History

CHAPTER IV

Neurotropic Virus Diseases

John R. Paul, M.D.

The group of diseases designated as neurotropic virus diseases in this chapter has been selected, for practical reasons, on a somewhat arbitrary basis. They include acute infections with the viruses that cause the arthropodborne virus encephalitides: poliomyelitis, rabies, and lymphocytic choriomeningitis. It is with some aspects of the clinical and epidemiological story of these virus infections, as they occurred in military personnel in World War II, that this chapter is concerned.

Numerically speaking, the recognized military cases of neurotropic virus infections have been insignificant, but from other standpoints these diseases have proved to be of some military importance. In the first place, any virus disease that attacks the central nervous system easily acquires a bad reputation. Furthermore, as a group, the mortality is apt to be high and the stigma of injured brain function accompanies them. In the case of poliomyelitis, not only does this disease carry a more serious prognosis when it occurs in young adults (of military age) than in children, but when a permanent Army post is involved, this disease presents a threat to dependents who may happen to be living within the epidemic area. And finally, as far as the arthropodborne virus encephalitides are concerned, any mosquitoborne disease is of military significance.

Early in World War II, the Medical Department of the U.S. Army recognized that this relatively new group of diseases might pose a number of problems, and to forestall them, Circular Letter No. 74 was issued on this subject by the Surgeon General's Office on 19 March 1943. This circular was followed by War Department Technical Bulletin (TB MED) 212, issued 16 January 1946. The bulletin reviewed information bearing on the common neurotropic virus diseases of man, including classification and diagnostic features. In addition, the bulletin described the circumstances under which the then available diagnostic procedures could be profitably utilized.

THE ARTHROPODBORNE VIRUS ENCEPHALITIDES

The arthropodborne virus diseases comprise a group whose membership has expanded greatly since the war, but even in 1941 the recognized members were eastern and western types of equine encephalomyelitis, St. Louis encephalitis, Japanese B encephalitis, and Venezuelan encephalitis. Others of less importance to U.S. Forces included Russian spring-summer encepha-

litis (and other types from Russia and Siberia), some types from Africa, andlouping ill from England. These will not be considered here.

The number of military cases of this group of diseases whichoccurred in World War II turned out to be few indeed, but besides the reasonsalready given that these few cases deserve attention here is that researchinitiated and promoted by the Preventive Medicine Division, Office of theSurgeon General, and the Army Epidemiological Board (Board for theInvestigation and Control of Influenza and Other Epidemic Diseases in the Army),contributed materially to the addition of knowledge about these importantinfections during World War II.

Military History Prior to World War II

In view of the fact that no member of this group of arthropodborne virus encephalitides had been discovered, nor had the diseases which they cause been recognized as such prior to the 1930's, there is nothing about them in the medical history of World War I; nor had there been in the post-World War I period any experience by the Armed Forces with these agents or with the diseases they cause. If cases of this group of illnesses had occurred and attracted attention in 1917-18, they would probably have been listed under the miscellaneous group of "encephalitis, type undetermined" or perhaps as "epidemic encephalitis." During the last year of World War I and the years immediately following, the type of encephalitis most frequently encountered in military populations was encephalitis lethargica, otherwise known as Von Economo's disease. The records from World War I show 80 admissions, and at least 79 secondary cases of encephalitis,reported for the period from 1 April 1917 to 31 December 1919 in the total U.S. Army of approximately 4million.^l In this group, 27 deaths occurred, giving a casefatality ratio of about 17 percent.The chances that a large percentage of these cases were examples of encephalitislethargica are good. However, as the etiological agent of that disease wasnever established, one cannot speak with any confidence that it was actually a virus disease and thereforedeserves discussion here. Furthermore and fortunately, the incidence ofencephalitis lethargica began to decline in the midtwenties, both in the United States andin Europe. By 1930, to all intents and purposes,classical cases of this disease had disappeared, so for the present at least,we need not pursue the discussion about it further, except to point out thatother new types of encephalitis were soon to supplant Von Economo's disease.

It was during the 1930's thatthe arthropodborne virus encephalitides came under scrutiny, the firstrecognition of any member of the group being that of the virus of westernequine encephalomyelitis, isolated with some difficulty, from a sick horsein California in 1931 by Dr. Karl F. Meyer of the University of California.,San Francisco. Later, Dr. Carl TenBroeck, of the

¹The Medical Department of the United States Army in theWorld War.Washington: Government Printing Office, 1925, vol. XV, pt. 2, pp. 90-138, 656.

Rockefeller Institute of Medical Research at Princeton, N.J.,found that strains of the equine encephalomyelitis viruses could be separatedinto eastern and western types. The "disease" for which these viruseswere responsible was regarded at that time primarily, if not entirely, as one ofhorses. A manifest interest by the Army in this matter accompanied the report in1934 by Lt. Col. (later Brig. Gen.) Raymond A. Kelser, VC, that these virusescould be transmitted from horse to horse by certain species of mosquitoes.

A second chapter in the story was written when it was found that this type ofillness affected man. In 1933, a severe outbreak of human encephalitis occurredin and about the city of St. Louis, Mo. More than 1,000 human cases werereported with about an 18 percent mortality. The virus of St. Louis encephalitiswas isolated in this epidemic more or less coincidentally by Drs. Ralph S.Muckenfuss and L. 'I'. Webster. Although sick horses received little noticeduring this epidemic, some of the investigators, including Maj. (later Brig.Gen.) James S. Simmons, MC, thought that St. Louis encephalitis might be relatedto one of the equine encephalitides and attempted to infect horses with the St.Louis virus. The assumption was correct, and the failure to substantiate itexperimentally at that time might have been due to the fact that the horses usedwere from the St. Louis area and they could well have been immune to thedisease.

It was also at about this time (1933-34) that U.S. investigators beganseriously to compare the St. Louis epidemic with the existing situation in Japanwhere endemic encephalitis had appeared in parts of the home islands almostevery summer since 1871. In 1924, there had been a particularly bad epidemic,and clinical studies had made, it possible for the Japanese to distinguish theirdiseases from epidemic encephalitis of the so-called A type (Von Economo'sdisease). For this reason, Japanese epidemic encephalitis has been termed type Bencephalitis. The epidemic of 1924 had spread through wide area resulting in aheavy mortality among 6,000 reported cases.During the period from 1924 to 1937, outbreaks occurred almost every summer inJapan, resulting in a total of some 21,000 reported cases for that period withthe heaviest concentration of cases occurring in the region of the InlandSea. Similar recurrent appearances of summer or autumn encephalitis were knownto have been reported from the Ryukyu Islands, as well as from FormosaManchuria, and the far eastern maritime districts of Soviet Russia. Opinion inJapan was divided as to the means of spread, and by 1938, although one grouphad suspected that it was mosquitoborne, the balance of Japanese medical opinionheld to the view that it was spread from the respiratory tract.

By 1938-39, relations between Japanese medical science andthat of the United States could hardly be described as close and shortlythereafter ceased altogether. Consequently, the up-to-date story on currentJapanese views as to how their type of encephalitis was transmitted and justwhere this disease could be expected to appear was not readily available tomedical intelligence officers during the war years.

The next development in this story took place in the United States in 1938, with the appearance in Massachusetts, Rhode Island, andConnecticut of a less extensive outbreak of acute encephalitis involving bothman and horses. The causative virus was identified as eastern equineencephalomyelitis virus. It also became apparent that here was a group ofdiseases that not only infected both man and horses, but perhaps other animals.More or less coincidentally, the discovery in 1937 ofthe spring-summer type of encephalitis in the forested, far eastern regions ofthe U.S.S.R. and the demonstration that it was caused by a new virus which wastickborne, all indicated the existence of a large group of related agentsextremely widespread geographically and with a variegated group of insects(arthropods) as vectors and several mammalian hosts. To this group were soonadded other strains of virus from South America (notably Venezuelanencephalitis), and subsequently several from Africa.

Early in the 1940's, informationabout these diseases was accumulating at a rather rapid rate, although much ofit was still theory. Birds had been found to be infected, which made theepidemiological picture still more complicated. Eventually, the epidemiology of some of this groupof diseases, as they occurred in the United States, was worked out largelythrough the efforts of Dr. William McD. Hammon at the University ofCalifornia, San Francisco. From his work, the concept gradually emerged that, inthis country at least, this group of infections, many of which were inapparent,was primarily one of birds and that the severe infections in man, horses, andother animals were what might be called casual, though spectacular, accidents.Apparently, the avian infection could be very widespread numerically but wasmild, causing little more than a viremia in certain members of the avian family.It was transmitted to various species of both birds and mammals usually throughthe agency of Culex mosquitoes.

This then was the background in 1941 withregard to the "new" neurotropic virus infections with which the U.S.Army might be confronted if it should engage in global combat. The threat wasappreciable in that any mosquitoborne disease recalled the destructive effectwhich malaria, yellow fever, or dengue had had upon troops in the field in thepast. In addition, a number of potential theaters of war, such as Japan,Manchuria, and elsewhere, were listed as endemic or epidemic areas and mightpossibly turn out to be hotbeds of infection by one of the worst members of thegroup, Japanese B encephalitis. These potentialities were further emphasized byan epidemic of western equine encephalomyelitis which swept over a largesection of Western Canada and many areas in the Western United States, includingthe Dakotas, Montana, and Colorado in the summer of 1941. Thousandsof civilian cases occurred, although the number of U.S. Army personnel involvedin this epidemic was insignificant. However, in Canada where it was estimatedthat there were more than 5,000 cases, mostly in Saskatchewan and Manitoba, theepidemic had also involved certain training areas where Canadian troops werestationed, and during the summer of 1941, anumber of cases occurred in the

Canadian Army.² It hardly could be questioned in the autumn of1941 that here was a new disease of potential military importance to U.S.troops.

Diagnosis.-It is important tomention here that not only in 1917-18 but in the subsequent 25 years theclinical diagnosis of encephalitis proved to be a loose one indeed, covering anumber of different entities. In another volume in the history of the MedicalDepartment in World War II, Sabin states:³

Clinical records from civilian as well as military medicalpractice indicate that the diagnosis of encephalitis is commonly made wheneverclinical manifestations suggestive of cerebral disturbance (ranging from mildlethargy to coma, from slight delirium to complete disorientation, fromrestlessness to convulsions) are associated with an otherwise undiagnosablefebrile illness. The diagnosis is not infrequently made when the syndrome ofaseptic meningitis is associated with what may be interpreted as lethargy orunusual restlessness. It is made not only when the cerebral disturbance isassociated with pleocytosis, but also in its absence, and indeed notinfrequently when toxic encephalopathy is associated with certain bacterialinfections.

In the period 1941-46, and subsequently, the exact method ofmaking adiagnosis of this group of virus diseases was by immunological and virologicaltests. Some of these became available during and immediately prior to World WarII. However, the utilization of these tests, which included neutralization orcomplement fixation tests on matched specimens of sera, was more or less in itsinfancy and hardly more than half a dozen laboratories in the United Statescapable of carrying them out.⁴

Experience During World War II

Most, although not all, of the apprehension aboutarthropodborne virus encephalitides proved to be unnecessary, for when theSecond World War was over the incidence of these infections in militarypersonnel turned out to be small. There were no large wartime epidemics in theUnited States involving the civilian population compared to those at St.Louis in 1933 and in the Northwest in 1941.

The final experience in World War II with these diseases both as to number ofrecognized cases, incidence rates, and deaths ascribed to encephalitis is listedin tables 10 and 11. It is clear that the figures suffer somewhat from theinaccuracies of diagnoses which are apt to beset all figures on the incidence ofthe encephalitides, infectious or otherwise. As just mentioned, Sabin has pointed out that the clinical diagnosis of any kind ofencephalitis

²Report,Commission on Neurotropic Virus Diseases, Board for the Investigation andControl of Influenza and Other Epidemic Diseases in the Army, 1 Dec. 1941-1 May1942.
³Sabin, Albert B.: Encephalitis. In MedicalDepartment, United States Army. Preventive Medicine in World War II. VolumeVII. Communicable Diseases: Arthropodborne Diseases Other Than Malaria. [Inpreparation.]
⁴Better known laboratories readilyavailable to the Medical Department of the U.S. Army for the diagnostic purposeof these diseases, in 1941-45, included that of the Army Medical School,Washington, D.C., the G. W. HooperFoundation of the University of California in San Francisco, the RockefellerInstitute for Medical Research in New York City (both of which facilities weremade available through the Commission on Neurotropic Virus Diseases of theArmy Epidemiological Board), and a few other laboratories, also connected withthe Army through that Board.

without the assistance of serological tests is notoriouslydifficult. In view of the fact that such immunological tests were not availablein many of the cases occurring in military personnel during wartime, the data intables 10 and 11 must be regarded as being approximate rather than definitive.It should be noted, however, that the rates for infectious encephalitis werehigher in 1944 and 1945 in the Pacific than in Europe. This is what should havebeen expected because, except for the presence of tickborne Russianspring-summer encephalitis in Czechoslovakia and in eastern Austria, thearthropodborne encephalitides as they are now known to occur in man are almostentirely absent from Europe.

TABLE 10.-Admissions forencephalitis in the U.S. Army, by diagnosis, selected area, and year, 1942-45

[Preliminary data based on sample tabulations of individual medical records]
[Rate expressed as number of admissions per annum per 1,000 average strength]

Diagnosis and area	1942-45		1942		1943		1944		1945
Diagnosis and area	Number	Rate	Number	Rate	Number	Rate	Number	Rate	Number	Rate
Infectious encephalitis:¹
Continental United States	187	0.01	44	0.02	65	0.01	43	0.01	35	0.01
Overseas:
Europe	(72)	0.02	(1)	0.01	(6)	0.02	(20)	0.01	(45)	0.02
Pacific	(107)	.03	(1)	.00	(5)	.01	(41)	.04	(60)	.04
Total overseas	247	0.02	4	0.01	14	0.01	94	0.02	135	0.03
Total Army	434	0.02	48	0.01	79	0.01	137	0.02	170	0.02
Postvaccinal encephalitis:²
Continental United States	(³)	(³)	(³)	(³)	(³)	(³)	1	0.00	---	0.00
Overseas:
Europe	(³)	(³)	(³)	(³)	(³)	(³)	---	0	---	0.00
Pacific	(³)	(³)	(³)	(³)	(³)	(³)	(6)	.01	(5)	.00
Total overseas	(³)	(³)	(³)	(³)	(³)	(³)	6	0.00	10	0.00
Total Army	(³)	(³)	(³)	(³)	(³)	(³)	7	0.00	10	0.00
Encephalitis, other and undetermined:⁴
Continental United States	953	0.06	272	0.10	355	0.07	211	0.05	115	0.04
Overseas:
Europe	(89)	0.02	(9)	0.11	(10)	0.04	(20)	0.01	(50)	0.02
Pacific	(138)	.04	(7)	.03	(17)	.04	(19)	.02	(95)	.07
Total overseas	394	0.04	26	0.04	101	0.06	97	0.03	170	0.04
Total Army	1,347	0.05	298	0.09	456	0.07	308	0.04	285	0.04

¹Includes infectious encephalomyelitisand Japanese B type encephalitis as well as other types of infectiousencephalitis. Excludes lymphocytic choriomeningitis.
²Includes postvaccinalencephalomyelitis.
³Dataare not available.
⁴Includes encephalomyelitis, other andundetermined. Excludes lymphocytic choriomeningitis.

NOTE.-Figures in parentheses are subtotals.

TABLE 11.-Deathsdue to encephalitis in the U.S. Army, by diagnosis, selected area of admission,and year of death, 1942-45

[Preliminary data based on tabulations of individual medicalrecords]
[Rate expressed as number of deaths per annum per 100,000 averagestrength]

Diagnosis and area	1942-45		1942		1943		1944		1945
Diagnosis and area	Number	Rate	Number	Rate	Number	Rate	Number	Rate	Number	Rate
Infectious encephalitis:¹
Continental United States	9	0.06	2	0.08	2	0.04	3	0.08	2	0.07
Overseas:
Europe	(4)	0.09	---	0	---	0	(1)	0.06	(3)	0.13
Pacific	(3)	.10	---	0	---	0	(2)	.20	(1)	.07
Total overseas	12	0.11	1	0.17	---	0	6	0.16	5	0.11
Total Army	21	0.08	3	0.09	2	0.03	9	0.12	7	0.09
Postvaccinal encephalitis:²
Total Army	(³)	(³)	(³)	(³)	(³)	(³)	---	0	---	0
Encephalitis, other and undetermined:⁴
Continental United States	57	0.39	7	0.26	20	0.39	23	0.58	7	0.24
Overseas:
Europe	(15)	0.34	---	0	(1)	0.37	(4)	0.24	(10)	0.42
Pacific	(19)	.61	(2)	.90	(1)	.21	(3)	.31	(13)	.92
Total overseas	55	0.51	2	0.34	11	0.65	15	0.39	27	0.58
Total Army	112	0.44	9	0.28	31	0.45	38	0.49	34	0.45

¹Includes infectious encephalomyelitis and Japanese B type encephalitis aswell as other types of infectious encephalitis. Excludes lymphocyticchoriomeningitis.
²Includes postvaccinal encephalomyelitis.
³Data are not available.
⁴Includes encephalomyelitis, other and undetermined. Excludes lymphocyticchoriomeningitis.

NOTE.-Figures in parentheses are subtotals.

No sizable epidemic due to one of the known encephaliticviruses was ever recorded in U.S. Forces stationed within the United Statesduring the period 1942-45. However,a possible outbreak, of which the agent was never identified, occurred duringthe summer of 1941, when 12 mildcases of encephalitis developed in a force of unknown size maneuvering nearSabinal, Tex.⁵ Sporadic cases of proved arthropodborne virusencephalitides occurred in western training areas during 1942-45, but the incidence never reachedanything comparable to that experienced by the Canadian troops in Manitoba in1941. Clinical descriptions of these sporadic cases in U.S. troops apparentlydid not differ from the usual textbook descriptions, and no unusual findings areknown to the author.

Outside the confines of the United States, a single case due to one of theexotic South American types of the neurotropic viruses was recorded of a

⁵Woodland, J. C., and Smith, E. M.:Acute Encephalitis; Mild Epidemic Observed at Station Hospital, Fort SamHouston, Texas. J.A.M. A. 120: 358-361, 3 Oct. 1942.

U.S. Navy seaman in Trinidad in 1943. Itproved to be due to the virus of Venezuelan equine encephalitis.⁶

By far the most important group of cases, however, which occurred during theSecond World War took place in an oversea theater. This was the small butimportant outbreak identified as Japanese B encephalitis which involved bothnatives and troops on the island of Okinawa in the summer of1945.

In the spring of 1945 andat the time of the occupation of islands north and northwest of Guam, theMedical Department recognized that U.S. troops were entering territory whereJapanese B encephalitis might be endemic. For this reason, knowledge of thedisease was summarized for use by medical officers in War Department TechnicalBulletin (TB MED) 181, July 1945. JapaneseB encephalitis had been previously reported as recurring not only in Japanproper but in the Ryukyu Islands, Formosa, Korea, eastern China, in certain ofthe far eastern maritime districts of the U.S.S.R., and in Manchuria. However,it was uncertain whether the Japanese B virus was the sole etiological agent ofencephalitis within all these areas.

The epidemic occurred during a combat period on the island ofOkinawa and has been well described by Sabin,⁷ so that his accountneed not be repeated here. It may suffice to say that the occupation of Okinawa,representing, as it did, a very strategic area, had been achieved in April1945, and during the entire spring and early summer months, fighting continuedsporadically on the island. Encephalitis first appeared among the nativepopulation early in July. The first native patients with severe encephalitisobserved by American medical officers in the Ryukyus were seen by Lt. L. M.Miller, MC, USNR (of the local military government) on 8 July 1945 on Heanza Shima, a small island about 2 miles east ofOkinawa. During the following 3 months,127 patients were seen by military government medical facilities onthe two islands; 66 of the 91 patientsfound on Okinawa were admitted to the isolation hospital for observation andtreatment. The etiological agent of the disease was first established by theresults of complement fixation and neutralization tests and by recovery of thevirus from a fatal case.

Two groups of workers participated in these identifications.The civilian cases were first identified by Hodes, Thomas, and Peck,⁸of the Naval Medical Research Unit No. 2, then established on the island ofGuam, and subsequently, military cases were identified by Lt. Col. Albert B.Sabin, MC,⁹ member of the Commission on Neurotropic Virus Diseases,Army Epidemiological Board. This achievement by American medical officers inrecognizing clinically and,

⁶Randall, R., and Mills, J. W.: Fatal Encephalitis in Man Due To VenezuelanVirus of Equine Encephalomyelitis in Trinidad. Science 99: 225-226, 17 Mar.1944.
⁷(1) Sabin, A. B.: EpidemicEncephalitis in Military Personnel; Isolation of Japanese B Virus on Okinawa in1945; Serologic Diagnosis, Clinical Manifestations, Epidemiologic Aspects andUse of Mouse Brain Vaccine. J.A.M.A. 133: 281-293, 1 Feb. 1947. (2) See footnote3, p. 83.
⁸Hodes, H. L., Thomas, L., and Peck, J. L.: Cause ofan Outbreak of Encephalitis Established by Means of Complement-Fixation Tests.Proc. Soc. Exper. Biol. & Med. 60: 220-225, November 1945.
⁹Sabin, A. B.: Outbreak of Encephalitis on Okinawa in 1945; Preliminary Report on Status as of August 27, 1945. J. Mil. Med. in Pacific 1: 79-84, November 1945.

subsequently, in identifying the etiology of Japanese Bencephalitis was accomplished under arduous combat conditions and was indeed anoteworthy event, both in military medicine and in the history of this diseasein general. At the time the disease was discovered, the island was the mostimportant advanced base in the Pacific area. Large forces of U.S. troops werealready assembled for the projected invasion of the home islands of Japanscheduled for the autumn. It was reasonable to assume that these troops were andwould be susceptible to neurotropic virus disease to which they had never beenpreviously exposed, and the danger of an epidemic was therefore a matter ofgreat concern to the Medical Departments of the Army and the Navy. The news ofthe epidemic of "a dread Japanese brain disease" on Okinawa had alsospread among the troops with demoralizing effect.

It is hard today to appreciate the difficulties whichconfronted medical officers at that time, but the story of these difficultieshas been well documented by Lt. Col. William D. Tigertt, MC, and Dr. Hammon.¹⁰They pointed out that in 1945, available information about the presence of thedisease on Okinawa was meager. Although Japanese B encephalitis had been statedto occur on Okinawa, the figures were difficult to assess since cases ofepidemic cerebrospinal meningitis, encephalitis lethargica, and malaria withcerebral symptoms were also reported, usually with the diagnosis made onclinical grounds. Furthermore, relatively few Japanese physicians had practicedon the island of Okinawa before World War II, and public health reports werefragmentary and incomplete there. Only later did it become known that Iimura hadreported 68 cases of Japanese B encephalitis on Okinawa in 1933 (cited byTigertt and Hammon) and that, in 1937, Takagi and others (cited by Tigertt andHammon) had shown that most of the human sera collected on Okinawa containedneutralizing antibodies.

Mosher¹¹has described how the situation washandled on Okinawa in July and August 1945. The investigation of encephalitiswas assigned to the Military Government Research Center, and on 18 July 1945, an isolationhospital for the study of the disease was opened at Gimbaru.By direction of the commandant of the U.S. Military Government, all nativepatients with cerebrospinal symptoms suggestive of encephalitis were referred tothe research center from all parts of the island by field dispensaries,hospitals, and other medical units established to care for the natives.Dispensary personnel were instructed in the recognition of the disease, and insome areas native police assisted in finding the sick. A visiting nurse programwas instituted by some of the dispensaries. While these nurses were largelyuntrained volunteers, they facilitated in some degree in case finding and inreferral of cases to the hospitals. Between early July and October, a total of91 natives of Okinawa

¹⁰Tigertt, W. D., and Hammon, W. McD.: Japanese B Encephalitis: AComplete Review of Experience on Okinawa, 1945-1949. Am. J. Trop. Med. 30:689-722, September 1950.
¹¹Mosher, W.E., Jr.: Japanese "B" Encephalitis; Epidemiological Report of the1945 Outbreak on Okinawa. U.S. Nav. M. Bull. 47: 586-593, July-August 1947.

were diagnosed as having encephalitis, the morbidity being 2.8 per 10,000, ascompared with 44.7 for the Heanza-Hamahika Islands.

Among U.S. military personnel, between July and mid-September, 38 militarypatients exhibited a variety of clinical manifestations and were investigated byserological methods for the diagnosis of Japanese B encephalitis. Of these,only 11 yielded unequivocal evidence of the specific infection. Two of theeleven died, and autopsy revealed cerebral lesions compatible with thediagnosis of viral encephalitis. It is highly probable that more than 11 casesoccurred.

In a report of the outbreak by Lewis and his associates,¹² which represents perhaps thefirst extensive clinical description of Japanese encephalitis made by U.S.physicians, the symptomatology of the disease was described as it occurred among Okinawan natives. The clinical features of the cases in U.S. militarypersonnel, as observed both on Okinawa and subsequently in Korea, have been welldocumented in War Department Technical Bulletin (TB MED) 181 on Japanese Bencephalitis, issued on 6 April 1947.

Although the clinical features of Japanese B encephalitis donot seem to differ materially from those of St. Louis encephalitis and westernequine encephalomyelitis, which were already in 1945 well described in U.S. textbooks of medicine, it may be worthwhile to mention something here of theclinical picture of Japanese encephalitis as it appeared on Okinawa. Mostimportant for diagnostic purposes was the appearance of the following signsduring the course of an acute febrile illness: Mental confusion, disorientation,purposeless movements, speech disturbances, and complete aphasia. Varyingdegrees of lethargy might be present ranging from abnormal somnolence tocomplete coma in patients who also exhibited high fever and nuchal and spinalrigidity. As a rule, there was a period of 2 or 3 days before the appearance ofany signs suggesting involvement of the nervous system. During this time,headache and low-grade fever were the only symptoms. Generalized convulsions ofthe grand mal or petit mal type were occasionally the first signs of involvementof the nervous system, with stiffness of the neck and back, and other signsalready mentioned, coming later. Flaccid paralysis, suggesting involvement oflarge numbers of lower motor neurons in the spinal cord or medulla, was notseen. Localized spastic paralysis was seen only once among 15 patients, althoughgeneralized rigidity was present in the more severe cases. Dissociated eyemovements were seen in only one patient, and diplopia did not occur. Pupilswere usually contracted and reacted poorly to light; a sticky exudate was notinfrequently seen about the eyes. The reflexes were variable and by themselvesof little aid in differential diagnosis. The abdominal reflexes were usuallyabsent while the tendon reflexes were most exaggerated; only occasionally didthey become diminished or absent. Babinski's sign was rarely elicited.

¹²Lewis, L., Taylor, H. G., Sorem,M. B., Norcross, J. W., and Kindsvatter, V. H.: Japanese B Encephalitis;Clinical Observations in an Outbreak on Okinawa-shima. Arch. Neurol. &Psychiat.57: 430-463, April 1947.

As a rule, the fever lasted from 7 to 11 days. It was high after theappearance of nervous signs and frequently remittent, although it is uncertainto what extent the administration of antipyretics may have affected thetemperature curve. A relative bradycardia was invariably present during thefebrile phase with a pulse rate of about 50 to 60 being common afterdefervescence. In fatal cases, death due to encephalitis occurred within thefirst 2 weeks and, as a rule, during the first 7 days after onset.

Convalescence was slow. Lethargy and incoordination, tremors and nervousness,and occasionally distinct personality changes persisted for some weeks afterdefervescence. Subsequently, it became apparent from observations by Japanesephysicians and by neurological consultants from the United States that residualsymptoms from this disease were noted in only a small percentage of patients.¹³These did not grow progressivelyworse as in the sequelae in encephalitis lethargica.

As to laboratory findings in the blood and spinal fluid, during the acutephase of the disease, the white blood cells in the former were likely to beincreased in the range of 10,000 to 25,000 cells per cubic millimeter of blood,with a definite increase in the number of mature and immature neutrophiles.Cerebrospinal fluid was clear, under normal or occasionally increased pressure,and pleocytosis, ranging from 22 to 1,450 white blood cells, was present in allof the military patients whose illness was definitely proved to be due to thisinfection. The cells were, as a rule, predominantly mononuclear, although inat least two of the group polymorphonuclear leukocytes predominated; spinalfluid sugar and chloride were in the normal range. Protein was normal or onlyslightly increased early in the disease, while during convalescence a 3 or 4plus Pandy reaction was not uncommon.

In American military personnel, poliomyelitis and"aseptic meningitis''¹⁴ offeredthe greatest problems of clinical differential diagnosis. Among the children andnatives of older age groups, tuberculous meningitis proved to be anotherimportant differential diagnostic consideration. Of aid in the diagnosis was theuse of neutralization and complement fixation tests and virus isolation fromfatal cases. It was fortunate indeed that, during the

¹³During World War II, and when thisdisease was first encountered, a subject of great interest was whether themilitary cases of Japanese B encephalitis would result in any residualdeficiencies in nervous function after the acute stage of the disease had beenpassed successfully. This was a matter which should call for preferablylong-term followup observations. One postwar study which can be mentioned isembodied in a report to the Surgeon General's Office by Dr. Charles D. Aring,Professor of Neurology, University of Cincinnati, Ohio, made under the auspicesof the Army Epidemiological Board in 1948 (published in Arch. Neurol. &Psychiat. 62: 759-765, December 1949). Dr. Aring examined 19 late cases ofJapanese B encephalitis in Americans at the 361st Station Hospital in Tokyo,as well as 12 late cases among Japanese. In only 1 American out of a total of 19 did he feel that it was possible that the patient was sufferingfrom residua, and even in this case it seemed probable that thesigns were attributable to an emotional disorder apart from his recent acutedisease. It was Dr. Aring's opinion that once the "dangerous period"had been passed without the appearance of crippling neurological signs, thepatient would go on to good recovery, with the possible exception of thedevelopment of parkinsonism, which had been reported in Japanese cases as an occasional occurrence.
¹⁴Several years later, it was shown that leptospirosiswas the cause of at least one outbreak of "aseptic meningitis" introops on the island of Okinawa.

combat conditions on Okinawa in the summer of 1945, not onlywere laboratory facilities made available for the carrying out of these tasksbut that personnel were also available to do the tests and to interpret them.This is a type of frontline scientific medicine which deserves special mentionin any military history.

Medical officers were aware that there was no specific treatment for JapaneseB encephalitis, but the following supportive measures were carried out. Duringthe period of coma, nutrition was maintained by gavage or by the parenteraladministration of fluids and the use of vitamin supplements. As depletion ofbody protein was sometimes extreme, plasma or amino acids were given.

Other special and general methods were used as a means of preventingdecubitus ulceration. The careful use of sedatives during periods ofrestlessness and irritability, with frequent changes of posture of comatose patients, tracheal aspiration, catheterization when indicated, and similar routineprocedures constituted almost all the therapeutic measures.

The treatment of complications with chemotherapeutic agents was regarded asof paramount importance, particularly with reference to pneumonia.

The pathology of Japanese B encephalitis was also described on the basis ofmaterial studied from the Okinawan epidemic. An excellent report was made byLt. Comdr. H. M. Zimmerman, MC, USNR, from the Naval Medical Research Unit No. 2¹⁵and, with the help of the Army Institute of Pathology (nowthe Armed Forces Institute of Pathology), Washington, D.C., another report wasmade by Haymaker and Sabin.¹⁶ Involvement of the brain proved to bevery extensive.

For preventive measures, the reader is referred to Sabin'schapter on encephalitis in another volume in the history of the MedicalDepartment in World War II.¹⁷ It is enough to say here that the useof mosquito control and a mouse-brain formalin (inactivated) vaccine were triedon Okinawa.

In summary, therefore, and in retrospect, it would appear thatduring World War II after considerable preparation with regard to thearthropodborne virus encephalitides this group of diseases turned out to be lessof a threat as a military disease than had been anticipated, but in this respectthere was feeling that the Armed Forces had been lucky. In any event,considerable was learned about arthropodborne virus encephalitides whichconstituted a group of what might be called new diseases as far as the MedicalDepartments of either the Army or the Navy were concerned. The first contact byAmerican troops with a most important member of this group, namely, Japanese Bencephalitis, became a landmark of some prominence

¹⁵Zimmerman, H. M.: The Pathology of Japanese B Encephalitis. Am. J. Path. 22: 965-991, September 1946.
¹⁶Haymaker, W., and Sabin, A. B.: TheTopographic Distribution of Lesions in Central Nervous System in Japanese B Encephalitis; Natureof the Lesions, With Report of a Case on Okinawa. Arch. Neurol &. Psychiat. 57: 673-692, June1947.
¹⁷See footnote 3, p. 83.

in the military history of virus diseases. That the diseaseshould have been promptly recognized, and the agent isolated by medical officersfrom the Army and the Navy working close to the combat areas, was a noteworthyachievement. Subsequent to World War II, important additions were made toknowledge about this disease, as a result of experiences in the army ofoccupation in Japan,¹⁸ but the introduction to this story came in July andAugust of 1945 on the island of Okinawa.

POLIOMYELITIS

Just prior to the onset of World War II, it was generallyagreed by medical officers in the Army that poliomyelitis was not a disease ofmilitary significance. This was based on the very low incidence of poliomyelitisin U.S. Army forces during and in the years immediately following World War I.It seemed justifiable to continue to regard this disease essentially, if notexclusively, as a disease of early childhood and not, to any appreciable degree,as a disease of men of military age.

By 1945, however, it was abundantly clear that this opinionneeded revision, for although the number of cases of poliomyelitis which hadoccurred in the Army during World War II was not very great (in the neighborhoodof about 1,000 covering the 4 war years), the disease had been responsible formany problems. The degree of crippling was high; the percentage of bulbar caseswas high; the mortality was high; and the element of panic which poliomyelitiscaused, either in outbreaks or in single cases within military units, had provedto be appreciable. Not only had this been so within the confines of the UnitedStates but, with the exception of the European Theater of Operations, U.S. Army,the incidence of poliomyelitis had been considerably greater in troops abroadthan at home (p. 99).

The statistics with regard to the prevalence of poliomyelitisin U.S. Army personnel preceding and during World War II have beenadmirably

¹⁸It will not be within the scope ofthis chapter to discuss postwar outbreaks of arthropodborne virus encephalitisor the experience with this disease by troops occupying Japan during the 2 yearsimmediately following 1945. Three cases did occur in U.S. troops in Korea in1946, one of them fatal. These occurred among 1,500 Americans stationed in anisolated camp near Kunsan (Sabin, A. B., Schlesinger, R. W., Ginder, D. R., andMatumoto, M.: Japanese B Encephalitis in American Soldiers in Korea. Am. J.Hyg. 46: 356-375, November 1947). No cases of encephalitis were found in thenative population coincidentally. Subsequently (1946-55), Korea has experiencedat least two large outbreaks of Japanese B encephalitis.

Also during the summer of 1946, an outbreak of illness amongU.S. Marines stationed in Tientsin, China, which at first was thought to beencephalitis and later regarded as poliomyelitis, led to certain investigationsby Sabin and his coworkers (Proc. Soc. Exper. Biol. & Med. 65: 183-187, June1947) which revealed that extensive previous inapparent infection with JapaneseB encephalitis virus existed among the populations of Shanghai and Tientsin,where no epidemics of encephalitis had been observed. The survey methodemployed by Sabin was one which had been followed by Japanese in Japan andelsewhere, for some years; namely, by determining the presence or absence ofneutralizing antibodies for the virus of Japanese B encephalitis in largenumbers of sera collected from various age groups of the local population livingin various locations. It was, however, one of the first of many subsequentexamples of the use of the serological antibody survey by U.S. investigators asa means of outlining the geographic distribution of epidemic encephalitis inwhat might be called unknown territory.

CHART 2.-Seasonal incidence ofpoliomyelitis in the Armyin the continental United States compared with contemporaneous civilian ratesduring the second half of each year, 1943-46

reviewed by Sabin in another volume in the history of theMedical Department in World War II.¹⁹ The attempt will not be made,therefore, to duplicate Sabin's figures to which the reader may be referred.There are, however, certain epidemiological points which deserve mention even atthe expense of reiteration because they represent new information about thisdisease acquired as a result of military experience. Primarily, it becameapparent during the years 1941-45 that men of military age, born and brought upin the United States during the 1920's and 1930's, were more susceptible topoliomyelitis than their fathers had been in 1917-18. This was unexpected. Themilitary rates for 1943-46 within the United States

¹⁹Sabin, Albert B.: Poliomyelitis. In Medical Department, United StatesArmy. Preventive Medicine in World War II. Volume V. Communicable DiseasesTransmitted Through Contact or By Unknown Means. Washington: U.S. GovernmentPrinting Office, 1960, pp. 367-400.

are shown in chart 2. In comparing the curves recording Armyand civilian incidence, respectively, in chart 2, one should recall that thecivilian population contains a much higher percentage of susceptibles (children)than does the military population. In terms of actual rates, the averagecivilian overall annual rate for poliomyelitis per 100,000 in the United Statesfor 1940-47 was about 10. This includes all ages, all months of the year, andboth paralytic and nonparalytic cases. It can be compared with the annual ratefor U.S. Army troops in the United States for the period 1940-47, which wasabout 3 per 100,000.

Another point that came out of the military experience wasthat in 1941 there was little appreciation that poliomyelitis could be atropical disease of any importance, or that it amounted to much in subtropicalareas. Local civilian public health statistics within the great majority oftropical areas had for years reported a dearth of epidemics and a very lowincidence of poliomyelitis in the native-born inhabitants.²⁰Therefore, it was naturally thought that this disease should not be ofparticular danger to troops in such areas. It was not long, however, before itbecame apparent that poliomyelitis could exist in poorly sanitated tropical orsubtropical areas as a hidden disease, hitherto unsuspected. Later, by thecopious use of hindsight, one could surmise that this might have been predictedon the basis of prewar experience with poliomyelitis in the Philippines. Asearly as 1936, Lt. Col. (later Brig. Gen.) Charles C. Hillman, MC, had reportedan interesting observation. which was to be repeated frequently during World WarII. In his account²¹ ofan outbreak of poliomyelitis which occurred in Manila, Philippine Islands, in1934, he described 17 patients with poliomyelitis who were admitted to theSternberg General Hospital in Manila; of these, 3 cases were in militarypersonnel, the remaining 14 being in dependents. Coincidentally, the number ofcases in the local Philippine civilian population was small, presumablyrepresented by only nine cases. Colonel Hillman commented on the fact that,considering the vast preponderance of natives to American-born people in thecommunity, there was indeed a striking discrepancy between the poliomyelitisincidence rate in the civilian population and that of the Americans. However,the extraordinary degree to which the immunity of the young adults in the twopopulations might differ was not appreciated at that time.

The idea should not be conveyed here that the MedicalDepartment of the U.S. Army was indifferent at the beginning of World War II tothe threat of poliomyelitis as a possible problem in military medicine, for thiswas not the case. During the summer of 1941, the Office of the Surgeon Generalof the Army prepared a statement about poliomyelitis and recommendations forits control in the Army. Again in 1943, at the request of

²⁰Since 1945, manyepidemics of poliomyelitis have been reported from tropical areas (Paul, J. R.,Ramirez Corria, F., and Horstmann, D. M.: Analyses From a Tropical Epidemic ofPoliomyelitis Which Occurred in Florida and Cuba in 1946. Am. J. Trop. Med. 29:543-554, July 1949).
²¹Hillman, C. C.:Poliomyelitis in the Philippine Islands. Mil. Surgeon 79: 48-58,July 1936.

The Surgeon General of the Army, the Division of MedicalSciences of the National Research Council sponsored a discussion by outstandingauthorities in the field of poliomyelitis, which again resulted in a number ofrecommendations used by military officers. These recommendations are recorded bySabin in another volume in the history of the Medical Department in World WarII.²²

Perhaps the first theater in which this disease became anappreciable problem was that of the U.S. Army Forces in the Middle East in 1943.Observations regarding the seriousness of poliomyelitis inBritish troops within the area during 1941-42 hadalready been made in 1943.²³ The situation was later reviewed by Caughey and Porteousin a postwar report of their experiences which includes a description of anepidemic of poliomyelitis which had occurred in 1940-41 inNew Zealand troops stationed in Egypt.²⁴ Similar British observationswere recorded in India with comments on the fact that poliomyelitis wasparticularly severe in foreign troops in India, whereas at the same time itseemed to be both uncommon and not severe in the natives there.

This early British experience in the Middle East was latershared by U.S. troops in North Africa, Egypt, and the Middle East generallyduring the summer of 1943. Thisjoint experience has been described²⁵with particular reference tothe high rate and high fatality of poliomyelitis in U.S. troops in contrast toits apparent rarity in the native adult Egyptians. Comment was also made on theabsence of epidemics of poliomyelitis in the local native population and thefact that the only examples of the disease which did appear in the localpopulation were in infants.

There was considerable difficulty with the diagnosis ofpoliomyelitis in U.S. troops stationed in this area during the summer of 1943. Medical officers had not been prepared for this diseaseand were very loath to accept suspicious cases as poliomyelitis. This may beunderstandable in that, at least at that period, the clinical picture ofpoliomyelitis in adults had received scanty treatment in American textbooks ofmedicine. At the 38th General Hospital near Cairo, Egypt, this author, inconsultation, saw at least a dozen cases of poliomyelitis, several of which werefatal. In the majority of patients, the disease was characterized by insidiousonset with 2 or 3 days of malaise,relatively little fever, but severe pain in the back. This is in some contrastto the textbook picture seen in children with an acute onset with fever andusually a biphasic course. Fortunately, at the 38th General Hospital, a viruslaboratory had been established in the sum-

²²See footnote 19, p. 92.
²³Van Rooyen, C. E., and Morgan, A. D.:Poliomyelitis; Experimental Work in Egypt. Edinburgh M.J. 50: 705-720, December1943.
²⁴Caughey, J. E., and Porteous, W. M.: An Epidemic ofPoliomyelitis Occurring Among Troops in the Middle East. M.J. Australia 1:5-10, 5 Jan. 1946.
²⁵Paul, J. R., Havens, W. P., Jr., andVan Rooyen, C. E.: Poliomyelitis in British and American Troops in the MiddleEast; Isolation of the Virus from Human Faeces. Brit. M.J. 1: 841-843, 24 June 1944.

mer of 1943. Monkeys were obtained locally and from Eritrea,where they had been trapped by members of the Army Veterinary Service, and theisolation of poliomyelitis virus by monkey inoculation with material from anumber of these cases during the summer of 1943 supported the diagnosis.²⁶

In the care of these patients, there is little to record other than the factthat here, as elsewhere in areas remote from the United States, tank respiratorsand other respiratory aids were seldom available. As a result, poliomyelitispatients who developed severe respiratory paralysis promptly died.

From theepidemiological standpoint, it was here in the Middle East that the idea firstemerged that the phenomena which had been observed by Hillman in the Philippinesin 1934 was one which could be repeated in a number of different areas,particularly in cities located in the tropics where sanitation was primitive. Inother words, among the native-born infants and young children in these areas,poliomyelitis was apt to be endemic with an exposure rate so high that theinfection was almost universally acquired by natives in infancy and was almostuniversally unrecognized. Consequently, by the time the native child had reachedthe age of 2 or 3 years, he had had the disease (rarely in either paralytic ornonparalytic form), but commonly in inapparent form and had thus acquired someimmunity. This immunity rate among the adult natives was high as opposed to thevisiting troops from northern Europe, the United States, Canada, Australia, andNew Zealand whose exposure to poliomyelitis at home had not been so heavy duringinfancy. When these troops entered these areas, poliomyelitis came to thesurface, as it were, because of heavy exposure of a moderately susceptiblepopulation coming into an infectious environment. As a result, not only wereappreciable numbers of cases of poliomyelitis acquired by the susceptiblemembers of the "immigrant" troops, but small epidemics in U.S. troopswere precipitated now and again of which notable examples appeared in 1944 and1945 in the Philippines.

It would also appear that the same unsanitary conditions andproximity to native populations, which gave rise to high attack rates ofbacillary dysentery and infectious hepatitis, were also associated with anincreased incidence of poliomyelitis. Thus, poliomyelitis and these otherdiseases did not often occur among the troops in various primitive, tropical orsubtropical, regions where the military installations were "beyond therange and influence of native villages." But where, as became particularlyevident in the Southwest Pacific Area and in the Philippines, U.S. troops movedinto the midst of congested native villages and towns with sanitation of theworst possible order, poliomyelitis appeared in unexpectedly high numbers ofcases, along with the other infections whose etiological agents were known tooccur predominantly in human feces.

²⁶Report, Commission on Neurotropic Virus Diseases,Army Epidemiological Board, to Office of the Surgeon General, U.S. Army, May1944, subject: Report of the Middle East Expedition of the Virus Commission.

In the Philippine Islands, for instance, the story was typical. Prior to theinvasion of the islands in 1944, theattacking force had spent a month on board ships without the appearance of asingle case of poliomyelitis. But shortly after the occupation of Leyte began inOctober 1944, casesappeared, and this was followed by a relatively high incidence of the disease.According to the statistical health report, 39 cases of poliomyelitis occurred,during the months of November and December 1944, in a force which varied from aninitial strength of about 200,000 to a little over 300,000 at the end of theyear. In the next year, there were 245 cases (for all of 1945) in a force with an averagestrength of around 600,000. Sabin states that there is good reason to believethat this does not include all the cases. Studies on the disease here werereported by the virus team of the 19th Medical General Laboratory, Leyte.²⁷It was noted by them that there was no uniform history of the increase of upperrespiratory infections in units involved, but several of the patients had haddiarrhea or dysentery subsequent to arrival on Leyte. Nonparalytic cases werealso recorded; several of them caused considerable difficulty in diagnosis.Coincidentally, no evidence of poliomyelitis appeared among the Filipinos sothat in the Philippine Islands poliomyelitis was considered to be a disease ofwhite people. In retrospect, the observations point to the fact that the localpopulation in Leyte was the hidden reservoir of the virus.

Another outbreak in the Southwest Pacific was investigated at Laoag Army AirBase in 1945 by Lt. Col. Adam J. French, MC.²⁸Twenty-two cases occurred, most of them during the month of May, with at least eight paralyticcases. Here again, it was not an isolated explosive outbreak but rather a groupof cases resulting from what seemed to be continuous exposure to a reservoir ofvirus.

Apart from the incidence of poliomyelitis in various oversea theaters, theincidence of poliomyelitis in troops in the continental United States wasappreciable (chart 2). As a rule, most of the cases were sporadic examples ofthe disease which were not followed by outbreaks in the units in which theyappeared. However, there were several small, sharp, and moderately seriousepidemics in the United States during the period 1941-46. These epidemics have beendiscussed with care by Sabin in another volume in the history of the MedicalDepartment in World War II.²⁹

The first of these was an epidemic in San Antonio, Tex., inDecember 1942.³⁰Although only 3 cases, 1 of them fatal, occurred in soldiers in the vicinity ofFort Sam Houston, San Antonio, there were a number of cases

²⁷Report, 19th Medical Service Detachment (GeneralLaboratory), to Chief Surgeon, Headquarters, U.S. Army Services of Supply, Southwest Pacific Area, 28 Dec. 1944, subject: Poliomyelitis and Other VirusDiseases in the Tacloban-Palo-Dulag area of Leyte.
²⁸Letter, Lt. Col. A. J. French, MC, to Chief Surgeon, U.S. Army Forces, Western Pacific, 25 June 1945, subject: Investigation of Poliomyelitis Outbreak at Laoag Army Air Base.
²⁹See footnote 19, p. 92.
³⁰Paul, J. R.: Preliminary Report on thePoliomyelitis Epidemic in San Antonio, Tex., September-December 1942. [Officialrecord.]

among the families of officers and men stationed in thatarea, 11 of which were admitted to the Brooke General Hospital at Fort SamHouston. This outbreak caused considerable concern locally and served as anillustration of the manner in which poliomyelitis can indirectly become a moraleproblem when it suddenly appears in the families of military personnel living ona large military post in this country.

A second outbreak, which was well described, occurred in a training unitdesignated as the STAR (Specialized Training and Reassignment) unit at PasadenaCollege, Pasadena, Calif. The STAR unit consisted of approximately 800 menamong whom an explosive epidemic occurred in mid-August 1943, just after 310 ofthe men had left for duty at Indiana University, Bloomington, Ind. The firstcase, which ended fatally, occurred on the train, and subsequently, there were16 other cases compatible with the diagnosis of paralytic or nonparalyticpoliomyelitis in the group which went to Indiana. Among the men remaining atPasadena College, there was only one case.

Another epidemic occurred at Fort McClellan, Ala., in the spring of 1945,which was apparently the only example of an outbreak of poliomyelitis in anisolated Army camp in the continental United States. Seventeen cases ofparalytic poliomyelitis occurred within a brief period of 2 months, yielding aparalytic attack rate of approximately 0.57 per 1,000 men. All the cases were insoldiers.

These last two small outbreaks which occurred in Army personnel in the UnitedStates were both explosive localized types, suggesting primary infection from acommon source over a limited period of time.

The incidence of poliomyelitis among American troops in theEuropean theater was of the same order of magnitude as in the United States,except that no outbreaks were recorded.

Diagnosis

During World War II, poliomyelitis proved to be a disease ofsome significance within several theaters. This had been more or lessunsuspected by medical officers, some of whom went to considerable lengths todetermine whether the case of acute paralysis seen in North Africa, forinstance, in 1943, might be due to some cause other than poliovirus. One of thereasons for the difficulties in making the diagnosis seemed to have been that atthat time, in the mid-1940's, the average medical or pediatric textbookdescription of acute poliomyelitis described the picture of the juvenile casecharacterized with initial signs and symptoms of acute fever (often in twobouts), headache, vomiting, and stiff neck. Textbook descriptions of adult caseswere few, and there was little awareness that adult cases could present apicture, quite different from the juvenile case, of insidious onset, often withlittle fever in the first few days and often with severe pain in the back.Consequently, it was with some reluctance that the diag-

nosis of poliomyelitis was made by medical officers in areaswhere poliomyelitis was said to be rare and where there was the possibility ofthe occurrence of one or more unusual diseases of local origin which mightsimulate poliomyelitis. This reluctance to diagnose poliomyelitis, because itwas a disease that was not supposed to occur in certain parts of the world andnot supposed to occur in soldiers, is understandable. By early 1944, cases ofpoliomyelitis in military personnel were becoming more familiar in theMediterranean area, and the diagnostic problems were soon resolved.

Treatment

It would not be profitable to review the various kinds oftreatment which patients with paralytic poliomyelitis received under widelydiffering circumstances in different theaters of war and in different kinds ofhospitals. During and immediately following World War II, current ideas as tothe symptomatic and supportive therapy of poliomyelitis were undergoing certainchanges. The abandonment of the prolonged and rigid splinting of paralyzed limbswas taking place, and the tendency was more in favor of the use of shell caststo protect the weakened or paralyzed limb rather than its fixation. Actually,the degree to which rigid splinting of paralyzed limbs during acute phases ofthe disease was carried out must have differed considerably in different places.Another innovation was just beginning to be used. This was the application ofmoist heat to the limbs and body in the painful stages of myelitis, theso-called Sister Kenny method, which also called for the reeducation of musclesearly in the postfebrile period.

Considerable improvements were to be made in the decadefollowing World War II in the development of various mechanical breathing aidsfor supporting patients whose life was threatened because of respiratory impairment as a result of paralysis to the respiratory muscles. During World War II,however, the main respiratory aid was the tank respirator, known as the Drinkerrespirator. This was a large, heavy piece of apparatus, bulky and difficult totransport. It was not standard equipment of many general hospitals.Nevertheless, a number of these tank respirators were available for hospitals inthe United States, and occasionally, the emergency transportation of a tankrespirator to a distant area was achieved. In retrospect and taking all thingsinto account, it is not believed that loss of life due to the failure ofavailability of respiratory aids was a serious situation.

Oversea patients with residual paralysis were eventually evacuated tohospitals in the Zone of Interior where they could have orthopedic supervisionand undergo a regimen of rehabilitation before discharge from the Army. Thislatter phase represents a different but important chapter in the handling ofthese cases.

In summary, therefore, it can be said that, before the close of World WarII, it had become apparent that, with the exception of northern Europe,

the rates of poliomyelitis for U.S. troops stationed abroadwere higher than in the United States, and in some instances far higher (chart3). In this chart, the rates are indicated at which poliomyelitis appeared inU.S. Army troops, which were low in the United States and the European theater,were higher in the Mediterranean, the Middle East, and China-Burma-Indiatheaters, and higher still in the Philippine Islands.

CHART 3.-Incidenceof poliomyelitis in the U.S. Army, by selected area and year, 1940-48

Unexpectedly, therefore, this military experience has added agood deal of knowledge to the epidemiology of poliomyelitis in general³¹butrelatively little to other aspects of this disease. This was because of thesmall number of cases and the insufficient volume of clinical material.

LYMPHOCYTIC CHORIOMENINGITIS

The story of this disease in World War II has been presented by Rasmussen andSmadel in another volume in the history of the Medical Department in World WarII.³² From their review, it appears that lymphocyticchoriomeningitis, which had been a popular diagnosis during the late 1930's,

³¹(1) Paul, J. R.: Poliomyelitis inJapan. Am. J. Hyg. 45: 206-218, March 1947. (2) Sabin, A. B.: Epidemiology ofPoliomyelitis; Problems at Home and Among Armed Forces Abroad. J.A.M.A. 134:749-756, 28 June 1947.
³²Rasmussen, Aaron F., Jr., and Smadel, Joseph E.: Lymphocytic Choriomeningitis. In Medical Department, United States Army.Preventive Medicine in World War II. Volume V. Communicable Diseases TransmittedThrough Contact or By Unknown Means. Washington: U.S. Government PrintingOffice, 1960, pp. 363-366.

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proved to be a much less common disease among U.S. military personnel thanhad been originally suspected.

Early in the war, this disease, which will be referred to here as LCM, hadbeen considered of sufficient importance to deserve detailed mention in CircularLetters Nos. 107 and 74, 21 October 1941 and 19 March 1943, respectively,pertaining to neurotropic virus diseases; later, these circulars were followedby TB MED 212, 16 January 1946. In all of these summaries, it was pointed outthat exact diagnosis was desirable and that aids to the clinical diagnosis ofLCM were available in the form of complement fixation tests, which couldpreferably be performed for diagnostic purposes on matched samples of sera.

These directives reflect the fact that the clinical diagnosis of LCM wasbeing made all too freely in the early 1940's and that the term had become acatchall to embrace the majority of cases of acute aseptic or lymphocyticmeningitis of undetermined etiology. This explains the report of admission toArmy hospitals of 758 cases of LCM in which the diagnosis was based on clinicalcriteria alone during the period. However, from the laboratory studies, reportedby Rasmussen and Smadel (in which only 31 of 276 suspected cases were proved tobe caused by LCM), it appeared that only 1 in 10 of these 758 cases reported inthe Army were actually caused by the virus of LCM, giving an estimated overallincidence of 76 cases during three of the war years, 1943-45.

The problem of differential diagnosis on clinical grounds in cases of asepticmeningitis was in the early 1940's, and still is, very appreciable, particularlyas the list of diseases which were considered in differentiating LCM from lymphocytic meningitis in military personnel waslong. It included mumps meningoencephalitis, nonparalytic poliomyelitis, centralnervous system syphilis, tuberculous meningitis, acute encephalitis of a varietyof causes, tetanus, brain abscess, rabies, lymphocytic meningitis associatedwith malaria, and infectious mononucleosis. At that time, the syndromeassociated with infections by a number of Coxsackie and Echo viruses was notknown, and it is highly probable that such cases were also included under theterm "acute benign lymphocytic meningitis." Furthermore, the syndromeof acute, benign lymphocytic meningitis encountered in leptospirosis was alsonot appreciated, and it is reasonable to suppose that such cases occurredbecause of their subsequent detection in areas where troops were stationedduring World War II.³³

In brief, then, it appears that although many cases of LCM were diagnosedclinically during the war, actually this disease was uncommon. The introductionof serological methods and the notification of medical officers that suchmethods were available did much to clarify this situation. It is quite clearthat in many theaters of operations it was difficult to have the

³³Professional History ofInternal Medicine in World War II, 1 Jan. 1940 to 1 Oct. 1945, The Panama CanalDept., vol. I, pp. 162-171. [Official record.]

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special type of laboratory determinations performed, such asthe serological diagnostic methods described in Circular Letters Nos. 107 and74, and TB MED 212.

Nevertheless, it was gradually brought home to medical officers, in thiscountry at least, that here was a disease of which, if loosely diagnosed, onecould find many examples, but if rigidly diagnosed, particularly with the use ofthe complement fixation test, 90 percentof the cases could be eliminated. The fact that these tests were more readilyavailable to physicians in the Medical Department of the Army than to manyphysicians in civilian practice indicates that here was a situation with certaineducational potentialities.

In retrospect, therefore, it would seem that LCM did notprove to be a disease of military importance in World War II. The number ofproved cases were few and scattered and, apparently, there was nothing specialor consistent about the circumstances under which they occurred. One noteworthyfeature about LCM during World War II was, however, that through thelaboratories of the Army Medical Department Professional Service Schools, ArmyMedical Center, Washington, D.C., and a few other special laboratories, thisproved to be one of the first of the virus diseases of the central nervoussystem in which an exact etiological diagnosis could be established byserological methods. Others in the group soon followed.

RABIES

Rabies among military personnel during World War II was rare and sporadic. Inthe U.S. Army, 1941-45, sevenrabies deaths were reported on individual medical records, five occurring in theUnited States and one each in Panama and the Philippine Islands. Of the fivepatients who died in the United States, one had contracted the disease in Italybut had not reported for treatment until after returning to the United States.

This author reviewed three case reports of patients who had contracted thedisease in the United States-one at Jefferson Barracks, Mo., in December 1941; one in Washington, D.C., inNovember 1943; andone at Chanute Field, Ill., in January 1944. The first two cases were due todogbites; the third, to the bite of a skunk.

In the three case reports reviewed, there were no specialfeatures with regard to the history, clinical course, and treatment. Theincubation period in two of the patients, one of whom received a full course ofantirabic inoculation, was from 3 to6 months; whereas, in the third patient, who was bitten on the lip and who hadreceived but three injections of vaccine, it was about 5 weeks. Once symptoms started, thecourse was rapidly downhill with death in 3 to 4 days. Initial symptoms includedmalaise, anxiety, and drowsiness. These were soon followed by nausea, pain inthe shoulders, increasing stupor, rapidly developing flaccid paralysis, andpharyngeal and

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laryngeal spasm. Paraldehyde and Avertin (tribromolthanol) were employed assedatives.

Despite the farflung activities of the U.S. Army during the course of thewar, the only areas other than the United States in which the disease wascontracted were, as just mentioned, Panama, the Philippine Islands, and Italy.This is extraordinary from the standpoint of the exposure which might haveexisted in North Africa and in the Middle East generally, but is of course notremarkable for Great Britain and France in the European theater.

Col. John E. Gordon, MC,³⁴ in a report from the European theater,noted that it was a novel sensation in the experience of most Americanphysicians to be able to look with complete equanimity on the occurrence of adogbite. Rabies had been so long absent from Great Britain by reason of thestringent quarantine practiced in that country that no need existed foradministration of antirabic vaccine after bites by dogs or other animals. Thelast rabies in Great Britain occurred at the time of World War I.

The rabies situation in France was almost as favorable, for apparently nodefinite cases of rabies had been detected in animals for some years, and nohuman had died from rabies in France for 16 years.

Rabies was, however, reported in Berlin, Germany, in 1945, and occasionalinfections among animals were recognized in northwestern European countries.Most American medical officers consequently returned to traditional practice inthe management of dogbites sustained in these areas.

Rabies transmitted by bats was a disease known to the Army,but was of no military significance since it did not produce human cases. Thisbat-transmitted disease is the cause of paralysis in livestock, principallycattle. It made its first appearance in Trinidad, in 1925, where, for 11 yearsthereafter, focal outbreaks reoccurred in cattle, with about 1,000 casesoccurring annually. The rigorous control measures which were brought to bear inTrinidad and Venezuela are described by Maj. Richard T. Gilyard, VC.³⁵

³⁴Gordon, John E.: A History of PreventiveMedicine in the European Theater of Operations, U.S. Army, 1941-45, vol. II,pt. III, p. 51. [Official record.]
³⁵Gilyard, R. T.: Bat TransmittedParalytic Rabies. Cornell Vet. 35: 195-209, July 1945.

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