Communicable Diseases, Table of Contents
CHAPTER XVII
VINCENT'S DISEASE
Vincent's disease, as it was known during the World War,was variously designated, according to location or pathological process, astrench mouth, trench gums, trench throat, ulcerative tonsillitis, Vincent'sangina, epidemic ulceromembranous stomatitis, ulcerative gingivitis, and anginanecrotica. As the disease first received attention on a large scale among troopswhile serving in the trenches, and it was thought that conditions incident tothis service at least predisposed them to infection, it was spoken of mostcommonly, during the war, as "trench mouth," "trenchthroat," and "trench gums." By some it was thought to be a newdisease. All authorities are not agreed as to the origin and cause of theaffection. Some contend that Vincent's angina almost invariably commences asgingivitis, acute ulcerative, sub-acute, or chronic;1others 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. Sobernheim2is often referred to as authority for the statement that the Wassermann reactionis positive in Vincent's angina. Further, there is dispute as to theetiological part played by B. fusiformis and Vincent's spiroch?ta, aswell as other spiroch?tes in the mouth, notably the S.dentium.
Vincent's disease is an acute or chronic, mildly contagiousdisease of the mucous membrane of the mouth, with occasional manifestations inthe throat, bronchi, eye, and genitalia. It is characterized clinically by arather slow or chronic onset, with a local lesion or lesions, pain in the acuteform and little or none in the ulcerative, lymphadenopathy of the glandsdraining the area involved, offensive breath, interference with deglutition whenthe lesion is located in the mouth or throat, and comparatively littleconstitutional disturbance. It is characterized pathologically by the formationof a pseudomembrane or "punched out" ulceration, with a red bleedingbase and the presence of the B. fusiformis and the Spiroch?tavincenti.
The number of cases of Vincent's disease reported inmedical literature prior to the war would indicate that it was rare until thewidespread occurrence among troops on the Western Front, described by Bouty.3Investigation showed that among the British and French troops, especiallyin the trenches, a disease of the mouth, gums, and tonsils, which came to becalled "trench mouth," "trench throat," and "trenchgums," was so common that it constituted 23 per cent of all throatcomplaints. It was found that these conditions were associated with an admixtureof fusiform bacilli and spirilla.
Before the entrance of the United States into the war, theulcerative form of Vincent's disease was practically unknown in the Army.Rarely cases of the acute type, characterized by presence of a pseudomembrane inthe throat (rarely on the gums), with severe angina and marked constitutionalsymptoms, were diagnosed as Vincent's angina. These cases were so few that itwas not deemed necessary to record this term in the Army list of diagnoses. Soonafter the arrival of American troops in Europe, cases of "trenchmouth" appeared on
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the sick and wounded reports and the number of reported casesof Vincent's disease greatly increased. Cases appearing under the terms"trench mouth" and Vincent's angina were tabulated and carriedseparately in the files; however, the statistical tables for the World War showonly cases reported as "trench mouth." In this chapter both trenchmouth and Vincent's angina will be considered as one and the same disease-Vincent'sdisease.
OCCURRENCE
IN CIVIL POPULATION
In modern American textbooks the statement is made that Vincent'sdisease is not common among the civilian population. Theisen4found that, between 1909 and 1910, 687 throat swabs were examined in theMichigan State Laboratory for diphtheria, and that 178 of the cases proved notto be diphtheria at all but were cases of Vincent's disease. Vincent himselffound the disease in 2 per cent of all cases of membraneous angina. One is ledto believe, therefore, that it is more common among civilians than heretoforebelieved.
IN ARMIES
Bouty,3 in 1917,stated that during the two preceding years there had been a gradual and markedincrease in the number of cases of Vincent's disease among the troops inFrance, both British and French. In times of peace the rate was from 2 to 3 percent of all throat complaints among French troops. Chalier5 reported46 cases of throat conditions among 2,500 men during 22 months. Of these, 26 percent were Vincent's disease, while Deglos6found 21 cases of ulceromembranous stomatitis, Vincent's disease, among 255men sent with sore throat to his contagious hospital. The acute ulcerative formof gingivitis was found present in about 0.7 per cent of the British troops inFrance seeking dental treatment, and in about 0.3 per cent among soldiers livingunder various conditions but not reporting for dental treatment.1
From the available fragmentary reports, it would appear thatVincent's disease, commonly designated by German and Austrian authors as Plaut-Vincentdisease, was prevalent among the German and Austrian forces. Sauerwald7described an outbreak of 45 cases among the German troops in 1917. These casesoccurred in a hospital center and were described as Vincent's angina and noma.Sachs8 demonstrated some cases in amilitary hospital in Vienna in April, 1917.
IN UNITED STATES ARMY
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 theWorld War. This table includes enlisted men only. It shows that the number ofcases of Vincent's disease, under the designation of trench mouth, was small,the majority having been reported from Europe, while the primary admissions forwhat was diagnosed Vincent's angina ran into the thousands and were aboutevenly 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 yearsincreased throughout the war, although the size of the Army fluctuated greatly,being considerably smaller in 1919 than during the preceding year.
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VINCENT'S ANGINA
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In 1917 there were 261 primary admissions for Vincent'sdisease 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. Ofthese, 857 were among enlisted men stationed in the United States and 848 inEurope. This increase continued during 1919, when the primary admissionsamounted to 4,159, with 1,770 in the United States and 2,272 in Europe. The Armyin Europe was much smaller in 1919, yet the number of primary admissionsmarkedly increased. Not only was the disease more prevalent in Europe, but thevast majority of cases reported from stations in the United States were amongtroops returning from Europe. It was of rare occurrence in the large militaryhospitals in the United States until patients were returned from Europe forfurther hospitalization and troops for demobilization. At the base hospital,Camp Grant, Ill., the disease was first noticed immediately upon arrival of thefirst consignment of patients from abroad, December, 1918.9Some 8,000 overseas patients were cleared through this base hospital, inaddition to approximately 35,000 patients admitted from commands that had notbeen abroad. The overseas patients were received between December, 1918, andJune, 1919. In addition to these troops, many thousands of overseas troops weresent direct to Camp Grant for demobilization. A chronic ulcerative condition ofthe gums and tonsils, especially the former, was noticed among the firstarrivals and received active attention of the dental surgeons. It was firstthought by the internist to be of syphilitic etiology and by the chief of thedental service to be a new disease. The patients spoke of their condition as"trench mouth" and some said it had been diagnosed as the "fourthvenereal disease." Finally the internist and the dental surgeons agreedthat the disease was Vincent's disease, described more particularly in foreignliterature. From January, 1919, until this base hospital closed during thefollowing summer, Vincent's disease was constantly present among overseaspatients, but nothing in the archives of this camp or hospital indicates spreadfrom one person to another.
The consensus of opinion among medical officers who servedwith troops at home before the war and with troops during the war not sentabroad is that Vincent's disease is a rare malady; however, it was quite acommon affection among American troops serving in Europe. It is furtherrecognized that the majority of cases did not seek admission to hospital;therefore, the number of admissions does not represent the occurrence. Thestatistics of an American base hospital at Coblentz, Germany, show Vincent'sdisease to have been very common and present in at least 20 per cent of casesadmitted to the throat wards.10 It is furthershown that this disease was not the cause of admission to hospital in themajority of cases.
As shown in Table 80, Vincent's disease was reported amongAmerican enlisted men serving elsewhere than in the United States and Europe. In1917 there were 29 primary admissions reported among such troops, 24 of whichwere in the Philippines, 2 in Hawaii, and 3 on transports. The same number ofprimary admissions was reported during the following year. Of these, 7 werereported in the Philippines, 3 in Hawaii, 2 in Panama, 3 on transports, and 14in countries not specified. In 1919 the number increased three or four fold. ThePhilippines reported 15 primary admissions; Hawaii, 7; Panama, 3; transports, 4;and countries not specified, 88.
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Although occurring among American troops serving in thePhilippines and Hawaii, Vincent's disease was of little or no importance amongthe native troops. There were 6 primary admissions among the Philippine Scoutsand 1 among the native Hawaiian troops during the period of the war.
The white American soldier was more commonly affected thanthe colored. There were 5,873 primary admissions among the former and 157 amongthe latter. In addition to these, 152 primary admissions were reported wherecolor was not stated. It is a recognized fact that the American negro suffersless from tooth and gum affections than the white man; therefore, it is notsurprising to find that the occurrence of Vincent's disease was no exceptionto the rule. Prevalence in Europe and in the United States, based upon thereported cases, was about evenly divided, not only in the total primaryadmissions, but also by race.
Vincent's disease was an appreciable cause ofnoneffectiveness among troops during the war. There were 92,690 days lost fromduty by the 6,189 primary cases, with an average of 14.97 days per case. Theaverage 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 thanfor colored troops. For the former the average was 14.60 and for the latter13.43 days. White enlisted men admitted to hospital on account of Vincent'sdisease 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 formercountry and 14.52 in the latter. When viewed by years of occurrence, it is seenthat 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 ofhospitalization was longer in Europe than in the United States. In this year itwas 6.33 and 9.84, respectively. Conditions were reversed the following twoyears. In 1918 and 1919, respectively, the average was 16.77 and 15.87 in Europeand 14.66 and 13.51, respectively, at home.
ETIOLOGY
The whole story in the etiology of Vincent's disease hasnot been told; however, since the report of Plaut, and later, the contributionsby Vincent, it is generally accepted that the Bacillus fusiformis and Spiroch?tavincenti are intimately associated as causal factors. Yet these organismsare normal inhabitants of the mouth. Nichols11states that some strains appear to take on virulent characteristics producingulceration and are capable of being spread to others. He asks: "How are thetwo organisms related to each other and to the disease?" "Are theyprimary or secondary causes? If primary, how can the epidemic beidentified?" There is no adequate answer at present to these crucialquestions. Fusiform bacilli, other than those of Vincent, have been found in themouth, some quite indistinguishable, morphologically, from the Vincent bacillus.
According to Zinsser,12the fusiform bacilli described by Vincent, Plaut, Babes, and others arefrom 3 to 10 micra in length, and have a thickness at the center varying from0.5 to 0.8 micron. From the center they taper gradually toward the ends, endingin blunt or sharp points. The length of these bacilli
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may vary greatly within one and the same preparation. Theyare usually straight, sometimes slightly curved. They do not stain very easilywith the weaker analine dyes, but are readily stained by L?ffler's methylene-blue,carbol fuchsin, or better, by Giemsa's stain. Stained by Gram, they areusually decolorized, though in this respect the writers have found them to vary.Stained preparations show a characteristic inequality in the intensity of thestain, the bacilli being more deeply stained near the ends, and showing a bandedor striped alternation of stained and unstained areas in the central body. Thestaining qualities in this respect are not unlike those of the diphtheriabacillus, and, according to Babes,13 thedark areas are to be interpreted as metachromatic granules. The bacilli are notmotile.
The spirilla found in Vincent's angina, according toZinsser, are usually somewhat longer than the fusiform bacilli, and are made upof a variable number of undulations, shallow and irregular in their curvaturesunlike the more regularly steep waves of Spiroch?ta pallida. They arestained with even more difficulty than the bacilli and usually appear lessdistinctly in the preparations. The stain, however, is taken withoutirregularity, showing none of the metachromatism observed in the bacilli.
The organisms conceded to give rise to Vincent's angina donot occur in the mouth alone, but are usually accompanied by such otherorganisms as the staphylococcus, the streptococcus, and, at times, thediphtheria bacillus. It has been said that the two organisms of Vincent exist insymbiosis. Whether they are primarily concerned in the cause of the disease, orare merely secondary invaders, has not been determined. Animal inoculation hasnot assisted in elucidating this factor; however, the consensus of opinion isthat the organisms of Vincent play an important r?le in the cause of Vincent'sdisease, yet the postulates of Koch have not been established with respect tothem.
Some workers, as noted, contend that Vincent's disease isnot a separate and distinct entity and that the ulcerative type is usuallysyphilitic. These suppositions are based upon appearance of the ulceration,chronicity, and Wassermann reaction. Diagnosis can not be made on appearancealone, and the disease, in its uncomplicated form, is neither preceded norfollowed by syphilitic manifestations. It yields to local treatment. There isample evidence to support the statement that the Wassermann reaction is negativein Vincent's disease unless the disease is superimposed on a syphiliticinfection.
Barnes14 statesthat the most destructive and fatal forms of gangrenous necrosis in which theseorganisms are found occur in subjects with leucemia or one of the other of theessential blood diseases.
Bouty3 remarks that abundant bacilli, mixed withcocci, are found in the pseudomembranous form of the disease, and that bacilliassociated with Gram-negative, mobile, flagellated spirilla are found in theulcerative form.
British observers regard Vincent's disease as being alwayspreceded by gingivitis.1 In an examination of3,000 men, in military hospitals of England during 1918, who were admitted onaccount of wounds and diseases other than gingivitis, 359 cases, or 11.9 percent, showed gingivitis, of which 354 were either subacute or chronic and 5ulcerative.1 Barker and Miller15regard Vincent's disease as being, in all probability, primarily aperidental gingivitis, and remark
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that it is associated with characteristic gum lesions andcapable of spreading to any part of the throat and mouth, possibly along thetrachea and bronchi into the lungs. McKinstry16believes that gingivitis is always the primary focus from which thedisease spreads to the tonsils, palate, etc. He examined 1,320 healthy soldiersand found the fuso-spirochetal organisms in 32; he also found 95 positives among230 recruits. The relationship of Vincent's disease to peridental gingivitisis the subject of a report by Taylor and McKinstry.17They made systematic examination of the gums in 70 cases of Vincent'sdisease and in every case found the gums to be infected. In the great majorityof cases there was a localized peridental or marginal gingivitis; and out of 150cases of fuso-spirillary gingivitis found, the characteristic lesions ofVincent's disease were present in the tonsil or pharynx in 70.
The organisms of Vincent have been shown in the mouths ofpersons suffering from the disease and also in normal mouths. If we accept theseorganisms as exciting cause, carriers, both acute and chronic, exist. But, aspointed out by Nichols,11 with our presentknowledge there is no scientific basis for carrier work. The exact mode ofspread and underlying factors that bring about outbreaks are not wellunderstood, yet the literature contains accounts of not infrequent epidemics. Anoutbreak in the German Army, Sauberwald7reported, started in one ward of a central hospital and suddenly appeared inother wards. Barker and Miller15 found thatthis disease may be very infectious, as shown by the occurrence of 200 casesamong 800 prisoners of a German camp in two days.
Predisposing factors are of importance equal to or greaterthan the presence of Vincent's organisms. The former may be controlled; thelatter can not be eradicated. Of first magnitude is faulty oral hygiene. Thepresence of dental caries, fermenting organic matter, faulty dentition, andneglect in oral hygiene lead to gingivitis, pyorrhea alveolaris, peridentalinfections, abscesses, etc. The resistance of the mucous membrane of the mouthand perhaps resistance of the entire body are lowered. The mouth becomes fouland in this condition the spirochete flourishes. Those who are in a physicallyrundown condition are very prone to develop the disease.
During the war, especially the early part, as mentioned atthe outset, Vincent's disease was often spoken of as trench mouth, trenchgums, etc. It is believed that nothing in trench service per se, otherthan the congregating of large numbers of persons and separating them from thenecessary means of maintaining clean mouths, played any part in causing thedisease.
The use of tobacco has been considered an important factor inincreasing susceptibility. Barker and Miller15refer to the importance of undernourishment, and Sauberwald7considers it an important factor in the outbreak above referred to. Generallyspeaking, the disease is more common as age advances. British statistics1show 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 onegroup and 33 per cent in another. No age, after dentition is established andbefore all teeth are lost, appears exempt. The part played by the vitamines aspredisposing factors appears unsettled.
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SYMPTOMS
After an unknown incubation period, the disease sets inslowly, as a rule, with the formation of a grayish, greenish, or yellowishdiphtheroid membrane situated more commonly on the tonsil, but also occurring onthe gums, uvula, pharynx; in fact, it may be found on the mucous membrane of thelarynx, bronchi, or trachea, usually by extension. The common sites are thetonsil and gums. This membrane is adherent and leaves a red bleeding surfacewhen removed. The breath is foul. Gingivitis and pyorrhea alveolaris arecommonly associated with Vincent's disease. The lesions are usuallyunilateral, but not always so. The lymph glands that drain the infected area areinvariably enlarged and usually painful; they do not suppurate. Swallowing iscommonly painful. The constitutional symptoms, as a rule, are neither marked norin proportion to the degree of pathological involvement seen in the mouth. It isnot uncommon for the temperature to be normal; however, 99? to 100? F. isusual, and occasionally 102? or higher is seen. Headache, anorexia, malaise,slight pains in the joints, lassitude, and some depression in variable degreeare common.
Ulceration usually follows the pseudomembrane formation. Theulcer has irregular, undetermined edges and a "punched out"appearance, and though it is usually confined to the soft parts, involvement ofunderlying bone has been reported. Pain is not a conspicuous symptom. Whenlocated on the tonsil the ulcer is usually unilateral and situated nearer theposterior pillar. Cases have been reported where the entire tonsil had beendestroyed by the process. These lesions contain the organisms of Vincent;however, other forms of bacteria are present in the smears which may requireconsideration in diagnosis. Large areas of the mouth may be involved. Infectionmay extend over the mucous membrane of the entire mouth.
Vincent classified the disease into two types: (a) Thesuperficial pseudomembranous, or diphtheroid type, in which a thin grayish-whitefilm usually starts over one tonsil and gradually spreads to adjacent tissue. Itis remarked that the membrane is easily removed, though not en mass, leaving ableeding base and shallow ulcer. (b) The ulcerative and more common formin which there is deep tissue ulceration covered by a thick, creamy, yellowexudate easily removed, leaving a red, granular, bleeding base. Both forms showa tendency to be unilateral. Vincent's classification is generally accepted,yet there are workers who have reported differently. Campbell and Dyas18divide the disease into types as follows: Type I, tonsil cases; type II, ulcerof the lower jaw immediately behind the last molar tooth; type III, gingivalcases; type IV, general infection of the buccal cavity. McKinstry16describes several types, namely, affections of the gums, affections of thetonsils (Vincent's angina), and affections of the mucous membrane of thebuccal cavity. This author emphasizes the statement that the commonest form ofthe disease is an ulcerative peridental gingivitis especially common around thelower incisors, posterior lower molars, crowned teeth, and between irregularones. Kiefer,19 remarking on Vincent'sclassification into diphtheroid and ulceromembranous types, says that this isdoubtful since we find vesicular, lacunar, membranous, and ulcerative formseither alone or in combination. Medical officers during the war accepted
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the original classification and noted that the majority ofcases were seen in ambulant persons during the ulcerative state.
Experience has proved that Vincent's disease is notconfined to the mouth and that it is at times a more serious malady thanformerly believed to be. Multiple lesions occur on the mucous membrane invarious parts of the body. A number of deaths have been reported. This will bediscussed more fully under prognosis. Bowman20reported a case with several lesions in different parts of the body. The primaryinfection was probably in the mouth, the glans penis, and conjunctiv? laterbecoming infected, probably by the fingers. Campbell and Dyas13reported seven cases of bronchial infection with a clinical picture of amoderately severe bronchitis, copious expectoration, little elevation oftemperature, and general depression; the sputum was loaded with Vincent'sorganisms. The infection was self-limited and lasted about three weeks. Theseauthors reported four cases of balanitis of Vincent origin. There was a longedematous prepuce whereon a membrane formed and extended to the glans. Corbus21described ulcerative balanitis due to Vincent's infection as the "fourthdisease." He expressed the opinion that this condition is often incorrectlydiagnosed as chancroid; however, it can be differentiated by the presence of theB. fusiformis and spirillum of Vincent in the former and the Ducrey-Unnabacillus in the latter. A case was reported from the base hospital in Coblenzwith ulceration of the meatus urethr? that showed the fusiform bacillus andspirillum. It yielded to local treatment and was diagnosed as Vincent'sdisease.
Recovery usually takes place in a week22 andrecurrences are not uncommon. According to Bouty,3 recurrences maytake place even three weeks after the first attack, in which case complicationsare more liable to occur. Recurrences were common among the American forces inGermany, yet there was nothing to indicate that these second attacks weredifferent from the primary ones in severity. Among the approximately 25,000patients that passed through the base hospital in Coblenz, there were two deathsattributed to Vincent's disease.10 In one, the direct cause ofdeath was suffocation following edema of the larynx; in the other, death wasattributed to streptococcic septicemia complicating Vincent's disease. Inboth cases there was extensive ulceration and membranous formation about thetonsil, hard and soft palates. The larynx became involved in the former case. Inthe latter, a severe streptococcic throat infection developed, complicating theVincent's disease. Abscess formation was suspected about the tonsils, butincisions revealed no pus. Before death the blood culture was positive for thestreptococcus.
DIAGNOSIS
The diagnosis of uncomplicated Vincent's disease is notdifficult. The comparatively slow onset, cervical lymph adenitis, foul breath,mild or absent constitutional symptoms, with unilateral lesions, constitutethe usual clinical picture. A positive diagnosis can be made only bymiscroscopic examination. Stained smears and dark field examination show thepresence of Bacillus fusiformis and Vincent's spirochete.
The ulceromembranous form must be differentiated fromdiphtheria, for the pseudomembrane in Vincent's disease is not unlike a truediphtheritic membrane. The ulcerative form of Vincent's disease must bedifferentiated from syphilis,
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It may be possible to make this differentiation on dark fieldexamination, as the Spiroch?ta pallida is morphologically different fromthe Vincent's spirochete is easily differentiated by those familiar with thecharacteristics of these organisms. This applies more particularly to theprimary lesion of syphilis when located in the mouth. In ulcerative tonsillitis,or ulcers of syphilitic origin located elsewhere in the mouth, the Wassermannreaction is of the greatest assistance, being positive in syphilis and negativein Vincent's disease. A history of specific infection and appearances ofsyphilis elsewhere in the body will support the diagnosis.
It must be remembered that Vincent's disease is at timessuperimposed upon both diphtheria and syphilis. It is also to be remembered thatVincent's disease may occur in a pure diphtheria carrier. All combinations ofthese conditions existed among American troops during the war.
Brumbaugh23 reports as follows on the dark fieldstudy of five cases of pseudomembranous oral infection diagnosed clinically asVincent'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 d?bris 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 ofthree weeks' duration. Pharynx and palate are granular and red and scatteredpatches of grayish exudate are present on the postpharyngeal wall and righttonsil. The gum about the two posterior lower right molars is reddish, swollen,projecting above the teeth and covered with grayish membrane. The lymph nodes atthe angle of the jaw are moderately enlarged; the inguinal and axillaries arealso readily palpable. Patient denies veneral infection. There are no scars onthe genitalia and the skin is clear. He smokes tobacco rather immoderately. Theteeth are clean and free from caries. Wassermann test: Negative. Throat smear:Stained preparation shows the presence of Vincent's organisms. Dark fieldexamination reveals very numerous coarse coiled spirochetes and a few fusiformbacilli, both forms very motile. Diagnosis of ward surgeon: Tonsillitis, acute,follicular. (2) Vincent's angina, right tonsil, moderately severe. Dark fielddiagnosis: Vincent's angina.
Case 3 -White; age, 23 years. His sore throat is of 10months' 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 Bacillusdiphtheri? 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 monthsago and three months ago and at the present time, are all negative. Dark fieldexamination revealed rapidly motile fusiform bacilli and coarse coiledspirochetes. Diagnosis
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of ward surgeon: Vincent's angina, severe, involving thefauces and soft palate. Dark field diagnosis: Vincent's angina.
Case 4 -White; age, 31 years. His sore throat began sixweeks ago. Both tonsils and soft palate are covered with a grayish whitemembrane, marked off with a narrow hyperemic zone. The lymphatics at the angleof the jaw and the postcervical chains are enlarged. The inguinal lymphaticsare slightly enlarged. The patient is obese, weighing 205 pounds. He has severalscars on the penis, which he attributes to soft chancres six weeks ago. His skinis clear. He complains of rheumatism of the ankles. He smokes very rarely. Histeeth are clean and free from caries. Throat culture showed hemolyticstreptococci. Throat smear: Stained preparation showed presence of Vincent's anginaorganisms, Gram-positive diplococci and diptheroid bacilli. Wassermann test,made recently, was negative. Dark field examination reveals the presence of avery 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 sixmonths' duration. He smokes considerably. His teeth are slightly tobaccostained and he had two carious molars. Otherwise his teeth are in goodcondition. The lesions consist of grayish white patches on the soft and hardpalate, 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 aboutthe palate lesion, but none around the tongue and lip lesions. The membrane istightly adherent and does not bleed readily if the surface is rubbed. He deniesvenereal infection and the skin of the body is free from eruptions. The glandsat the angle of the jaw are markedly enlarged. The axillaries and inguinals arealso moderately enlarged. The genitalia are free from scars. Throat culture oneweek previously showed bacillus diphtheri? absent. Throat smear: Stained preparation showed Vincent's angina organismspresent. Wassermann test one week previously was mildly positive. Dark fieldexamination revealed a few typical Treponema pallida. Diagnosis of wardsurgeon: Acute catarrhal pharyngitis and Vincent's angina. Dark fielddiagnosis: Secondary syphilis.
Blood changes in Vincent's disease are of but slightdiagnostic importance. There is but little change in the number of white cells.A leucocytosis of over 10,000 is rare. Deglos,6 reporting 21 casesobserved in his hospital, remarks that the white counts were about 10,000 andthe red cells usually were reduced to 3,000,000. Anemia was not a conspicuoussign among the American cases, as shown by review of the clinical records. Allcases were not clear-cut in their symptomatology, as shown by the followingcase abstracted from the records of the base hospital at Camp Grant, Ill.Although several diagnoses were suggested by various consultants, the finaldiagnosis was Vincent's angina.
Corporal V-, Company A, 333d Machine Gun Battalion.Admitted May 2, 1918. Died August 16, 1918. The chief complaints on admissionwere: Pains in the stomach, chest, back, and head, vertigo, and slight cough,for the past two weeks. There was no expectoration. Examination of the clinicalrecord shows a continuous temperature of the septic type throughout the courseof the disease. The general condition on admission was good. The throat wascongested and lymph glands negative. The genitourinary system was negative forpathological findings. The patient denied all venereal diseases. Otherwise thephysical examination was negative. Based upon the physical examination andlaboratory reports, the following diagnoses were made: (1) Fermentation,intestinal; (2) Vincent's angina.
On May 4 the right tonsil was red, swollen, and covered withan exudate. The tongue was red and coated; the breath was foul; the heart showedno abnormal findings; the spleen was palpable; a few coarse moist r?les wereheard over the base of both lungs. On May 12 diagnosis was made of a dento-alveolarabscess 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 wereenlarged and tender. The intestinal fermentation was recorded as cured.
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Necrosis of the upper left maxillary bone was later recorded,extending upward from the left second bicuspid tooth. The condition of thepatient did not improve and on July 17 was such that transfusion of blood wasthought advisable. A 250 c. c. citrated transfusion was administered. It wasrepeated 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 leftupper maxilla. The patient was pale and felt weak. The tonsil was covered withan exudate and the urine showed albumin. Frequent consultations among thechiefs of services were held. The X ray showed osteomyelitis.
On July 15 a portion of the alveolar processshowedsequestration. Blood examination this date showed 792,000 red cells, 13,000white cells, and 30 per cent hemoglobin. The differential count showed 90 percent large mononuclear, 5 per cent small mononuclear, and 5 per centpolymorphonuclear cells.
Condition generally improved following eachtransfusion,but improvement of short duration, usually lasting about three days. The redcell count remained about 1,000,000 hemoglobin per cent low; local conditionshowed a tendency to improve; the general condition did not improve. The patientbecame weaker, temperature continued elevated, and he died August 16, 1918.
The patient received five blood transfusions and two doses ofarsenobenzol, in addition to various local applications. Several operations wereperformed to remove dead bone. The smears were negative for diphtheriabacilli. The Wassermann reaction was negative; also Widal reaction, and bloodotherwise negative. Syphilis was excluded. The glands of the neck did notsuppurate. 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 percent; large mononuclears, 58 per cent; small mononuclears, 31 per cent;polymorphonuclears, 11 per cent. A further study of the blood pictures of thispatient shows that he has an index of 1.25; that he has many large, deeplystained red cells such as are commonly seen in advanced anemia of the splastictype. His blood cells have recently been as high as 24,000 which is decidedlyagainst 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 beclassed as myelocytes; and there are others less mature. I take thelatter to be myeloblasts and premyeloblasts. There is also a decided relativeincrease in the number of lymphocytes. The total white count is low. This,however, is not an impossible finding in leukemia. On the whole, the bloodpicture might be interpreted as a myelogenous leukemia. Smears which Itook from the mouth this morning show: (1) Nothing suggestive of Vincent'sangina; (2) a diplococcus which in some places is seen in chains of from 4 to 8organisms and which may be a streptococcus.
This patient was in hospital 107 days. The report of necropsyand histological reports are as follows:
AUTOPSY No. 81
On this the 16th day of August, 1918, I held in themorgue 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 thanthe right, and there is a definite swelling of the tissue about the superior maxilladownward to the angle of the jaw. There is no recent blood in the nostrils orthe external auditory canals. On the left side from a point directly behind theupper 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 mucousmembrane along the gum margin of the teeth practically everywhere, but mostlythose 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 verypale. The neck is fairly long and there is an enlargement of the cervical lymphglands particularly on the left side.
* * * Upon eviscerating the chest and abdomen in the usualway there are found no injuries on the inside of the thorax other than such asmight have been produced by tearing of the adhesions between the parietal andvisceral pleura. The lining of the aorta is very pale, quite smooth, androughened only by scattered areas of subintimal fatty infiltration. The lymphglands along the aorta everywhere are increased in size, and for the most partare rather dark brown or cyanotic in color; they are also fairly firm. Thelymph glands at the bifurcation of the trachea are small and on the surfacesmade by sectioning there are firm
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gray pale white nodules 1 mm. in size. The lining of theesophagus is very pale, otherwise it is normal save for a slight epitheliosis ofits lining. The lymph glands at the bifurcation of the trachea are moderatelyincreased in size and are fairly large. On the left side there is a mass ofglandular tissue very much increased in size; the section surfaces of thisgland being very firm and pale. This mass of glandular tissue is rough, 3 by 4by 2 cm. and extending out onto the pleural surface just above the region of thepericardium, and on the outer surface of the pericardium there are translucentwhite 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 abovethe point where the left bronchus enters this organ.
The lining of the trachea and main bronchi is very pale. Onthe outer surface of the right lung there are numerous subpleural petechialhemorrhages. The posterior portion of this lung is somewhat boggy, but containsair throughout. The anterior margin of the left lung is adherent to thepericardial sac, and on the surface made by sectioning this tissue this organis very pale. The anterior margin of the left lung is firmly adherent to thepericardial sac. In the region of the thymic body there are lymph glands, some ofthem very red but containing on the surfaces made by sectioning pale whitenodules from 1 to 2 mm. in diameter. In one of the lymph glands there isa small caseous calcified spot 1 mm. in diameter. * * *
* * * On the right side the lymph glands of the cervicalregion are large and form a mass along the course of the deep vessels of theneck. The thyroid gland is very pale, but otherwise is quite normal. On the leftside the cervical lymph glands are also enlarged. The enlargement extendsupward. There are no changes in the esophagus, or pharynx. The larynx is verypale, but there is no disease of this organ. The section surfaces of the lymphglands removed from the left cervical region are large and pale white; they arevery firm. On the surface made by sectioning the septa of the glands extend downinto their substance dividing the firm pale areas, already mentioned, into areasof tissue completely or partially separated from each other. In such lymphglands where the enlargement has not completely destroyed the gland there arewhite areas from 1 to 2 mm. in diameter. Both sera maxillary glands, on bothsides, are incapsulated, but otherwise appear quite normal.
No further examination of the body was made.
ANATOMIC DIAGNOSIS
1. Extensive chronic suppurative necrosis of the alveolarprocess of the left superior maxillary bone.
2. Chronic suppurative sinusitis of the left antrum ofHighmore.
3. Numerous absent teeth.
4. Chronic generalized suppurative gingivitis and pyorrheaalveolaris.
5. Chronic inflammatory edema of the left side of the face.
6. Marked chronic nonsuppurative adenitis of the right andleft cervical and of the parabronchial lymph glands.
7. Marked emaciation.
8. Marked generalized anemia.
9. Multiple petechial hemorrhages and smallsuggillations ofmany tissues of the body.
10. Cloudy swelling and acute fatty changes of the myocardiumand parenchymatous organs.
11. Marked hyperplasia of the spleen, biliary,mesenteric,and abdominal aortic lymph glands.
12. Chronic nodular caseous and calcified tuberculosis of theparabronchial lymph glands.
13. Left chronic nodular fibrous tubereculosispleuritis.
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 ven? and hypodermic needle puncture wounds ofboth arms.
27. Old circumcision scar of the foreskin of the penis.
28. Slight decubital necrosis over the sacrumand leftposterior superior iliac spine.
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HISTOLOGICAL REPORT
L-- V--. Autopsy No. 81.
(A) Lymph gland: There is a marked increase in themononuclear cells of this lymph gland. These cells are relatively large with afairly abundant margin of cytoplasm and a relatively clear vesicular andslightly mottled nucleus. The lymph gland for the most part consists of thesecells which resemble in many respects endothelial cells as they are found inlymph glandular tissue. So profound are the changes in this lymph gland thatthere is very little lymphoid cells as such, the tissue consisting essentiallyof these large mononuclear cells packed very closely. Even the capsule of thelymph gland in places has been invaded by these cells.
(B) Lymph gland: Around the lymph gland there is a certainamount of edematous adipose tissue. It too contains many large mononuclearcells. These cells have penetrated into the adipose tissue surrounding the lymphgland.
(C) Lymph gland: The description as given in A and B holdstrue for C, with this exception, that the density in the arrangement of thelarge mononuclear is greater and in the centers of the more densely arrangedportions there are areas of about one-fifth millimeter and smaller where thecells have undergone necrosis. The nuclei of these cells are pycnotic,fragmented, or entirely missing, the cytoplasm of the cells being pinklystained. These areas of necrosis are fairly abundant. The lymphoid cells in thisgland too are arranged in nodules, relatively small.
(D) Lymph gland: The same as A and B, without areas ofnecrosis.
(E) Lymph gland: Contains areas of necrosis, the strikingfeatures of which is that the outline of the cells in the destroyed tissue isstill present.
(F) Lymph gland: Similar to A and B, with very littlenecrosis.
(G) Lymph gland: Similar to A and B, with small hemorrhagesin one spot.
Liver: The uniformity of the liver structure under themicroscope is broken by collections of mononuclear cells in numbers from about ahalf dozen to others in areas fully 1 millimeter in maximum dimensions. Theseareas are usually perilobularly arranged along the portal canals or occasionallyappearing toward the center of the lobules. The latter condition is theexception rather than the rule. These mononuclear cells are as given in A, B, Cof the lymph glands described, namely, cells with circular nuclei and a moderateamount of cytoplasm. The sinusoids of the liver for the most part are widelydistended, around the peripheral portions of the lobules, they being less widethan toward the centers. The liver chords diminish in width toward the center ofthe lobules where the cytoplasm of the cells is practically gone. Where presentthe cytoplasm is vacuated. These retrogressive liver changes in the liver chordsextend fully two-thirds to three-fourths of the distance from the center to theperiphery of the lobules.
Testicle: There is a marked atrophy of the testicularepithelium, with absolutely no or very little spermatogenisis. The tubules arevery small and between the tubules there is an extensive infiltration of thetissue with mononuclear cells such as have been described in several placesabove.
Spleen: In the spleen, too, there is a profound proliferationof endothelial cells. Many of the endothelial cells are pigmented a light brownand contain either injected red cells or circular, irregular masses of a brownamorphous substance. Some of these are light brown on yellow granules.
Adrenal: The cells of the adrenal cortex are markedlyvacuolated. This is true almost throughout the entire substance of the organ.
Accessory spleen: There is a decidedhyperplasia ofendothelial cells of this organ similar to the description given for the spleenproper. There is a small area of necrosis about one-half millimeter in diameterin this section.
Kidney: There is a moderate interstitial edema in this organ,and there are scattered areas of endothelial mononuclear cell infiltration insize from a few cells to others one-fourth of a millimeter in diameter. Theseare commonly found around the glomnerul? and along the vessels. The tubularepithelium of the convoluted tubules is fairly low, and in the lumina of thesetubules there are pinkly stained granules. There are pink granules in thecapsule spaces of the glomerular spaces also.
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PROGNOSIS
The majority of cases terminate in complete recovery. The average durationamong American soldiers during the World War was 14.97 days.
Among 6,189 primary admissions for Vincent's disease in the Army during thewar, 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 thefollowing year there were 4 deaths among white enlisted men. Eight of the deathsoccurred in the United States and 4 in Europe. All were reported among casesprimarily admitted to hospital on account of Vincent's disease, and inprobably all instances, the deaths were due to complications.
As a basis for discharge from the service on surgeon's certificate ofdisability, Vincent's disease was of minor importance. The records of theSurgeon General's Office show four enlisted men discharged from the service onthis 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'sdisease is self-limited, beyond doubt the soldiers were discharged for someassociated condition or complication; however, the records do not permit ofanalysis to determine this matter in detail.
PREVENTIVE MEASURES
No specific preventive measures were known before the war and none developedduring that period. It has been established that the disease is an infection;however, the method of transmission is unknown. The organisms of Vincent areconstantly present where Vincent's disease exists, but are also normalinhabitants of the mouth. The important factor seems to be in the prevention oflowered local and constitutional resistance. The best results are accomplishedby proper oral hygiene. Accepting the British point of view, if the gums andteeth are kept clean, there can be no marginal gingivitis, and if no marginalgingivitis develops, pyorrhea and Vincent's disease do not develop. Since theorganisms are contained in discharges from the lesion, which is commonlylocated in the mouth, the proper care of drinking cups and eating utensils is ofimportance.
In some camps during the war attempts were made to quarantine contacts merelyon account of the presence of a few Vincent organisms in the throat. In view ofour incomplete knowledge of the transmission of Vincent's disease from oneindividual to another, and in view of the presence of the causative organisms inthe mouths of many normal individuals, quarantine is not considered practicable.
TREATMENT
Specific and empirical treatment have been advocated by contributors to theliterature of the therapeutics of Vincent's disease. In the specific treatmentarsenic is used both locally and intravenously, while in the empirical treatmentsuch medicaments as silver salts, methylene blue in alcohol, liquor potassiiarsenitis, and salicylic acid are recommended.
In 1910, Ehrlich24 called attention to the value of salvarsan in thetreatment of Vincent's disease. On account of the specific action of this drug uponspirochetes, especially the Spiroch?ta pallida, many clinicians haveused it in the treatment of Vincent's disease, especially in its severerforms. The drug, how-
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ever, is expensive and acts best only when givenintravenously. Partly on this account and partly because the vast majority ofcases recover under simple local treatment and the correction of faulty oralhygiene, it has not been used as a routine.
It has been said that a good dentist is the best therapeuticmeasure. Filthy mouths must be cleaned up, and gingivitis and pyorrheaalveolaris must be adequately treated, if satisfactory improvement is to beexpected. Local application of drugs, curettement, and intravenous therapy aremerely adjuncts.
Intravenous administration of salvarsan or neosalvarsan wasused in the Army in protracted cases; however, only rarely was it necessary.Generally speaking, patients suffering from Vincent's disease were admittedto wards set aside for patients suffering from inflammation of the throat. Nospecial attempt was made to quarantine them, and if detected in other wardswhere they happened to be for a concurrent disease, they were allowed to remainin these wards as long as the primary cause of admission was the more importantfrom the treatment standpoint. The records of several hospitals show specialcare taken in the handling of eating utensils. There is nothing in the availablerecords to indicate that any patient contracted Vincent's disease while inhospital.
Mercury in any form is contraindicated for these patients onaccount of its physiological action on gum tissue. It is best to refrain fromthe use of tobacco while under treatment. The use of the toothbrush must beencouraged; Vincent's disease is more common in those who are lax in thisrespect. In some hospitals, patients suffering from this disease were lined upafter meals, each with his toothbrush, and marched to the toilet or other placewhere they could clean their teeth, the cleaning being supervised by one inauthority. Further, they were taken to the dental surgeon at regular intervals.In this manner proper oral hygiene was soon established and maintained. This isthe most important phase of the treatment.
REFERENCES
(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 f?r 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 Progr?s M?dical, Paris, 1918, No. 20, 174.
(6) Deglos, E.: Quelques observations a propos de l'angine de Vincent. Un cas compliqu? de sphac?le grave des tissus voisins. Lyon m?dical, 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.
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(11) Nichols, Henry J.: Carriers in Infectious Diseases. Williams and WilkinsCo., Baltimore, 1922, 98.
(12) Zinsser, Hans: A Textbook of Bacteriology. D. Appletonand Co., NewYork, Fifth Edition, 1922, 867.
(13) Babes, V.: Spindelf?rmige Bazillen. Handbuch der Pathogenen Mikroorganismen. Erg?nzungsband 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, M?nchen, 1910, lvii, part 2, No. 43, 2268.
