organisms conceded to give rise to Vincent's angina do not occur in the mouth alone, but are usually accompanied by such other organisms as the staphylococcus, the streptococcus, and, at times, the diphtheria bacillus. It has been said that the two organisms of Vincent exist in symbiosis. Whether they are primarily concerned in the cause of the disease, or are merely secondary invaders, has not been determined. Animal inoculation has not assisted in elucidating this factor; however, the consensus of opinion is that the organisms of Vincent play an important rôle in the cause of Vincent's disease, yet the postulates of Koch have not been established with respect to them.

Some workers, as noted, contend that Vincent's disease is not a separate and distinct entity and that the ulcerative type is usually syphilitic. These suppositions are based upon appearance of the ulceration, chronicity, and Wassermann reaction. Diagnosis can not be made on appearance alone, and the disease, in its uncomplicated form, is neither preceded nor followed by syphilitic manifestations. It yields to local treatment. There is ample evidence to support the statement that the Wassermann reaction is negative in Vincent's disease unless the disease is superimposed on a syphilitic infection.

Barnes14 states that the most destructive and fatal forms of gangrenous necrosis in which these organisms are found occur in subjects with leucemia or one of the other of the essential blood diseases.

Bouty3 remarks that abundant bacilli, mixed with cocci, are found in the pseudomembranous form of the disease, and that bacilli associated with Gram-negative, mobile, flagellated spirilla are found in the ulcerative form.

British observers regard Vincent's disease as being always preceded by gingivitis.1 In an examination of 3,000 men, in military hospitals of England during 1918, who were admitted on account of wounds and diseases other than gingivitis, 359 cases, or 11.9 per cent, showed gingivitis, of which 354 were either subacute or chronic and 5 ulcerative.1 Barker and Miller15 regard Vincent's disease as being, in all probability, primarily a peridental gingivitis, and remark


that it is associated with characteristic gum lesions and capable of spreading to any part of the throat and mouth, possibly along the trachea and bronchi into the lungs. McKinstry16 believes that gingivitis is always the primary focus from which the disease spreads to the tonsils, palate, etc. He examined 1,320 healthy soldiers and found the fuso-spirochetal organisms in 32; he also found 95 positives among 230 recruits. The relationship of Vincent's disease to peridental gingivitis is the subject of a report by Taylor and McKinstry.17 They made systematic examination of the gums in 70 cases of Vincent's disease and in every case found the gums to be infected. In the great majority of cases there was a localized peridental or marginal gingivitis; and out of 150 cases of fuso-spirillary gingivitis found, the characteristic lesions of Vincent's disease were present in the tonsil or pharynx in 70.

The organisms of Vincent have been shown in the mouths of persons suffering from the disease and also in normal mouths. If we accept these organisms as exciting cause, carriers, both acute and chronic, exist. But, as pointed out by Nichols,11 with our present knowledge there is no scientific basis for carrier work. The exact mode of spread and underlying factors that bring about outbreaks are not well understood, yet the literature contains accounts of not infrequent epidemics. An outbreak in the German Army, Sauberwald7 reported, started in one ward of a central hospital and suddenly appeared in other wards. Barker and Miller15 found that this disease may be very infectious, as shown by the occurrence of 200 cases among 800 prisoners of a German camp in two days.

Predisposing factors are of importance equal to or greater than the presence of Vincent's organisms. The former may be controlled; the latter can not be eradicated. Of first magnitude is faulty oral hygiene. The presence of dental caries, fermenting organic matter, faulty dentition, and neglect in oral hygiene lead to gingivitis, pyorrhea alveolaris, peridental infections, abscesses, etc. The resistance of the mucous membrane of the mouth and perhaps resistance of the entire body are lowered. The mouth becomes foul and in this condition the spirochete flourishes. Those who are in a physically rundown condition are very prone to develop the disease.

During the war, especially the early part, as mentioned at the outset, Vincent's disease was often spoken of as trench mouth, trench gums, etc. It is believed that nothing in trench service per se, other than the congregating of large numbers of persons and separating them from the necessary means of maintaining clean mouths, played any part in causing the disease.

The use of tobacco has been considered an important factor in increasing susceptibility. Barker and Miller15 refer to the importance of undernourishment, and Sauberwald7 considers it an important factor in the outbreak above referred to. Generally speaking, the disease is more common as age advances. British statistics1 show that the age group under 25 years furnished the lowest percentage of cases-i. e., 6.7 per cent-and those over 35 the highest, namely, 19.2 per cent in one group and 33 per cent in another. No age, after dentition is established and before all teeth are lost, appears exempt. The part played by the vitamines as predisposing factors appears unsettled.



After an unknown incubation period, the disease sets in slowly, as a rule, with the formation of a grayish, greenish, or yellowish diphtheroid membrane situated more commonly on the tonsil, but also occurring on the gums, uvula, pharynx; in fact, it may be found on the mucous membrane of the larynx, bronchi, or trachea, usually by extension. The common sites are the tonsil and gums. This membrane is adherent and leaves a red bleeding surface when removed. The breath is foul. Gingivitis and pyorrhea alveolaris are commonly associated with Vincent's disease. The lesions are usually unilateral, but not always so. The lymph glands that drain the infected area are invariably enlarged and usually painful; they do not suppurate. Swallowing is commonly painful. The constitutional symptoms, as a rule, are neither marked nor in proportion to the degree of pathological involvement seen in the mouth. It is not uncommon for the temperature to be normal; however, 99° to 100° F. is usual, and occasionally 102° or higher is seen. Headache, anorexia, malaise, slight pains in the joints, lassitude, and some depression in variable degree are common.

Ulceration usually follows the pseudomembrane formation. The ulcer has irregular, undetermined edges and a "punched out" appearance, and though it is usually confined to the soft parts, involvement of underlying bone has been reported. Pain is not a conspicuous symptom. When located on the tonsil the ulcer is usually unilateral and situated nearer the posterior pillar. Cases have been reported where the entire tonsil had been destroyed by the process. These lesions contain the organisms of Vincent; however, other forms of bacteria are present in the smears which may require consideration in diagnosis. Large areas of the mouth may be involved. Infection may extend over the mucous membrane of the entire mouth.

Vincent classified the disease into two types: (a) The superficial pseudomembranous, or diphtheroid type, in which a thin grayish-white film usually starts over one tonsil and gradually spreads to adjacent tissue. It is remarked that the membrane is easily removed, though not en mass, leaving a bleeding base and shallow ulcer. (b) The ulcerative and more common form in which there is deep tissue ulceration covered by a thick, creamy, yellow exudate easily removed, leaving a red, granular, bleeding base. Both forms show a tendency to be unilateral. Vincent's classification is generally accepted, yet there are workers who have reported differently. Campbell and Dyas18 divide the disease into types as follows: Type I, tonsil cases; type II, ulcer of the lower jaw immediately behind the last molar tooth; type III, gingival cases; type IV, general infection of the buccal cavity. McKinstry16 describes several types, namely, affections of the gums, affections of the tonsils (Vincent's angina), and affections of the mucous membrane of the buccal cavity. This author emphasizes the statement that the commonest form of the disease is an ulcerative peridental gingivitis especially common around the lower incisors, posterior lower molars, crowned teeth, and between irregular ones. Kiefer,19 remarking on Vincent's classification into diphtheroid and ulceromembranous types, says that this is doubtful since we find vesicular, lacunar, membranous, and ulcerative forms either alone or in combination. Medical officers during the war accepted


the original classification and noted that the majority of cases were seen in ambulant persons during the ulcerative state.

Experience has proved that Vincent's disease is not confined to the mouth and that it is at times a more serious malady than formerly believed to be. Multiple lesions occur on the mucous membrane in various parts of the body. A number of deaths have been reported. This will be discussed more fully under prognosis. Bowman20 reported a case with several lesions in different parts of the body. The primary infection was probably in the mouth, the glans penis, and conjunctivæ later becoming infected, probably by the fingers. Campbell and Dyas13 reported seven cases of bronchial infection with a clinical picture of a moderately severe bronchitis, copious expectoration, little elevation of temperature, and general depression; the sputum was loaded with Vincent's organisms. The infection was self-limited and lasted about three weeks. These authors reported four cases of balanitis of Vincent origin. There was a long edematous prepuce whereon a membrane formed and extended to the glans. Corbus21 described ulcerative balanitis due to Vincent's infection as the "fourth disease." He expressed the opinion that this condition is often incorrectly diagnosed as chancroid; however, it can be differentiated by the presence of the B. fusiformis and spirillum of Vincent in the former and the Ducrey-Unna bacillus in the latter. A case was reported from the base hospital in Coblenz with ulceration of the meatus urethræ that showed the fusiform bacillus and spirillum. It yielded to local treatment and was diagnosed as Vincent's disease.

Recovery usually takes place in a week22 and recurrences are not uncommon. According to Bouty,3 recurrences may take place even three weeks after the first attack, in which case complications are more liable to occur. Recurrences were common among the American forces in Germany, yet there was nothing to indicate that these second attacks were different from the primary ones in severity. Among the approximately 25,000 patients that passed through the base hospital in Coblenz, there were two deaths attributed to Vincent's disease.10 In one, the direct cause of death was suffocation following edema of the larynx; in the other, death was attributed to streptococcic septicemia complicating Vincent's disease. In both cases there was extensive ulceration and membranous formation about the tonsil, hard and soft palates. The larynx became involved in the former case. In the latter, a severe streptococcic throat infection developed, complicating the Vincent's disease. Abscess formation was suspected about the tonsils, but incisions revealed no pus. Before death the blood culture was positive for the streptococcus.


The diagnosis of uncomplicated Vincent's disease is not difficult. The comparatively slow onset, cervical lymph adenitis, foul breath, mild or absent constitutional symptoms, with unilateral lesions, constitute the usual clinical picture. A positive diagnosis can be made only by miscroscopic examination. Stained smears and dark field examination show the presence of Bacillus fusiformis and Vincent's spirochete.

The ulceromembranous form must be differentiated from diphtheria, for the pseudomembrane in Vincent's disease is not unlike a true diphtheritic membrane. The ulcerative form of Vincent's disease must be differentiated from syphilis,


It may be possible to make this differentiation on dark field examination, as the Spirochæta pallida is morphologically different from the Vincent's spirochete is easily differentiated by those familiar with the characteristics of these organisms. This applies more particularly to the primary lesion of syphilis when located in the mouth. In ulcerative tonsillitis, or ulcers of syphilitic origin located elsewhere in the mouth, the Wassermann reaction is of the greatest assistance, being positive in syphilis and negative in Vincent's disease. A history of specific infection and appearances of syphilis elsewhere in the body will support the diagnosis.

It must be remembered that Vincent's disease is at times superimposed upon both diphtheria and syphilis. It is also to be remembered that Vincent's disease may occur in a pure diphtheria carrier. All combinations of these conditions existed among American troops during the war.

Brumbaugh23 reports as follows on the dark field study of five cases of pseudomembranous oral infection diagnosed clinically as Vincent's disease at the base hospital, Camp Dodge, Iowa:

Case 1 -White; age, 22 years. Soreness of the mouth dates from the extraction of a molar tooth one month ago; dysphagia, but no pain; smokes considerably, but teeth are sound and clean. The lesions consist of several grayish white patches on the right tonsil and a large patch of similar color involving the right side of the soft palate, extending to the gum of the upper jaw and the cheek, having a sharply defined margin and a narrow reddish zone of hyperemia around it. The base of the ulcer bleeds readily when the membrane is scraped off. The lymph nodes at the angle of the jaw on both sides are enlarged, especially on the right. The axillary and inguinal glands are moderately enlarged and easily palpable. A pigmented scar is found on the shaft of the penis. The patient claims it was caused by chancroid one year ago. His skill is clear of eruption. Wassermann test: Negative. Throat smear: Stained preparations showed the presence of the spirochetes and fusiform bacilli characteristic of Vincent's angina. Dark field examination of secretion from the lesions revealed the presence of enormous numbers of motile fusiform bacilli and coarse coiled spiral organisms, both forms being very active and darting across the microscopic field so rapidly that their morphology could be distinguished only when they are slowed up at clumps of cells or débris in the preparation. Diagnosis of ward surgeon: Vincent's angina. Dark field diagnosis: Vincent's angina.

Case 2 -White; age, 23 years. His sore throat is of three weeks' duration. Pharynx and palate are granular and red and scattered patches of grayish exudate are present on the postpharyngeal wall and right tonsil. The gum about the two posterior lower right molars is reddish, swollen, projecting above the teeth and covered with grayish membrane. The lymph nodes at the angle of the jaw are moderately enlarged; the inguinal and axillaries are also readily palpable. Patient denies veneral infection. There are no scars on the genitalia and the skin is clear. He smokes tobacco rather immoderately. The teeth are clean and free from caries. Wassermann test: Negative. Throat smear: Stained preparation shows the presence of Vincent's organisms. Dark field examination reveals very numerous coarse coiled spirochetes and a few fusiform bacilli, both forms very motile. Diagnosis of ward surgeon: Tonsillitis, acute, follicular. (2) Vincent's angina, right tonsil, moderately severe. Dark field diagnosis: Vincent's angina.

Case 3 -White; age, 23 years. His sore throat is of 10 months' duration. Lesions consist of a granular ulceration of the soft palate, having a reddish base, with scattered irregular areas of grayish pseudomembrane. He smokes moderately and his teeth are good and clean. Throat culture: Showed Bacillus diphtheriæ absent; a few hemolytic streptococci present. Throat smear: Stained preparation three months previously showed Vincent's angina organisms. Two weeks ago none was present. Wassermann tests, made, respectively, two months ago and three months ago and at the present time, are all negative. Dark field examination revealed rapidly motile fusiform bacilli and coarse coiled spirochetes. Diagnosis


of ward surgeon: Vincent's angina, severe, involving the fauces and soft palate. Dark field diagnosis: Vincent's angina.

Case 4 -White; age, 31 years. His sore throat began six weeks ago. Both tonsils and soft palate are covered with a grayish white membrane, marked off with a narrow hyperemic zone. The lymphatics at the angle of the jaw and the postcervical chains are enlarged. The inguinal lymphatics are slightly enlarged. The patient is obese, weighing 205 pounds. He has several scars on the penis, which he attributes to soft chancres six weeks ago. His skin is clear. He complains of rheumatism of the ankles. He smokes very rarely. His teeth are clean and free from caries. Throat culture showed hemolytic streptococci. Throat smear: Stained preparation showed presence of Vincent's angina organisms, Gram-positive diplococci and diptheroid bacilli. Wassermann test, made recently, was negative. Dark field examination reveals the presence of a very few typical Treponema pallida and a few Vincent's organisms. Diagnosis of ward surgeon: Vincent's angina. Dark field diagnosis: Secondary syphilis.

Case 5 -White; age, 22 years. His sore throat is of six months' duration. He smokes considerably. His teeth are slightly tobacco stained and he had two carious molars. Otherwise his teeth are in good condition. The lesions consist of grayish white patches on the soft and hard palate, the lateral and inferior surface of the tongue, and on the lower lip. They have smooth serpiginous margins and a very narrow zone of hyperemia about the palate lesion, but none around the tongue and lip lesions. The membrane is tightly adherent and does not bleed readily if the surface is rubbed. He denies venereal infection and the skin of the body is free from eruptions. The glands at the angle of the jaw are markedly enlarged. The axillaries and inguinals are also moderately enlarged. The genitalia are free from scars. Throat culture one week previously showed bacillus diphtheriæ absent. Throat smear: Stained preparation showed Vincent's angina organisms present. Wassermann test one week previously was mildly positive. Dark field examination revealed a few typical Treponema pallida. Diagnosis of ward surgeon: Acute catarrhal pharyngitis and Vincent's angina. Dark field diagnosis: Secondary syphilis.

Blood changes in Vincent's disease are of but slight diagnostic importance. There is but little change in the number of white cells. A leucocytosis of over 10,000 is rare. Deglos,6 reporting 21 cases observed in his hospital, remarks that the white counts were about 10,000 and the red cells usually were reduced to 3,000,000. Anemia was not a conspicuous sign among the American cases, as shown by review of the clinical records. All cases were not clear-cut in their symptomatology, as shown by the following case abstracted from the records of the base hospital at Camp Grant, Ill. Although several diagnoses were suggested by various consultants, the final diagnosis was Vincent's angina.

Corporal V-, Company A, 333d Machine Gun Battalion. Admitted May 2, 1918. Died August 16, 1918. The chief complaints on admission were: Pains in the stomach, chest, back, and head, vertigo, and slight cough, for the past two weeks. There was no expectoration. Examination of the clinical record shows a continuous temperature of the septic type throughout the course of the disease. The general condition on admission was good. The throat was congested and lymph glands negative. The genitourinary system was negative for pathological findings. The patient denied all venereal diseases. Otherwise the physical examination was negative. Based upon the physical examination and laboratory reports, the following diagnoses were made: (1) Fermentation, intestinal; (2) Vincent's angina.

On May 4 the right tonsil was red, swollen, and covered with an exudate. The tongue was red and coated; the breath was foul; the heart showed no abnormal findings; the spleen was palpable; a few coarse moist râles were heard over the base of both lungs. On May 12 diagnosis was made of a dento-alveolar abscess about the upper left first molar tooth. This was incised and drained. The wound received regular daily treatment. Smears showed Vincent's organisms. Arsenobenzol, 0.49 gram, was given intravenously. The glands of the neck were enlarged and tender. The intestinal fermentation was recorded as cured.


Necrosis of the upper left maxillary bone was later recorded, extending upward from the left second bicuspid tooth. The condition of the patient did not improve and on July 17 was such that transfusion of blood was thought advisable. A 250 c. c. citrated transfusion was administered. It was repeated on July 26 with 500 c. c. and again on August 5 with 350 c. c.

On July 20 there was a large sloughing area about the left upper maxilla. The patient was pale and felt weak. The tonsil was covered with an exudate and the urine showed albumin. Frequent consultations among the chiefs of services were held. The X ray showed osteomyelitis.

On July 15 a portion of the alveolar process showed sequestration. Blood examination this date showed 792,000 red cells, 13,000 white cells, and 30 per cent hemoglobin. The differential count showed 90 per cent large mononuclear, 5 per cent small mononuclear, and 5 per cent polymorphonuclear cells.

Condition generally improved following each transfusion, but improvement of short duration, usually lasting about three days. The red cell count remained about 1,000,000 hemoglobin per cent low; local condition showed a tendency to improve; the general condition did not improve. The patient became weaker, temperature continued elevated, and he died August 16, 1918.

The patient received five blood transfusions and two doses of arsenobenzol, in addition to various local applications. Several operations were performed to remove dead bone. The smears were negative for diphtheria bacilli. The Wassermann reaction was negative; also Widal reaction, and blood otherwise negative. Syphilis was excluded. The glands of the neck did not suppurate. Lymphosarcoma was suggested and X-ray treatments were given. Leukemia and pernicious anemia were also suggested, but not concurred in.

On July 11, the chief of laboratory reported as follows:

Red cells, 1,040,000; white cells, 8,400; hemoglobin, 35 per cent; large mononuclears, 58 per cent; small mononuclears, 31 per cent; polymorphonuclears, 11 per cent. A further study of the blood pictures of this patient shows that he has an index of 1.25; that he has many large, deeply stained red cells such as are commonly seen in advanced anemia of the splastic type. His blood cells have recently been as high as 24,000 which is decidedly against this as a diagnosis. The white cells show a very remarkable condition. There are, at this time, almost no polynuclear cells to be seen. There are, however, cells evidently of bone marrow origin in the blood which can be classed as myelocytes; and there are others less mature. I take the latter to be myeloblasts and premyeloblasts. There is also a decided relative increase in the number of lymphocytes. The total white count is low. This, however, is not an impossible finding in leukemia. On the whole, the blood picture might be interpreted as a myelogenous leukemia. Smears which I took from the mouth this morning show: (1) Nothing suggestive of Vincent's angina; (2) a diplococcus which in some places is seen in chains of from 4 to 8 organisms and which may be a streptococcus.

This patient was in hospital 107 days. The report of necropsy and histological reports are as follows:


On this the 16th day of August, 1918, I held in the morgue of the base hospital a postmortem examination upon the body of Corp. V-- , Company A, 333d Machine Gun Battalion, who died in ward 32, August 16, 1918, with the clinical diagnosis of Vincent's angina. * * *

The left side of the face is swollen more than the right, and there is a definite swelling of the tissue about the superior maxilla downward to the angle of the jaw. There is no recent blood in the nostrils or the external auditory canals. On the left side from a point directly behind the upper canine tooth and extending backward to the last molar, which is loose, there is a necrosis into the antrum of Highmore through an opening fully 1 cm. in diameter. There is a bluish discoloration and a loosening of the mucous membrane along the gum margin of the teeth practically everywhere, but mostly those teeth which are posterior and below. The first lower left molar is loose, the second is absent, and the third is also loose. The mucous membrane is very pale. The neck is fairly long and there is an enlargement of the cervical lymph glands particularly on the left side.

* * * Upon eviscerating the chest and abdomen in the usual way there are found no injuries on the inside of the thorax other than such as might have been produced by tearing of the adhesions between the parietal and visceral pleura. The lining of the aorta is very pale, quite smooth, and roughened only by scattered areas of subintimal fatty infiltration. The lymph glands along the aorta everywhere are increased in size, and for the most part are rather dark brown or cyanotic in color; they are also fairly firm. The lymph glands at the bifurcation of the trachea are small and on the surfaces made by sectioning there are firm


gray pale white nodules 1 mm. in size. The lining of the esophagus is very pale, otherwise it is normal save for a slight epitheliosis of its lining. The lymph glands at the bifurcation of the trachea are moderately increased in size and are fairly large. On the left side there is a mass of glandular tissue very much increased in size; the section surfaces of this gland being very firm and pale. This mass of glandular tissue is rough, 3 by 4 by 2 cm. and extending out onto the pleural surface just above the region of the pericardium, and on the outer surface of the pericardium there are translucent white nodules which lie close to the mass of glandular tissue just described. There are also gray areas on the pleural surfaces of the left lung, just above the point where the left bronchus enters this organ.

The lining of the trachea and main bronchi is very pale. On the outer surface of the right lung there are numerous subpleural petechial hemorrhages. The posterior portion of this lung is somewhat boggy, but contains air throughout. The anterior margin of the left lung is adherent to the pericardial sac, and on the surface made by sectioning this tissue this organ is very pale. The anterior margin of the left lung is firmly adherent to the pericardial sac. In the region of the thymic body there are lymph glands, some of them very red but containing on the surfaces made by sectioning pale white nodules from 1 to 2 mm. in diameter. In one of the lymph glands there is a small caseous calcified spot 1 mm. in diameter. * * *

* * * On the right side the lymph glands of the cervical region are large and form a mass along the course of the deep vessels of the neck. The thyroid gland is very pale, but otherwise is quite normal. On the left side the cervical lymph glands are also enlarged. The enlargement extends upward. There are no changes in the esophagus, or pharynx. The larynx is very pale, but there is no disease of this organ. The section surfaces of the lymph glands removed from the left cervical region are large and pale white; they are very firm. On the surface made by sectioning the septa of the glands extend down into their substance dividing the firm pale areas, already mentioned, into areas of tissue completely or partially separated from each other. In such lymph glands where the enlargement has not completely destroyed the gland there are white areas from 1 to 2 mm. in diameter. Both sera maxillary glands, on both sides, are incapsulated, but otherwise appear quite normal.

No further examination of the body was made.


1. Extensive chronic suppurative necrosis of the alveolar process of the left superior maxillary bone.

2. Chronic suppurative sinusitis of the left antrum of Highmore.

3. Numerous absent teeth.

4. Chronic generalized suppurative gingivitis and pyorrhea alveolaris.

5. Chronic inflammatory edema of the left side of the face.

6. Marked chronic nonsuppurative adenitis of the right and left cervical and of the parabronchial lymph glands.

7. Marked emaciation.

8. Marked generalized anemia.

9. Multiple petechial hemorrhages and small suggillations of many tissues of the body.

10. Cloudy swelling and acute fatty changes of the myocardium and parenchymatous organs.

11. Marked hyperplasia of the spleen, biliary, mesenteric, and abdominal aortic lymph glands.

12. Chronic nodular caseous and calcified tuberculosis of the parabronchial lymph glands.

13. Left chronic nodular fibrous tubereculosis pleuritis.

14. Serous atrophy of the peritoneal adipose tissue.

15. Slight left hydrothorax.

16. Slight hydropericardium.

17. Chronic diffuse nephritis-large white kidney.

18. Slight subintimal fatty infiltration of the aorta.

19. Persistent musculomembranous Eustachian valve.

20. Fibrous patches in the tricuspid leaflets.

21. Fenestration of the cusps of the aortic semilunar valve.

22. Bilateral fibrous pleuritis.

23. Left intersigmoid fossa.

24. Fibrous adhesive perisplenitis.

25. Multiple accessory spleens.

26. Numerous venæ and hypodermic needle puncture wounds of both arms.

27. Old circumcision scar of the foreskin of the penis.

28. Slight decubital necrosis over the sacrum and left posterior superior iliac spine.



L-- V--. Autopsy No. 81.

(A) Lymph gland: There is a marked increase in the mononuclear cells of this lymph gland. These cells are relatively large with a fairly abundant margin of cytoplasm and a relatively clear vesicular and slightly mottled nucleus. The lymph gland for the most part consists of these cells which resemble in many respects endothelial cells as they are found in lymph glandular tissue. So profound are the changes in this lymph gland that there is very little lymphoid cells as such, the tissue consisting essentially of these large mononuclear cells packed very closely. Even the capsule of the lymph gland in places has been invaded by these cells.

(B) Lymph gland: Around the lymph gland there is a certain amount of edematous adipose tissue. It too contains many large mononuclear cells. These cells have penetrated into the adipose tissue surrounding the lymph gland.

(C) Lymph gland: The description as given in A and B holds true for C, with this exception, that the density in the arrangement of the large mononuclear is greater and in the centers of the more densely arranged portions there are areas of about one-fifth millimeter and smaller where the cells have undergone necrosis. The nuclei of these cells are pycnotic, fragmented, or entirely missing, the cytoplasm of the cells being pinkly stained. These areas of necrosis are fairly abundant. The lymphoid cells in this gland too are arranged in nodules, relatively small.

(D) Lymph gland: The same as A and B, without areas of necrosis.

(E) Lymph gland: Contains areas of necrosis, the striking features of which is that the outline of the cells in the destroyed tissue is still present.

(F) Lymph gland: Similar to A and B, with very little necrosis.

(G) Lymph gland: Similar to A and B, with small hemorrhages in one spot.

Liver: The uniformity of the liver structure under the microscope is broken by collections of mononuclear cells in numbers from about a half dozen to others in areas fully 1 millimeter in maximum dimensions. These areas are usually perilobularly arranged along the portal canals or occasionally appearing toward the center of the lobules. The latter condition is the exception rather than the rule. These mononuclear cells are as given in A, B, C of the lymph glands described, namely, cells with circular nuclei and a moderate amount of cytoplasm. The sinusoids of the liver for the most part are widely distended, around the peripheral portions of the lobules, they being less wide than toward the centers. The liver chords diminish in width toward the center of the lobules where the cytoplasm of the cells is practically gone. Where present the cytoplasm is vacuated. These retrogressive liver changes in the liver chords extend fully two-thirds to three-fourths of the distance from the center to the periphery of the lobules.

Testicle: There is a marked atrophy of the testicular epithelium, with absolutely no or very little spermatogenisis. The tubules are very small and between the tubules there is an extensive infiltration of the tissue with mononuclear cells such as have been described in several places above.

Spleen: In the spleen, too, there is a profound proliferation of endothelial cells. Many of the endothelial cells are pigmented a light brown and contain either injected red cells or circular, irregular masses of a brown amorphous substance. Some of these are light brown on yellow granules.

Adrenal: The cells of the adrenal cortex are markedly vacuolated. This is true almost throughout the entire substance of the organ.

Accessory spleen: There is a decided hyperplasia of endothelial cells of this organ similar to the description given for the spleen proper. There is a small area of necrosis about one-half millimeter in diameter in this section.

Kidney: There is a moderate interstitial edema in this organ, and there are scattered areas of endothelial mononuclear cell infiltration in size from a few cells to others one-fourth of a millimeter in diameter. These are commonly found around the glomnerulæ and along the vessels. The tubular epithelium of the convoluted tubules is fairly low, and in the lumina of these tubules there are pinkly stained granules. There are pink granules in the capsule spaces of the glomerular spaces also.



The majority of cases terminate in complete recovery. The average duration among American soldiers during the World War was 14.97 days.

Among 6,189 primary admissions for Vincent's disease in the Army during the war, the records show 12 deaths. No deaths were reported during 1917. In 1918, there were 8 deaths, 7 among white troops and 1 among colored. During the following year there were 4 deaths among white enlisted men. Eight of the deaths occurred in the United States and 4 in Europe. All were reported among cases primarily admitted to hospital on account of Vincent's disease, and in probably all instances, the deaths were due to complications.

As a basis for discharge from the service on surgeon's certificate of disability, Vincent's disease was of minor importance. The records of the Surgeon General's Office show four enlisted men discharged from the service on this account, all white. In 1918, there was one such case in the United States. In 1919, there were three cases, also in the United States. Since Vincent's disease is self-limited, beyond doubt the soldiers were discharged for some associated condition or complication; however, the records do not permit of analysis to determine this matter in detail.


No specific preventive measures were known before the war and none developed during that period. It has been established that the disease is an infection; however, the method of transmission is unknown. The organisms of Vincent are constantly present where Vincent's disease exists, but are also normal inhabitants of the mouth. The important factor seems to be in the prevention of lowered local and constitutional resistance. The best results are accomplished by proper oral hygiene. Accepting the British point of view, if the gums and teeth are kept clean, there can be no marginal gingivitis, and if no marginal gingivitis develops, pyorrhea and Vincent's disease do not develop. Since the organisms are contained in discharges from the lesion, which is commonly located in the mouth, the proper care of drinking cups and eating utensils is of importance.

In some camps during the war attempts were made to quarantine contacts merely on account of the presence of a few Vincent organisms in the throat. In view of our incomplete knowledge of the transmission of Vincent's disease from one individual to another, and in view of the presence of the causative organisms in the mouths of many normal individuals, quarantine is not considered practicable.


Specific and empirical treatment have been advocated by contributors to the literature of the therapeutics of Vincent's disease. In the specific treatment arsenic is used both locally and intravenously, while in the empirical treatment such medicaments as silver salts, methylene blue in alcohol, liquor potassii arsenitis, and salicylic acid are recommended.

In 1910, Ehrlich24 called attention to the value of salvarsan in the treatment of Vincent's disease. On account of the specific action of this drug upon spirochetes, especially the Spirochæta pallida, many clinicians have used it in the treatment of Vincent's disease, especially in its severer forms. The drug, how-


ever, is expensive and acts best only when given intravenously. Partly on this account and partly because the vast majority of cases recover under simple local treatment and the correction of faulty oral hygiene, it has not been used as a routine.

It has been said that a good dentist is the best therapeutic measure. Filthy mouths must be cleaned up, and gingivitis and pyorrhea alveolaris must be adequately treated, if satisfactory improvement is to be expected. Local application of drugs, curettement, and intravenous therapy are merely adjuncts.

Intravenous administration of salvarsan or neosalvarsan was used in the Army in protracted cases; however, only rarely was it necessary. Generally speaking, patients suffering from Vincent's disease were admitted to wards set aside for patients suffering from inflammation of the throat. No special attempt was made to quarantine them, and if detected in other wards where they happened to be for a concurrent disease, they were allowed to remain in these wards as long as the primary cause of admission was the more important from the treatment standpoint. The records of several hospitals show special care taken in the handling of eating utensils. There is nothing in the available records to indicate that any patient contracted Vincent's disease while in hospital.

Mercury in any form is contraindicated for these patients on account of its physiological action on gum tissue. It is best to refrain from the use of tobacco while under treatment. The use of the toothbrush must be encouraged; Vincent's disease is more common in those who are lax in this respect. In some hospitals, patients suffering from this disease were lined up after meals, each with his toothbrush, and marched to the toilet or other place where they could clean their teeth, the cleaning being supervised by one in authority. Further, they were taken to the dental surgeon at regular intervals. In this manner proper oral hygiene was soon established and maintained. This is the most important phase of the treatment.


(1) History of the Great War (British), Medical Services, Pathology. His Majesty's Stationery Office, London, 1923, 533.

(2) Sobernheim, W.: Kurze serologische Mitteilung zur Angina Vincenti-Frage. Archie für Laryngologie und Rhinologie, Berlin, 1909, xxi, Heft 3, 504.

(3) Bouty, R. J. C.: Vincent's Angina among the Troops in France. The British Medical Journal, London, November 24, 1917, ii, 685.

(4) Theisen, C. F.: Report of Some Interesting Cases of Vincent's Angina. Annals of Otology, Rhinology and Laryngology, St. Louis, 1918, xxvii, No. 2, 594.

(5) Chalier, J.: A propros de l'angine de Vincent. Le Progrès Médical, Paris, 1918, No. 20, 174.

(6) Deglos, E.: Quelques observations a propos de l'angine de Vincent. Un cas compliqué de sphacèle grave des tissus voisins. Lyon médical, 1918, cxxvii, No. 1, 3.

(7) Sauerwald: Ueber, Angina Vincenti und Noma. Berliner klinische Wochenschrift, Berlin, 1917, liv, No. 5, 111.

(8) Sachs, Otto: Demonstrationsabend im k. u. k. Garnisonsopital Nr. 2 in Wien, April 2, 1917. Wiener klinische Wochenschrift, Wien, 1917, xxx, No. 35, 1122.

(9) Based on History of Base Hospital, Camp Grant, Ill., by Lieut. Col. H. C. Michie, M. C. On file, Historical Division, S. G. O.

(10) Personal observation of the author.


(11) Nichols, Henry J.: Carriers in Infectious Diseases. Williams and Wilkins Co., Baltimore, 1922, 98. 

(12) Zinsser, Hans: A Textbook of Bacteriology. D. Appleton and Co., New York, Fifth Edition, 1922, 867.

(13) Babes, V.: Spindelförmige Bazillen. Handbuch der Pathogenen Mikroorganismen. Ergänzungsband I, Jena, 1907, Heft 2, 271.

(14) Barnes, H. A.: Vincent's Angina. The Medical Clinics of North America, Philadelphia, 1918, i, No. 4, 997.

(15) Barker, L. F., and Miller, S. R.: Perforating Ulcer of the Hard Palate Resembling Tertiary Syphilis. The Journal of the American Medical Association, Chicago, 1918, lxxi, No. 10, 793.

(16) McKinstry, W. H.: Vincent's Disease of the Mouth and Pharynx. Practitioner, London, 1917, xcix, December, 507.

(17) Taylor, F. E., and McKinstry, W. H.: The Relationship of Vincent's Angina to Peridental Gingivitis. Journal of the Royal Army Medical Corps, London, 1918, xxx, No. 5, 512.

(18) Campbell, A. R. and Dyas.: Epidemic Ulceromembranous Stomatitis (Vincent's Angina) Affecting Troops. The Journal of the American Medical Association, Chicago, 1917, lxviii, No. 22, 1596.

(19) Kiefer, H. A.: Vincent's Angina. The Laryngoscope, St. Louis, 1919, xxix, No. 3, 150.

(20) Bowman, F. B.: A Case of Vincent's Infection Involving Mouth, Eyes, and Penis. The Lancet, London, October, 6, 1917, ii, 536.

(21) Corbus, B. C.: Erosive and Gangrenous Balanitis. The Fourth Veneral Disease. A Further Report. Journal of the American Medical Association, Chicago, 1913, lx, No. 24, 1769.

(22) Stevens, A. A.: Vincent's Angina. In The Practice of Medicine. Philadelphia, W. B. Saunders Co., 1922, 400.

(23) Brumbaugh, A. S.: Dark Field Study of Five Cases of Pseudomembranous Oral Infection Diagnosed Clinically as Vincent's Angina, at Base Hospital, Fort Dodge, Iowa. Survey of Head Surgery, September, 1918, i, No. 2. On file, Historical Division, S. G. O.

(24) Ehrlich, P.: Aerztlicher Verein in Frankfurt a. M. Erfahrungen mit Ehrlich-Hata 0.5 geheilt. Diskussion. Muenchener medizinische Wochenschrift, München, 1910, lvii, part 2, No. 43, 2268.