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Chapter 2



Epidemic Keratoconjunctivitis

Murray Sanders, M.D.


When a clinical entity makes its appearance de novo, it becomes a subject of interest to the entire medical profession. When such a phenomenon occurs precipitously in the industrial heart of a newly organized war effort, spreading its unpleasant and incapacitating effects with great speed, then it can assume proportions of a national problem affecting all military and civil departments. This, for a time, was the history of epidemic keratoconjunctivitis. It was these wartime potentialities which led the Preventive Medicine Service, Office of the Surgeon General, to initiate investigation of this disease.

As far as can be determined by medical record, epidemic keratoconjunctivitis first made its appearance in the continental United States sometime during the summer of 1941. The epidemic nature of the disease had been recognized in 1889 by Ernst Fuchs, who described a superficial keratitis somewhat similar to herpes simplex infections of the eye but not associated with the formation of vesicles.1 He emphasized the consistent appearance of symptoms of an acute conjunctivitis with subsequent spread to the cornea, frequent appearance in only one eye, and persistence of pain, photophobia, and lacrimation. Other authors have reported similar outbreaks from 1900 to 1930 in Bombay and Madras. These outbreaks were considerably more extensive than the one reported by Fuchs but appeared to be clinically related to it. An outbreak in London in 1933 was minor, but there were subsequent extensive epidemics in India in 1933 and 1934, in China in 1936, in Germany from 1938 to 1940, in Malaya from 1935 to 1938, and in Tasmania in 1941.

By 1941, the disease had appeared in epidemic proportions in Oahu , Hawaii , and consequently became of increasing interest to the United States. In the summer of 1941, 10,000 cases occurred in Oahu,2 and in the late summer and early fall of the same year the disease made its first appearance in continental United States, when 16 cases were reported in a veterans' hospital in San Fernando, Calif. The disease then spread with devastating rapidity up and down the coast, appearing especially in industrial areas. Only those who have witnessed its explosive onslaught in a crowded factory can appreciate the enormity of the psychological effect on the industrial population.

1Fuchs, Ernst: Lehrbuch der Augenheilkunde. Leipzig and Wien: Franz Deuticke, 1889.
2Holmes, W. J.: Epidemic Infections Conjunctivitis. Hawaii M.J. 1: 11-12, November, 1941.


The apparently inexplicable spread of the disease through all departments of a factory and the inability of medical departments to cope with the epidemic quickly reduced the efficiency of industrial centers.

The situation became considerably aggravated when, in the early months of 1942, epidemic keratoconjunctivitis made its appearance on the east coast. Here, the acute symptoms became more severe and were followed by complications which lasted longer and which occurred in a much greater percentage of cases than on the west coast. By the fall of 1942, when approximately 4,000 cases developed in one of the most important defense factories, the situation became critical. It was at this time that the Office of the Surgeon General began a concerted, disciplined attack on the problem based on studies which had been initiated with considerable foresight by the Preventive Medicine Division in March 1942 at the College of Physicians and Surgeons, Columbia University, New York. The disease practically disappeared within 3 months after the isolation of the etiological agent. After January 1943, it was no longer a source of concern, and incidence was of such a low order in the few instances where epidemic keratoconjunctivitis still persisted that the threat was considered nullified.3


There is no doubt that epidemic keratoconjunctivitis is a distinct clinical entity. However, until fully developed cases appear in epidemic numbers, the wide variability of introductory signs and symptoms may lead to confusion with other acute conjunctivitides. Perhaps the one factor that may be considered a valuable warning in a preepidemic period is the persistence of an acute conjunctivitis for more than 10 days with little or no secretion present but with considerable lacrimation and soreness in the preauricular or submandibular areas. Such systemic signs as headaches, rhinitis, or malaise should add to, rather than detract from, the suspicion of this disease.

The clinical appearance of epidemic keratoconjunctivitis to an examining physician is that of an acute conjunctivitis, frequently follicular in type. Hyperemia and edema (especially of the upper lid) are predominant signs. It has been said that the follicular hypertrophy is due to a local proliferation of lymphoid cells within the stroma of the conjunctiva.4 As a result of the proliferation, small areas of glistening, raised mucous membrane can be seen. In this early stage, the patient complains frequently of a foreign-body sensation, and, although lacrimation is marked, secretions are minimal. Often, symptoms may appear before marked physical changes occur. On the other hand, fully developed follicles may be disguised by the edema of the surrounding tissue, with the lymphoid hyperplasia appearing diffusely in the

3Between 1943 and 1951, epidemic keratoconjunctivitis appeared sporadically in different parts of the Nation, but, in each instance, the successful application of the lessons learned during the epidemic months resulted in limitation of the number of cases and averted a major epidemic.
4Sanders, M.: Epidemic Keratoconjunctivitis. Scient. Monthly 57: 469-472, November 1943.


deeper connective tissue. Where the latter picture is seen, there may be noted a massive pouching out of the palpebral mucous membrane which becomes dramatically apparent when the lower lid is pulled down. Involvement of the bulbar conjunctiva is usual, and the chemosis may be sufficiently severe to produce a projection of the bulbar mucous membrane between the lids that is visible when the patient's lids are at rest. When fully developed, an acute case of epidemic keratoconjunctivitis can present a fearsome picture.

Lymphadenopathy of varying degree almost inevitably accompanies acute signs and symptoms. The glands which are usually involved are the preauricular, cervical, and submental. One, two, or all three groups of glands may be involved, and the tenderness may be so extreme that chewing becomes painful. Referred pain along the mandible is not unusual. Lymphadenopathy may be present for only a few days or may persist for weeks after subsidence of other acute signs. Laboratory tests made during this stage of the disease are not particularly diagnostic. Conjunctival scrapings may show occasional lymphocytes or large mononuclears. If a secondary invader is present, a polymorphonuclear reaction may be apparent. Bacteriologic studies of secretions are negative or result in the demonstration of what are apparently secondary invaders.

Although unilateral involvement is the rule, the disease may involve both eyes. If both eyes are involved, however, it is usual for the second eye to show a milder infection. The intensity of clinical signs and the severity of the disease vary greatly from patient to patient within the same epidemic or within the same household, and it is impossible to prognosticate the outcome or the expected duration of the acute disease on the basis of early clinical appearance.

The association of systemic signs and symptoms with the acute ocular symptoms should be mentioned. In several hundred cases, headaches were associated with the ocular disease, and, in one study,5 it was noted that the headaches started within 36 hours after the onset of the conjunctivitis, were fronto-occipital in distribution, and could not be relieved by analgesics. In the same outbreak, rhinitis and pharyngitis were frequently seen in the early stages of the disease. In two cases seen in Schenectady , N.Y.,6 there was possible nervous-system involvement marked by a persistent and extreme somnolence. One of the patients was drowsy and exhibited emotional disturbance in association with the onset of the eye disease. There were additional systemic signs of malaise and fever, sometimes in conjunction with considerable nasal discharge which was usually serious in character.

It will be recalled that the first epidemic began on the west coast of the United States and then spread to the Atlantic coast. It is of interest, there‑

5Sanders, M., Gulliver, F. D., Forchheimer, L. L., and Alexander, R. C.: Epidemic Keratoconjunctivitis; Clinical and Experimental Study of an Outbreak in New York City : Further Observations on the Specific Relationship Between a Virus and the Disease. J.A.M.A. 121: 250-255, 23 Jan. 1943.
6Symposium on Epidemic Keratoconjunctivitis, 4 Dec. 1942, held at the College of Physicians and Surgeons, Columbia University, New York.


fore, to compare the two outbreaks since there is a suggestion that the eastern form, while apparently due to the same infectious agent, was more virulent than that encountered on the Pacific coast. On the west coast, the patients were usually incapacitated for 1 or 2 weeks, and corneal opacities of a transient character appeared in 40 percent to 75 percent of the cases. On the east coast, on the other hand, subjective symptoms were considerably more distressing in the majority of cases, and the acute stage lasted frequently for 2 or 3 weeks or longer. Furthermore, corneal opacities were observed in as many as 85 percent of the cases and persisted for many months.

As the name of the disease suggests, the cornea usually becomes involved as the acute phase of the disease passes, or within 7 to 10 days after the appearance of the first signs. The inception of this stage of the disease may be marked by a sudden ocular pain, by photophobia, or by both. However, in a fairly large number of cases, the infiltrates appear subtly, and the patient may notice only gradual blurring of the vision or a foggy halo around lights. The characteristic pathologic picture of the opacities is one of multiple subepithelial infiltrates tending to be localized in the pupillary area and appearing from one to several weeks after the onset of the acute conjunctivitis. It is interesting to note that patients with severe conjunctival involvement may go on to spontaneous recovery in approximately 10 days without development of corneal opacities. On the other hand, in some cases of mild conjunctivitis, the acute stage may persist for weeks and may ultimately resolve with the formation of many opacities and impairment of vision. As a rule, ulceration of the cornea does not occur in true, uncomplicated epidemic keratoconjunctivitis.


Before 1942, the disease entity known as epidemic keratoconjunctivitis spread without hindrance, and the only medical reports were clinical records in industrial centers, particularly west coast shipyards, describing the incapacitating effect of the disease on thousands of essential workers. However, in March 1942, at the College of Physicians and Surgeons, a virus was isolated from the eyes of two patients suffering from the disease. It was not surprising that a transmissible agent could be isolated from these patients since the disease was obviously of infectious origin. Furthermore, the scrapings from the conjunctival surfaces of patients with acute cases, which usually revealed lymphocytes in association with monocytes, were consistently free of significant bacteria and pointed to a probable viral causation.

The initial isolations of the virus were accomplished not by direct animal inoculation but by incidental passage to tissue cultures into which conjunctival scrapings from the patients were placed.7 After incubation in the tissue

7(1) Sanders, M.: Epidemic Keratoconjunctivitis ("Shipyard Conjunctivitis"). I. Isolation of a Virus. Arch. Ophth. 28: 581-586, October 1942. (2) Sanders, M., and Alexander, R. C.: Epidemic Keratoconjunctivitis : I. Isolation and Identification of a Filterable Virus. J. Exper. Med 77 : 71-96, January 1943. (3) See footnote 5, p. 5.


cultures, it was possible to transmit a fatal disease to Swiss white mice by intracerebral injection.8 Further investigation with unweaned Swiss white mice proved the virus pathogenic by intranasal, intraperitoneal, and intracerebral routes. For adult mice, however, only the intranasal and intracerebral routes could be used for transmission of the agent, and in the case of rabbits only the intracerebral route was effective. Once the agent was isolated so that it could be transmitted from mouse to mouse, a characteristic picture of a mouse meningoencephalomyelitis was observed. While this was not typical of any specific pathologic entity, it indicated neurotropic attack, which was substantiated by the fact that only brain tissues were consistently pathogenic for mice.

It is notable that, in the six strains isolated at the College of Physicians and Surgeons, a transmissible agent could be obtained only by inoculation of conjunctival scrapings into mouse brain-tissue cultures. In the case of serial tissue culture, a transmissible agent could be maintained only after 6 days of incubation at room temperature and when the culture-to-culture inoculum consisted of ground-up cells as well as fluid medium.

The specific nature of the experimentally isolated agent was suggested by the high degree of consistency with which serum from convalescent patients neutralized the virus. Through the use of the neutralization techniques, it was noted that the eastern and western outbreaks appeared to be due to the same agent, since the New York virus was neutralized by convalescent serums from both areas. As a matter of fact, as the disease spread over the country, convalescent serums obtained from all areas neutralized the New York virus.

Two other observations are of interest in relation to the specific nature of the virus. In filtration experiments, the virus passed without difficulty through an E.K. Seitz filter (double pads) and through all grades of Berkefeld filters. In more quantitative filtration analyses, the agent passed consistently through graded collodion membranes with an a.p.d. (average pore diameter) of from 75 to 100 millimicrons and to a lesser extent through membranes with an a.p.d. of from 50 to 75 millimicrons. When the a.p.d. of collodion surfaces was less than 50 millimicrons, the virus was retained.

The second observation of interest is that the inoculation of the experimentally isolated agent onto the conjunctival surfaces of a human volunteer reproduced a mild but characteristic picture of epidemic keratoconjunctivitis. Furthermore, the serum of the human volunteer, while not neutralizing the mouse virus before infection, contained neutralizing antibodies for it 1 month after infection.

8Since the original work was carried out in the isolation of a mouse virus from patients suffering from epidemic keratoconjunctivitis, there has been great difficulty in isolating similar strains. There is a possibility that identical or similar mouse viruses were isolated, but statements to this effect are based on personal correspondence. According to the Review of Medical Microbiology, Second Edition, 1956, one strain of CPC virus type 8 has been associated with outbreaks of the disease.


Although four additional isolations were made at Columbia and confirmation was reported by Braley,9 the question has been raised whether the virus isolated in New York is a new one or is a variant of herpes simplex. Evidence for the latter view has been recorded by the group at the Wilmer Ophthalmological Institute and the Department of Medicine, the Johns Hopkins Hospital and University, Baltimore, Md.,10 who believed that the agent isolated at that institution was related to herpes simplex. Their conclusions were based on partial cross-neutralizations between herpes simplex and epidemic keratoconjunctivitis viruses.

The evidence for specific neutralization of the virus isolated in New York is strong. No neutralizing antibodies were demonstrated in so-called normal populations. In a study carried out with the cooperation of the New York State Health Department, 118 serums from one of the worst outbreaks were studied by number at Columbia University. In this group of serums were included those of normal individuals, those of epidemic keratoconjunctivitis patients in the acute and in the convalescent phase of the disease, and those of contacts of such patients. The laboratory tests were carried out by number and entirely without knowledge of the history of the individual serum. Following the laboratory procedure, correlations were made between the presence or absence of neutralizing antibodies and the history of the patient. The final results are presented in table 1.

TABLE 1.-Extent of neutralization to the virus of epidemic keratoconjunctivitis shown by selected serums

Titer of serum

Number of neutralizing doses





Early (1st week)

Convalescent (6-10 weeks)

Late (4-5 months)

Intimate (5 months after onset of case)


































































Source: Korns, R. F., Sanders, M., and Alexander, R. C.: Epidemic Keratoconjunctivitis: Correlation of Epidemiologic Data and Results of Serum Virus Neutralization Tests. Am. J. Pub. Health 34: 567-571, June 1944.

9Braley, A. E.: Epidemic Keratoconjunctivitis. Tr. Am. Acad. Ophth. 48 : 153-174, January-February 1944.
10Maumenee, A. E., Hayes, G. S., and Hartman, T. L.: Isolation and Identification of the Causative Agent in Epidemic Keratoconjunctivitis (Superficial Punctate Keratitis) and Herpetic Keratoconjunctivitis. Am. J. Ophth. 28: 823-839, August 1945.


Neutralization results from the use of the New York virus against acute and convalescent serums from both east and west coasts suggest an immunologic relationship between the virus isolated in laboratory animals and the disease known as epidemic keratoconjunctivitis.

In addition, the filtration activity of the New York virus should be emphasized. It will be noted that the epidemic keratoconjunctivitis virus can pass without difficulty through a double Seitz filter. This has never been recorded for the recognized strains of herpes simplex virus. Furthermore, it will be remembered that, in the quantitative graded collodion-membrane tests, the epidemic keratoconjunctivitis virus passed through membranes with very low a.p.d. values. On the basis of Elford's calculations, this virus can be considered as being in the group of small viruses, such as that of the encephalitides.

While the result of the human volunteer inoculation should not be considered conclusive, nevertheless it is noteworthy that the volunteer in question had herpes simplex neutralizing antibodies prior to infection with the epidemic keratoconjunctivitis virus and had no neutralizing antibodies to the latter virus before infection. It was only during the convalescent phase of his illness that antibodies to the last-named virus appeared in his blood.

The possibility that the Johns Hopkins group dealt with either an incidental herpes virus or mixed viruses, that is, herpes mixed with epidemic keratoconjunctivitis, cannot be disregarded. It is of interest that their observations included positive fluorescent staining opacities, revealing a rupture of the conjunctival epithelium, characteristic of herpetic ulceration. In contrast, in the New York studies, all opacities were noted to be subepithelial in character, and no fluorescent staining was ever demonstrated.

Actually, the possibility of a relationship between the virus of epidemic keratoconjunctivitis and herpes simplex has become very remote, in view of recent work by Cheever11 and Ruchman.12 Both investigators demonstrated conclusively that the virus of epidemic keratoconjunctivitis is closely related immunologically to St. Louis encephalitis. In fact, epidemic keratoconjunctivitis could not be differentiated from St. Louis encephalitis by intracerebral neutralization tests. Cheever and Ruchman also found a similar but more distant, relationship between epidemic keratoconjunctivitis and Japanese and West Nile encephalitic viruses. It was noted, however, that the virus of epidemic keratoconjunctivitis had an increased pathogenicity for rabbits in contrast to the classical St. Louis encephalitis virus. These findings are consistent with the report by Heyl, Allen, and Cheever13 who also found no

11Cheever, F. S.: Studies on Possible Relationship Between Viruses of St. Louis Encephalitis and Epidemic Keratoconjunctivitis. Proc. Soc. Exper. Biol. & Med. 77: 125-129, May 1951.
12Ruchman, I. : Immunological Relationship Between Epidemic Keratoconjunctivitis and St. Louis Encephalitis Viruses. Proc. Soc. Exper. Biol. & Med. 77: 120-125, May 1951.
13Heyl, J. T., Allen, H. F., and Cheever, F. S.: Quantitative Assay of Neutralizing Antibody Content of Pools of Gamma Globulin From Different Sections of the United States Against the Viruses of Herpes Simplex, Lymphocytic Choriomeningitis and Epidemic Keratoconjunctivitis. J. Immunol. 60 : 37-45, September 1948.


antigenic relationship between the viruses of herpes simplex and epidemic keratoconjunctivitis when they correlated neutralizing antibodies in pools of gamma globulin from different sections of the United States. When tested against herpes simplex, neutralizing antibodies were found, whereas none could be demonstrated against the epidemic keratoconjunctivitis virus. The observations by Cheever and Ruchman tend to clarify studies carried out by Sanders on the specific relationship between the New York disease and the clinical entity of epidemic keratoconjunctivitis (particularly with reference to possible encephalitic involvement in some patients, as noted in the clinical description of the disease), as well as the filterable activity of the New York agent. The relationship between the epidemic keratoconjunctivitis and St. Louis encephalitis has, of course, raised an interesting question on the adaptation of human viruses to ocular tissue. This subject is comprehensively discussed in an editorial in the 7 July 1951 issue of the Journal of the American Medical Association, in which attention is brought to the biphasic activity of the epidemic keratoconjunctivitis and St. Louis encephalitis viruses.


It is an interesting commentary on the limitations in the practice of medicine that many months had elapsed after the first cases of epidemic keratoconjunctivitis had been noted in the United States and thousands of patients had been infected before the epidemiologic significance of contact infections was appreciated. It was only after the disease had increased in virulence and had spread to the east coast that the efforts of workers in the New York State Department of Health revealed the uncomplicated picture of transmission of the disease. The first significant evidence was found in an occupational analysis of one of the most heavily involved factory areas. As can be seen from table 2, which reports incidence of epidemic keratoconjunctivitis among employees in a plant in Schenectady, N.Y., in 1942, the 31.3 percent incidence among physicians and nurses was outstanding, since the second most heavily infected group (welders, cutters, solderers, and babbitters) showed an incidence of only 6.5 percent or 6.3 percent.14 Considerable additional evidence soon made its appearance in the form of individual case histories, as reported by Braley, as well as in further epidemiologic studies, reported by Sanders and coworkers. The conclusion was inevitably reached that any assembly point for patients with traumatized or infected eyes served as an efficient focus for dissemination of the disease as long as an occasional person infected with epidemic keratoconjunctivitis was present. In view of the important role which contact infections played in the spread of epidemic keratoconjunctivitis, it was not surprising that the virus could be demonstrated in solutions commonly used for treatment of ocular infections. It thus became of paramount importance to institute and

14Perkins, J. E., Korns, R. F., and Westphal, R. S.: Epidemiology of Epidemic Keratoconjunctivitis. Am. J. Pub. Health 33: 1187-1198, October 1943.


maintain strict, albeit simple, hygienic procedures and aseptic techniques in factory clinic and in private medical practice. The program for dissemination of information set up by the Preventive Medicine Division, Office of the Surgeon General, was admirably suited for this purpose.

TABLE 2.-Incidence of epidemic keratoconjunctivitis, by occupational group

Occupational group

Attack rate

Occupational group

Attack rate





Physicians, nurses


Stockroom keepers


Welders, cutters




Solderers, babbitters




Crane, followers


Receivers, shippers


Chippers, filers, grinders




Sheet-metal workers


Laborers, porters


Painters, varnishers






Plates, dippers, polishers


Maintenance and repair workers


Miscellaneous workers


Machine and press operators








Toolmakers and diemakers





It is axiomatic that, in those fortunate instances in which medicine has specific therapy available to combat infection, prescriptions are few and brief. The wide variety of the prescriptions used in the attempt to arrest the progress of epidemic keratoconjunctivitis in 1942 and 1943 is evidence of the paucity of our knowledge of therapy with respect to this disease. The whole gamut of symptomatic treatments and chemical agents was used, from hot and cold compresses to all forms of sulfonamides. Little or no success attended these efforts, and the disease ran a self-limited course with the incidence of the complication of corneal opacities running as high as a discouraging 85.5 percent in the Schenectady outbreak.

Possibly, the first therapeutic success was noted in 1943,15 following the use of convalescent serum of high titer. But even in this instance, the series of cases was admittedly small, and only the prompt application of plasma or serum before the fifth day of the disease appeared useful. In a final evaluation of this convalescent serum therapy, Braley chose the incidence of opacities as a criterion for therapeutic success or failure. He stated that opacities occurred in 99 percent of his patients treated symptomatically. In contrast, he found an incidence of opacities of 30 percent in those epidemic keratoconjunctivitis patients treated with convalescent plasma.

15(1) Braley, A. E., and Sanders, M. : Treatment of Epidemic Keratoconjunctivitis ; Preliminary Report of Ten Cases. J.A.M.A. 121: 999-1000, 27 Mar. 1943.
(2) See footnote 8, p. 7.


Since the advent of the newer antibiotics, there is some reason to hope for discovery of an effective therapeutic agent. In studies in New York and Miami, the possibility of Aureomycin as such an agent was raised.16 But again, the number of patients treated was small and evidence suggested that only administration of large amounts of the antibiotic intravenously in conjunction with its local application is effective during the first week of the disease.

In the evaluation of the therapy of epidemic keratoconjunctivitis, it cannot be stated too strongly that prevention of the disease is at present much simpler than its cure. Prompt initiation of hygienic or aseptic procedures when the first cases of the disease are recognized can save many hours of essentially unrewarding treatment.


Few other diseases studied during World War II can be evaluated in relation to the military effort as clearly as epidemic keratoconjunctivitis. Apparently nonexistent in the United States as a clinical entity before the war effort was launched, this disease emphasized the importance of industrial effort in modern warfare by incapacitating numerous skilled, essential workers. The rapidity with which the Preventive Medicine Division, Office of the Surgeon General, nullified the threat to industry was dramatic, and it is of decidedly more than historical interest to note the action taken as well as the results obtained. Control of the disease was undertaken by means of the mobilization of trained personnel and by the rapid dissemination of technical information to physicians, particularly those having industrial responsibilities.

In March 1942, studies concerned with the then unknown etiology of epidemic keratoconjunctivitis were initiated through the Commission on Neurotropic Virus Diseases of the Board for the Investigation and Control of Influenza and Other Epidemic Diseases in the Army, at the College of Physicians and Surgeons, Columbia University. The project was placed in the hands of Dr. Murray Sanders of the Department of Bacteriology, who discovered that the causative agent was a virus. Dr. Sanders was later appointed consultant to the Secretary of War and a member of the Commission on Neurotropic Virus Diseases. Thus, the Office of the Surgeon General was constantly in touch with the investigative program.

When the nature of the disease was appreciated, highly effective epidemiologic studies were made possible because of the centralization of authority through the Office of the Surgeon General. Thus, when epidemics occurred in industrial plants engaged in warwork at Hartford and Schenectady, it was possible to authorize Dr. Sanders to work with health authorities in both areas, who cooperated to obtain data permitting an effective check on new

16(1) Braley, A. E., and Sanders, M. : Aureomycin in Ocular Infections ; A Preliminary Report. J.A.M.A. 138: 426-427, 9 Oct. 1948 . (2) Braley, A. E., and Sanders, M.: Aureomycin in Ocular Infections ; A Study of Its Spectrum. Ann. New York Acad. Sc. 51 : 280-289, 30 Nov. 1948.


cases. There is little doubt that the teamwork among physicians, research investigators, epidemiologists, and other skilled investigators accelerated a solution to many aspects of the problem.

The Preventive Medicine Division was in a position to disseminate the new information at hand to civilian physicians (through the Industrial Medicine Section) and to medical officers in the various branches of the Armed Forces. This phase of the work was carried out in the following manner:17

1. On 21 November 1942, letters concerning the potential danger of epidemic keratoconjunctivitis were sent from the Office of the Surgeon General to the Chief of Ordnance, the Air Surgeon, the Surgeon General of the Navy, and others, calling attention to the disease and stating : "It is felt that it is highly important that medical officers and medical directors at arsenals, depots, and munition works become fully acquainted with this entire subject."

2. On 4 December 1942, a symposium on epidemic keratoconjunctivitis was held at the College of Physicians and Surgeons under the auspices of the Preventive Medicine Division. Arrangements for this symposium were made primarily by Col. Anthony J. Lanza, MC, Chief, Occupational Hygiene Branch, Preventive Medicine Division, who wished to bring the disease to the attention of medical officers and physicians in industrial plants. Col. (later Brig. Gen.) James S. Simmons, MC, Director, Preventive Medicine Division, Office of the Surgeon General, made the opening remarks at the meeting. The symposium was well attended and had immediate effect in arousing several State and industrial medical organizations to a recognition of the importance of the disease.

3. During November and December 1942, a circular letter on epidemic keratoconjunctivitis was drafted and submitted to numerous authorities for criticism and revision. This resulted in the distribution of Circular Letter No. 14, Office of the Surgeon General, dated 11 January 1943, to all medical officers.

4. The Preventive Medicine Division not only accumulated and distributed widely all publications and proceedings of meetings but also arranged for further meetings similar to the New York symposium in Chicago, St. Louis, and various other centers potentially important to the war industrial effort.

The quick removal of epidemic keratoconjunctivitis from the list of important problems in civilian life attests to the effectiveness of the program of The Surgeon General. Furthermore, the approximate total of 1,000 cases in the Armed Forces, with rapid control in the affected units, was considered a highly satisfactory minimum against the potential damage that could have occurred in such crucial elements as air or mechanized groups.

17Letter, Col. J. S. Simmons, MC, Director, Preventive Medicine Division, Office of the Surgeon General, to Dr. W. C. Davison, National Research Council, 12 Jan. 1943.